Ramblings of a carnivore

Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle.

2012-01-19T10:50:00.000+01:00

It's not a new study [1] and many know it well, but it's such a simple and in many ways beautiful study, so I thought it an appropriate time for a revisit.

Australian researcher Kerin O'Dea proposed that, "...temporarily reversing the urbanization process in diabetic Aborigines should improve all aspects of their carbohydrate and lipid metabolism that are linked to insulin resistance."

She then asked 10 diabetic Aborigines to live as hunter-gatherers for 7 weeks in their traditional country in north-western Australia. The Aborigines were middle aged overweight when they started. After 7 weeks of traditional lifestyle they were still middle aged, but carried an average of 8 kilos less body weight. Fasting glucose went from diabetic 11,6mM to non-diabetic 6,6mM. Postprandial glucose clearance improved, fasting insulin fell from 23mU/L to 12mU/L and triglycerides went from 4mM to 1,2mM.

An analysis of food intake over 2 of the 7 weeks revealed that 64% of the energy came from animal foods. Energy intake was calculated to be only 1200kcal/day which is not surprising as they obviously obtained a lot of their energy from body fat.

It's as simple as it gets really.

1. O'Dea K: Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes 1984, 33: 596-603.

The carnivore connection hypothesis

2012-01-14T17:45:00.000+01:00

I just came across this article [1] and found that it's really quite interesting. It's about why we are insulin resistant. Even though the term "insulin resistance" is mostly used to describe a pathological condition, all tissues that can respond to insulin are, to some extent, insulin resistant and so we are all displaying various degrees of insulin resistance in various tissues all the time. Insulin resistance is simply when a tissue do not respond to insulin or responds poorly. So when muscles, for example, become insulin resistant, they do not take up as much glucose from the blood despite high blood insulin level. And they will keep burning a larger proportion of fat despite insulin trying to make them burn sugar.

"Certain metabolic adaptations were necessary to accommodate low carbohydrate intake because the brain and reproductive tissues had evolved a specific requirement for glucose as a source of fuel."

"The amount of carbohydrate may have ranged from as little as 10 g up to 125 g a day, much lower than the typical 250 to 400 g per day consumed in modern diets."

Brand-Miller, Griffin and Colagiuri looks at insulin resistance from an evolutionary perspective. The basis for the article is that the last 2 million years of human evolution was dominated by a low carbohydrate intake. This may have caused a selective pressure for insulin resistance. In addition, environmental pressures such as geographic isolation and/or starvation may have further increased the prevalence of insulin resistance genes in certain populations. The reason is that when carbohydrate intake is low it is important that the tissues that do not need to burn glucose and can burn fat become insulin resistant, thus freeing glucose for the tissues that need glucose and cannot burn fat.

"With the first severe Ice Age, global temperatures fell dramatically and resulted in moist African forest becoming dry, open woodland and savannah. Hominids that were unable to utilize grasslands became increasingly carnivorous."

"In Africa and Eurasia, hunted animals displaced gathered plant foods as the principal source of food, leading to a diet low in carbohydrate and high in protein for most of the year. Increased meat intake from wild terrestrial and marine animals would have also provided greater amounts of omega-3 fatty acids such as docosahexaenoic acid essential for brain development, facilitating the larger brain size of H. sapien."

The authors further hypothesize that the selective pressure for insulin resistance was relaxed with the advent of agriculture and the increasing amounts of carbohydrate in the human diet. Domestication of cereal grains first began in the Middle east, some 12 000 years ago, and spread across to Europe and East Asia. The logic thus goes that populations that only recently have adopted agriculture are more likely to become insulin resistant, overweight and at ill health than those populations longer exposed.

As examples of such cultures the authors mention the Pima Indians, Nauruans, and Australian Aboriginals. The Pima only adopted agriculture some 5000 years ago, about the same time as us Norwegians.

According to the authors the carnivore connection hypothesis hinges on five lines of evidence:

(1) During the last two million years of evolution, humans were increasingly carnivorous, that is, consumed a low-carbohydrate, high-protein diet.

(2) A low-carbohydrate, high-protein diet requires profound insulin resistance to maintain glucose homeostasis, particularly during reproduction.

(3) Genetic differences in insulin resistance and predisposition to type 2 diabetes can be explained by differences in exposure to carbohydrate during the past 12,000 years.

(4) Changes in the quality of carbohydrate can explain the higher prevalence of type 2 diabetes in susceptible populations.

(5) Habitual consumption of a high-glycemic-load diet worsens insulin resistance and contributes to the obesity and type 2 diabetes in all populations.

Food

As there are some tissues that are in great need of glucose, mostly those with few or no mitochondria, insulin resistance is a key mechanism by which these tissues are properly fed. But now a days insulin resistance occurs in combination with a high carbohydrate diet and is a sign of something being very wrong - the reason being that when carbohydrate intake is high, insulin sensitivity needs to be high in order to keep us from being sugar poisoned. Usually when we talk of insulin resistance we are referring to liver insulin resistance. Glucose is an important fuel for fetal growth and insulin resistance thus ensures enough glucose is directed at this process. Pregnant women naturally become more insulin resistant, but if you are already insulin resistant this may develop into gestational diabetes, a form of diabetes that normally improves after pregnancy. Women with polycystic ovarian syndrome are insulin resistant and PCOS can be seen as just another manifestation of the metabolic syndrome in women. Brand-Miller and coworkers believe that these women may represent a group that was highly fertile in a low carbohydrate environment. There is much indicating that insulin resistant mothers have insulin resistant babies and that each new generation is more metabolically challenged that the former. So in individuals well adapted to low carbohydrate living, increasing insulin resistance is caused by continuous high carbohydrate dieting.

"We propose that the selection pressure for insulin resistance was relaxed first in Europeans when dietary carbohydrate increased 12,000 years ago with the advent of agriculture. In accordance with this long-term exposure, Europeans have experienced a lower prevalence of diabetes, even when overweight and obese (see Section 6), compared to other population groups."

One aspect of this article I particularly liked, was that they did not adhere to a common misconception of food availability. They mention Neel’s thrifty gene hypothesis which suggests that cycles of "feast and famine selected for a quick insulin trigger." They also mention Gerald Raven's similar hypothesis that suggests that "muscle insulin resistance was the key to survival during food scarcity because it conserved glucose by minimizing gluconeogenesis and preserving lean body mass." Both of these hypotheses are based on an assumption that food must have been hard to come by during our recent evolution. To me this is a serious underestimation of humans and suggests that those doing the hypothesizing have themselves not spent much time outdoors. Luckily, Brand- Miller and coworkers are aware of the shortcomings of these hypotheses and write: "However, this is not supported by the scientific literature. While hunter gatherers would have been exposed to seasonal and geographical changes in food supply, severe food shortages or starvation were rare and more likely to occur after the transition to agriculture (preindustrialization)."

The authors also spend some time discussing types of carbohydrate and the transition from complex unrefined to refined easily digestible and the concomitant change in glycemic index. This might have further enhanced the insulin resistance promoting effects of our high carbohydrate diet.

Humans are well adapted low carbohydrate intakes, but it seems this ability might have come at a cost. Anyway, it seems many of us are fighting our genetic disposition by stuffing ourselves with carbohydrates. All in all a really interesting article and well worth a read.

1. Brand-Miller JC, Griffin HJ, Colagiuri S: The carnivore connection hypothesis: revisited. J Obes 2012, 2012: 258624.

A little something to learn from McArdle's disease

2011-12-03T10:28:00.001+01:00

“Muscle glycogen phosphorylase deficiency (glycogenosis type V or McArdle’s disease) is a disorder characterized by marked exercise intolerance—that is, premature fatigue and cramps during exertion, with frequent episodes of rhabdomyolysis.”

“Unfortunately, sedentary behavior may worsen exercise intolerance by further reducing the limited oxidative capacity caused by blocked glycogenolysis.” [7]

Glycogen matters. Having chronic full glycogen stores, while continuing to consume ample amounts of carbohydrates, is a bad idea, especially if your fat tissue does not easily expand.

Glycogen is a treat the body gives us when we need extra and fast energy. Even on a low carb diet we never fully deplete our glycogen stores (skeletal muscle and liver) and high intensity exercise on a low carb diet still makes you dig into your glycogen stores. But what if you were all out of glycogen and tried to exercise? There are in fact people who are unable to use glycogen during exercise. Some of these people lack myophosphorylase, an enzyme that breaks glycogen down to glucose-1-phosphate. These people have what is known as glycogen storage disease type V, commonly called McArdle’s disease. The disease was recognized by Dr. Brian McArdle who first noticed it when he came across a patient who experienced pain and weakness after exercise. McArdle did an exercise test on the patient and noticed that he failed to increase lactate levels. This prompted him to believe that the patient had a glycogen breakdown problem.

If you are one of the 1:100 000 who has McArdle’s, proper warm up is very important. Gradual warm up causes a gradual increase in fat metabolism which reduces the need for glycogen. This is also a tip to everyone on ketogenic diets who like to engage in vigorous exercise. Proper and gradually increasing warm up exercises makes sure as much fat as possible is ready for use. Patients with McArdle’s are known to experience a “second wind” which happens when alternative sources of energy are increasing in availability.

Keeping muscle glycogen stores from being full is perhaps one of the most important strategies when it comes to treating insulin resistance. Once glycogen stores are full, the muscles become insulin resistant, to keep from getting “sugar poisoned.” When glycogen stores are low, muscles increase the uptake of glucose from the blood by increasing the glucose transporter GLUT4 in the cellular membrane. This protects us from high blood sugar. In patients with McArdle’s, due to their inability to convert glycogen to glucose-1-phosphate, the muscles increase GLUT4 in order to get enough fuel [1]. But in McArdle's the glycogen stores are full, and so they have impaired glucose tolerance and are in fact insulin resistant, despite increased GLUT4[2] .

One of the problems with not being able to break down glycogen is that the body must burn alternative fuels. These fuels are proteins or fats. For those of you reasonably versed in physiology you probably see how this can be problematic. On a high carbohydrate diet and little or no ability to break down glycogen, protein breakdown will be high. As the body breaks down proteins to glucose, the McArdle’s patients experience muscle wasting and renal failure due to myoglobinuria (muscle form of hemoglobin in the urine).

There is more to learn from these strange myopathies. For one, it is postulated that the exercise induced growth hormone (GH) response is stimulated by lactate. Lactate is produced when the muscles break down glycogen. Thus, exercising patients with McArdle’s disease should provide a clue. This was the reasoning of a research group from the UK [3]. They exercised 11 patients with McArdle’s and found that lactate remained at a resting level throughout the exercise and 9 of the 11 patients failed to show a significant exercise induced increase in growth hormone. Thus, it seems likely that lactate really is an important growth hormone stimulus.

If you are interested in a large GH response, high intensity does it. Although circulating levels of GH rise in response to low intensity exercise, a sevenfold and sustained rise (60–90 min post-exercise) in GH is observed with exercise above the lactate threshold.

You would think that if you can’t rely on glycogen for fuel, it would be wise to optimize fat burning, for example going on a ketogenic diet. And a few observations suggest that you would think right. A ketogenic diet seems to help [4,5], as does a high fat diet [6]. Also, if you have trouble using glycogen, insulin should be reduced to a minimum, as insulin inhibits glycogen breakdown. German researchers report of a

“...55 year-old man with McArdle disease. By increasing the fat content of his diet to 80% with 14% protein (1 g/kg/d) to totally 1.760 kcal, ketosis of 2-6 mmol/l 3-OH-butyrate was established. The principal effects comprise absence of carbohydrate-based stimulation of insulin secretion leading to activation of glycogen synthesis, and repletion of the tricarboxylic cycle with acetyl-CoA from ketone bodies. With a continuous one-year diet his exercise tolerance was 3- to 10-fold increased dependent of the endurance level.”[4]

McArdle’s patients easily become sedentary. This just serves to exacerbate muscle breakdown and worsen muscular quality. But you don’t need glycogen to exercise or build muscles. Simple running has proven very effective in one case report [7]. Running also involves eccentric exercise which has a low energy cost for a given level of muscle force.

From Perez et al 2007

Although a ketogenic diet seems the natural choice for patients with McArdle’s, there are no real good studies of the strategy. A few small studies have examined high protein feeding with some very modest results [8], but high protein seems a bit of, as fat and ketones can replace glycogen more easily than proteins. Other strategies such as supplementing with creatine or vitamin B6 or ingesting glucose prior to exercise has been tested, but with varying results.

References

1. Robertshaw HA, Raha S, Kaczor JJ, Tarnopolsky MA: Increased PFK activity and GLUT4 protein content in McArdle's disease. Muscle Nerve 2008, 37: 431-437.

2. Nielsen JN, Vissing J, Wojtaszewski JF, Haller RG, Begum N, Richter EA: Decreased insulin action in skeletal muscle from patients with McArdle's disease. Am J Physiol Endocrinol Metab 2002, 282: E1267-E1275.

3. Godfrey RJ, Whyte GP, Buckley J, Quinlivan R: The role of lactate in the exercise-induced human growth hormone response: evidence from McArdle disease. Br J Sports Med 2009, 43: 521-525.

4. Vorgerd M, Zange J: Treatment of glycogenosys type V (McArdle disease) with creatine and ketogenic diet with clinical scores and with 31P-MRS on working leg muscle. Acta Myol 2007, 26: 61-63.

5. Busch V, Gempel K, Hack A, Muller K, Vorgerd M, Lochmuller H, Baumeister FA: Treatment of glycogenosis type V with ketogenic diet. Ann Neurol 2005, 58: 341.

6. Viskoper RJ, Wolf E, Chaco J, Katz R, Chowers I: McArdle's syndrome: the reaction to a fat-rich diet. Am J Med Sci 1975, 269: 217-221.

7. Perez M, Moran M, Cardona C, Mate-Munoz JL, Rubio JC, Andreu AL, Martin MA, Arenas J, Lucia A: Can patients with McArdle's disease run? Br J Sports Med 2007, 41: 53-54.

8. Quinlivan R, Beynon RJ: Pharmacological and nutritional treatment for McArdle's disease (Glycogen Storage Disease type V). Cochrane Database Syst Rev 2004, CD003458.

Low fat – we're gonna need more nails

2011-11-19T17:17:00.001+01:00

Low fat dieting for weight loss doesn’t work. That is, it works, just very very poorly. In fact it works just enough for confused obesity researchers to call the weight loss significant. Somewhere along the way, it was decided that a 5% loss of initial body weight is to be considered clinically significant [1]. So if you weigh 100kg and work your butt of (which is what you are not really doing) to get rid of 5kg, scientifically speaking that's a success. When Bray, Bouchard and James wrote the Handbook of Obesity [2] they presented pretty compelling evidence that traditional weight loss does not work. They still continued recommending low fat for weight loss. The 2002 Cochrane meta-analysis titled “Advice on low-fat diets for obesity” by Pirozzo and coworkers [3] was recently withdrawn. The Cochrane organization claims the conclusions are out of date. What the metaanalysis showd was that

“...fat-restricted diets are no better than calorie restricted diets in achieving long term weight loss in overweight or obese people.“

And the authors concluded that both strategies produced a weight loss that was

“...so small as to be clinically insignificant.”

This conclusion was reached by looking at the best studies available up till 2002. No new studies have provided evidence the conclusion of the meta-analysis was wrong, but it seems the Cochrane Collaboration could not live with such a politically incorrect conclusion.

In a new study, and a pretty damn large one at that, the researchers went out of their way to resurrect the dead, but sadly not buried lowfatforweightlossworksgoddamnit-hypothesis.

Enter the Look AHEAD Study. The study was a “…multicenter randomized clinical trial to examine the effects of a lifestyle intervention designed to achieve and maintain weight loss over the long term through decreased caloric intake and exercise.”

Here’s how the authors view the study:

“As perhaps the most extensive test of long-term multidisciplinary lifestyle intervention to date, the Look AHEAD (Action for Health in Diabetes) trial presents a unique opportunity to examine the long term viability of lifestyle intervention as a clinical and public health strategy for obesity and type 2 DM.”

A total of 5,145 overweight/obese men and women with type 2 diabetes were randomly assigned to an intensive lifestyle intervention (ILI) or a usual care group, referred to as Diabetes Support and Education (DSE).

“The ILI included diet modification and physical activity and was designed to induce at least a 7% weight loss at year 1 and to maintain this weight loss in subsequent years. The ILI participants were assigned a calorie goal (1200- 1800 kcal/d based on initial weight), with less than 30% of total calories from fat (<10% from saturated fat) and a minimum of 15% of total calories from protein.”

“The exercise goal was at least 175 minutes of physical activity per week, using activities similar in intensity to brisk walking. Behavioral strategies, including self monitoring, goal setting, and problem solving, were stressed. The ILI participants were seen weekly for the first 6 months and 3 times per month for the next 6 months, with a combination of group and individual contacts. During years 2 through 4, participants were seen individually at least once a month, contacted another time each month by telephone or e-mail, and offered a variety of ancillary group classes. At each session, participants were weighed, self-monitoring records were reviewed, and a new lesson was presented, following a standardized treatment protocol.”

Bet you wonder what kind of marvelous results you can get from this intensive intervention. Bet you think all the participants in the ILI group came out of the study looking like Greek gods. I mean, 4 years of exercise, diet and pampering…

At the end of the 4 year period the participants in the ILI group, whose average baseline weight was 95kg in women and 109kg in men, reduced their weight by 4.7%. Actual weight loss was 4,9kg.

Here’s nice graph from the study

This figure shows how 74% of the participants in the ILI group lost weight while 26% gained weight. Only 46% of the group lost more than 5% body weight:

So there you have it. These are the grand effects of 4 years of intensive lifestyle changes. I'm not impressed.

PS.

Funny thing. If you read the abstracts, the article in which the main results were published [4] states that the average weight loss was 6,15%, yet in a more recent article addressing what factors correlated with long term success, the number is 4,7% [5]. It turns out that the number 6,15% is an average of the weight lost at 1, 2, 3 and 4 years which is not a very nice way to present data. I would say it’s a pretty poor way to present data. You have to read the entire article to find that “…the ILI group maintained a mean weight loss of 4.7% at year 4.”

Literature

1. J. Stevens et al., "The Definition of Weight Maintenance," Int J.Obes.(Lond) 30, no. 3 (2006): 391-399.

2. George A. Bray, Claude Bouchard, and W. P. T. James, Handbook of obesity, ed. George A. Bray, Claude Bouchard, and W. P. T. James. (New York: M. Dekker, 1997), xii, 1012.

3. S. Pirozzo et al., "Advice on Low-Fat Diets for Obesity," Cochrane.Database.Syst.Rev., no. 2 (2002): CD003640.

4. R. R. Wing, "Long-Term Effects of a Lifestyle Intervention on Weight and Cardiovascular Risk Factors in Individuals With Type 2 Diabetes Mellitus: Four-Year Results of the Look AHEAD Trial," Arch.Intern.Med. 170, no. 17 (2010): 1566-1575.

5. T. A. Wadden et al., "Four-Year Weight Losses in the Look AHEAD Study: Factors Associated With Long-Term Success," Obesity.(Silver.Spring) 19, no. 10 (2011): 1987-1998.

Low fat - another nail in the coffin

2011-11-15T17:07:00.001+01:00

So here’s an interesting study: "Effects of a lifestyle intervention in metabolically benign and malign obesity."

From the intro:

“In the last few years it has been shown that metabolically healthy obese (MHO) individuals comprise roughly 30% of obese people and 10% of the adult general population [1– 5]. In addition to having insulin sensitivity that is similar to non-obese individuals, MHO individuals have lower liver fat content and lower intima media thickness (IMT) of the common carotid artery than obese insulin-resistant (OIR) individuals [6].”

A group of German researchers put 262 non-diabetic people on a 9 month lifestyle intervention. The intervention was of the traditional (insane) type:

“Counselling was aimed to reduce body weight by ≥5%, to reduce the intake of energy from fat to <30% and particularly the intake of saturated fat to ≤10% of energy consumed and to increase the intake of fibre to at least 15 g/4,184 kJ (1,000 kcal). Individuals were asked to perform at least 3 h of moderate sports per week. All participants completed a standardised self-administered and validated questionnaire to measure physical activity and a habitual physical activity score was calculated.”

262 participants entered the study. Of these, 43 were normal weight and 116 were overweight. The remaining 106 were obese.

The point of the study was to see how this lifestyle intervention affected people with different insulin sensitivity (IS). The obese individuals were (BMI≥30.0 kg/m2) were grouped, based on their IS and IS was estimated from an oral glucose tolerance test (OGTT). Those with the best insulin sensitivity were labeled metabolically healthy obese (MHO, n=26) while those with poor IS were labeled obese insulin-resistant (n=77, OIR).

More from the intro:

“Data about the effects of lifestyle modifications specifically in MHO and OIR populations are sparse: two small studies implemented energy-restriction diets for 12 weeks and 6 months in women [8, 9], and one a 6 month exercise intervention programme, also in women[10]. All three studies showed an improvement in cardiovascular risk profile in OIR, but not in MHO, women, despite similar weight loss [8–10].”

So apparently traditional dieting does not do much for 70% the obese people. Anyway, weight loss was unimpressive as always with these strategies. The obese insulin resistant lost 3,3kg and the obese metabolically healthy lost a whopping 2,4kg of the average starting weight of 100kg. Remember this is 9 months of dieting. The difference between groups was not significant and the total body fat loss in the MHO didn’t even reach statistical significance.

However, fasting glucose (5.42 - 5.26 vs 5.07 - 5.17) and insulin (91.43 - 77.10 vs 38.33-39.70) both decreased more in the insulin resistant obese (there was a non-significant increase in both in MHO). This is perhaps not surprising as they had a much higher baseline level in both factors. Insulin sensitivity (OGTT) improved in the OIR group, but decreased (non-significant) in the MHO. Homeostatic model assessment (HOMA) also showed a decrese (2.98- 2.44) in the OIR group and an increase in the MHO group (1.16-1.23). Liver fat was high in the OIR and also decreased a bit in this group.

None of the cholesterol markers were interesting, but the authors noted that:

“Unexpectedly, there was a small reduction in HDL-cholesterol levels in both groups. However, this was statistically not significant, indicating that these changes are not clinically relevant.”

The end results show that despite a small weight loss, traditional calorie reduction can improve several markers of insulin resistance, but only if you are very resistant. And even though insulin sensitivity improved in the OIR group, their end level was still only 9,3 wheras the baseline level in the MHO group was 17,5.

The study illustrates that traditional lifestyle treatment only works (marginally) if your metabolism is really messed up. If not, there is little to gain from this strategy, and the study indicates that it might even make things worse. Though unfortunately not the final one, this is another nail in the coffin for traditional lifestyle treatment and a good reminder that overweight and obese people are a pretty heterogenic group that may respond quite differently to similar treatments. So don’t mess around with this nonsense. Go paleo instead.

The authors weren't that impressed with the results either, writing:

"For MHO individuals, the option of a lifestyle intervention seems to be less effective if the target is to improve insulin sensitivity, although it may positively affect non-metabolic causes of morbidity and mortality in obesity, such as cancer and traumatic incidences. For OIR people, a lifestyle intervention clearly has positive effects. However, their insulin sensitivity remains very low even after the intervention compared with the MHO group, which indicates putative inadequate protection from type 2 diabetes and cardiovascular disease."

And their solution to the problem? Drugs:

“Thus, an early pharmacological treatment of obese insulin-resistant people, additional to the lifestyle intervention, may be considered as an appropriate therapeutic approach. “

Do you exercise like a predator or prey?

2011-11-08T15:47:00.000+01:00

I have little time for writing these days. I mostly hover quietly in the background of the blogosphere and the twittering realm, plotting for the lifestyle revolution to come.

But a thought hit me in the shower one day.

Exercise is stress. It is a voluntarily induced stressing of our physiology which triggers certain responses. It is usually the response were after, though the exercise in itself can be very rewarding. What we want is for our body to grow stronger and fitter, which it does in response to exercise. It is the rest following exercise that makes us stronger, not the exercise in itself. That is all well and good, but I’ve been wondering how much our mental state while exercising affects the exercise and thus the response. I have often said that if exercise is nothing but a stressful element in your life, something you dread and that gives you no pleasure at all, then don’t exercise. Life's too short and mental stress is so harmful I am unsure if there’s a point in exercising if you hate it.

This got me thinking of people I know who do not exercise, but still lead relatively active lives. These are people who walk and half run through the day, rarely having time even to eat sitting down. Although they are fairly non sedentary and probably have an energy expenditure easily exceeding that of many healthy hunter gatherers, they are not very fit. Then I realized that much of the “exercise” they do, happens while being in a state of mental stress – hastening from meeting to meeting or from any other A to B. Some of these people almost never have time to walk calmly, do some thinking or enjoy the scenery. In these peoples’ lives there is also a relationship between the intensity of an activity and the amount of mental stress – the highest intensities are reached when things are crazy stressful.

These people remind me of prey animals. This form of physical activity is like that of a nervous prey animal running for its life several times a day. And this is why I am wondering if there is anything to gain, even in pure physiological factors. Does exercise while being stressed negate the normal positive effects of exercise?

Although I don’t know the answer to the above question, the way I would like people to exercise is like a predator. Do some workouts on an empty stomach like you would if you needed to hunt for food. Exercise with high intensities and reward yourself with a big slice of meat and total relaxation after. And don’t exercise like this every day. Like a predator we may move around a lot when we don’t hunt, but we don’t hunt every day.

Exercise...

...eat...

...then rest.

The fittest person in the morgue

2011-10-07T11:50:00.000+02:00

I have to admit that the title is stolen from an article by Mary Sheppard. The article is about the strange phenomenon of athletes keeling over and dying during strenuous exercise. The irony is that a marathoner will probably be the most worn out specimen at the morgue despite having a high VO2max before death.

The Hormesis

“If we accept the validity of the general concept of physiological hormesis as being the phenomenon of achieving health beneficial effects by exposure to mild stress, then hormesis is being applied already and successfully to humans. The evidence for this is the well-demonstrated health benefits of regular and moderate exercise.”[1]

Running is good for us. It has to be, we've been told so for years and years. There’s just no doubt about it. There usually isn’t much need for running in a modern society, except for perhaps trying to catch a bus or escaping the occasional bully or mugger. But despite the lack of need to run, many of us still prefer to run, and some run a lot. We even learn to enjoy the burning lungs, the taste of blood and a heart rate that would otherwise have us seriously worried. We are mimicking the thrill of the hunt. Humans are truly made to run. But, contrary to our hunting forefathers there is no reward following the hunt. No big mammoth to cut up and bring home. No great mammal that feeds your family for a week and that makes running unnecessary until the meat is gone.

Modern humans do things differently. Instead of following the natural evolutionary approach and wait with exerting ourselves until more food is needed, we run again the very next day, and the day after that, and the day after that. The total amount of physical activity is staggering. There is nothing natural about it. Recreational joggers and marathon runners burn through an extreme amount of energy, usually supported by a high carbohydrate diet. Many also claim they do it for their health. But is it really that healthy?

Exercise is the perfect example of the principle of hormesis. The term is usually used to describe favorable effects of small amounts of something that is unfavorable in larger amounts, like a toxin or a stressor. Exercise is a stressor. If you want to test it, you can start exercising and don’t stop. You will get weaker and weaker until you fall and your body will be in a far worse shape than when you started. Exercise is really and truly bad for us, but only acutely and only if we forget to rest after.

“…the occurrence of SCD [Sudden Cardiac Death] associated to training and competitions for athletes is increased by 2.8 times compared to the average relative risk of non-competitive practitioners, hence giving rise to the following question: Does sports activity causes sudden death in young people?”[2]

It is important to remember that it is the physiological response to exercise, the repairing of damaged tissues, and increasing of tolerability that causes exercise to make us stronger. It is the rest, the restitution that increases our potential, our endurance and our strength. Exercise makes us weak, rest makes us stronger.

Energy and glucose restriction has been shown to increase the lifespan of several species. It also increases formation of reactive oxygen species (ROS) in the mitochondria. The organism however, seem to adapt and acquire an increased resistance to oxidative stress. Antioxidants, which decrease ROS levels, limit the life extending effects of glucose restriction and exercise [3]. It has also been suggested that high antioxidant intakes lessens the adaptive response to exercise. But not all data show this [4].

The bottom line is that if you want exercise to be healthy, you better learn to rest.

The Metabolism
Everybody is free to do what they want and to exercise as they please. But the marathon runner lies, consciously or not, if he says he runs for his physical health. Although top athletes are marvelous examples of how far we can push the boundaries of the human body, they are not in it for the health. Injuries, wear and tear, infections and long term side effects are all part of the deal. This deal also needs to be remembered by recreational runners.

If you run for hours a day, you do it for the joy of exercising. You do it for the brake it gives you from the everyday hassle. You do it for shear competitiveness. But you do not do it for your physical health. That is bollocks.

From a metabolic standpoint is makes little sense to participate in long duration exercise of an intensity that is way over in the carbohydrate burning zone. Our carbohydrate fuel stores are quickly depleted. From en evolutionary standpoint these stores are there for short and intense bouts of exercise. As a hunter or gatherer we would spend most of our time in a fat burning low intensity zone and only occasionally do shorter high intensity work. Imagine foraging or tracking prey or working around the camp – all low intensity physical activities. Or you can watch Robb Wolf and his “caveman” friends hunting big game with atlatls. There is little sprinting involved.

Many runners (or other endurance athletes) however, spend much of their time in a carbohydrate burning zone. I was taught in school that intensities around the anaerobic threshold, where much of the energy (ATP) is produced outside of the mitochondria, are ideal for improving endurance performance. But the long time spent exercising at these intensities, may cause serious problems.

One obvious aspect is that the high intensity exercise many do requires them to stuff themselves with carbohydrates. Stuffing yourself with carbs is probably more of a problem if you don’t exercise much, but it might still be problematic. High carbohydrate for an endurance performer is usually synonymous with high sugar high starch which will in itself have a negative impact on the body. What’s worse is that high starch usually means high grain low fat. The stage is set for gut problems, infections, allergies and asthmas, muscle cramping and soreness, slow wound healing and general poor health. Remember, the apparent absence of disease does not equal good health. Poor diet might be the reason why the 50 year old marathon runner often does not look anything like a healthy human specimen.

The Body
But there are other problems, directly related to the exercising itself. One obvious aspect is the amount of wear and tear. The higher intensity exercise you perform the longer restitution needed to fully repair the body. Injuries and frailty is part of the deal. Endurance athletes are more osteoporotic than the rest of us [5-8].

Too little rest and too much exercise results in increased cortisol and other stress parameters. Marathon running is a huge stress to the body. One group of researchers from Canada used data from magnetic resonance imaging (MRI) to find out how marathon running affects the heart over time. Headed by Dr. Eric Larose, the group found that the magnitude of abnormal heart segments was more widespread and significant in a group of less fit runners. Runners with lower VO2max showed more signs of heart injury than more fit runners.

Wu et al [9] found that a 24hour ultra marathon damaged about every part of the body measured, including the liver and gallbladder. They also found that HDL decreased, LDL increased, red and white blood cell count decreased as well as testosterone. Their conclusion: “Ultra-marathon running is associated with a wide range of significant changes in hematological parameters, several of which are injury related.”

Lippi et al noticed that enzyme biomarkers indicating liver damage are increased after a half marathon run to such a degree that there is no point testing for liver damage close to a race [10].

Skenderi et al [11] examined thirty-nine runners competing in the Spartathlon race (a 246km continuous race from Athens to Sparta) who managed to complete the race within a 36h time limit. They found that “Muscle and liver damage indicators were elevated at the highest level ever reported as a result of prolonged exercise…”

There is more data showing muscle damage from this kind of exercising. Warhol et al [12] found that the muscles of veteran runners had intercellular collagen deposition suggesting repeated injury. Tissue from non runner controls did not show this.

“Since oxidative modifications of DNA can lead to mutations and exceptionally high volumes of exercise are also associated with a substantial oxidative stress, concerns have arisen about the health effects of competing in endurance and ultraendurance exercise events, particularly when participants are not optimally trained.”[13]

As if damaging your muscles and organs weren’t enough, both ultra endurance exercise and half marathon results in DNA damage [13,14]. There is however need for follow up studies of DNA damage and instability. So far the effects are only proven acutely. Rae et al fount that telomere length in the vastus lateralis muscle in experienced endurance runners was inversely related to years spent running and hours spent training [15]. Shortening of telomere length is a sure sign of aging. Collins et al [16] found that Athletes with exercise-associated fatigue (fatigued athlete myopathic syndrome) had significantly shorter telomere length in their vastus lateralis compared to matched controls. Results from Ludlow et al suggest that hormesis is in fact a factor and that when it comes to telomere length moderate physical activity is better than both low and high levels [17].

As heart-healthy as running is supposed to be the heart is still one of the body parts placed under the most pressure and cardiac damage is easily measured [18,19]. I was taught in school that endurance exercise increases left ventricular volume and thus produces a greater cardiac output. Strength exercise on the other hand was supposed to increase heart wall thickness because of the high blood pressure, and thus increase the risk of cardiac arrhythmias. I think this is what is called the “Morganroth hypothesis.” Trouble is that much data refute the hypothesis. The most recent comes from Australia, showing increased left ventricular wall thickness after endurance exercise, but not after strength exercise.

Cardiac troponin (part of contraction process in skeletal and cardiac muscle) increases greatly after a half marathon in young runners, and “…reach levels typically diagnostic for acute myocardial infarction…”[20]. The level is higher in less trained athletes [21]. Whether cardiac injury markers are indicative of real damage is uncertain. Jassal et al puts it this way “Elevations of cardiac injury markers in non-elite athletes are extremely common following the completion of endurance events and correlate with the increased endurance time. Whether the increase in the levels of these enzymes represents true myocardial injury or a result of the release of cTnT from the myocytes requires further investigation.”[21].

“The clinical significance of chronic exposure to endurance exercise is unknown. The development of myocardial fibrosis has been suggested as a long-term outcome to chronic exposure to repetitive bouts of endurance exercise and has been linked to an exercise-induced inflammatory process observed in an animal model. This hypothesis is supported by a limited number of studies reporting postmortem studies in athletes and an increased prevalence of complex arrhythmia in veteran athletes.”[22]

There are other parts of the cardiovascular system negatively affected by extreme exercise. A 96 fold increased serum level of calprotectin after both half and full marathon is indicative of damage to the vascular endothelium and microthrombi [23].

Marathon running has also been shown to induce kidney damage/renal abnormalities [24], and especially if you get dehydrated.

It has been suggested that marathon running also induce brain damage, as measured by increase levels of S100beta, a common marker of brain damage. A study from 2004 however, indicates that the increased S100beta levels come from extracranial sources [25]. But it’s still tissue damage. By the way, S100beta is also a marker of cancer.

The Conclusion
Exercise breaks us down. Rest is what makes us stronger. There is little indication that marathon running is worth participating in for health reasons. Running is in itself fine, but too much and too high intensity combined with an unnatural diet makes it very unhealthy. If I was to give an advice based on the best of my knowledge for optimal health I would recommend short high intensity exercise such as interval or strength training. Do this 2-4 times a week and keep any other exercise you partake in in a fat burning, moderate intensity zone. This is also an exercise advice that can be easily coupled with low carbohydrate dieting.

References

1. Rattan SI, Demirovic D: Hormesis can and does work in humans. Dose Response 2009, 8: 58-63.

2. Ferreira M, Santos-Silva PR, de Abreu LC, Valenti VE, Crispim V, Imaizumi C, Filho CF, Murad N, Meneghini A, Riera AR, de Carvalho TD, Vanderlei LC, Valenti EE, Cisternas JR, Moura Filho OF, Ferreira C: Sudden cardiac death athletes: a systematic review. Sports Med Arthrosc Rehabil Ther Technol 2010, 2: 19.

3. Ristow M, Zarse K: How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis). Exp Gerontol 2010, 45: 410-418.

4. Higashida K, Kim SH, Higuchi M, Holloszy JO, Han DH: Normal Adaptations to Exercise Despite Protection Against Oxidative Stress. Am J Physiol Endocrinol Metab 2011.

5. Campion F, Nevill AM, Karlsson MK, Lounana J, Shabani M, Fardellone P, Medelli J: Bone status in professional cyclists. Int J Sports Med 2010, 31: 511-515.

6. Smathers AM, Bemben MG, Bemben DA: Bone density comparisons in male competitive road cyclists and untrained controls. Med Sci Sports Exerc 2009, 41: 290-296.

7. Burrows M, Nevill AM, Bird S, Simpson D: Physiological factors associated with low bone mineral density in female endurance runners. Br J Sports Med 2003, 37: 67-71.

8. Schmitt H, Friebe C, Schneider S, Sabo D: Bone mineral density and degenerative changes of the lumbar spine in former elite athletes. Int J Sports Med 2005, 26: 457-463.

9. Wu HJ, Chen KT, Shee BW, Chang HC, Huang YJ, Yang RS: Effects of 24 h ultra-marathon on biochemical and hematological parameters. World J Gastroenterol 2004, 10: 2711-2714.

10. Lippi G, Schena F, Montagnana M, Salvagno GL, Banfi G, Guidi GC: Significant variation of traditional markers of liver injury after a half-marathon run. Eur J Intern Med 2011, 22: e36-e38.

11. Skenderi KP, Kavouras SA, Anastasiou CA, Yiannakouris N, Matalas AL: Exertional Rhabdomyolysis during a 246-km continuous running race. Med Sci Sports Exerc 2006, 38: 1054-1057.

12. Warhol MJ, Siegel AJ, Evans WJ, Silverman LM: Skeletal muscle injury and repair in marathon runners after competition. Am J Pathol 1985, 118: 331-339.

13. Wagner KH, Reichhold S, Neubauer O: Impact of endurance and ultraendurance exercise on DNA damage. Ann N Y Acad Sci 2011, 1229: 115-123.

14. Niess AM, Baumann M, Roecker K, Horstmann T, Mayer F, Dickhuth HH: Effects of intensive endurance exercise on DNA damage in leucocytes. J Sports Med Phys Fitness 1998, 38: 111-115.

15. Rae DE, Vignaud A, Butler-Browne GS, Thornell LE, Sinclair-Smith C, Derman EW, Lambert MI, Collins M: Skeletal muscle telomere length in healthy, experienced, endurance runners. Eur J Appl Physiol 2010, 109: 323-330.

16. Collins M, Renault V, Grobler LA, St Clair GA, Lambert MI, Wayne DE, Butler-Browne GS, Noakes TD, Mouly V: Athletes with exercise-associated fatigue have abnormally short muscle DNA telomeres. Med Sci Sports Exerc 2003, 35: 1524-1528.

17. Ludlow AT, Zimmerman JB, Witkowski S, Hearn JW, Hatfield BD, Roth SM: Relationship between physical activity level, telomere length, and telomerase activity. Med Sci Sports Exerc 2008, 40: 1764-1771.

18. Whyte GP, George K, Sharma S, Lumley S, Gates P, Prasad K, McKenna WJ: Cardiac fatigue following prolonged endurance exercise of differing distances. Med Sci Sports Exerc 2000, 32: 1067-1072.

19. Dawson EA, Whyte GP, Black MA, Jones H, Hopkins N, Oxborough D, Gaze D, Shave RE, Wilson M, George KP, Green DJ: Changes in vascular and cardiac function after prolonged strenuous exercise in humans. J Appl Physiol 2008, 105: 1562-1568.

20. Nie J, George KP, Tong TK, Gaze D, Tian Y, Lin H, Shi Q: The influence of a half-marathon race upon cardiac troponin T release in adolescent runners. Curr Med Chem 2011, 18: 3452-3456.

21. Jassal DS, Moffat D, Krahn J, Ahmadie R, Fang T, Eschun G, Sharma S: Cardiac injury markers in non-elite marathon runners. Int J Sports Med 2009, 30: 75-79.

22. Whyte GP: Clinical significance of cardiac damage and changes in function after exercise. Med Sci Sports Exerc 2008, 40: 1416-1423.

23. Fagerhol MK, Nielsen HG, Vetlesen A, Sandvik K, Lyberg T: Increase in plasma calprotectin during long-distance running. Scand J Clin Lab Invest 2005, 65: 211-220.

24. Neviackas JA, Bauer JH: Renal function abnormalities induced by marathon running. South Med J 1981, 74: 1457-1460.

25. Hasselblatt M, Mooren FC, von Ahsen N, Keyvani K, Fromme A, Schwarze-Eicker K, Senner V, Paulus W: Serum S100beta increases in marathon runners reflect extracranial release rather than glial damage. Neurology 2004, 62: 1634-1636.

Carbs and cancer

2011-09-11T19:38:00.000+02:00

This is not one of those “carbs cause cancer” posts. I though “Carbs and cancer” had a better ring to it than for example “Metabolism and cancer”, what with the alliteration and all. Still, it's important to remember that although carbohydrate restriction is an effective treatment for cancer, this does not mean cancer is caused by consumption of carbs.

Our diet determines our health, even our risk of getting cancer and our risk of surviving it. Her are some reasons macronutrients matter:

The cause

- Humans who live on natural diets seem free of many cancers and also free of metabolic diseases [1]. Metabolic diseases such as obesity, diabetes, insulin resistance and heart disease, also coexist with cancer.

- A high body mass index increases the risk of most cancers [2].

- Cancer cells are normal cells that grow too fast and the cells need both energy and growth factors to grow at an increased pace. A logical theory of treatment would be to take away the energy and growth factors and starve the cancer cells.

- Hanahan and Weinberg suggested that six essential alterations in cell physiology could underlie malignant cell growth [3]. These six alterations were described as the hallmarks of nearly all cancers and included, 1) self-sufficiency in growth signals, 2) insensitivity to growth inhibitory signals, 3) evasion of programmed cell death (apoptosis), 4) limitless replicative potential, 5) sustained vascularity (angiogenesis), and 6) tissue invasion and metastasis.

- Cancer cells crave glucose. Aerobic glycolysis, the breaking down of glucose in the presence of oxygen, but with high lactic acid production in the cytoplasm (the Warburg effect), is a metabolic hallmark of most tumors [3]. Almost all cancers express aerobic glycolysis, regardless of their tissue or cellular origin.

- Enhanced glycolysis (the breakdown of glucose) is required for the rapid growth and survival of many tumor cells.

- People with type 2 diabetes are at increased risk of getting pancreatic, liver, colorectal, and bladder cancers, and non-Hodgkin lymphoma [4]. But if you have type 1 diabetes you have a reduced risk of lung cancer, Hodgkin’s lymphoma and prostate cancer.

- Mitochondrial dysfunction is a key element in most cancers.

- One of the problems if you are insulin resistant is that the mitochondria are bombarded with energy and pushed to the max. This causes them to produce reactive oxygen species (ROS). Increased ROS production can impair genome stability, tumor suppressor gene function and control over cell proliferation [3].

- The glycolytic enzyme "glyceraldehyde-3-phosphate dehydrogenase" potential is upregulated in many common tumors. GAPDH is also a transcription activator and link the metabolic state to gene transcription.

- The integrity of the nuclear genome is largely dependent on the functionality and energy production of the mitochondria.

- Impaired mitochondrial function can also induce abnormalities in tumor suppressor genes and oncogenes.

- Some viruses are associated with certain cancers. Several of these viruses are known to affect the mitochondria.

- While the mutator phenotype of cancer can be linked to impaired mitochondrial function, normal mitochondrial function can suppress tumorigenesis. We can suppress cells capability of causing tumors by fusing cytoplasm from normal cells without a nucleus with tumor cells. This suggests that normal mitochondria can suppress the tumorigenic phenotype [3].

- The function of a tumor suppressor gene called p53 is linked to cellular respiration. Damage to the respiration will gradually reduce p53 function.

- The study of cancer and metabolism involves such fancy words as "the Warburg effect" and "von Hippel-Lindau," so there's got to be something to it :-)

If cancer is a disease of energy metabolism, then a rational approach to cancer management can be found in therapies that target energy metabolism.

The cure

- Growth and progression of cancers of the mammary, brain, colon, pancreas, lung, and prostate has been reduced following energy restriction.

- Due to accumulated genetic mutations, cancer cells lack metabolic flexibility, so shifting the metabolism makes sense.

- Many tumors have abnormalities in the genes and enzymes needed to metabolize ketone bodies for energy so ketogenic diets are especially potent.

- It is well established that dietary energy restriction protects against cancer in many animal models, but…

- Freedland and coworkers transplanted prostate cancer cells into mice. The mice were then divided into one ketogenic group, one low fat group and one western diet. After 51 days the tumor volume in the low carb mice was 33% smaller than the other two groups, despite similar energy intake [5].

- Zhou and coworkers put mice with malignant brain cancer on a ketogenic diet meant for epilepsy and showed that the diet decreased the intracerebral growth by 65% compared to mice on control diet [6].

- LJ Martin and coworkers randomized women to a low fat diet or a control group, hoping to affect the risk of breast cancer. They did. But not how they wanted. Over an average of 10 years low fat eating led to 118 invasive breast cancers while the control had 102. Carbohydrate intake was found to correlate with cancer risk [7].

- A group of Japanese researchers [8] hypothesized that the increase in colorectal cancer in Japan could be due to increased fat intake. So they told 373 people with previous cancer to restrict their fat energy ratio to 18-22%. After 4 years the researchers were surprised to find that fat restriction had increased the risk of cancer recurrence.

- A group of Italian researchers found direct relations between dietary GI and GL and risk of renal cell carcinoma [9].

- In 1995, two pediatric patients with malignant Astrocytoma tumors were put on a 60% MCT diet to induce ketosis. PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects One patient exhibited significant clinical improvements in mood and new skill development during the study- continued the diet and remained free of cancer progression [10].

- An Italian case control study from 1996 found that the risk of breast cancer decreased with increasing total fat intake and that the risk increased with increasing intake of available carbohydrates [11].

- Eugene Fine at Albert Einstein College of Medicine of Yeshiva University, have been using a 1 month Atkins diet in cancer patients, hoping to see a reduction in tumor size. Results have not been published yet.

- Stephen J. Freedland at Duke Univeristy is currently testing the hypothesis that an Atkins diet will prevent or at least minimize the metabolic consequences of androgen deprivation therapy in prostate cancer treatment.

- The University of Würzburg Hospital has recommended a low carb, ketogenic diet for cancer patients since 2007

- Other studies are testing ketogenic diets in relation to cancer treatment. There's much interesting knowledge to come.

Impaired mitochondrial energy metabolism seems to underlie the origin of most cancers. To improve mitochondrial function: avoid toxic foods, read the Perfect Health Diet, avoid foods that induce inflammation, make sure to produce ketones now and then and remember to exercise.

References

1. Lindeberg S: Food and western disease: health and nutrition from an evolutionary perspective. Chichester: Wiley-Blackwell; 2010.

2. Renehan AG, Tyson M, Egger M, Heller RF, Zwahlen M: Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet 2008, 371: 569-578.

3. Seyfried TN, Shelton LM: Cancer as a metabolic disease. Nutr Metab (Lond) 2010, 7: 7.

4. Tabares-Seisdedos R, Dumont N, Baudot A, Valderas JM, Climent J, Valencia A, Crespo-Facorro B, Vieta E, Gomez-Beneyto M, Martinez S, Rubenstein JL: No paradox, no progress: inverse cancer comorbidity in people with other complex diseases. Lancet Oncol 2011, 12: 604-608.

5. Freedland SJ, Mavropoulos J, Wang A, Darshan M, Demark-Wahnefried W, Aronson WJ, Cohen P, Hwang D, Peterson B, Fields T, Pizzo SV, Isaacs WB: Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate 2008, 68: 11-19.

6. Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN: The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer. Nutr Metab (Lond) 2007, 4: 5.

7. Martin LJ, Li Q, Melnichouk O, Greenberg C, Minkin S, Hislop G, Boyd NF: A randomized trial of dietary intervention for breast cancer prevention. Cancer Res 2011, 71: 123-133.

8. Nakamura T, Ishikawa H, Takeyama I, Kawano A, Ishiguro S, Otani T, Okuda T, Murakami Y, Sakai T, Matsuura N: Excessive fat restriction might promote the recurrence of colorectal tumors. Nutr Cancer 2010, 62: 154-163.

9. Galeone C, Pelucchi C, Maso LD, Negri E, Talamini R, Montella M, Ramazzotti V, Bellocco R, Franceschi S, La Vecchia C: Glycemic index, glycemic load and renal cell carcinoma risk. Ann Oncol 2009, 20: 1881-1885.

10. Nebeling LC, Miraldi F, Shurin SB, Lerner E: Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports. J Am Coll Nutr 1995, 14: 202-208.

11. Franceschi S, Favero A, Decarli A, Negri E, La Vecchia C, Ferraroni M, Russo A, Salvini S, Amadori D, Conti E, Montella M, Giacosa A: Intake of macronutrients and risk of breast cancer. Lancet 1996, 347: 1351-1356.

http://www.time.com/time/health/article/0,8599,1662484,00.html

Exercise zen – this is my habitat

2011-09-10T10:58:00.000+02:00

"Because it's there"

George Mallory, when asked why he wanted to climb Mount Everest.

Between the productive factory and the setting sun the rusty old metal offered me exercise. I accepted, but not for the exercise.

Shoot the messenger

2011-08-18T13:37:00.000+02:00

The blogosphere is buzzing with new theories, discussions, disagreements and downright squabbles. What better time to look at some of the ways to make your case. There are many ways to lose an argument, these are just a few examples.

Argumentum ad hominem (to the man)

When you have no basis for an argument, abuse the plaintiff.

Cicero

It can be surprisingly easy to attack a person or a person’s traits rather than that person’s arguments. When arguing ad hominem you are linking a negative trait, characteristic or belief to the truthfulness of that persons claim. Contrary to what many people think, calling someone an asshat is not argumentum ad hominem. That’s just a good old insult. If however, you were to say that your opponent cannot be takes seriously because he smokes joint now and then, you are making a logical fallacy.

In the nutrition blogosphere one ad hominem argument is often repeated.

Remember Matt Stone's “Poor Poor Jimmy Moore “ post where he linked Jimmy’s weight to the truthfulness of his weight loss claims? Although he never directly said, "Jimmy is fat, therefore his low carbohydrate diet advice does not work" – it was strongly implied.

After the death of Robert Atkins many have tried to undermine his message by referring to images showing he was not very lean.

Anthony Colpo wrote, amongst much other silliness, this about Richard Nikoley:

…apparently there is an angry post written by some overweight joker who runs what would appear from its URL to be an animal liberation blog …

Once again, Colpo did not say Richard is fat therefore he is wrong, but it was implied and could thus be filed under the ad hominem label.

A fat dietician or nutritionist is actually not any less trustworthy than a lean one, although we easily feel it is so. If you reject a person’s claim due his weight it is a logical fallacy. Sadly, when you work with nutrition, you gain more acceptance if you yourself look fit.

Calling another person fat is only a logical fallacy if it is formulated such as: “You are fat therefore you must be wrong.” But the “therefore” can often be implied.

The above examples are forms of ad hominem arguments called “Tu quoque”, meaning “you to”.

The uncrowned king of logical fallacies and ad hominem arguments in the nutrition blogosphere is Durianrider

Here are a few examples from his blog:

Durianrider is the type of person who makes me want to commit logical fallacies myself. Oh, what the hell: Durianrider is an asshat, so you cannot take anything he says seriously.

Here’s another example of Tu quoque:

Bob: "Smoking is a highly addictive habit and causes health problems. You should not smoke."

Alice: "But you yourself smoke!"

The fact that Bob smokes doesn't mean that he is wrong about the effects of smoking.

Imagine for example that you move to a new town that has two dentists, of which one has poor teeth and one has good teeth. Who do you choose as your dentist? The one with the poor teeth of course, because chances are that he does the teeth of the dentist with the fine smile.

Similarly if you are joining a gym, join the one with the lean customers and the fat instructor rather than the one with fat customers and a lean instructor.

Overweight has a large range of causes, nutrition being but one. We all know that knowing what is smart to do is not enough to do what is smart. Especially we need to remember psychological issues that are usually at play. Overweight people can give just as good nutritional advice as lean people.

There are other forms of ad hominem arguments. If you claim that an argument is incorrect due to its source; for example saying your trainers claim that “proteins are good for you” must be wrong because the trainer sells protein supplements, it is a logical fallacy called Ad hominem circumstantial. You might want be skeptic, but scepticism it is no ground to dismiss his argument. We cannot dismiss a scientific article because it is funded by Pepsi because even Pepsi might be right.

Guilt by association can also be a type of ad hominem fallacy. An example:

Person P makes claim C to paleo blogger.

Vegans, a group which is viewed negatively (nutjobs) by the paleo blogger, also makes claim C.

Therefore, person P is also viewed as a nutjob and claim C is dismissed.

Argumentum ad ignorantiam

Appeal to ignorance – the claim that whatever has not been proved false must be true, and vice versa (e.g., there is no compelling evidence that UFOs are not visiting the Earth; therefore UFOs exist – and there is intelligent life elsewhere in the Universe. Or: there may be seventy kazillion other worlds, but not one is known to have the moral advancement of the Earth, so we're still central to the Universe.) This impatience with ambiguity can be criticized in the phrase: absence of evidence is not evidence of absence.

Carl Sagan

People often arrive at the wrong conclusions simply because of ignorance or lack of knowledge. A creationist may argue that evolution must be wrong based on the complexity of nature, thus illustrating his lack of understanding.

I feel that the oft-used “we don’t know the long term effects of carbohydrate restriction, therefore we consider it unhealthy and recommend against it” falls under the above category. If however carbohydrate restriction was always found to be unhealthy in short term trials, claiming it is unhealthy long term, is not a fallacy.

The argumentum ad ignorantiam can go two ways. Arguing that a central control of obesity is nonexistent because no one has proven it beyond a doubt is a fallacy. It is also a fallacy to say that a central control of obesity exist because its non-existence has not been proved.

Post-hoc ergo propter hoc

The human brain is in many ways designed specifically to se correlations and to assess causality. When the stone age man learned that bear cubs alone in the forest meant get the hell out of there before mother bear comes, it saved his life. It can also be life saving to associate the moldiness of food with abdominal pain. We look for associations everywhere and all the time, but we also often fail miserably. Correlation does not prove causation.

Many people will argue from their own experience that homeopathic medicine works, even though most studies show that they don’t. It you get well after doing or eating something out of the ordinary you are likely to believe that particular action caused the improvement rather than thinking you would have gotten better anyway. This illustrates the dangers of advise based on n=1 experimenting.

If you make the observation that fat people are more sedentary than lean people and that people are thus fat because they are sedentary, you are making a logical fallacy. There is always the chance that obesity makes people sedentary and that leanness makes people move.

When the low carber finds his symptoms of poor health disappear, he argues that carbohydrates caused the poor health. This too can easily be a fallacy.

Straw men

By reducing an opponent’s arguments into simplified versions easier to dismantle you are building straw men. Nutritional researchers are exceptionally good at making straw men. You can find several studies claiming dietary fat reduction cause all sorts of good things, even though the studies did much more than just reduce dietary fat.

Some studies claim to have disproven the effectiveness of low carbohydrate diets by using a diet with quite a lot of carbohydrates but labeling it low carb. They have then created an illusion of having refuted a proposition by replacing it with a superficially similar yet unequivalent proposition (the "straw man"), and refuting it, without ever having actually refuted the original position.

Tautology

If you say that obesity is caused by an excessive calorie intake, this can be considered a tautology. Obesity by definition means calorie intake has been high, at least higher that calorie expenditure, so the claim is meaningless and nonsensical.

Argumentum ad verecundiam (Argument from authority)

In any decent discussion the discussing parts needs to have a certain degree of knowledge. James Krieger says Gary Taubes is wrong. As a consequence less knowledgeable people appear and say that Taubes is wrong because Krieger says so. This is a logical fallacy. Whether Taubes is right or not is beside the point.

How often do you think a politician commits a logical fallacy by arguing from authority? Whatever your view is, it is never hard to find an “expert” to lean on. In nutritional politics this logical fallacy is common. When the politician says you should eat more grain because ADA says so, this is a logical fallacy, albeit a rather necessary fallacy.

The Golden Mean

The golden mean argument bugs the hell out of me. The golden mean fallacy says that the truth must be somewhere between the extremes, often right in the middle. Most people have a tendency not to believe in anything extreme. But the truth is the truth, extreme or not.

Political correctness often ends up in a golden mean argument. Official dietary guidelines are pretty much based on the golden mean fallacy.

Argumentum ad populum (appeal to the people)

Even bad ideas and untruths can be accepted by the majority, this however does not make the idea any more valid.

All your friends say cholonics are a good idea and very healthy so it must be true, is a prime example.

I Norway, leading nutritional experts will say that almost every government in the world agrees that the human diet should be grain based, implying that it must thus be true.

In health and nutrition ad populum arguments are very common so watch out.

False Dichotomy

Saying fat is either good or bad for you is a false dichotomy, and do not believe the answer to overweight is either food reward or macronutrients.

Anyone who has worked with exercise or nutrition knows how people will make false dichotomies all the time. “Is this food healthy or unhealthy? Is this exercise effective or ineffective?”

As always, there are links in the text even though they are not highlighted by a different color. If you’d like to watch the full range of logical fallacies live, watch Fox News.

A spark of reason

2011-08-16T20:28:00.000+02:00

I’ve been reading through many (not all) of the comments on Guyenet’s rebuttal of the carbohydrate hypothesis. Although it can be rather tedious, especially because of the apparent mental hospital escapee ItsTheWoo2 (who does have a few good points but a complete lack of putting those point out there in a sane way), but Stephan finally got to his senses and blocked the comments from her (him?).

After reading both the blog post and the comments I find that I am rather unsure of what we are discussing. It seems we are dealing with to poorly defined theories and that much of the seemingly contradictory nature of those theories stem from a lack of clear definition.

The only comment I felt was really worth noting was that of Dave “Spark of reason” Dixon who had this to say:

@Stephan,
Just to clarify (and apologies if already discussed, I haven't gone through all of the comments): what precisely is the "carbohydrate hypothesis" under discussion? Is it that carbohydrate is *necessary* for obesity, or *sufficient*? My reading of Taubes is the former, that you need carbohydrate to drive fat storage, but not that just eating carbohydrates will make you fat.
I don't find anything in what you presented which is inconsistent with that view, e.g. examples of lean cultures with traditionally high-carbohydrate diets may simply indicate that other factors are needed to drive obesity, and particularly metabolic syndrome. Are there any examples of obesity occurring in the absence of dietary carbohydrate?

Isn’t this actually an important point? Does the carbohydrate hypothesis being discussed say that carbohydrates are necessary or sufficient for causing obesity? If, as Dave interprets GCBC, the theory says carbohydrates are necessary, then what exactly are people arguing about?

I don’ get it!

Macronutrients and food reward

2011-08-13T19:03:00.000+02:00

If you see one bright red swan, you are not likely to give up a theory that says that all swans are white; you will instead go looking for the person who painted it.

Imre Laktos

Much is being said on this subject. Bet many are getting pretty fed up by now. But I still think this is an interesting discussion and so I will take this opportunity to add some thoughts. After all, the goal here is to find the truth; to find out how the world works. In that respect, I would also like to say that I do not agree with any one side in this discussion. Scientifically speaking, agreeing is not very scientific. That would mean confusing matters of opinion with matters of fact. Things are just what they are.

Chris Kresser is of course right in that there is no single cause of obesity. In animal studies obesity can be induced in a number of ways, just as in humans. The fat tissue is a large part of our body and it has a wide range of receptors and interesting signaling, so it should not come as a surprise that there are many ways to become fat.

If we are to look for a general cause, we could say that western, post agriculture lifestyle is to blame for obesity and our lifestyle diseases. But that does not mean you cannot get fat eating paleolithic foods, although if you did, you should blame your parents for the lousy chromosomes.

Neither carbohydrates nor food reward is able to explain all the observations. They both explain a part of the observations and so are both likely influential factors. Just how big a role each plays is an extremely difficult question to answer. Thus the current discussion.

The key question is: Why is not hunger down-regulated in humans becoming fat?

The Guru Walla
From what I can see, the Cameroonian Guru Walla is a bland food, overeating, fat gaining rite.

In the Guru Walla ritual, young Cameroonian men consume a diet made of red sorghum and cow milk (makes up over 95% of calories). The young men isolate themselves in different houses with a female attendant devoted exclusively to the preparation of Guru Walla meals. The diet and exclusion is supposed to lead to a certain level of purity. The men eat every 3 hour for 60 days, during which time body-weight can increase by an average of 17kg. Only 64-75% of the weight gain is fat [1].

Traditional food amongst these Cameroonians is about 75% CHO, 10% fat and 15% protein. During the Guru Walla it is 70% CHO, 15% fat and 15% protein.

The Guru Walla food is obviously fattening; at least if force fed and combined with minimal physical activity. The question we need to ask is: Would the Cameroonians be overweight if all they consumed was the Guru Walla diet?

It seems that the Cameroonians do not get fat because of the food itself. Rather they become fat because they force feed themselves. The newly gained weight is also lost after the ritual.

The reason I called the Guru Walla food bland, is that it most likely is very bland after the first few days. Try eating any one food exclusively for 2 months, and eat it even though you are not hungry (vomiting is also a part of the Guru Walla). The dopamine reward response should be minimal. Remember the Twinkie Professor who ate nothing but Twinkies, Oreos, donuts and similar crap but who lost 27 pounds in a 10 week experiment. He did consciously under eat, but my point is that we need to ask ourselves how lack of variation affects reward.

Food reward
While food reward might help explain why we overeat at a biochemical level, there is little evidence to indicate that a fat loss diet needs to be unrewarding, if by unrewarding we mean less palatable. We also need to know if it is possible to unconsciously overeat (become fat) on rewarding foods if we have a working metabolism and the rewarding foods do not mess with our metabolism. If not, whatever caused the metabolism to go out of whack is the real problem.

Stephan’s bland food through a straw experiment does not necessarily support a theory claiming that the study participants lost weight because of an inherently unrewarding quality of that particular diet. The finding could easily also support the theory that eating only one food, no matter how rewarding it may be when consumed intermittently, will make people lose weight because the rewarding quality of that food declines with increasing intake.

So we need to know if people could lose similar amounts of weight eating other foods exclusively.

Leptin
I am still having trouble seeing what's the big fuzz about leptin. It is a signaling molecule. It signals energy surplus and the lack of leptin signals lack of energy. Leptin also increase fat oxidation. The leptin deficient animal models, that are obese, act and behave as they were starving and administering leptin normalize their behavior and induce weight loss. Either the body just needed to be told that it had stored energy to use, or we just needed to increase fat oxidation. If you increase fat oxidation by other means such as GH, ob/ob mice lose weight just as with leptin.

If for example high insulin levels cause leptin resistance, focusing on leptin does not add anything to obesity treatment. High insulin levels can also be caused (or at least be exacerbated) by factors other than carbohydrates. For example factors that messes with liver function.

“In particular, protein-rich foods such as beef can increase insulin secretion as much as certain starch foods such as pasta, or more.”

The quote takes the results from trials out of context. It is an unfair statement, just like “proteins are inherently satiating” statement. A few days of beef eating will likely lead to lower insulin than a few days of pasta. I’ve written some about satiating proteins here.

In overweight people, as in overweight animal models, the key issue seems to be a reduced fat oxidation. Reduced fat oxidation with a high energy intake cause fat deposition in most all tissues and also insulin resistance.

Anything that increase fat oxidation in overweight animal or humans, cause weight loss and reduced food intake.

Lessons from insulin resistance
Stephan claims that overweight people have high serum free fatty acids. This is not completely true, at least if we are to listen to Keith Frayn at [2]. The claim may be true in general, but there are lots of overweight people with normal FFA levels. This however does not change Stephan’s argument. Generally the fat tissues of the overweight give out more FFA indicating adipose tissue insulin resistance.

Here is how we imagine insulin resistance to occur (roughly):

The pancreas has a direct route to the liver. The reason for this direct route is that the liver controls blood sugar level through its production of glucose. When blood sugar rises, the pancreas notice and secretes insulin. When the liver receives this insulin, glucose production is reduced. As the cells in the body are utilizing glucose for fuel, blood glucose level drop.

Somehow the liver becomes insulin resistant and keeps sending out glucose despite the insulin being sent from the pancreas. The reason seems to be inflammation and/or buildup of fat (NAFL). In this insulin resistant state, the muscles also fill up with fat. Once glycogen stores are full they become insulin resistant to avoid sugar poisoning, but keep taking up fatty acids. Because of the high carb diet and/or lack of physical activity the muscles do not burn fat and so it builds up. Also, there is some loss of muscle and liver mitochondria function and probably fatty acid transport into mitochondria.

The fat tissue takes up both glucose and fatty acids and expands if it takes up more than it gives out. The expansion of fat tissue eventually cause fat cells to send out stress signals (probably caused by endoplasmatic reticulum stress) and macrophages invade the tissue, gathering around dying fat cells. In this state, the fat tissue secretes a lot of fatty acids that wreak havoc around the body. But if free fatty acids are not burned they need to be re-esterefied. A high FFA level does not mean that we are not gaining weight or that we are losing weight (that more fat is leaving than entering the fat tissue). FFA are measured fasting and although the level might be higher in overweight and insulin resistant in that fasted state, this does not mean that over time more fat is leaving the fat tissue than are entering.

Stephan Guyenet takes the high FFA-level often observed in the overweight to mean that the fat tissue is insulin resistant and that they could not be gaining weight. This might be a wrong assumption. They have definitely been gaining weight and most overweight people are either weight stable or gaining weight. Is it impossible to gain weight while still having high FFA level?

Lean people also get insulin resistant. As do animals and humans with lipodystrophies. Many massively overweight do not become insulin resistant, and it seems that what causes the overflow of free fatty acids from adipose tissue is that it reaches its limit – a limit of course determined by both genetics and lifestyle.

In the insulin resistant state (metabolic syndrome), free fatty acids are usually high and fat builds up everywhere. Anything that increases fat oxidation helps. Pharmacological inhibition of the oxidation of fatty acids in the liver stimulates food intake in both humans and rats and stimulation of hepatic fatty acid oxidation reduces food intake, weight gain and adiposity in rats with diet-induced obesity [3].

FFA’s come from food, the liver or fat tissue. Carbohydrates are largely responsible for the amount secreted by the liver. At a cellular level, insulin resistance/metabolic syndrome seem to come from a high total energy intake. There is a surplus of both glucose (glycogen) and fat and the body can’t handle it all. Reducing the dietary fat load helps (at least if hypocaloric), but reducing dietary carbohydrate is the most efficient treatment to date. The question, though, is still why these people overeat.

Insulin

“…for insulin to cause fat gain, it must either increase energy intake, decrease energy expenditure, or both.”

“If calories and protein are kept the same, high-carbohydrate meals cause equal or greater satiety than high-fat meals, and equal or less subsequent food intake, despite a much larger insulin response)”

Stephan Guyenet

Insulin will reduce hunger as long as there is energy coming from ingested food. Once that flow of energy stops or is reduced, a high insulin level cause hunger. In order for insulin to cause overweight, the level only needs to be high enough for allowing fat oxidation to be less than fat storage in that particular individual over time.

Injecting both glucose and insulin reduce hunger. Injecting insulin alone increase hunger. Long term satiety is better with low carbohydrate diets than high. We need to remember that we adapt to burning different fuels. If we normally eat high carb and suddenly eat high fat we are likely to be poor fat burners and thus more likely to get hungry. This might also explain higher leptin levels after high fat meals in acute feeding studies.

“If blood glucose decreases enough, it activates a system called the "counter-regulatory response", designed to maintain blood glucose at all costs to protect the brain from the effects of hypoglycemia. Part of this response is hunger and increased food intake. However, this system is not activated except in severe hypoglycemia, which is rare except in diabetics, thus it is not relevant to common obesity.”

This quote seriously needs references. It seems very unlikely.

These are just some thoughts. Nothing more.

References

1. Pasquet P, Brigant L, Froment A, Koppert GA, Bard D, de G, I, Apfelbaum M: Massive overfeeding and energy balance in men: the Guru Walla model. Am J Clin Nutr 1992, 56: 483-490.

2. Taubes G: Insulin resistance. Prosperity's plague. Science 2009, 325: 256-260.

3. Ji H, Friedman MI: Reduced capacity for fatty acid oxidation in rats with inherited susceptibility to diet-induced obesity. Metabolism 2007, 56: 1124-1130.

Science and religion

2011-08-07T11:11:00.000+02:00

He held forth on a great range of topics, on some of which he was thoroughly expert but on others of which he may have derived his views from the few pages of a book at which he had happened to glance. The air of authority was the same in both cases.

Roy Harrod about John Maynard Keynes

Science is what scientists do. It is difficult to find a better definition of the word. No one agrees completely on what methods and rules should make up science. But there are still aspects of science that are generally agreed upon and that make more sense than others. One goal, if not the only goal of science, is to find facts and explain the world as it really is. Science is searching for truths rather than lies and untruths. Interestingly, a whole field of intellectuals work and live as scientists without actually having a clear definition of the word science. But it is not given that we need a strict definition. We generally know what people are talking about when they say something is true or false. Our language often works perfectly fine in conveying such vague ideas “truth.” Leaving out deeper philosophical considerations, words like truth, reason and fact actually make sense to most of us. It is true that the earth is round (or more correctly closer to an oblate spheroid) and it is false that the earth is at the center of our solar system. Natural selection is a fact and so the creation of all living beings by a god is a lie.

Dean Ornish

Whenever I write about many of the “scientists” in the field of nutrition, I often feel compelled to put the word “scientist” in quotes. I know they work as scientists, but are they following scientific principles? Are their results, scientific results? Is, for example, Dean Ornish a scientist? Is his work focused on finding truths and facts based on logic and reason? Because it seems to me that he disregards a great deal of data when he comes to his conclusions and that he has a great ability to cherry pick and interpret any cherry picked data to fit his existing world view. This makes many of his conclusions wrong, and many have argued correctly that he is in fact wrong about many things.

Ornish works as a scientist, even if he has not always followed agreed upon principles designed to filter out the truth. Should I then disregard anything he says? No, of course not. That would mean to disregard basic aspects of human nature, one of which is our great ability to screw things up. We all do, but unfortunately, some more than others. Thus, I have to consider anything Ornish has to say. This does not, however, mean that he has earned my trust.

Ornish is just an example here, and is in no way unique in his field. Scientists regularly work in unscientific ways. As Thomas Sowell puts it:

The ignorance, prejudices, and groupthink of an educated elite are still ignorance, prejudice and groupthink…

Although scientists should always put new theories to the test and assess their validity, this is not always done. Ideas are often accepted more on the basis of resonance with peers than empirical verification. In fact, as Sowell puts it, scientists act just like the rest of us:

If they are simply people who are like-minded in general, then the consensus of the group about a particular new idea depends on what that group already believes in general- and says nothing about the empirical validity of that idea in the external world.

The fact that ideas are wrong does not mean they can’t be accepted by a great many people, and even sometimes by the majority of people. The ideas of Hitler, Lenin and Mao for example, was and are still accepted by millions as being very good ideas indeed, despite their lack of logic and empirical testing. The belief that humans are cured of illness because needles are jammed into immeasurable magical energy points or that homeopathy makes any sense at all, are also beliefs with numerous followers despite being completely devoid of reason. Religions, as the prime example, gather millions of followers without being in anyway rational.

By no means does working as a scientist or working in a scientific field mean that you are a reasonable person. Religion is in many ways the opposite of reason as it usually requires a lack of, or disregard of reason to exist. It is then difficult to understand how someone can work as a scientist or in a scientific field and at the same time believe in a higher power when there is absolutely no evidence for the existence of such a higher power.

An important part of science is the falsifications of hypotheses. Not every theory needs to be falsified, but many theories will be nonsensical if they cannot be falsified. The existence of a god cannot be falsified, that is, one cannot prove that there is no god. That, however, does not make the existence of a deity any more plausible. Although the existence of a god cannot be falsified, we do know enough about the human psyche, the history of the earth and the universe and the history and evolution of religions to say that any of the proposed gods are extremely unlikely to exist. I will not do the whole discussion of why religion is nonsensical. Others have done so before and have done so far better than I ever could. I can, however, recommend and refer to writers such as Sam Harris, Richard Dawkins, Christopher Hitchens and Daniel Dennet. (Here is a short talk by Dennet, and while at TEDs, make sure to also watch Dawkins talk on militant atheism.)

Writing critically about religion is going to hurt many people’s feelings. Religion is personal. It is at the core of the identity of many, and challenging religion is challenging who people are. But religion is a part of human existence. It affects us personally and as a society, and most importantly, there is no reason to think that religions are benign or that they do not affect the wellbeing of humans negatively. So religions should be discussed and I am taking the side of the critic.

Isn't it enough to see that a garden is beautiful without having to believe that there are fairies at the bottom of it too?

Douglas Adams

Although Norway is one of the least religious countries in the world, I am afraid that the recent atrocities in Oslo, which turned out to be a one man crusade against both democracy and Islam, will make it even harder to publically being critical towards religion. Suddenly one fears being grouped with such lunatics. But falling silent is not a good response. Nothing has changed, but being the critic still has its dangers. Ayaan Hirsi Ali, for example, has written some wonderful literature and is an extremely intelligent person, but she is also openly criticizing Islam and has thus been forced to live large parts of her life in hiding and under protection. There are many like her and openly criticizing religions, especially Islam, can often be a death sentence.

Even in countries like Norway where freedom of speech is a virtue held high, being publically critical of religion is severely frowned upon and like in so many other countries, blasphemy has long been a crime. Norwegians in general are naïve people and are often so afraid of stepping on any toes that we are willing to sacrifice even a freedom of speech to avoid it. Monty Pythons “Life of Brian” was originally banned in Norway. When finally released a few years later it was with an NC-18 rating and a text on the cover explaining that Brian was not really Jesus.

Religion, and any other unsubstantiated beliefs, should be put under the same scientific scrutiny as a scientific claim, or any claim at all for that matter. Reason and objective analysis tells us that religions greatly differ in their ability to make as many people as possible as happy as possible. Thus some religions must be characterized as better than or worse than others and some thus pose greater threats to our well-being than others, despite all being equally devoid of reason. To say that one religion by nature is better or worse than others is perhaps the greatest tabu. It is still a reasonable conclusion.

In “The Moral Landscape – How Science Can Determine Human Values”, Sam Harris argues that if our goal is to maximize the well being of humans, then religions fall severely short of science and reason. In particular, religions are horrible moral guidelines. This, of course, will strike many as odd, given that they believe religion to be the only place to look for moral guidance. Writes Sam Harris:

For nearly a century, the moral relativism of science has given faith-based religion – that great engine of ignorance and bigotry – a nearly uncontested claim to being the only universal framework for moral wisdom. As a result , the most powerful societies in on earth spend their time debating issues like gay marriage when they should be focused on problems like nuclear proliferation, genocide, energy security, climate change, poverty, and failing schools.

In his “The year of living biblically” experiment, A.J. Jacobs attempted to follow all the rules of the Old Testament (view his talk on TED Here). This proved an impossible mission, as it would have made him into a murdering lunatic. He did however give some of the rules a try, such as not shaving the corners of his beard, stoning an adulterer, not sitting in a place where a menstruating woman had sat and only wearing clothes made from the same fabric.

Religion does undoubtedly not originate from reason or science, but from the lack of it. There is thus no way religion and science can coexist in a person without being at conflict with each other. Says Sam Harris about the oft perceived unproblematic uniting of religion and science:

…this is based on a fallacy. The fact that some scientists do not detect any problem with religious faith merely proves that a juxtaposition of good ideas and bad ones is possible.

Francis Collins

How then should we respond when a person like the director of the National Institutes of Health, physician-geneticist Francis Collins, described by the Endocrine Society as "one of the most accomplished scientists of our time", head of the Human Genome Project, goes religious, publishes a book about his strong faith in the Christian God and claims that science points to the existence of God and that God himself does not need an explanation since he is beyond the universe?

When Collins, in 2006, published “The language of God” the result was remarkable. Rather than being an intellectual suicide, he continued as before and received praise for his attempt to reconcile and unite science and religion (or rather Christianity). Collins probably has more responsibility for biomedical and health related research than any other person on earth. He is controlling an annual budget of more than $30 billion, and yet he believes God created the universe some 14 billion years ago, that breaking God’s moral law will lead to the estrangement from God and that Jesus is the solution, that God created evolution and that a virgin gave birth to the son of God and that Jesus was actually resurrected some 2000 years ago.

The insanity of all of this is overwhelming. You can see it live here, and you can see him make an ass of himself for Bill Maher here.

According to “The Diagnostic and Statistical Manual of Mental Disorders" (DSM-IV), published by the American Psychiatric Association, delusion is a “false belief based on incorrect inference about external reality that is firmly sustained despite what almost everyone else believes and despite what constitutes incontrovertible and obvious proof or evidence to the contrary.”

According to this definition Collins is delusional. The fact that others around him also firmly sustain this belief does not make it less delusional, although most scientists are not religious.

The problem here is not so much that Collins is delusional but that the system allows him to be delusional in the position he holds. Would he still be in his job had he been a devout Muslim or Hindu? Of course not. Because the religion he happened to fall upon was a type of Christianity approved of by a majority, no one much cared that Collins would take the texts of the bible as certain proof just as he would laboratory observations.

Most any time someone is critical towards religion, opponents invariably bring up the “but-why-does-it-matter-that-some-people-are-religious "argument and the "they-are-not-hurting-anyone" argument.The quick answer is that, although they may not be directly hurting anyone with their belief, there is no reason to think that religious belief is benign. Religions are without reason, and Collins will and do argue falsely and irrationally when discussing religion while arguing rationally and logically when discussing many scientific matters. That affects people.

“So he found God and faith. Good for him?” Yes perhaps, but bad for us. Because it means that he is willing, in some respects and circumstances, to put aside reason and logic and believe in farfetched ideas despite all the evidence pointing to the contrary. Collins judgment cannot be trusted.

A person's private beliefs should not keep him from a public position, but Collins is an advocate of profoundly anti-scientific beliefs, and it is reasonable for the scientific community to ask him how these beliefs will affect his administration.

Steven Pinker

It is reasonable to ask why Collins was not fired from his position when he turned Christian when he definitely would have been fired had he claimed to believe in Thor or Zeus.

Being open to the possibility of a intelligent higher power is in itself not that big of a threat to reason. On can for example be open to the possibility that such a power started what lead to the known universe. This cannot yet be disproved, but it still makes no sense. Why choose to believe this over non-theist explanations? But if a person believes that the universe was created by any of the already know gods, that belief comes with a package called religion. A package containing farfetched beliefs in magic rituals, nonsensical moral laws and a whole range of extra beliefs that flies in the face of logic. This is what Collins do when he assumes the universe is created by the christian god and he must also then accept and buy into (which he admittedly does) the other parts of the christianity package.

The fact that we do not know something is no reason to conjure up a god as an answer. In addition, the belief that a god created the universe may take away the curiosity and incentive to try and figure out, using science, what actually did start it all. In this way religion is corrosive to science.

Science is also corrosive to religion. There are far more atheists and agnostics amongst the highly educated and especially those educated in the natural sciences, then amongst the general public. Religion is corrosive to science and reason. Of course we cannot leave important decisions about future human flourishing and well being, like for example that of how to use embryonic stem cell research, in the hands of a devote Christian or Muslim. Religious people will often believe in a soul, no matter how unlikely the existence of such a thing might be, and they will also believe that embryonic stem cell research is wrong simply because writings from a primitive Bronze Age community are interpreted to mean that an almighty god says it is wrong. No logic or reason required. It is simply wrong. When Francis Collins was appointed head of NIH, the Times featured a story where many prominent scientists spoke up against it. Writes The New Yorker:

Steven Pinker, a cognitive psychologist at Harvard, questioned the appointment on the ground that Collins was “an advocate of profoundly anti-scientific beliefs.” P. Z. Myers, a biologist at the University of Minnesota at Morris, complained, “I don’t want American science to be represented by a clown.”

Collins, who founded the BioLogos Foundation dedicated to "the integration of science and Christian faith," sees no conflict between science and religion and believes that God is outside of time and space, or put in more reasonable terms, nonexistent. In his work to unite religion (Christianity) with science he undermines and mocks the very key concepts of science he should be representing.

Food reward, a factor in obesity

2011-07-06T11:01:00.000+02:00

“I think food reward offers the most compelling explanation for the US/global obesity epidemic.”

Stephan Guynet

“In studies where the food intake and energy expenditure of subjects are carefully monitored over a period of weeks to months (which tends to average out day-to-day fluctuations) a remarkable balance between calories consumed and calories burned was observed. When various mammals, from mice to monkeys, are either overfed or starved for a few weeks, their weight soon returns to normal levels when free access to food is resumed. Crucially, our mammalian bodies seem to be able to regulate feeding based on the amount of energy available in the food we consume, not just on the volume of that food.”

The above quote David Linden, suggests the body controls body weight by registering the amount of energy in food. This theorizing usually leads to the white adipose tissue derived hormone leptin and particularly its effect on the hypothalamus. Leptin, in general, correlate with adipose tissue mass. But the energy the body needs comes from two places: food and stored energy. Increasing use of stored energy will make animals and human eat less. Any energy-sensing control system must register the total amount of energy available, both from foods and from fat and glycogen stores. From this point of view, obesity could to be caused by the body not having access to its own stored energy and so continues to signal for food intake. Alternatively, the stored energy is readily available, but somehow an obese person experience feelings of hunger and craving that overpower any signal telling the brain that there is enough energy available. This scenario makes it likely that obesity is caused by a malfunctioning control system.

Stephan Guyenet has created quite a stir lately with his posts about food reward. Several of the posts have over 100 comments, some more rational than others, but people clearly have strong feelings about this. I think one of the reasons some people feel personally offended by his writing, is that they feel food reward lends support to overweight being caused by lack of willpower. This is definitely not Stephan’s intent, nor does his reasoning indicate willpower as a major factor. Nevertheless, willpower is a major part of food reward, as one of the opposing forces to a physiological drive to consume rewarding foods.

The theory of food reward is a theory of how foods affect our feelings, stimulate our behavior and how some foods appear addictive and promote addictive behavior. This seems lost on many. Food reward does not and cannot explain how we fatten. To find the answer to this we need to look at the physiology of the fat cells. Basic biochemistry still applies and some foods are more fattening than others, although as it seems, Stephan does not think so and he even uses his belief that macronutrients doesn’t matter as an argument in favor of the food reward theory. But the theory itself is a theory of why we (over)eat, not a theory of how we gain fat.

Even though the theory of food reward is not about willpower, willpower invariably enters into the equation. Many physiological drives can be affected by conscious thought. Stick your hand in ice water and your head tells you to pull it out (or your spine), but you can keep it submerged by willpower, some longer than others. Highly rewarding foods do, according to Guyenet, cause obesity in susceptible people, just like drugs may make addicts of some (often the same people). Still, I cannot see that food reward argues more strongly for willpower as a part of obesity, than other rational theories.

The theory of food reward is actually mostly about carbohydrates as most of the data relating to it is from the studying of sweet foods. As Hans-Rudolf Berthoud put it

“For nonsweet palatable foods (typically high-fat foods), there is less convincing evidence for development of dependence…” [1]

So it seems the key questions are:

- do sweet foods cause addiction and increased energy intake with subsequent obesity?

or
- do sweet foods cause obesity (fat storage) with following addiction or addiction like behavior possibly caused by metabolic clues?

As we undoubtedly fatten differently and not everyone becomes obese despite similar obesogenic environments, we can conclude that addiction to high palatability foods is 1) genetic and that preexisting differences in reward functions cause obesity; 2) intake of palatable foods is in itself addictive and leads to obesity; or 3) obesity (the excess storage of energy in fat tissue) cause changes in reward functions thus further accelerating obesity.

As many lean people also eat large amounts of highly rewarding foods, it seems unlikely that the food itself can be to blame. So, either food reward is secondary to the harmful effects of sugars/grains (sweet food not found in hunter gatherers): these foods create excessive fat storage in obesity prone people and this cause addictive behavior towards the very same foods; or it is the primary cause of obesity: people prone to weight gain have physiological measurable differences in parts of the brain that cause an addictive intake of fattening foods.

Although I enjoyed the posts about food reward I was left with very many unanswered questions after reading:

The reasoning
Stephan uses the fact that hunter-gatherers are lean in support of rewarding foods causing obesity in non HG societies, arguing that one of the reasons hunter gatherers are lean is because their diets are bland (although I think many HG’s would disapprove of their diets being called bland). This argument could go both ways. Because if the foods that drive fat gain also promote addictive intake of the same foods, then traditional diets can be as tasty as any, just as long as they do not contain these particular foods. As long as they don’t, there is no reason to think blandness is the cause of leanness.

Although lean traditional people’s diets are more unrewarding then say a SAD diet, this does not mean that we in the west become obese because our foods are not.

Also we have to ask: if obese people remove fattening foods, which are the same as those considered highly rewarding, will the addictive behavior/strong cravings for the fattening foods subside? I know from experience that many who struggle with strong cravings, lose their cravings when switching to a LCHF diet. The fact that some feel cravings even after some time on low carb diets, does not favor a set-point hypothesis. It could just indicate a dietary insufficiency, like the lack of salts or some fatty acids. As the cravings usually disappear before a considerable weight is lost, it is unlikely that the cravings were caused by the obesity itself. Often, it seems that cravings disappear when people regain the ability to burn fat.

Burning fat, or having a functional metabolism will make us eat less. The oxidation of fat in the liver offers a strong satiety signal [2]. So, even if lipolysis is high in obese, hunger will not go down if somehow the burning of fat in the liver is restricted. This is sort of a “metabolism argument”: One of the things that separate those prone to obesity and insulin resistance from the rest, is a poor and broken metabolism. They rely on glucose (glycogen) for fuel and have poor fatty acid oxidation in combination with blood sugar fluctuations and cravings, so fat is stored rather than burned as it should. Resolving the metabolism issues will in many reduce the cravings and rewarding foods are no longer an issue.

Another important question to ask is: how often during the day and how much hyperpalatable, highly rewarding foods do people who become obese actually eat?

If people become obese without consuming highly rewarding foods (something I consider very possible) then the theory of food reward argues strongly that this type of obesity is mostly due to lack of willpower, as there is no addiction to blame.

The “bland food” study from 1965 Stephan writes of can be used to support a “food reward” theory, but there are many other ways of explaining why the overweight people lost weight while the lean did, not. If the obese ate high sugar/grain and franken-fat diets, that also happen to be palatable once you get used to it, then of course they lost weight on the liquid diet.

“The first volunteer continued eating bland food from the machine for a total of 70 days, losing approximately 70 pounds. After that, he was sent home with the formula and instructed to drink 400 calories of it per day, which he did for an additional 185 days, after which his total weight loss was 200 lbs. The investigators remarked that "during all this time weight was steadily lost and the patient never complained of hunger or gastrointestinal discomfort." This is truly a starvation-level calorie intake, and to eat it continually for 255 days without hunger suggests that something rather interesting was happening in this man's body.”

This isn’t really that interesting. With all likelihood the man could have lost an equal amount of weight eating real foods that are far more rewarding but not fattening. It has been known to happen.

“I think decreased fasting insulin occurs as a result of weight loss…”

Stephan Guyenet

Another important point is that the body fat “setpoint” is still a theoretical point, and any theory based on the setpoint hypothesis is equally hypothetical.

“As one would expect if food reward influences the body fat setpoint, lean volunteers maintained starting weight and a normal calorie intake, while their obese counterparts rapidly lost a massive amount of fat and reduced calorie intake dramatically without hunger. This suggests that obesity is not entirely due to a "broken" metabolism (although that may still contribute), but also at least in part to a heightened sensitivity to food reward in susceptible people. This also implies that obesity may not be a disorder, but rather a normal response to the prevailing dietary environment in affluent nations.”

Lean people have good access to their own body fat and high fat oxidation rates. They have a better working liver than obese, and they definitely had a better pre experiment diet than the obese. The above results can be explained exclusively by a broken metabolism theory. There is no need to involve food reward.

“Some people may be inclined to think "well, if food tastes bad, you eat less of it; so what!" Although that may be true to some extent, I don't think it can explain the fact that bland diets affect the calorie intake of lean and obese people differently.”

Most diets affect lean and obese differently. These people are per definition quite different metabolism wise, and foods affect metabolism. Once again, the fact that one of the many diets that affect lean and obese differently are bland, does not lend much evidence for palatability playing a major part in obesity.

Although the rewarding abilities of different foods might explain some of the reason we overeat on fattening foods there are very many other ways you are likely to gain weight. As David Pier points out in the comments section:

“Excess fructose? Too high an omega-6/omega-3 ratio? Too much omega-6? Too little omega-3? Too much polyunsaturated fat in general? Too little saturated fat? Micronutrient (choline, minerals, etc.) deficiencies? Excess total carbohydrate? Superstimulating hyperpalatibility? Over-availability? Excess insulin (cause and/or effect)? Gut flora (cause and/or effect)? Lack of fiber (insoluble and/or soluble)? Multi-generational epigenetic changes? Artificial sweeteners? Endocrine disruptors? Sleep disturbances? Psychological causes essentially independent of all hormonal homeostatic mechanisms?”

In his third post, Guyenet writes about the review of low fat non energy restricted diets where overweight lost more weight than lean:

“In other words, low-fat groups reduced their calorie intake by an average of 271 calories per day, and lost 7.5 pounds (3.2 kg). When they considered only people who started off overweight, they lost 12.8 pounds (5.8 kg). The investigators noted that the results were similar no matter what the duration of the trial, because weight loss plateaued fairly quickly.”

Then he writes

“This is all without any instruction to reduce calorie intake, therefore we can assume these dieters were eating to fullness.”

No you can’t assume that. These are participants included in non blinded weight loss trials. I would say it’s a safer bet that they were in fact restricting their food intake.

“The best low-carbohydrate diet study I've seen was published in 2008 in the New England Journal of Medicine (3). 322 "moderately obese" participants were placed on a low-carbohydrate diet, a calorie-restricted low-fat diet, or a Mediterranean diet, for two years. The low-carbohydrate group's carbohydrate intake decreased by 130 grams per day, which is about half of a typical person's total intake, and neatly corresponds to the reduction in calories of 561 per day, despite not being instructed to reduce calorie intake.

At two years, the low-carbohydrate group had lost 10.4 lbs (4.7 kg), which is very similar to the average weight loss seen in low-fat diet trials.”

There are two major issues here. 1) The study by Shai et al is a horrible study: The Atkins based diet came with recommendations of getting fat from vegetable sources; By 24 months, carbohydrates constituted 40% in the low carb group and 50% in the low fat group. The low fat diet went from baseline fat intake of 31,4% to 30% (no reduction at all); the aurhors left out baseline energy intakes and only reported reductions; The study also used intention to treat analyses. The weight loss in the low carb group for the 272 who completed the study was 5.5kg in the “low carb” and 3.3kg in the “low fat” group. After 6 months the study diets were not very dissimilar.

If this is the best low-carbohydrate study Guyenet has read, he needs to read the other studies. Low-carbohydrate diets usually outperform low fat diets, as long as carbohydrate intake is kept restricted. This outperformance is despite low fat groups having caloric restrictions while low carb groups can stuff themselves as much as they want. His reasoning that low carb and low fat perform equally is flawed in so many ways, and he uses this reasoning to support a food reward hypothesis.

“I think the reason very low-carb ketogenic diets cause fat loss is the same reason extreme low-fat diets cause it: they have a greatly reduced reward value.”

Stephan Guyenet

The fact that participants in the Lindberg study lost weight without caloric restrictions does not mean food reward had anything to do with it. Once again, if certain foods themselves cause fattening, and we restrict these foods, weight loss is likely to occur. There is no need to blame blandness.

Messing about with dopamine signaling can cause obesity in animal models, and there are differences in dopamine receptors between "normal" people and those prone to addictive behavior. It is not strange that messing about with the brain will cause all sorts of things, but it does not mean obesity is caused by food reward.

There is more reasoning to discuss, but this post is getting way to long. Is there really enough available evidence to justify calling food reward a dominant factor in obesity? If there is, I can’t say I found evidence of this in Stephan’s posts.

And as Paul Jaminet pointed out:

“Likewise, we’re all familiar with young people who eat massive quantities of junk food and remain slender. The high food reward diets, even toxic and malnourishing diets, seem not to cause weight gain until some kind of metabolic damage occurs.

It seems that metabolic damage – the disease of obesity – is a prerequisite for food reward to matter.”

Obese people should eat boring diets
Guyenet even offers tips on how to make food less palatable and more bland. But does this mean that there are people out there who have tried all the obvious ways to lose weight, like reducing inflammation and cutting back on carbs, who have not succeeded and are left with trying to make food not taste good?

The most palatable foods are those packed with fat and sugar. These foods are the first to go on any dietary strategy. Do we need to make the rest of the diet bland?

Guyenet offers a range of advice for losing weight based on food reward theory. For example:

“Don't snack. In France and many other countries with strong food traditions, snacks are for children. Adults eat at mealtime, in a deliberate manner.”

And yet, if snack in itself do not seem to cause obesity, why not snack?

“Don't add fat to your food. That doesn't mean don't eat fat, it just means keep it separate from your cooking. If you want to eat butter, eat it separately rather than mixing it in with your dish.“

…I don’t know what to say about this…but I know I don’t like it.

Some of his advices are meant mostly for those who struggle to lose weight, but I fear if anyone would follow them, they would die of boredom instead:

“Eat only single ingredients with no flavorings added. No spices, herbs, salt, added sweeteners, added fats, etc. If you eat a potato, eat it plain. If you eat a piece of chicken, eat it plain. It can be in the same meal as other foods, but don't mix anything together. If you would like to keep salt in your diet, dissolve it in water and drink it separately.”

There are more of course. Most make sense, but they also make sense without considering food reward.

Importantly, all the studies used to support the award theory can also be used to support different theories. While they do no not falsify a reward theory they do not provide strong supportive evidence. But this is how science works. Stephan is right in offering the theory and he might turn out to be spot on. It will be interesting to see what future studies will reveal. We need some RCT’s to enlighten the causation between food and dopamine response and function, well any kind of RCT in this field would be important. I would like to make foods that are highly rewarding (measured by dopamine response or something fancy, that make people crave them, and that does not contain anything inherently fattening. Then I would give people free access to it to see if they got fat. Wonder what it could be?

"Some people have lost fat simply by avoiding carbohydrate or fat. I've heard people say that a low-carbohydrate diet in particular curbs their cravings and allow them to have a healthy relationship with food again (although others have developed strong cravings on low-carbohydrate diets). I believe this is mostly, if not exclusively, driven by the fact that carbohydrate and fat are major reward factors."

Stephan Guyenet

References

1. Berthoud HR, Lenard NR, Shin AC: Food reward, hyperphagia, and obesity. Am J Physiol Regul Integr Comp Physiol 2011, 300: R1266-R1277.

2. Friedman MI, Harris RB, Ji H, Ramirez I, Tordoff MG: Fatty acid oxidation affects food intake by altering hepatic energy status. Am J Physiol 1999, 276: R1046-R1053.

I see naked people

2011-06-29T22:52:00.000+02:00

A little while back I wrote a post entitled “Feet on ground.” It was meant as a reminder, mostly to myself, about not getting caught by the paleo hype, if such a hype exists.

My experience and observations of the people around me, is that many (by this I mean more than one would think, but it’s not a great number) people who live non-paleo lives, who eat lots of grains and low fat products, still seem perfectly fine.

As some commenters suggested, this might be just an illusion. The effects of far from optimal diets become increasingly pronounced with increasing age. However, I must still admit that there are several people I know, that surprises me with regards to their health, even old people.

Admittedly, Norway is far from being the worst when it comes to diet and health. We are in general grain based, but we are still far from USA or UK, where things are truly bad.

But, I’m rambling. What I wanted to say, was that I've found a very subjective and entertaining way of getting a feel of how deteriorating a modern western lifestyle can be. This thought experiment can be done anywhere, but it might be easiest where people wear little clothes.

When in a place where there are lots of ordinary people (non paleo people) try to remember all those nature shows (best are from BBC and Human Planet is highly recommended, oh and David Attenborough rules) where you’ve seen human tribes living traditional lives.

The slender yet muscular fit looking people – of the type that climbs high trees and goes through much pain just for some honey, or that hunt lions on foot with a wooden spear – that likely come to mind, are likely nude or at least severely underdressed for a tea party, unless you are thinking of Inuit, Lapps or someone similar.

Now, look around, and imagine all the people around you similarly naked and in the bush or on the savannah. If the thought of these people in such a situation seem like some horrible joke of evolution, then we have reason to worry about our general health.

Without seeming like some pervert, I actually think there are things to learn from these thought experiments. Mostly what I keep feeling is not that we are particularly fat (in Norway), but what strikes me, is how little muscular and fit people seem. This is more pronounced from middle age and up. Most of the lean people are either strikingly skinny and unhealthy looking, or lean in the female-westerner-with-high-body-fat-percentage-unable- to-do-a-single-push-up sort of way.

Too much fat, and too little muscle

The lack of visual muscular fitness, often combined with poor body posture, surprises me more than the overweight.

Well, in other news, yet another study finds that overweigh people have higher life expectancy than their lean counterparts, albeit with greater risk of disabilities. Perhaps our focus should be on natural foods and exercise, rather than on the significance of some extra padding. (study here)

Unnecessary starvation cures diabetes

2011-06-25T17:01:00.000+02:00

If I wanted to find out if I could reverse the progressive development of type 2 diabetes with energy restriction, I would conduct a clinical trial.

I would need a group that reduced their energy intake, but if I wanted to make sure an effect wasn’t caused by the reduction in a specific macronutrient (and if I had the recourses) I would need more groups; one who reduced fat intake while keeping calories stable, one reduced proteins and one who reduced carbohydrates. I still couldn’t be sure if an effect was due to a specific macronutrient – it could just as well be because of the relationship between nutrients – but I would be more sure.

Now, recourses are usually sparse but a study could be done with only one group also. I would just have to make very sure to write in the discussion that an effect could be due to the specific lowering of one nutrient as opposed to lowering of total calories.

A group of researchers at Newcastle University did the above mentioned study. They hypothesized that

“…both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake.”

To test the hypothesis, eleven people with type 2 diabetes ( mean BMI 33.6, nine male and two female) were studied before and after 1, 4 and 8 weeks of a 600 kcal)/day diet.

600 kcal is not much and as Peter at Hyperlipid noted, one of the participants found the diet difficult to handle:

"It was very tough. I was hungry all the time. It was a starvation diet and food was on your mind all the time,"

said Gordon, the retired lorry driver.

This was actually a study that looked at beta cell function, and it came to be because one of the authors had read about the miraculous healing of T2D that occurs with bariatric surgery.

Writes Lim et al

“However, type 2 diabetes is clearly reversible following bariatric surgery. The normalisation of plasma glucose concentration follows within days of surgery, long before major weight loss has occurred…”

Which means the pathology of T2D is not caused by overweight itself, because the normalization of glucose is vital in losing the T2D diagnosis.

The experimental diet was a liquid diet formula (46.4% carbohydrate, 32.5% protein and 20.1% fat, 510 kcal/day) sponsored by Nestlé Nutrition. This was supplemented with three portions of non-starchy vegetables so that total energy intake was about 600 kcal/day.

I won’t dwell on the details; it’s an open access article so anyone can read.

Anyway, the diet caused a significant reduction in plasma glucose (9.2 to 5.9 mmol/l) and insulin (151 to 73 pmol/l after 1 week and to 65 pmol/l by 8 weeks.

These remarkable changes happened after just one week, before much fat was lost (2,4kg), confirming that T2D is not caused by overweight.

From Lim et al 2011

“In the first 7 days of the reduced energy intake, fasting blood glucose and hepatic insulin sensitivity fell to normal, and intrahepatic lipid decreased by 30%.”

Lim et al writes that the study

“…supports the accumulating information on the inhibitory effect of fatty acids on insulin secretion in vitro and in vivo and is the first direct evidence in humans that the beta cell defect of type 2 diabetes is reversible by sustained negative energy balance. Prolonged elevation of plasma fatty acids in humans decreases insulin secretion, and it has previously been shown that there is an association between pancreatic fat content and type 2 diabetes. Prior to the onset of spontaneous diabetes in rodents, both total pancreatic fat and islet triacylglycerol content increase sharply. In vitro, chronic saturated fatty acid exposure of beta cells inhibits the acute insulin response to glucose, and removal of fatty acids allows recovery of this response.”

They may be right, in that fatty acids all over the place are to blame, but I still don’t see the need for starvation. What about just reducing carbs? It has been done before, and it has also been found to cure diabetes, despite ad libitum eating. No need for starvation.

The discussion chapter includes the necessary limitations section, where the authors are supposed to say something about the role the different macronutrients has on the pathology discussed and whether the effects can be attributed to the reduction in one of these. But there is no such discussion. Starvation cures diabetes.

Writes Lim et al

“This study demonstrates for the first time the time course of a return of normal beta cell function and hepatic glucose output by acute restriction of dietary energy intake in individuals with type 2 diabetes.”

And

“This new insight allows an understanding of the causality of type 2 diabetes in individuals as well as in populations.”

In other words; diabetes is caused by eating to damn much. Because eating less cures it.

Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R: Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia 2011.

The satiating effects of protein

2011-06-22T13:26:00.000+02:00

"The mechanisms by which protein may affect satiety remain elusive."

Halton and Hu 2004 [1]

“Although the immediate satiating effect of dietary fat may be comparatively weak, there is no doubt that ingested fat does inhibit feeding.”

Leonhardt 2004 [2]

LCHF opponents keep throwing out the same old argument, that fat is the least satiating macronutrient and that all that fat might thus make people hungry and unable to stay with the strategy. Eventually the low satiating effect of fat will cause people to gain weight. This is claimed despite the existence of several studies showing that people put on ad libitum high fat diets experience less hunger, lose weight and all over seem perfectly fine.

Protein, it is said, is the most satiating macronutrient. So the best dietary strategy is replacing fat with proteins and keeping carbs high.

My colleagues in dispute seem very eager to have me agree that protein is very satiating and that we at least should have this as common ground.

But my own experience urges me not to agree. If I reduce my fat intake and eat more protein, as I sometimes do, for example in periods of stress where I eat too much eggs and lean meat and forget about the fat, I feel horrible. My blood sugar drops and over time lethargy hits in. What’s more, I soon feel hungry and start craving fat/carb combos. Simply eating fat eases my symptoms. Eating carbohydrates would probably also ease my symptoms, but we all know that is no good long term solution.

So are proteins especially satiating?

Weigle et al [3] placed 19 subjects sequentially on the following diets: a weight-maintaining diet (15% protein, 35% fat, and 50% carbohydrate) for 2 wk, an isocaloric diet (30% protein, 20% fat, and 50% carbohydrate) for 2 wk, and an ad libitum diet (30% protein, 20% fat, and 50% carbohydrate) for 12 wk.

Weigle is good for a laugh. Here’s from the introduction of the article

“Both low-fat diets (2– 4) and low-carbohydrate diets that are high in fat and protein have been shown to cause a decrease in ad libitum caloric intake and significant weight loss in humans. Thus, it appears that diets with fat contents at opposite extremes have the same therapeutic result, despite evidence that excessive dietary fat intake promotes obesity. This paradox could be explained if it is the high protein content rather than the lower carbohydrate content of low-carbohydrate diets that offsets the deleterious effect of high fat intakes and results in weight loss.”

Quite the paradox there. Hope someone will resolve it someday.

Weigle is often cited for showing that proteins are satiating. But measurements of hunger and fullness showed that even though hunger was reduced and fullness increased during the isocaloric diet, they returned to baseline with the ad libitum diet despite constant protein content. The reason the study is sited is because calorie intake dropped with higher protein. However, satiety and calorie intake did not seem to correlate.

As in all similar studies, the high protein diet differed from the low protein diet in many aspects even though carbohydrate intake remained constant. Below is an example of what the two different diets might contain.

So can we conclude that the hunger (temporarily) and body weight dropped because of the higher protein content? Of course not. That would be silly. It might be the proteins, but it might be any one of the other differing dietary factors.

Weigle and colleagues also wrote that

“It is likely that a reduction in dietary fat by 15% of total energy contributed to weight loss in the present study.”

This is a very strange thing to claim, as several studies where subjects are put on high fat diets reports significant weight loss and reduced hunger.

Weigle concluded thusly

“An increase in dietary protein from 15% to 30% of energy at a constant carbohydrate intake produces a sustained decrease in ad libitum caloric intake that may be mediated by increased central nervous system leptin sensitivity and results in significant weight loss. This anorexic effect of protein may contribute to the weight loss produced by low-carbohydrate diets.”

Skov et al [4] randomized 65 subjects to two ad libitum fat reduced (30%) diets for six months. One with 12% energy from protein and one with 25% from protein. Weight loss in the low protein group was 5.1kg and 8.9kg in the high protein group. By labeling the diet higher in protein a “high protein diet” our focus is drawn away from the fact that the high protein diet also had significantly less carbohydrates. This is a recurring problem; how should the diets be labeled? The labeling wouldn’t actually be problem if the researchers remembered to properly discuss the effects of reduced carbohydrate intake or reduced glycemic index. This, however, is often not done and when a diet labeled “high protein diet” is discussed the protein content usually get the major part of the attention.

Skov and his Danish research fellows later wrote that

“The mechanisms responsible for the larger weight loss caused by an HP diet may be attributed to a greater satiety and fullness, and also the thermogenic effect of protein.”

But of course, they might be right. A number of studies have compared hunger and satiety in the hours following consumption of a single meal, and have come to the conclusion that a high-protein meal is more satiating. So to say that a high protein diet suppresses hunger might be a correct statement, but it’s still a bloody unfair statement. Because what matters is the long term effect on hunger, and what actually cause the decreased hunger. The studies looking at single meal effects are usually poorly controlled and there are many confounding factors. Also, the protein content of high protein meals is often very high, ranging from 40% to 75%, and most of the studies have very few participants.

One of these studies, from Stubbs et al [5] (60% protein), found that there was no difference in subsequent energy intake despite acutely reduced hunger following a high protein meal. This was one of the more well controlled single meal studies.

Thomas Holton [1] notes that

“There are, however, some methodological issues concerning this type of research. Satiety appears to be influenced by a wide variety of factors including palatability, food mass, energy density, fiber and glycemic index. When using real foods, it is difficult if not impossible to control for all of these influences at the same time while still delivering different amounts of protein.”

Fat is often considered the least satiating macronutrient from these single meal studies. But it might not be that simple. Mark I Friedman found that hepatic ATP, or the energy availability of the liver, exerts a strong effect on feelings of hunger. What is important, is that there’s fuel available, be it glucose or fat. A theoretical satiating effect of proteins is their conversion to glucose by gluconeogenesis thus providing more fuel for the liver.

A quote from Friedman

“Hyperphagia associated with the development of obesity is accompanied by a metabolic state that fosters the deposition of fat in adipose tissue, the largest fuel storage compartment. This shift in fuel partitioning toward storage is independent of and occurs before the change in food intake in nearly every animal model studied. According to the model presented here, overeating results because fuels that would otherwise be oxidized to produce ATP in a detectable manner are redirected into fat stores.” [6]

And what redirects fuel into fat stores? I’ll leave it to you to figure this one out yourself. The point is that according to Friedman’s work, a higher fat diet will reduce hunger by making both glucose and fat more available for oxidation.

Daniel H. Bessesen [7] also believes that what separates obesity prone and those prone to leanness are differences in the trafficking of fat. He writes

“It may be that a preferential delivery of dietary fat to metabolically active tissues including liver and skeletal muscle allows more accurate sensing of dietary fat in a manner that promotes more accurate coupling between dietary fat intake and oxidation. Conversely, preferential delivery of dietary fat to adipose tissue may impair nutrient sensing and promote weight gain.”

On low carb ketogenic diets, hunger is often drastically reduced within a matter of a few days after initiation of carb restriction. With fasting or starvation we see a drop in hunger with increased ketone body concentration. This satiating effect is often attributed to the ketone bodies themselves, in particular beta-hydroxybutyrate, but according to Friedman’s theory it could just as likely be caused by the increased internal energy availability that occurs when lipolysis and fat oxidation (with a subsequent increased ketone body production) are increased.

Some studies also suggest that you will experience a stronger hunger if you eat some food as mostly carbs, than if you eat no food at all.

The belief that high protein diets are especially satiating seem similar to the belief that high fat diets are fattening. Of course they might be, but as I said, it would be a bloody unfair statement. In animal studies high fat diets often do cause obesity, but normally only in the presence of a substantial amount of carbohydrates (or crazy amounts of frankenfats). The term “high fat diet” does not imply minimal carbohydrates. High protein diets might decrease hunger, but higher protein diets are usually lower in carbohydrates, sugars and have a lower glycemic index. Attributing the decreased hunger to the proteins might be just as much off target as attributing weight gain to fat.

Halton and Hu illustrates this point when they term many low carb study diets, high protein, low carb diets. Like the much sited study by Samaha et al [8]. In this study the low carb diet was a 1630kcal, 22% protein, 41% fat and 37% carbohydrate diet. Protein intake was well below 1g per kilo body weight. It produced a greater weight loss than a 1576kcal, 16% protein, 51% carbohydrate and 33%fat diet. The results can hardly be attributed to the proteins alone. Holtan and Hu, in their review of high protein diets and satiety, forget to discuss the potential long term satiating effects of increased fat intake.

Monika Leonhardt [2] seem more open and writes

“Fat seems to be less satiating than carbohydrate and might therefore lead to passive overconsumption [4]. Yet, in rodents, the efficacy of a high-fat diet to induce hyperphagia appears to be related to the energy and carbohydrate content of the diet. Therefore, overeating of high-fat diets is presumably not due to the high fat content alone. This assumption is in line with recent studies in humans showing that a high-fat, low-carbohydrate diet reduced rather than increased voluntary energy intake.”

Leonhardt continues to suggest that overeating on a high fat diet might be, amongst others, due to

“the high energy density of such diets in combination with their carbohydrate content”

“the usually low postprandial oxidation of ingested fat in the presence of carbohydrates.”

That protein exerts some acute satiating effect compared to carbohydrate and fat is hardly a good point. It is an interesting observation, but not an argument in favor of high protein diets. People put on high fat low carbohydrate diets also feel their hunger disappear and shed weight without caloric restriction. The high protein diets seem to stem from the cognitive dissonance of the upholders of the traditional dietary dogma. First fat was fattening, now it seems carbs are equally so. What they are left with are diets low in both fat and carbohydrates, diets that do not consider any of the important roles of the vast variety of fatty acids available to the body. I’ll eat my hat the day some anthropologist can show me a traditional human population thriving on a high protein, low fat, low carbohydrate diet. Fat matters.

References

1. Halton TL, Hu FB: The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr 2004, 23: 373-385.

2. Leonhardt M, Langhans W: Fatty acid oxidation and control of food intake. Physiol Behav 2004, 83: 645-651.

3. Weigle DS, Breen PA, Matthys CC, Callahan HS, Meeuws KE, Burden VR, Purnell JQ: A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. Am J Clin Nutr 2005, 82: 41-48.

4. Skov AR, Toubro S, Ronn B, Holm L, Astrup A: Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity. Int J Obes Relat Metab Disord 1999, 23: 528-536.

5. Stubbs RJ, van Wyk MC, Johnstone AM, Harbron CG: Breakfasts high in protein, fat or carbohydrate: effect on within-day appetite and energy balance. Eur J Clin Nutr 1996, 50: 409-417.

6. Friedman MI: Control of energy intake by energy metabolism. Am J Clin Nutr 1995, 62: 1096S-1100S.

7. Bessesen DH: Update on obesity. J Clin Endocrinol Metab 2008, 93: 2027-2034.

8. Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L: A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003, 348: 2074-2081.

Feet on ground

2011-06-17T16:35:00.000+02:00

When loading regular non paleo hot dogs, which besides meat were stuffed with nitrates, glucose, starches and all things horrible, I experienced a fleeting moment of guilt. I should be eating some real food. Like some grass fed beef and butter soaked veggies.

But then I started thinking about all the people in the world who continually eat corns, vegetable oils, legumes, sugars, toxic additives and so on who live long lives and who most of the time do not appear very sick.

Reading paleo health literature you might get the impression that everyone who bases their diet on the things we learn should be avoided would simply fall apart, rot from the inside out and become inflamed to the point of combustion.

But they don’t. There are people all around me living on what I would call a crappy diet, and they are fine. Sure some infections and pains could probably be avoided and perhaps they could feel just a little better, but that’s not the point. The point is that they’re fine. Most people around me are grain based. Athletes and sedentary alike on low fat, high fructose, high corn diets, and their doing fine most of the time.

I know we are sick animals, us industrialized humans. Most of us probably do not know what it feels like to be in good health most of the time. But knowing what I do about nutrition and the effects of food on the body I am surprised at how little I or any other paleo(ish) stand out. Where are the superpowers? Why aren’t we more different?

Even considering that most people are sick most of the time or that we are only beginning to see the ill effects of the way we live, I have to admit to myself, that the difference between those living on healthy diets and people living on diets composed of the thing I shun, are not as big as I might be inclined to think.

I am not trying to, nor do I want to downplay the effects of healthy diets. Diet matters and it matters more to those dealt the worst genetic cards.

I just realized that this perspective was missing in my mind and that it should be there to keep me from getting airborne. To keep my feet on the ground, as I am constantly fighting an urge to be carried away and at the same time I’m truly baffled by the results some achieve by lifestyle changes.

Just a thought…

The As Good Health As Possible Diet

2011-06-14T12:17:00.000+02:00

Never eat more than you can lift

– Miss Piggy

I think some who decide to write a diet book, hope that it will be the diet book to end all diet books. The final solution. I also believe that most who publish diet books are more interested in earning quick bucks than putting a final end to obesity and poor health.

I do feel that there is no need for any more diet books. The multitude of diet books with different strategies serve only to confuse the masses. Books about nutrition are a different issue. The field of nutrition is scattered with holes of ignorance desperately needed to be filled by new knowledge.

Still, I would like there to be one diet book. One book that is constantly updated with new research. It would be The Diet Book. The book that made all other diet book superfluous. The go to place for everyone interested in achieving good health. The only book we would need.

It would not have to contain all aspects of nutrition, only the most important parts, and the parts we know for surest. It would also have to be understandable for most people, perhaps come in a simplified short version.

This vision is of course what governments are going for in making nutritional guidelines. Guidelines composed to give us as good health as possible and at the same time presented in an easy to understand form. The trouble is that national dietary guidelines will not get you close to optimal health. They can only improve your health if your diet is already complete crap.

The one book I’ve found that comes closest to being the diet book to end all other diet books is Perfect Health Diet. Had it replaced the official dietary guidelines we might actually be getting somewhere. The Perfect Health Diet book is not a perfect book, nor should it be. I think that some of the composition could be improved as well as the lay out and I would’ve liked to see some statements moderated, but content wise and information wise, Perfect Health Diet appear as a good first draft of a book with the potential to end the need for any more diet books.

I am excitedly looking forward to the second edition. In the meantime I will enjoy the Perfect Health Diet blog which today celebrate its one year anniversary.

Fat people are liars

2011-06-10T15:58:00.000+02:00

Obviously! Obesity is a remarkably simple problem to solve. Eat less and move more. When energy expenditure exceeds energy intake, you lose weight. Many people claim to have tried eating less and exercising more and claim that it does not work. As this would be a violation of the laws of thermodynamics it is quite unlikely.

Not only do overweight people claim to break the fundamental laws of nature they also constantly lie about how much they actually eat.

Elaine Prewitt and coworkers examined the effect of a 37%-fat (HF) diet for 4 weeks followed by a 20%-fat diet (LF) for 20 weeks on body composition and weight in 18 premenopausal women with body mass index (BMI) of 18-44. They found that

Despite adjustments in energy intake to maintain weight throughout the study, by the end of the LF period, energy intake had increased significantly in comparison with the HF diet (119% of the HF intake, P < 0.0001).

The authors knew what kind of people they were dealing with and wrote

We have no means of assessing the degree of food waste by subjects when meals were taken out but there was no reason to attribute the magnitude of energy increase we observed to overreporting of dietary infractions. By contrast, one would expect the subjects, particularly obese subjects, to underreport extra foods eaten.

W. Daniel Schmidt and coworkers exercised overweight women. All study groups were put on an energy restricted diet. The control group only dieted without changing exercise routines, but somehow they didn’t lose any weight. The authors write

The fact that the control subjects in our study did not lose weight is perplexing and conflicts with other research that generally supports weight loss with caloric restriction [17, 18]. One explanation may be that subjects simply underreported the amount of calories consumed, thus making this an issue of noncompliance.

Not only are fat people liars, but fat people on low fat diets are the worst. James Krieger, everyone’s favorite researcher suggests that

…subjects on low-fat diets systematically underreport energy intake compared with subjects on low carbohydrate diets.

In support of his theory he cites a study where weight loss from a low fat diet did not turn out as predicted.

Fat people on low fat diets are not only the worst liars around, they are also not very smart. Kelly A Meckling and coworkers compared a low fat diet to a low carbohydrate diet in overweight men and women. They write

Energy restriction alone predicted a weight loss of 5.5. and 6.9 kg, respectively, in the LF and LC groups, which was close to the observed values of 6.8 and 7 kg for the same groups. Slight differences, particularly for LF subjects might be explained by underreporting of habitual diets, as the subjects became better able to estimate their intakes and keep better food records as the trial proceeded.

Those put on a low carb group obviously nailed the food reporting task right away, even before they actually were put on the diet, and missed the predicted weight loss by a mere 100 grams.

Everyone knows low fat fatties are the worst. Thermodynamics applied to food and the body is very simple, yet predicted weight loss are often not achieved by low fat fatties.

Writes Jennifer B Keogh and colleagues (when a low carb group lost more weight than a low fat group in their study)

Greater weight loss with a low-carbohydrate diet than with a conventional low-fat diet has been reported previously (2– 4, 57). Subjects in these studies reported similar energy intakes despite differences in weight loss, which suggests that the conventional diet group underreported their intake (3, 4, 57).

A group of Dutch researchers set out to test the extent of underreporting in 30 obese men. Their conclusion:

Total underreporting by the obese men was explained by underrecording and undereating. The obese men selectively underreported fat intake.

Not only did these men lie about how much they were eating, they didn’t even eat as much as they should have. They underrate. Those bastards!

If by chance you are wondering if the methods of the Dutch researchers were bulletproof, they weren’t. Still…

It is possible that overweight people underreport more than lean people. But people seem to think that the underreporting somehow is the reason they are fat. They don’t know how much they eat and so they stuff themselves and grow fat.

But are fat people fat because they underreport and lie, or are they perhaps underreporting because they are fat and afraid of being stigmatized as gluttonous and desperately trying to keep some of their dignity?

Listen to your body, but question its objectivity

2011-06-06T17:11:00.000+02:00

I’ve not much to say these days and I believe that when there’s nothing more to say, a good rule is to shut up.

Luckily there are others who still have working brains and who have something interesting to say. Also, shutting up and reading goes great together. I'll finish up the Perfect Health Diet book, which so far is great. But all those skilled bloggers out there (the Jaminets included) make it difficult to find time for book reading.

Dr.Eades tells us not to listen to our body, or at least not act on what it tells you, in what might be a great new series.

Jamie reminds us that ingestion does not mean absorption. Although he's talking about zink, the rule is general and worth remembering.

Stephan brought up a really interesting, but controversial aspect relating to overweight recently. Food reward. Paul and Emily, among others, keep the discussion going, and I'm looking forward to Stephans future reflections.

Richard D. Feinman gives you a reason not to trust us Norwegians, which you shouldn't (those socialist bastards).

Toms "wheat is murder" t-shirts are hilarious.

Oh, and remember to always stop by Hyperlipid for some nerdy fun.

PS. Names are for clicking.

What drives me to move

2011-05-23T17:35:00.000+02:00

’I can’t tell you how wonderful it was’, she told me. ‘I walked into this room, and it was full of people like me. People who couldn’t sit still. People who had to move to think.’

Ken Robinson, The Element

I do some temp work at a local school. Noticed a boy in the top of a school yard tree the other day. I know he is one of those 14 year old boys who are completely unable to sit still for an entire class. That day, the first thing he did during break was to climb a tree. Because the tree was there.

If you place a running wheel in a rodent cage the animals will run. They will expend more energy and of course increase their food intake. But there is no need for rewards or incentives to get them to run. They thoroughly enjoy it. There is an inherent drive to run. It is in their nature.

A good fat metabolism will most likely make you active. Some people just can’t sit still. They are fat driven machines. If they can’t run they radiate heat and fidget non stop. These people are usually lean, which is the reason they can't sit still.

Adam Kennedy and colleagues put mice on a ketogenic diet, a common obesogenic high-fat, high-sucrose diet, a 66% caloric restriction diet or control chow.

Mice on the ketogenic diet ate the same amount of calories as both the mice on control diet and the high fat/high sugar diet, but their weight dropped and stabilized at 85% of initial weight.

Analysis of energy expenditure in the high fat/high sugar and the ketogenic groups revealed an increase in energy expenditure in ketogenic diet animals. Total heat output was 15% higher in the ketogenic group.

Some nice quotes from the study authors.

Somewhat reduced exploratory activity was seen in HF [High Fat] animals compared with C-fed [chow] animals.

The somewhat surprising preservation of fat mass in calorie-restricted animals has been described previously.

Thus, although severe caloric restriction is known to cause fat mass loss in rodents, metabolic adaptations prevent fat mass loss during moderate CR in mice and even permit a small weight gain...

Insulin levels were somewhat reduced in calorie-restricted animals compared with the chow-fed group, whereas insulin levels in ketogenic diet-fed animals were dramatically lower to a level that was only 10% of that seen in the calorie-restricted group.

Give rats sugar, and they become passive, give them fat and they radiate heat. I am not sure if Kennedys rats had access to a wheel, but it would have been interesting to also have measured voluntary wheel running, which is easier to measure than exploratory activity.

You can breed mice to become wheel runners. These are so called “High Runner lines.” It is probably much worse for these mice to be deprived of their wheel than it is for other mice. It is also much worse to ask a human with an effective fat metabolism to sit still, than one operating on a lower gear.

In a somewhat interesting article entitled, The biological control of voluntary exercise, spontaneous physical activity and daily energy expenditure in relation to obesity: human and rodent perspectives, the authors note that:

...food consumption increases in the presence of wheels, at least in rodents.

I do not get leaner and leaner the more I exercise, and this seems to be quite a universal human trait. This means that there must be a compensatory mechanism, and this mechanism has to be increased food intake or decreased non exercise energy expenditure.

In studies of human subjects confined within metabolic chambers for 24h, Ravussin et al. found that SPA [Spontaneous Physical Activity] varied widely and was a rather strong positive predictor of DEE [Daily Energy Expenditure] (Ravussin et al., 1986). They commented (p. 1577) that: “Because the subjects were not allowed to carry out physical exercise such as isometric exercises or calisthenics, it is possible that such activity represents an unconscious need to be active.” The implication is that forced reduction in voluntary exercise may lead to an increase in other types of physical activity.

Garland et al 2011

We move to little and this is making us fat. At least this is what those less informed are trying to convince us.

Westerterp and Speakman provide evidence that physical AEE [Activity Energy Expenditure] has not declined over the same period that obesity rates have increased, and argue that it is unlikely that decreased DEE has been a major contributor to the human obesity epidemic.

Garland et al 2011

Even though obesity rates seem to increase universally, reduced physical activity do not seem to be a universal phenomenon. In Canada and Finland physical activity trends seem to be increasing while USA has hit a plateau. England and Australia though seem to have decreasing physical activity trends.

Based on this retrospective application of the energy balance equation, many investigators and public health officials have used the same energy balance equation in a prospective manner to predict that the obesity epidemic can be addressed by initiating changes in energy expenditure or energy intake as small as 25–50 kcal/day. From the energy expenditure side of the equation, 25–50 kcal/day can be spent by walking an additional 750–1500 steps per day. From the energy intake side of the equation, energy intake can be reduced by 25–50 kcal/day or by eating one less cookie, or forkful of food each day. Although this use of a valid retrospective application of the energy balance equation to a prospective prediction appears quite valid, it is not an equivalent situation. The prospective application of the energy balance equation for a single change in energy intake assumes that energy expenditure will not change in response and that a simple change in energy expenditure assumes that energy intake will not change in response. Evidence, however, does not support this assumption.

Schoeller 2009

The world is a funny place, but exercise will not make a fat person lean and simply eating less is a poor weight loss strategy. This, at least, we know.

Physical activity and weight loss

2011-05-12T13:00:00.000+02:00

Physical activity is a poor strategy for weight loss. Still, all around the world, clinicians and health personnel are chasing fat people around, getting them to move, move and move even more. When, in the end it becomes clear that moving more doesn’t affect weight, the blame is often put on the overweight. They must be doing it wrong, they’re too lazy between exercise bouts and they are obviously stuffing themselves.

Jakicic et al recently conducted a trial where participants were divided into three physical exercise groups differing in activity doses. With no dietary change recommendations they wanted to show the 18 month effects of either 150 min PA/week, 300 min PA/week or a self help group provided a self help intervention to increase PA.

278 overweight subjects were included. The PA interventions included behavioral interventions, individual exercise and some group sessions. The self help group were given a manual and a monthly newsletter, seemingly to inspire change.

So how much weight do you lose if you exercise 150 min/week for 18 months? 0,7kg!

Then what about 300 min/week? 0,8kg!

Being given newsletters and a pamphlet results in 0,5kg weight loss.

To be fair, these are intention to treat analyses, and so the results show the effect of being told to exercise rather than actually doing the exercise. Still, reported increased caloric expenditure per week was 442kcal for self help, 348kcal for 150 min/week and 832kcal for 300 min/week.

The authors did a secondary analysis where participants were grouped based on whether there was weight gain, weight loss, or weight stability. This analysis showed that a small weigh loss is possible and managed to obscure cause and effect completely. Luckily the authors are aware of this and writes:

Despite these findings, concluding that PA alone can result in the magnitude of weight loss observed in WT-LOSS within the retrospective secondary analysis may be misleading. There is some indication that participants classified as WT-LOSS, who lost 7.4% of their body weight compared to baseline (Table 3 and Figure 2) also made significant changes in their eating behavior as measured by the EBI questionnaire (Table 3), despite the lack of an intervention promoting a reduction in energy intake.

And how do they conclude?

In summary, the mean change in body weight resulting from an intervention that promotes 150–300 min/week of moderate- intensity PA with no reduction in energy intake is <2.0 kg. However, ~25% of subjects lost >3% of their initial body weight in this study, with these subjects categorized retrospectively as WT-LOSS for secondary analysis. Individuals categorized as WT-LOSS for these secondary analyses do appear to be more compliant with initially increasing PA by 245 min/ week and maintaining an increase of at least 161 min/week at the conclusion of this 18-month study.

In somewhat simpler terms, physical activity can produce a small weight loss and if you don’t lose any weight you’re not doing it right.

Lack of balls or lack of brains?

2011-04-10T18:58:00.000+02:00

In my last post I hinted strongly at the occurrence of cognitive dissonance in a recent editorial. I don’t actually think there is much dissonance out there in the world of science. People aren’t really suffering emotional distress from feelings of holding conflicting ideas. Those who sense something is wrong usually acknowledge it and resolve their confusions. Most often when we find obvious contradictions in the same texts in scientific journals I think there are two main reasons; Lack of balls and lack of brains.

Lack of balls is a naturally occurring phenomenon due to the peer review system. If the editorial mentioned in my last post had concluded that carbohydrate restriction is the solution to all our problems it probably wouldn’t have been published, and we would have missed out on all the good stuff that was also in it. Somewhere along the way the writer possibly swallowed a medium sized camel and experienced the consequent testicular shrinkage.

Lack of brains is also no rare happening. Either as lack of actual thinking power or lack of brains for dinner, the two are closely related. Still, dissonance is rare. Pure stupidity, I believe, more frequent. Many, simply do not know any better.

I finally finished Lindebergs “Food and Western Disease: Health and nutrition from an evolutionary perspective." Despite the joy of finally reading this exiting book, at closing the book after reading its last page I felt a strong sense of disappointment. Lean meat! LEAN MEAT! Come on, Staffan.

Here is a book with tons of great science, nearly two thousand references and a great and interesting study to top it off, but when the author seem to miss some of the absolute basics about fat and disease, I find it unlikely this is due to fear of not getting published. It seems his honest opinion. On top of it all, Lindeberg clearly over interprets many studies. Often, the references do not support the statement they accompany and the belittling words that should have been there with the statement, are left out.

So I’ve been thinking a lot lately. Are my standards to high? How can I get so disappointed because of a few blunders in an otherwise great book? Nobody’s perfect, I know, but I just so much want someone to get everything right, or at least all the important stuff. Reading books about diet can be tedious, as I am sure many of you agree with. We're all looking for that one book to make all other books in it's field superfluous.

The one thing I do know is that I can't keep going with my standards at the currant level. It'll only make me an angry, stressed out old man. Right now there is too much non sense out there, and I need to find a way to deal with it.

So I'm taking a break right now.

You want cognitive dissonance? I’ll give you cognitive dissonance!

2011-03-28T18:26:00.000+02:00

The latest issue of Obesity offers both welcome rationality, important discussions and good chances of some decent hair pulling.

It features an editorial by Jean-Pierre Flatt from the Department of Biochemistry and Molecular Biology, University of Massachusetts.

Flatt gives us an insight into some important misconceptions about obesity. He even made us a list of contents:

1. Problems in applying the energy balance concept

2. Problems with the metabolic efficiency concept

3. The misleading emphasis on the importance of low resting metabolic rates

4. Misleading expectations about the importance of adaptive thermogenesis

5. Problem in judging the importance of de novo lipogenesis and of its metabolic cost

6. The irrelevance of the “nutrient partitioning” concept

7. Failure to recognize the greater impact of energy intake than energy expenditure

8. Difficulties in understanding food intake regulation

9. Conditions for body weight stability: settling point vs. set point

10. Problems with the application of the RQ/FQ concept

11. The “defense of body weight” concept

12. The different roles played by CHO and fat in energy metabolism

13. Food intake regulation and carbohydrate balance

14. The difficulty in obtaining experimental evidence about the role of carbohydrate balance in food intake regulation

15. The need to distinguish between the role of carbohydrate balance in food intake regulation and the role of habitual glycogen levels in body weight regulation

16. Understanding the recent increases in the preponderance of obesity

17. Why don’t people eat even more?

18. Confusion about the leverage of exercise on body weight

19. Is dietary fat or is dietary CHO the major culprit in causing weight gain?

20. How can inherited traits influence body weight regulation?

21. The leverage of inherited vs. noninherited factors

22. BMI vs. % ideal body weight

Lots of interesting stuff right? Right. There is lots of interesting food for thought in the editorial and much is welcome food. For instance the problems with the energy balance concept, and:

The use of settling point rather than set point:

This corresponds to a “settling point” (20). Such a view accommodates the fact that circumstances cause weight stability to occur for various degrees of adiposity. Thus it seems to fit reality much better than the concept of a "set point" or "ponderostat".

It has sometimes been considered that “set-points” are reset for different conditions, but in effect this argument reduces the set-point phenomenon to a settling point.

I agree with him that saying the body is "defending" itself against body weight change is not a very helpful thing to say:

The common tendency of individual body weights to return to their original value after a weight-changing intervention is often explained as the manifestation of a mechanism tending to “defend” a particular body composition. The problem with this concept is that it appears to imply that mechanisms exist to actively drive the fat mass to a particular level, much as one would expect if a set-point mechanism existed (21). It fails to take into consideration that before the intervention, body composition for a given individual had already evolved until a steady state of weight maintenance had become established.

He even mentions Mark Friedmans work on how liver substrate oxidation rates affect hunger, work I have previously written about on this blog.

And he even acknowledges that exercise reduces weight by glycogen depletion and increased fat oxidation rather than by acutely increased energy expenditure.

But most of all, he talks about the importance of glycogen storage in obesity.

Thus, the role which increased habitual glycogen levels will play in promoting obesity in humans needs to be recognized!

And the dissonance?

After elaborating thoroughly on the importance of glycogen stores:

“In view of the considerations made above, it is not surprising that a high incidence of obesity is typically encountered in sedentary populations consuming diets providing substantial amounts of fat.” (my bold)

You can pull your hair now. It never seizes to surprise me how so much smart and something so incredibly stupid can be crammed into the same text.

Heres another brainmusher for you:

Thus the answer to the question asked above is that the major culprit is the unrestricted and ubiquitous availability of a mixed diet, offering numerous appetizing foods, often in large portions, in which sugar, and to an even greater extent fat, contribute to raise the energy density.

Spring cleaning, truth and disagreements

2011-03-26T21:24:00.001+01:00

There!

Spring cleaning. All freshened up – away with bricks and Banksy and bombing.

The truth
We are all confused (some more than others) about what to eat – which foods are good for us and which are not. We’d all like to know this, to learn once and for all which foods give us the best health. It’s all just so bloody confusing.

There is one thing, though, that we have to keep in mind if we want to know the truth about healthy foods. Or rather, there is something to realize. And here it is:

Some things are right and some things are wrong. Sometimes there is only one right answer, and when one thing is right, everything else is wrong. Sometimes things are either black or white with no shades of grey. There are such things as truths.

Only very narrow minded people think that there are always more nuances. They are narrow minded because they exclude the possibility of non gradation. This is a problem. It is a problem because this idea of there always being more sides to a story gives rise to the idea of everything in moderation – the golden mean. There is nothing strange about this response to confusing information. We are not all experts and most of us do not have the time to dig into the literature and by ourselves solve any disagreements. So we keep away from extremes. It’s a balancing act.

But if your goal is optimal nutrition and optimal health, the middle way is the wrong way. Nothing in nutritional science indicates that this is an effective way to reach our goals. Most likely you will end up eating too little of some nutrients and too much of others. And I know many nutrients are essential in one dose, optimal in another and toxic in higher doses. Still, this does not in any way indicate the middle way to be a good general rule. For optimal health you need the right amount of nutrients, nothing more nothing less.

Unfortunately, government nutritional guidelines are a version of “everything in moderation.” Not too much fat, a little sugar, some fiber and some protein and a little salt. This means that if your diet is utter crap, starting eating as official guidelines recommends, will likely improve your health. However, you will never have an optimal diet. This requires rather more rationality than what is offered by the official guidelines.

The disagreements
What appear to be scientific disagreements confuse us into dietary mediocrity. But the disagreements themselves are rarely scientific. Whenever you see two “experts” arguing about what constitutes a good diet, remember that any scientific data by itself is objective. It is what it is. But the data has to be interpreted by people, thus making it subjective. It is interpreted by people with very different amounts of total and subject specific knowledge, and with varying potential for rational thinking.

This means that whenever “experts” disagree on basic knowledge there are two likely scenarios. Either one of them is right, which means the other is wrong. Or they are both wrong. I’ve said it before and I’ll say it again. We cannot disagree more than the evidence permits. A disagreement is not a matter of opinion. There is no room for opinion in science. A disagreement is either a sign of lack of knowledge in one or more of the disagreeing parts or a sign of an underlying agenda not related to science in one or more of the parts.

Taubes and Oz disagreed about the dangers of saturated fat. They might both be wrong, but they can’t both be right.

My beloved science and me

2011-03-11T23:43:00.000+01:00

I am no expert on anything, except perhaps on being me, of which I have an entire lifetime of experience. I don’t know much about biochemistry, about anthropology, anatomy or physiology in general. I got through my entire low quality typically Norwegian education in sport sciences almost completely without taking notes (it’s difficult to listen to a lecturer, think, and take notes at the same time) and without top scores. I have a terrible memory and often read my own blog to learn new things. In fact one of the reasons I started writing things down here was simply to have a place to put down my thoughts so that I could find them again. I am no expert and no one reading this blog should make the mistake of considering anything here expert advice.

But I like science. The reason is that I’d just like to know the truth. I am not interested in believing and the only way to find truth, as far as I know, is to use science. We all start out as scientists and we all know how to use science when we are born. From day one we are doing our very own n=1 study. What happens when I eat this? What sort of reaction do I get when I pull this down? The results are recorded in neurons and we test and test and test.

After a while though the brain starts living a life of its own, and we believe things not tested, we suppose and assume and depend on rational guidance to not lose touch with reality.

The urge to believe is strong. Superstition, which is one of those evolutionary obstacles on the course to rationality, is a good example of this. You wore your blue shirt to that meeting that went just perfect, and when it is time for a new meeting there is an urge to yet again pull out the same shirt, because it might be that the shirt matters. Another great meeting and the likelihood of a different shirt being worn to an important meeting gradually diminishes. Athletes engaging in competitive sports seem particularly prone to superstitious thoughts.

Superstition still makes perfect sense in light of evolution, as most things do, but luckily we can fight even evolution. Our irrationality can also be blamed on evolution. Believing that the stars are fires on the eternal hunting grounds of the afterlife or that somehow everything is linked to a carpenter being nailed to a piece of wood for saying people should just try to get along, is believed because our brains have evolved little protection against these sorts of thoughts. But this lack of an irrationality force field can make the search for truth difficult.

I am no expert, but I’d still like to know the truth and I fight the propensity to believe every day. That being said, I don’t think you have to be an expert to understand the general theme of healthy living. Much of it makes perfect sense and much of the rest requires a strong belief held despite the nature of the evidence.

Eating foods found in nature and not those invented by humans makes a lot of sense. Not accepting this requires some faith. Eating animals also makes a lot of sense as most data suggest it to be wise, while not eating animals requires belief in something other than nature (if you ask a vegan he might say he believes in nature, but that’s just self delusion. He believes in his self delusion).

Grains worry me. Admittedly I haven’t looked at the data on this subject very thoroughly. It seems to me the data arguing against grain intake is not that strong. I would have liked to have some RCT’s and some more anthropologic data from hunter gatherers. But the data are strong enough to have me worried, and strong enough to make grains nothing more than an occasional exception to my diet.

In all likelihood you do not have to eat a low carb diet to be healthy. Anthropologic data has shown us that humans can and do live as hunter gatherers on a relatively high carbohydrate diet without being plagued by the diseases of civilization.

I feel there are two important notes shat should be made regarding optimal diets. Firstly, although humans can thrive with good health on high carbohydrate diets, this does not exclude the possibility that we can thrive even more and improve our health more by replacing some of the carbohydrate with fats and protein. The Kitawans were healthy, but could they have been healthier? Secondly, although the evidence clearly indicate a natural, Paleolithic like diet with minimal grains, plant oils and processed foods as the optimal diet for maximal health, as a (wannabe)scientist I cannot take this to mean that we will not find an even better alternative. I am, and have to be, open to the possibility that we in the future might grow meat in the laboratory that far exceeds the nutritional quality of any natural meat, that we may make genetically modified foods that should replace natural foods or that we in the end will compose our diets of highly processed even plant based foods which might be the best human diet ever achieved. Technology is cool and the speed of scientific progress is astounding. I can’t wait to see what the future will bring. For now though, natural paleo like diets are our best alternative.

Science like most human endeavors is also affected by fashion and trends. There are even scientific journal with names like “Trends in molecular medicine” and “Trends in cell biology.” The latest environmental fashion is climate, which seems to be changing rather more than most people like it to. It’s a fashion though, and I dislike the reduced focus on other major environmental disasters. Physics has string theory, which has been all the hype for some time. Paleo is a trend in nutritional science and I think leptin perhaps is losing its popularity.

Strangely, it took a fashion designer (my wife) to give me a good scientific analogy for the changing of trends and how we perceive them. Fashion is after all both defined and plagued by ever changing trends. She proposed that trends are like the ever moving tectonic plates, but there is always a constant and stable core. Sometimes we get caught up in the ways of the plates and forget about the core.

The important thing to remember about trends in science is to not confuse popularity with importance. A new and exciting theory can shift our focus like a pair of boobs passing through the vision of a human male, but its importance must be questioned.

I sometimes think that as a scientist I should be open to anything. If new data emerge from good methods they should be accepted despite any of my previous certainties. I also think that not all things need to be studied. We do not need to do a scientific study to find out if it is dangerous to jump out of an airplane without a parachute, because common sense, a well developed human ability, predict the outcome of these actions and tells us what the result might be.

Unfortunately, this view – the conviction that some things need not be tested because rationality and common sense dictate them to be true – can also be used to halt science. This has happened in some scientists who do not think any more dietary trials are necessary because we already know fat is fattening. Or that no more trials of physical activity to treat obesity are necessary because we already know exercise makes us thinner. It is common sense and regarded as established as gravity.

So we need to have an open mind, albeit not so much that our brains fall out, the prime example being alternative medicine which in all aspects apart from a deity seems equal to religion.

Nutritional science like any science is a mental obstacle course where the true way is along a rope that is not spanned high in the air, but only just above the ground. It seems intended more to cause stumbling than to be walked upon.*

*Franz Kafka

The setpoint hypothesis revisited

2011-02-26T17:45:00.000+01:00

The homeostasis

(hō'mē-ō-stā'sĭs): The ability or tendency of an organism or cell to maintain internal equilibrium by adjusting its physiological processes.

Humans are warm blooded and the enzymes that make us, require a certain temperature to operate optimally. The water and ion concentration of cells must remain at a certain level to allow for normal cellular processes to occur. Homeostatic processes make us able to adapt to environmental changes. Feedback mechanisms are responsible for maintaining particular levels of processes. Most processes allow for some variation, but if pushed too far in one direction the process may break down.

Body temperature is maintained by thermoreceptors communicating with our hypothalamus, by sweating, vasoconstriction and dilation, hairs standing on end, shivering, shifts in metabolism and other. All of these factors work in unison and affect each other and by doing so maintain our body temperature at around a rough mean.

During energy restriction we get hungry, our thyroid hormone levels decrease, non essential processes like that of reproduction is down regulated, and energy expenditure goes down. It is difficult to make people gain weight by overfeeding and it is difficult to make people lose weight by underfeeding. The feeding always affects energy expenditure. Thus body weight or some level of cellular mass is required for survival and the body is self regulating to make sure sufficient tissue mass is present for survival and eventually reproduction.

None of this justifies the use of the term “setpoint” in body weight regulation.

The set point

“Again, this supports the idea that the body has a body fat mass 'set point' that it attempts to defend against changes in either direction. It's one of many systems in the body that attempt to maintain homeostasis.”

Stephan Guyenet

Although I have much respect for Stephan Guyenet and appreciate his very fine blog, I don’t understand his focus on the body fat setpoint. I don’t understand anyones focus on body fat setpoint for that matter. I’ve never felt comfortable using the “setpoint” word when it comes to body weight regulation. It makes me think of a glowing red number etched into my hypothalamus. “15 kg fat” NO MORE, NO LESS. It does not feel very “organic” to have a set point and I’m pretty sure I am organic. But of course, no one is claiming there is a number etched in my brain.

When it comes to the body fat setpoint, I rather like the lake comparison. A lake can for those less informed seem to have a set point of water level. Despite rather large fluctuations in temperature, evaporation and water going into and out of the lake, the lake maintains it water level because the factors mostly responsible for the level influence each other. This does not mean that it is difficult to change the level, nor does it mean the lake "attempts to defend against change." Build a damn dam and the water level will go up. Drain it, and the level goes down. It’s not very hard, you just have to push the right buttons.

If our fat mass changes through life and in various situations and in fact is not that difficult to change, then why the hell say it’s a set point? It’s obviously not very set, is it? Most of the time we are gaining and losing fat at pretty much equal speeds, although with constant variations around the mean. The fact that the fat storing and fat using process does not spiral out of control either way, that most of us don’t get very lean or very obese, would mean that there is a control mechanism, a feedback loop or a set point. But all the body’s processes are regulated. We are self regulated and all processes work best around a given mean determined by the nature of the very process and the processes it affects or is affected by.

A homeostatic process must have a level to operate on. It’s the way the world works. The level can usually be changed by modifying the factors that make the process.

Stephan Guyenet claims that one criterion for the cause of modern fat gain is that it “…has to cause leptin resistance or otherwise disturb the setpoint.”

What I don’t understand is, why can’t we say disturb the “regulation of body weight”, “the metabolism” or “the process.” Why “disturb the setpoint”?

The language

“..the body doesn't want to lose weight. It's extremely difficult to fight the fat mass setpoint, and the body will use every tool it has to maintain its preferred level of fat: hunger, reduced body temperature, higher muscle efficiency (i.e., less energy is expended for the same movement), lethargy, lowered immune function, et cetera.”

Stephan Guyenet

Whenever body fat setpoint is discussed it seems the body is at war with one of its processes. Why turn it into fight? Obviously it is not that difficult to “fight the fat mass set point”. I’ve asked people who’ve lost weight who said it was easy. What’s more is that they have stayed lean with ease. The setpoint hypothesis was invented mostly because people didn’t lose weight by eating low fat and that they often regained lost weight. Now, I could try to change the water level of a lake by drinking the water through a straw, and when failing I could conclude that the water level is “extremely difficult to fight”, but it wouldn’t be a very good conclusion.

I believe firmly that our language is a great obstacle for scientific progress. The main reason is that it is very hard to imagine things that cannot be put into preexisting words. Also our minds operate within the boundaries of our language and language will limit the things we can imagine. I think quantum physics is a good example of an area in which the language simply is not sufficient. The electrons can be in several places in the same time. Some things are both particles and waves. Matter consists mostly of empty space and so on. On top of it all, once words are set, once something is described in a particular way, it usually stays that way.

In Guyenets posts about the body fat setpoint, the word setpoint is often given with quotation marks, like in the above quote. I can only assume that this means that the word setpoint is not an accurate description of what he is talking about, that it is not actually a set point, but that it is used for the lack of a better word.

Guyenet also writes extensively about leptin. Leptin is an interesting protein, but it is just one of those signaling molecules involved in the homeostatic regulation. Of course weight will change if we or nature messes with leptin, its receptors in the hypothalamus or any other involved part. But the existence of leptin does not justify the use of the setpoint term.

Body fat mass can be quite easy to change so why the hell do we need the setpoint? I feel the word contributes nothing to our understanding and if anything just complicates the matter more than necessary. How about adding a muscle mass setpoint and a bone mass setpoint? How about a hair growing speed setpoint or a saliva setpoint? Does it help our understanding?

I do not think the use of the word setpoint is neutral. It affects out thinking and I am afraid its existence is a net negative contributor to the science of body weight.

On the website of one of the leading obesity clinics in Norway we are told that the clinic bases its work on the setpoint theory. They call it theory, but talk about it as an undeniable fact. This is a problem because the hypothesis rests on the assumption that weight loss is inherently difficult and that the body (in the words of Guynet) “will fight” that weight loss. It is not a very positive attitude. Remember that the setpoint hypothesis saw light of day partly because losing weight through traditional (eating less) methods did not give the expected (based on thermodynamics) results and that people constantly regained lost weight. The clinic thus operates on the assumption that it may take years of hard work to change the setpoint downwards and that it takes a very short time to change the setpoint upward (that the body "gets used" to a new higher level of fat mass).

What if the obesity clinic, instead of basing its treatment on setpoint theory (forcing overweight people to starve and doing insane amounts of exercise), said that weight loss does not have to be difficult and lasting weight loss is possible? What if they read some real science, pushed the right buttons and stopped torturing people? The studies are out there. It really does not have to be difficult. The metabolism must be altered, mostly through changing the hormonal milieu and reducing inflammation thus achieving a homeostatic regulation at a lower amount of body fat mass. And there is little evidence it has to take years to do so.

The conclusion

"When something seems ‘the most obvious thing in the world’ it means that any attempt to understand the world has been given up."

Bertolt Brecht

If the point of this rambling is lost on you, let me try to sum it up.

The body fat “setpoint” is just a word used to describe a level of a self regulating biological process.

To call a certain mean level of a homeostatic regulation a set point is unproblematic. As far as I can see, this is how Stephan Guyenet uses the term. But when medical professionals use the setpoint hypothesis to argue that body weight loss by nature is difficult and near impossible, we have a problem. The continued use of the expression seems to affect both medical professionals and researchers in a negative way, because it closes their mind for other possibilities, among them that weight loss from a physiological point of view is easy if you just push the right buttons. That we do not always know what these buttons are does not mean weight loss must be difficult, only that we are ignorant. Many aspects of metabolic regulation are under our control. Most important of all is that the level of homeostatic regulation of body fat called the setpoint, seems to be determined by what we eat.

Kurt Harris, the messiah, the hype and the throwing of scales

2011-02-12T22:07:00.000+01:00

I think Kurt Harris is a smart man and makes some very good points now and then, not to mention his reading list resembles my own. But reading his blog recently I keep thinking of Monty Pythons Life of Brian. For those less versed in the film (shame on you!), Brian is mistaken for the messiah and tries his best to convince a rapidly growing crowd that he’s not. But whatever he does, it is taken as a sign and further confirmation that he is the messiah and he can do nothing wrong.

Dr. Harris stopped blogging for a while, which somehow seemed to increase his blogging status. He disabled his comments section and I bet that also increased his standing. In a recent post he talks about the important fact that people are focusing too much on stupid details and forgetting about true science, the bigger picture and how to relax and enjoy life. According to Harris in the “do no harm” post: “I've had more laudatory emails and fresh donations (Thank you all!) as a result of this post than any I've written in a long time.”

Kurt is the new Brian. “Therapy versus Life,” has an important message and despite how obvious it is, it needs to be repeated. Worrying about the lectins in the beans you just ate or whether or not you should add an extra t-spoon of coconut oil to your daily diet will only take down a road you really don’t want to go. It will not make you live longer or happier!

Sure, a good diet can make life better, you might lose weight and be more toned. But life’s there to be lived. I advocate a diet mostly free of modern foods and I am really interested in finding answers about what foods affect the body in what way and what exercise is the most effective and so on. But I’m constantly working hard not to lose my head (and perhaps overcompensating a bit) and under no circumstance am I willing to give up beans with my bacon, beer or ice-cream or sugar (yeah that’s right, glucose AND fructose) in my daily cup of earl gray tea. Oh, and I’ve been exercising regularly once a week for about the last six months. Why? Because it doesn’t matter.

I’m not saying it’s easy to be happy. I’m saying we will definitely not get any happier by focusing on minor and insignificant details relating to diet or exercise.

Paleo is fad (fad = a temporary fashion; a craze, interest or activity that (some) people follow enthusiastically, but lasts for a short period of time). Sure it’s a good idea to not eat modern foods, but we must not start suggesting that a food is bad because it is modern. And we must not forget that a paleo diet is not actually a defined diet, but rather a some general guidelines based on not so strong evidence about what our ancestors ate.

Paleo is likely a fad because humans are crazy about inventing new words, labeling everything and grouping things together. The world is to complex not to make subgroups of everything and we’re so bloody good at it. Don’t get me wrong, I actually like the word paleo, but I bet a new craze will take over; the paleo group feel will dilute and hopefully integrate more into standard dietary advice.

But what about the throwing of scales? Talking to more and more people trying to lose weight just further convinces me that weighing is an obstacle for success. The first thing you should do if you want to lose weight is to chuck the old measuring tool in the trash. As I said, humans get to caught up in details and especially numbers on a scale. Have patience, in time you’ll know if you are losing fat. You were clothes, don’t you? Your clothes are the only reference you need. If you can't get in or out of them, you've gained weight. Oh, and perhaps some getting to know your body and how you actually feel might help to.

And as for me? I feel an overpowering urge to tackle the “set-point” hypothesis issue. Something smells fishy about the standard theory which Harris and Guyenet, amongst others, find the most fitting.

Hva er egentlig problemet med rødt kjøtt? (In Norwegian)

2011-02-08T11:26:00.000+01:00

istockphoto

Mandag 31. januar la Nasjonalt råd for ernæring frem rapporten, ”Kostråd for å fremme folkehelsen og forebygge kroniske sykdommer.” Rapporten er en vitenskapelig gjennomgang av kostens påvirkning på en rekke sykdommer og helsetilstander, og gir konkrete råd om forebygging. Blant rådene er en anbefaling om restriksjon i inntaket av rødt kjøtt. Begrunnelsen er at rødt kjøtt øker risikoen for tykk- og endetarmskreft. Så sikre er rådet i saken at de sier det er en ”overbevisende” årsakssammenheng mellom de to faktorene. Det vil si, det er egentlig ikke Nasjonalt råd for ernæring som er sikre. De gjengir bare konklusjonen fra en rapport fra World Cancer Research Fund (WCRF) fra 2007 [1]. Det var denne rapporten som konkluderte med en overbevisende sammenheng mellom inntak av rødt kjøtt og kreft i tykk- og endetarm og det er denne rapporten de norske anbefalingene hviler tungt på.

Sentralt i den delen av vitenskapen som dreier seg om kostholdsfaktorers påvirkning på helse er spørsmålet om kausalitet, d.v.s. hvilken faktor som direkte forårsaker en helseeffekt. Det er kun en type vitenskapelige studier som med god sikkerhet kan vise kausale årsakssammenhenger. I tilfellet med rødt kjøtt ville en slik type studie bestå av minst to grupper med mennesker som er like på alle måter bortsett fra i inntaket av rødt kjøtt. Om en gruppe spiser mye kjøtt og en annen lite, kan vi følge gruppene over tid og etter hvert registrere hvor mange i hver av gruppene som får tykktarmskreft. Om gruppen som spiste mye kjøtt fikk så mye mer kreft enn gruppen som spiste lite at det ikke kan anses å være tilfeldig, kunne vi anta at kjøtt fører til kreft. Det vil si, selv da hadde vi ikke bevist noe, for selv et slikt resultat betyr lite inntil noen gjør akkurat den samme studien om igjen og får et tilsvarende resultat. Kausalitet, det at kjøtt faktisk fører til kreft, krever at resultater i slike studier er reproduserbare. En slik studie har aldri og vil aldri bli gjort. Selv om det kunne gitt oss et endelig svar en gang for alle, er slike studier altfor dyre og resurskrevende å gjøre over lang tid på mange mennesker. I stedet gjør man det som av mange regnes som det nest beste - epidemiologiske eller observasjonelle studier. Slike studier deler gjerne ut spørreskjemaer til en stor gruppe mennesker med spørsmål om hva og hvor mye de spiser. Disse menneskene følges så opp over mange år og man registrerer sykdommer etter hvert som de oppstår. Deretter kan man gjennom statistiske metoder se om det er en sammenheng mellom inntak av rødt kjøtt og kreft. Det viktigste å huske på med slike studier, og gjerne det første man lærer i metodefag på skolen, er at de ikke sier noen ting om kausalitet. De kan ikke under noen omstendigheter fortelle oss om kjøttspising fører kreft, kun at de to faktorene kan opptre sammen i en befolkning. Man kan finne at rødt kjøtt korrelerer (opptrer sammen med) med kreftforekomst, men det kan godt tenkes at de som spiser mest rødt kjøtt også røyker mer eller er mer utsatt for en miljøfaktor som kan gi kreft. Dermed er det en annen faktor som er sannsynlig årsak til kreften, selv om kjøtt og kreft korrelerer. Man kan for eksempel, gjennom å bruke en slik studie, finne at det er en sammenheng mellom fotstørrelse og intelligens. Man bør likevel være forsiktig med å kirurgisk øke fotstørrelsen for å få økt intelligens, fordi korrelasjonen mest sannsynlig kommer av at voksne med store føtter skårer høyere på tester enn barn med små føtter.

I et merkelig sitat fra den nye norske rapporten skrives det at det tyske Bundesinstitut für Risikobewertung, ” ...konkluderer at de epidemiologiske studiene ikke dokumenterer entydig at sammenhengen er kausal.” Grunnen til at setningen er rar er som nevnt over at epidemiologiske studier ikke kan dokumentere kausalitet. Dette er vitenskapelig metode for nybegynnere.

Ettersom alle studier som finnes om sammenhengen mellom inntak av rødt kjøtt og tykktarmskreft er i gruppen epidemiologiske studier, kan vi ikke si at rødt kjøtt fører til kreft. Men om alle våre data, selv om de som er epidemiologiske, tyder på at det finnes en sammenheng og vi i tilegg har svært sannsynlige årsaksforklaringer fra for eksempel dyrestudier eller cellestudier, så kan man si at det er overbevisende sannsynlig at høyt inntak av rødt kjøtt fører til tykk- og endetarmskreft.

Så hva er egentlig grunnlaget for konklusjonen i den norske repporten?

I hovedsak er den norske anbefalingen basert på rapporten fra World Cancer Research Fund fra 2007. Denne rapporten hevder også at det er en overbevisende sammenheng mellom rødt kjøtt og tykk- og endetarmskreft. Stewart Truswell skrev i 2009 en sterk kritikk av rapporten til WCRF i American Journal of Clinical Nutrition [2]. Truswell stiller seg undrende til at rødt kjøtt ble flyttet fra å ha en sannsynlig (probable) sammenheng med tykk- og endetarmskreft i rapporten fra 2002, til å ha en overbevisende (convincing) sammenheng i 2007.

Truswell trekker blant annet frem at WCRF har utelukket 13 studier med til sammen 1.578.970 deltakere, hvorav kun to av disse fant en positiv sammenheng mellom rødt kjøtt og kreft. Michael Marmot og Martin Wiseman som medforfattet WCRF-rapporten hevder at flere av disse studiene ikke så på rødt kjøtt direkte, men at noen så på bearbeidet kjøtt og rødt kjøtt sammen og andre på kjøtt generelt [3]. WCRF tok heller ikke med en oppfølgingsstudie av 5 grupper vegetarianere som var sammenlignet med sosialt like altetere. Denne fant ingen forskjell i dødelighet fra tykk- og endetarmskreft [2]. I et tilfelle rapporterte WCRF direkte feil, da de hevdet at i en finsk studie av Pietinen og kolleger, var den relative risikoen for tykk- og endetarmskreft for storfe, svin og lam 1.2, når den i virkeligheten var 0.9 eller 0.8. Marmot og Wiseman innrømmet dette, men unnskyldte seg med at de ikke hadde tatt så mye hensyn til denne studien likevel.

WCRF valgte bort én stor studie som viste en lav risiko for kreft, til fordel for en metodisk dårligere studie som vist langt høyere risiko, fordi den sistnevnte passet bedre inn i den statistiske metoden de brukte. I tilegg til feilmerking av en studie og andre mer eller mindre grove feil fra forfatterne av WCRF-rapporten, minner Truswell oss på at i CD-en som fulgte med rapporten ble det hevdet at ”…mechanisms for involvement of meat in colorectal cancer are far from plausible.”

I tilegg til WCRF refereres det i kostholdsanbefalingene til en metaanalyse (analyse av analyser) av 15 prospektive studier som fant en positiv sammenheng mellom risiko for tykk- og endetarmskreft og inntak av rødt kjøtt. Relativ risiko var 1.28 for høyt mot lavt inntak av rødt kjøtt – et tall som er alt for lavt for å vekke oppmerksomheten til forskere som ikke allerede har et forutinntatt forhold til rødt kjøtt.

Den norske rapporten viser også til en ny og svært stor studie av Amanda Cross og medarbeidere [4]. Denne studien undersøkte hele 494036 deltagere over 6.8 år (Rapporten fra Nasjonal råd for ernæring sier at studien hadde 545653 deltakere og kikk over 10år, men dette er misvisende). Denne studien er et godt eksempel på datagrunnlaget for kostholdsanbefalinger ettersom den brukte en svært vanlig epidemiologisk metode. Studien baserte sine funn på spørreskjemaer som ble delt ut i oppstarten av studien. Spørreskjemaene innholdt spørsmål om hva deltakerne vanligvis spiste. Etter ca 7år sjekket man om det var en sammenheng mellom sykdom og det som ble oppgitt i disse skjemaene. Denne metoden tar ikke hensyn til kostholds- og livsstilsfaktorer som endrer seg i løpet av studien, men dette er dessverre likevel en helt vanlig metode å bruke. De i studien som spiste mest kjøtt hadde mindre utdannelse, var yngre, røykte mer og var generelt mer overvektige. Disse faktorene ble kontrollert for i analysen, men faktorer som sukkerinntak som er nært knyttet til overvekt, brydde ingen seg om. Næringsstoffgruppen som kalles karbohydrater er spesielt interessant og burde kontrolleres for, fordi man vet at senkning av blodsukkeret reduserer vekst og utvikling av tykktarmskreft [5]. Uansett, forskerne fant at høyt inntak av rødt kjøtt var forbundet med økt risiko for tykk- og endetarmskreft (Hazard Ratio=1.24, for de som er interessert.)

Truswell er ikke den eneste som er kritisk til hvor mye som tolkes inn i dataene som finnes. I “Red meat and colorectal cancer: a critical summary of prospective epidemiologic studies”, fra 2010 [6] fremmer Alexander og Cushing en viktig innvending. Det at andre faktorer enn rødt kjøtt, for eksempel vestlig livsstil og et høy inntak av raffinert sukker, også korrelerer med kreft, begrenser muligheten til å isolere effekten av rødt kjøtt. I sitt grundige review konkluderer Alexander og Cushing med at de tilgjengelige epidemiologiske bevis ikke er nok til å støtte en uavhengig positiv sammenheng mellom rødt kjøtt og tykk- og endetarmskreft.

Hvis rødt kjøtt forårsaker kreft i tykktarmen, vil man forvente å finne at økende inntak av kjøtt gir økende forekomst av kreft. Altså jo mer kjøtt, jo mer sykdom, en såkalt dose-respons sammenheng. Nasjonalt råd for ernæring sier i rapporten sin at en slik dose-respons sammenheng finnes, men de oppgir ingen kilde med uttalelsen. Jeg sjekket, og fant at noen studier har et dose-respons forhold mens andre ikke har det.

Den norske rapporten fremhever flere ganger at de epidemiologiske studiene støttes av mekanistiske studier. Problemet er bare at de mekanistiske studiene omhandler teorier som er svært dårlige, så dårlige at de ikke kan brukes til å støtte noe som helst. I rapporten står det, ”Mekanismer for utvikling av kreft og de mulige kostfaktorer som kan påvirke risiko for kreftutvikling er grundig diskutert i rapporten fra World Cancer Research Fund rapporten (1) og den medfølgende CD.” Jeg synes konklusjonen angående mekanismer som gis på denne CD-en er verdt å gjenta, ”…far from plausible.”

Så de vitenskapelige ”bevisene” som finnes for sammenhengen mellom rødt kjøtt og tykk- og endetarmskreft er kun fra studier som ikke egentlig kan si noe om årsaken til kreft. Noen av disse studiene viser ingen sammenheng, mens noen finner en sammenheng og ofte er sammenhengen svak. Epidemiologiske studier har en mengde svakheter, kanskje først og fremst det man kaller ”confounding factors.” For at ikke andre faktorer enn kjøtt, for eksempel røyking eller fysisk aktivitet, skal være årsaken til en eventuell sammenheng, kontrollerer man for disse faktorene i de statistiske utregningene. Men hvilke faktorer man kontrollerer for er fullstendig opp til de respektive forskere. Det er for eksempel vanlig å kontrollere for inntak av mettet fett, fordi man har en oppfatning om at mettet fett er farlig. Andre faktorer som godt kan tenkes å være den egentlige årsaken til en positiv sammenheng kan bli oversett, enten på grunn av forutinntatthet eller på grunn av manglende kunnskap, og det er ikke usannsynlig at rødt kjøtt blir uskyldig dømt. Disse studiene blir sett i sammenheng med dyre- og cellestudier som heller ikke kan si noe om årsaken til kreft, og som er basert på relativt dårlige biologiske hypoteser.

Man skulle kanskje tro at for å kunne si at det er en overbevisende sammenheng mellom to faktorer, måtte man ha flere gode randomiserte kontrollerte studier som er gullstandarden når det kommer til å peke på årsaker. Men slik er det ikke. Ingen slike studier finnes og vi må nøye oss med det nest beste.

Interessant nok står det i ”Kostråd for å fremme folkehelsen og forebygge kroniske sykdommer” at ”Ut fra en helhetlig vurdering av forskningsfeltet, inklusive manglene på klare mekanismer, kan man reise spørsmål ved om sammenhengen heller burde kategoriseres som sannsynlig.” Rådet kommer dermed med selv med en innvending reist av mange andre, men unnlater å ta hensyn til den.

Samtidig med de norske anbefalingene kom det også ut nye kostholdsanbefalinger i USA. I USA valgte de en mer moderat tilnærming til kjøtt og kreft og skriver, “…moderate evidence suggests an association between the increased intake of processed meats (e.g., franks, sausage, and bacon) and increased risk of colorectal cancer and cardiovascular disease.” Rødt kjøtt gis tilnærmet ingen oppmerksomhet.

Til syvende og sist er bevisene for en sammenheng mellom rødt kjøtt og kreft i tykktarm og endetarm dårlige. Dette betyr ikke at sammenhengen ikke finnes, og det er fortsatt mulig at kjøtt faktisk gir oss kreft. Så valget må bli opp til den enkelte av oss. Jeg kommer til å fortsette med å spise kjøtt, mye kjøtt og aller helst rødt kjøtt. Mitt eneste håp er at myndighetenes ensidige fokusering på korn, frukt og grønt gjør at kjøttprisene går ned så jeg kan fortsette å nyte min dagelige porsjon rødt kjøtt.

Litteratur

1. Food, nutrition, physical activity, and the prevention ofcancer: a global perspective. Washington DC: American Institute for Cancer Research; 2007.

2. Truswell AS: Problems with red meat in the WCRF2. Am J Clin Nutr 2009, 89: 1274-1275.

3. Marmot M, Wiseman M: Reply to AS Truswell. The American Journal of Clinical Nutrition 2009, 89: 1275-1276.

4. Cross AJ, Leitzmann MF, Gail MH, Hollenbeck AR, Schatzkin A, Sinha R: A prospective study of red and processed meat intake in relation to cancer risk. PLoS Med 2007, 4: e325.

5. Seyfried TN, Shelton LM: Cancer as a metabolic disease. Nutr Metab (Lond) 2010, 7: 7.

6. Alexander DD, Cushing CA: Red meat and colorectal cancer: a critical summary of prospective epidemiologic studies. Obes Rev 2010.

New dietary guidelines - the fairies are rejoicing

2011-02-01T15:48:00.001+01:00

Nonsense, n; That which is not sense; spoken or written words which make no sense or convey absurd ideas; also, absurd or senseless action.

I am writing nonsense, but it is because no sense within my mind will answer the purpose.

Hawthorne (1871)

All around are heated discussions and angry tweeters, heads are being slammed on desks, palms being slammed on faces (preferably ones one) and Einstein’s definition of madness is being quoted frequently.

Ladies and gentlemen, I give you the new and updated dietary guidelines.

Someone once said that science pretends to be more reasonable than it is, and so ends up being more unreasonable as a consequence. I am more inclined to replace science with scientists.

There is so much to be said about dietary guidelines and I am sure much will be said in the near future. I will not go into details and argue what statements are sound and supported by science and which are not. But I do find the entire process very interesting and I wonder if a time comes when people will look back at this while giving themselves a good facepalm and thinking, “What the hell were they thinking?” I can’t wait till the future gets here.

I was at the Norwegian Health Directorate yesterday to get a copy of the new national guidelines and to hear what the perpetrators had to say. As expected, they served fruit and bad coffee. It was interesting to hear how the authors boasted about the foolproof methodology they had used. How only the best information from the best sources, like the World Health Organization and the World Cancer Research Fund, was used. It got me thinking how remarkable it is that in some peoples mind, as long as the methodology is good the conclusion is equally good. But good methodology does not translate into good science. It might help, but in the case of WCRF report, for example, it clearly did not. I checked, and it is full of arbitrary mess ups like translating correlation directly into causation, not to mention its use of thermodynamics and its cherry picking articles and miss referencing.

The Norwegian guidelines were neatly divided into 13 simple, easy to follow points (loosely translated):

1: Diet should be primarily plant based and contain lots of vegetables, fruit, berries, whole grain and fish, and contain limited amounts of red meat, salt, added sugar and energy dense foods.

2: It is recommended to maintain a balance between energy intake and energy expenditure.

3: Eat 5 portions of vegetables, fruit and berries a day.

4: Eat minimum 4 portions of whole grain products each day.

5: Eat the equivalent of 2-3 dinner portions of fish per week.

6: It is recommended that low fat dairy products be a constituent of the daily diet.

7: It is recommended that one chooses lean meat and meat products and limit the intake of red and processed meat.

8: It is recommended that one choose plant oils and margarines.

9: Drink water.

10: Limit intake of added sugar.

11: Limit intake of salt.

12: Supplements might be necessary to ensure nutrient intake for parts of the population.

13: A minimum of 30 min of physical activity per day is recommended.

There you have it. The recipe for good and healthy living. The diet should be plant based. I know there are humans in the world and even small societies that do live on a primarily plant based diet and who seemingly are in good health. But in no way does this imply that a plant based diet is healthier than one animal based. It doesn’t even prove that a plant based diet is healthy, just that it might be possible. Of course the guidelines are not based on anthropologic evidence, but on a fear of animal fat and meat. It is not based on scientific data supporting a link between the intake of animal fats and disease, but on a completely irrational fear that fat might be deleterious to health, a fear created by a wonderful combination of a scientific field consisting of people who have forgotten what science is but who are still constantly cheering each other on in close cooperation with media and marketing interests.

The one vital part missing in the dietary guideline picture is what we do when the brilliant foolproof methodology gives us a conclusion. This is not when we rest on our laurels, but the time for some actual science to take place. This is when we have to check if the conclusion makes sense in light of what we know from all the different areas of science.

There is no evidence of this last part taking place in the guideline process. But the guidelines are not worthless. In fact a good and scientifically sound way to base your diet and lifestyle would be to use the guidelines in the following way:

Mind the advice about cutting sugar as well as the advice about exercising. Don’t mind the fish and the water and the vegetables, do the complete opposite of the rest:

- Diet should be animal based.

- Grain intake should be minimal

- Butter and animal fats should be substituted for plant oils and margarine.

- Do not pay attention to energy intake and expenditure,

and remember to get enough salt.

What is the best exercise for fat loss? Part V - the conclusion

2011-01-30T17:41:00.000+01:00

I wondered what the best exercise for fat loss was. I honestly didn’t know the answer, but now feel I have acquired a more thorough understanding. As a scientist I ask questions I want answered and work to find the answers. However, all this digging in the details and nerding about does not mean fat loss should be a primary motivation for exercising. On the contrary, if the only reason that you exercise is to try to lose weight and everything else about exercising is a pain in the ass, I would recommend you to stop exercising. No matter your external motivation for exercising, be it health in general, weight loss, muscle strength or flexibility, if you want exercise to be a positive part of your life you need to find an exercise form that gives you something more, that is motivated by internal factors, preferably that you enjoy the actual exercising. If you want to lose weight and you know high intensity strength based exercise is the most effective exercise, but you would rather swim because you really like swimming, than the choice is simple. Swim!

That being said, for the sake of curiosity, let’s see what the best exercise for fat loss is.

There is not enough data to say much about what exercise form is more efficient, whether running is better than cycling for example or a step machine better than elliptical trainer. There are just too many other variables. There is however enough data to make a calculated guess about aerobic versus resistance exercise, and about exercise amount and intensity.

Just wanted to illustrate the expected effects of exercising without dieting. The below table gives a few examples of just how much weight and fat you can expect to lose. Results are not god, and tend to become poorer in time in the longer lasting trials. Many of the results are non significant. What this tells us is that diet matters. A lot.

It seems that resistance exercise is or can be just as effective as aerobic exercise in improving body composition. Resistance exercise usually cause some fat loss while also increasing muscle mass. Aerobic exercise usually causes larger loss of fat, but also larger loss of muscle. High intensity aerobic exercise causes less lean mass loss than low intensity.

The best exercise for fat loss should:

- be of medium to high intensity (frequently bring you above lactate threshold)

- include resistance exercises

- be interval based (30 min of sprint intervals is most likely better than 60 min jogging)

- not be performed every day (rest is important and more is not better than the right amount)

- exercise the whole body

- be combined with a high protein low glycemic diet for maximal improvement in body composition.

That’s it, as far as I can tell. Feel free to disagree. Tomorrow I’m off to the Norwegian Directorate of Health and the unveiling of the new national dietary guidelines. The snack there is crap (usually fruit), but hopefully there’s coffee and plenty of it.

What is the best exercise for fat loss? Part IV

2011-01-20T19:45:00.000+01:00

The bias
I have this theory. In the last post I concluded that there is sufficient data for recommending high intensity exercise in favor of low intensity for fat loss. Admittedly, the data in support of this is not strong. It is there, but I would not bet my life on it yet.

I might be a bit biased in favor of high intensity because of my theory that seems rigidly stuck in my brain. From the world of resistance exercise, we know that you can use a number of strategies to build muscles. Some use slow movements with relatively low resistance where the muscles are activated for a long time. Others use quick movements with high loads allowing for a greater workload to be performed in a shorter amount of time. Some simply cut blood flow to the working muscles which also will make them grow. The bottom line is that the one important factor when it comes to muscle hypertrophy seems to be the amount of physiologic stress placed on the working muscles during exercise. So you can stress a muscle or muscle group by making it work for a long time like in static strength training or you can do the standard high load high repetition fast movement exercise. You can even do pure eccentric exercises rather than the usual concentric/eccentric. All of this and pretty much everything in between will cause muscle growth. It is the total workload, the time multiplied by load, that matters.

The concept is very similar to the energy hypothesis that claims it is the amount of energy spent during exercise that determines fat loss, rather than intensity or time by itself. The difference is that the hypertrophy theory is supported by science whereas the energy hypothesis is not.

Although hypertrophy can be achieved in many ways, there is a limit to the equation, workload = time x load. It is not only the amount of work done that determines muscle growth. Running, for example will not build significant amounts of muscle even if some of the muscles involved perform a great workload. The reason is that somewhere in the area between multiple repetition resistance exercise and endurance exercise the stimulus changes and thus the physiological adaptations.

Most people are aware of this and know that walking or running is a poor strategy for building muscles.

My theory is that the whole "exercise intensity and fat loss" issue is of a similar nature, that to a certain degree, it is the amount of work performed that matters the most. Both low and high intensity exercise cause fat loss, but somewhere in the declining intensity area the stimulus becomes different and fat loss is reduced. Shopping, gardening and other everyday activities with low intensity, but often of long duration seem poor strategies for weight loss. Likely, we are working to close to the body’s comfort zone to make it adapt. Or put in better words, the body does not adapt to these activities because it doesn’t need to, it already has.

This means that high or low intensity might not matter that much, as long as the tissues are exposed to new stimuli, forcing them to adapt. However, this is not to say that high intensity is not better than low, the question is how much better.

As with muscle hypertrophy, if the goal is to maximize all factors, then high intensity, high workloads and variation in stimuli is important. I believe it is the same with exercise intensity and fat loss. This might explain some of the variation in results found in different trials.

The losing of fat and not muscles
Loss of muscle mass is common with weight loss, independent of dietary approach. Some diets seem to lead to better muscle mass retention and some exercise forms will prevent muscle loss. But we must make sure not to assume that all muscle loss is a negative thing. The size of our muscles will determine our appearances while their function is what will affect our health.

In school I was taught that one important factor for skeletal muscle hypertrophy was positive energy balance. You had to take in more than you expended. This however, turned out to be wrong. The muscles might need a readily supply of fuel, but they couldn’t care less if the energy comes from glycogen and fat stores or from food. Thus it is theoretically possible to lose fat mass while increasing muscle mass.

Fleck and Kraemer [1] concludes that in untrained individuals doing regular resistance exercise you can expect a 2kg increased muscle mass in 14 weeks. That’s about 0.06kg per exercise session. If we consider the women only trials the number is about 0.04kg per session.

Resistance exercise builds muscles when we’re not dieting, but does this hold true when we are simultaneously losing fat mass? Short answer, yes. We can. But, you would not come to that conclusion if you put together a meta-analysis of decent trials. The reason is that in several studies fat loss is significant while muscle growth is not. However, when the mean is zero change, the individual data will show that many did increase their lean mass while losing fat.

I know this is a statistical quagmire, but part of my conclusion will still be based on individual results rather than the reported means. The reason is that when several people in a resistance exercise study build muscle, it is very likely that the exercise is to blame. This is not a strategy I would use when for example looking at weight loss results from low fat diet studies that show a mean zero improvement. If finding that half the participant lost weight and the other half did not, it would not be smart to claim that low fat diets works. There are a great many things that lead us to lose weight, although it almost always involves some reduction in dietary carbs. But as I said, when people gain muscle in a resistance exercise trial, the gain is extremely likely to come from the resistance exercise.

There is another issue as well. Many body composition studies are done with DEXA (dual energy x-ray absorptiometry). Because adipose tissue mass is considered 85% lipid and 15% water, and because DEXA measurement of fat free mass includes this adipose tissue water, a loss of adipose tissue without loss of fat free mass suggests favorable changes in muscle mass.

When I did a small study in 2009 I found that in eight women who did regular resistance exercise in combination with a ketogenic diet, four of them increased lean body mass, while four reduced it. The study was not large enough to indicate what factors were responsible for the lack of muscle mass gain in the other four. I guess anything from dietary protein (amino acids), thyroid issues to stress might contribute [2].

Figure 2 from Jabekk et al 2009. Lc+Ex= Low carb + resistance exercise. Ex=resistance exercise.

Shadid and Jensen [3] compared 20 weeks of pioglitazone with exercise and diet. Diet and exercise resulted in 11.8kg mean weight loss. The group was instructed in a 500kcal deficit diet and in an exercise program starting with 15min of aerobic exercise three times per week at 50% of each individual’s heart rate reserve. This was gradually increased to 45min aerobic exercise four times a week at 60–70% of heart rate reserve. The surprising find in the study was that the intervention caused a mean 9.5kg fat loss and a non significant 0.5kg reduction in fat free mass, which is an unusually small reduction.

Barbara A. Gower et al [4] also got surprisingly good results from a traditional very low energy diet in overweight women. Mean fat mass lost was 11.2kg. White women in the trial lost a non significant 0,77kg lean mass while the African American women lost 1.53kg (non significant) lean mass.

In both the above trials, several individuals managed to increase their lean mass while reducing fat mass. This was even done without any reported resistance exercise. Most if not all of the participants in the trials were insulin resistant, which if improved, I suspect can cause muscle growth by itself.

Gary Hunter [5] who coauthored the Gower trial found that in women who lost 12kg of weight, resistance exercise conserved lean mass. The women were randomized to diet only, diet and resistance exercise or diet and aerobic exercise.

Figure 1 from Hunter et al 2008. FFM=fat free mass. AA=african-american. EA=european-american

In a study from 1988 Douglas L. Ballor et al [6] concluded similarly to Hunter and stated that “In conclusion, data from this study indicate that weight training added to a caloric restriction program results in maintenance of LBW [Lean Body Weight] and regional increases in muscle area. When diet plus weight-training exercise is compared with exercise without caloric restriction, there is no difference in the rate of strength gain or magnitude of upper-arm muscle area increase."

From Ballor et al 1988. C=control. DO=diet only. DPE=diet plus exercise. EO=Exercise only.

It might seem counterintuitive, but finding that endurance exercise increases lean mass or attenuate lean mass loss is quite common. Janssen et al [7] found that aerobic and resistance exercise did equally well in preserving muscle mass with dieting in premenopausal obese women. This finding reflected their previous (1999) trial with both men and women, which also found preservation of lean mass with both resistance and aerobic exercise.

Contrary to Janssen et al, Geliebter et al [8] and Bryner et al [9] did find that resistance exercise was more effective in improving lean mass with weight loss than aerobic exercise.

The combination of resistance training with aerobic training has been shown to be superior for body weight and fat loss and to result in greater lean body mass compared to aerobic exercise alone in several randomized controlled trials.

Park et al [10] for example, found that aerobic exercise reduced fat percentage by 9.2 while combining it with resistance exercise reduced fat percentage by 10.3. Lean mass increased by 0.9kg with aerobic exercise and by 5.6kg with combined exercise. This trial did not use a dietary intervention and the subjects had a mean BMI of 25. But it is an interesting example of how the exercise did not cause a weight change but still caused a significant body composition change.

Using a combination of high protein diet and resistance exercise Wycherley et al [11] demonstrated an 11.4kg fat mass reduction in 16 weeks. The reduction was accompanied by a 2.4kg reduction in fat free mass. The body composition results are impressive, but as I said we rarely if ever find a significant mean fat loss in combination with significant mean fat free mass gain.

Saving the best for last, Kevin David Ballard and colleagues is responsible for a meeting abstract from 2008 titled “Effects of diets restricted in fat and carbohydrate with and without resistance training on body composition and cardiovascular risk.” Ballard reports results from the Department of Kinesiology at University of Connecticut were heavyweights like Jeff Volek and William Kraemer reside. They report having examined the effects of carbohydrate restricted (CRD) and low fat diets (LFD) alone and in combination with resistance training (RT) in 47 overweight men.

The results state that “Reductions in body mass, fat mass, percent body fat and abdominal fat were greater in the CRD than the LFD (p<0.001).” and that “Gains in lean body mass were demonstrated in the RT groups only (p=0.004).” Their conclusion: “Resistance exercise is an effective strategy to combat diet induced losses of lean body mass.”

On the matter of resistance exercise and fat-free mass Donnely and ACSM [12] concludes thusly: “…most studies combining resistance training with energy restriction report improved lean body mass compared to dieting alone.” They continue; “In summary, resistance training does not seem to be effective for weight reduction in the order of 3% of initial weight and does not add to weight loss when combined with diet restriction. Resistance training increases fat-free mass when used alone or in combination with weight loss from diet restriction. Resistance training may increase loss of fat mass when combined with aerobic exercise compared to resistance training alone.”

Petra Stiegler and Adam Cunliffe [13] did a very good job addressing the evidence for the effect of exercise and diet on anthropometric variables. They conclude that: “…it becomes clear that a combination of modest caloric restriction combined with endurance exercise or endurance and physical training of different modes is preferable over dietary modification alone to induce favorable changes in body composition accompany ing weight loss.”

The Conclusion
It is possible to increase lean mass while losing fat mass. There are many factors at play but a high animal protein diet and resistance exercise is the best strategy we know of. Resistance exercise is very effective at increasing lean body mass, and it seems that this effect remains even if people are dieting and the effect is observed in both low and high carbohydrate diets. The addition of endurance exercise to diet and resistance exercise seems to slightly increase fat mass loss, but has little effect on lean mass.

The references

1. Fleck SJ, Kraemer WJ: Designing resistance training programs. Champaign, IL: Human Kinetics; 2004.

2. Jabekk PT, Moe IA, Meen HD, Tomten SE, Hostmark AT: Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing body fat. Nutr Metab (Lond) 2010, 7: 17.

3. Shadid S, Jensen MD: Effects of pioglitazone versus diet and exercise on metabolic health and fat distribution in upper body obesity. Diabetes Care 2003, 26: 3148-3152.

4. Gower BA, Weinsier RL, Jordan JM, Hunter GR, Desmond R: Effects of weight loss on changes in insulin sensitivity and lipid concentrations in premenopausal African American and white women. Am J Clin Nutr 2002, 76: 923-927.

5. Hunter GR, Byrne NM, Sirikul B, Fernandez JR, Zuckerman PA, Darnell BE, Gower BA: Resistance training conserves fat-free mass and resting energy expenditure following weight loss. Obesity (Silver Spring) 2008, 16: 1045-1051.

6. Ballor DL, Katch VL, Becque MD, Marks CR: Resistance weight training during caloric restriction enhances lean body weight maintenance. Am J Clin Nutr 1988, 47: 19-25.

7. Janssen I, Fortier A, Hudson R, Ross R: Effects of an energy-restrictive diet with or without exercise on abdominal fat, intermuscular fat, and metabolic risk factors in obese women. Diabetes Care 2002, 25: 431-438.

8. Geliebter A, Maher MM, Gerace L, Gutin B, Heymsfield SB, Hashim SA: Effects of strength or aerobic training on body composition, resting metabolic rate, and peak oxygen consumption in obese dieting subjects. Am J Clin Nutr 1997, 66: 557-563.

9. Bryner RW, Ullrich IH, Sauers J, Donley D, Hornsby G, Kolar M, Yeater R: Effects of resistance vs. aerobic training combined with an 800 calorie liquid diet on lean body mass and resting metabolic rate. J Am Coll Nutr 1999, 18: 115-121.

10. Park SK, Park JH, Kwon YC, Kim HS, Yoon MS, Park HT: The effect of combined aerobic and resistance exercise training on abdominal fat in obese middle-aged women. J Physiol Anthropol Appl Human Sci 2003, 22: 129-135.

11. Wycherley TP, Noakes M, Clifton PM, Cleanthous X, Keogh JB, Brinkworth GD: A high-protein diet with resistance exercise training improves weight loss and body composition in overweight and obese patients with type 2 diabetes. Diabetes Care 2010, 33: 969-976.

12. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK: American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2009, 41: 459-471.

13. Stiegler P, Cunliffe A: The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss. Sports Med 2006, 36: 239-262.

What is the best exercise for fat loss? Part III

2011-01-11T13:43:00.000+01:00

For some reason it makes intuitive sense to me that high intensity exercise is better for fat loss than low intensity, but I do not quite know how this came to make sense.

High intensity exercise will cause a primary burning of glucose and so high intensity exercise will make our muscles better at taking up and burning glucose thus theoretically making us more glucose tolerant. Then again, during low intensity endurance exercise we primarily burn fat. Endurance exercise will make us better at burning fat, and fat is undoubtedly the thing to burn if we want to lose weight.

Generally speaking high intensity exercise will increase our muscle-neuron cooperation, improve factors related to anaerobic fuel utilization, improve our glucose metabolism and if performed with some resistance, increase our muscle size and strength. Lower intensity exercise will improve our aerobic fuel utilization, increase blood flow by increasing numbers of capillaries and increase the number and size of mitochondria – the powerhouse of the cells that are responsible for burning fat.

In the 2001 version of the ACSM position stand “Appropriate Intervention Strategies for Weight Loss and Prevention of Weight Regain for Adults,” the authors could say little on the effect of exercise intensity [1]. Lucky for us, several studies have come out since then that help paint a clearer picture. Despite these recent publications, the new and updated 2009 ACSM position stand contain no discussion on exercise intensity at all and the subject seems forgotten [2].

No doubt, if physical activity is to affect weight loss or weight loss maintenance it invariably has to affect the very same factors we try to affect by diet. As overweight is a condition of excessive fat storage we want to increase lipolysis (the release of fat) from fat cells and we want to reduce storage of fat in the fat tissue. This does not however necessarily mean low intensity endurance exercise that increases our fat burning abilities.

The two major factors at play here are insulin and glucose levels in the blood. Because the fat tissue is guarding us against the dangers of high blood glucose by taking up excess it will grow as it is protecting us, making us burn glucose to reduce blood levels and storing fatty acids for later as they pose no immediate threat. If our muscle and liver glycogen stores are full (as they will be with high carb diets and little exercise) excess carbohydrate intake will force the body to turn glucose into fat to get it out of the way.

It is well known that even a single exercise session is associated with a significant improvement in insulin-stimulated glucose uptake. Training, in making us better at taking up glucose, will also improve glucose uptake into the fat cells by increasing GLUT-4. This is a good thing.

The antidiabetic drug Metformin (Glucophage) for example will increase glucose uptake by fat cells by increasing GLUT-4 mRNA expression and cellular protein content, leading to increased GLUT-4 protein content in the plasma membrane. GLUT-4 is a glucose transporter which allows glucose to travel across membranes. Metformin also stimulates glucose oxidation in fat cells.

It is also likely that increased lipolysis and fat oxidation will reduce hunger. The result is that a greater amount of the energy needed to sustain your daily life will come from your own fat stores rather than from food. Increased lipolysis and fat oxidation may even make you want to move around more. I think Albert Pennington hit the nail on the head when he said, "Energy expenditure is an index of calorie nutrition at a cellular level."

The Intensity
First let’s look at some studies. (If you find yourself fighting the urge to fall asleep, just skip to the conclusion)

Coker et al tested the differential effects of moderate (50% of Vo2max) versus high-intensity (75% Vo2max) exercise in 18 overweight (BMI=30) elderly (71ys). The training was endurance exercise designed to expend 1000kcal per week. There was no significant change in body weight, BMI or percent fat, but the high intensity group experienced a significant reduction in visceral fat and a significant increase in thigh muscle attenuation [3].

A study published in the latest European Journal of Internal Medicine, reports putting twenty-two women with type 2 diabetes in a supervised group exercise program for six months. The program combined endurance and resistance exercise and the duration and intensity of exercise for each subject was recorded. The subjects were then divided with respect to training volume in a high training volume group and a low training volume group [4].

Although exercise capacity did not change significantly during the training period, insulin sensitivity increased significantly and HbA1c decreased significantly from baseline in the high volume group but not in the low volume group. A large part of the improvement in insulin resistance was explained by exercise intensity. It is likely that an improvement in insulin resistance will affect the amount of fat mass lost over time.

Contrary to the above finding, Emmanuel G. Ciolac found that equal volume of high-intensity interval (aerobic interval training 80–90% of Vo2max) and moderate-intensity continuous exercise training (50–60% of Vo2max) elicited equal improvements in insulin sensitivity in healthy women [5].

Grediagin et al [6] did a small study where twelve untrained, moderately overweight women were randomly assigned to a high-intensity (80% Vo2max) or low-intensity (50% Vo2max) exercise group. The subjects trained four times per week for 12 weeks in sessions with duration sufficient to expend 300 kcal. The subjects were further instructed to maintain their normal diet and activity patterns. By the end of twelve weeks there were no significant between-group differences for change in weight, percent body fat, fat mass, fat-free mass, skin fold measurements or circumference measurements.

The above study however, because of its small number of participants may have type 2 error in it. Although the differences did not reach statistical significance, the mean weight loss was 0.7 lb for the high-intensity group and 3.3 lb for the low-intensity group. Hydrostatic data revealed that both groups lost 5.0 lb of fat, but the high-intensity group gained more than twice as much fat-free mass (4.3 vs 1.8 lb).

Brian Irving and colleagues [7] did a study where twenty-seven middle-aged obese women (51ys, BMI=34) with the metabolic syndrome completed one of three 16-week aerobic exercise (walk/run) interventions: no-exercise training (Control), low-intensity exercise training (<lactate threshold 5days per week) and high-intensity exercise (>lactate threshold, 3days per week). Exercise time was adjusted to maintain caloric expenditure (400 kcal per session). The researchers found that high-intensity significantly reduced total abdominal fat, abdominal subcutaneous fat and abdominal visceral fat. These changes were not observed in the control or the low intensity group.

Similar to Irving, Bryner et al [8] found that in 15 women randomized to exercise with a mean heart rate of 132 or 163 for 45 minutes 4 times per week, high intensity did cause a significant reduction in percent body fat not observed in the low intensity group.

Nicklas et al [9] randomized 112 overweight and obese postmenopausal women to one of three 20-week interventions of equal energy deficit: calorie restriction, calorie restriction plus moderate-intensity aerobic exercise (treadmill walking at an intensity of 45-50% heart rate reserve), or calorie restriction plus vigorous-intensity exercise (70-75%). Exercise was 3 days per week.

The exercise groups lost significantly less lean mass than the diet only group. The vigorous intensity group increased Vo2max more than the other groups and changes in visceral fat were inversely related to increases in Vo2max. However, the groups lost equal amounts of total and regional fat.

Slentz, who coauthored the Houmard study mentioned in the last post, reported that low-amount/moderate-intensity and low amount/vigorous intensity endurance training (i.e., activity equivalent to ~12 miles per week of walking or jogging) were equally effective in reducing percent body fat mass, waist circumference and abdominal circumference in overweight middle-aged adults. They also reported that high-amount/vigorous-intensity endurance training (activity equivalent to ~20 miles per week of jogging) was more effective in reducing percent body fat and fat mass compared with the two low-amount training groups [10].

These results are of course used to justify the claim that it’s the amount of calories burned or the volume of exercise that matters.

In a more recent trial Slentz et al [11] demonstrated that in middle-aged overweight/obese individuals who were randomized to three 8-month exercise programs: low amount/moderate intensity, low amount/vigorous intensity, or high amount/vigorous intensity, the moderate intensity improved pancreatic β-cell function more than vigorous intensities. However, vigorous intensity caused a 7% reduction in visceral fat whereas moderate intensity gave no reduction. Also, only the high-amount/vigorous-intensity group showed a decreased insulin response to a glucose challenge. There was no decrease in insulin response in the low amount/moderate intensity group that had the greatest improvement in insulin sensitivity index.

Whyte et al [12] tested the effect of 2 weeks of sprint interval training on ten overweight (BMI=31) men. The exercise comprised of 6 sessions of 4 to 6 repeats of 30-second Wingate anaerobic sprints on a cycle ergometer, with 4.5-minute recovery between each repetition. Despite the short intervention time, both waist and hip circumferences decreased compared with baseline.

It is important to remember that these acute (2 weeks) responses to exercise are not necessarily transferable to long term responses. However, acute responses are sometimes all we’ve got and should be considered.

Chambliss et al did a 1 year intervention study with four different exercise interventions as a part of a standard calorie restricted diet. They found no significant differences between low and moderate intensities on weight loss [13].

Jakicic et al [14] also did a 1 year study where 201 women were randomized to 1 of 4 exercise groups: vigorous intensity/high duration; moderate intensity/high duration; moderate intensity/moderate duration; or vigorous intensity/moderate duration. The participants also followed a low energy diet. The authors did not find any differences in weight loss after one year.

The conclusion
There are a few things I find important to keep in mind when interpreting results from exercise trials. First, an improvement in a factor related to metabolic health may not cause a significant short term effect on weight or fat mass. It is still theoretically plausible that improvements in fat mass may come in time because of the improvements in the related metabolic parameters. Simply speaking, I don’t expect big results on fat mass from any form of exercise lasting only a few months.

Also, some of these studies use intension to treat analyses, and so the actual effect of doing the different exercises is not reported.

All in all, and as far as I can tell, there is sufficient data to support a recommendation of high intensity exercise over low intensity exercise for maximal loss of body fat. Not all trials find a difference, but several do, and some of those that do not find anthropometric differences find metabolic differences likely to affect weight loss over time. In addition, risk factors for cardiovascular disease are improved more with high intensity than low intensity.

Although most studies looking at exercise intensity in relation to fat loss use endurance exercises some studies still show an increased growth or reduced loss of muscle tissue with high intensity training. In fact, it is quite possible to lose fat while gaining muscle even while doing low resistance high intensity exercise. I think the whole topic of gaining muscle while losing fat deserves a separate post so…

Next: The losing of fat, not muscles.

References:

1. Jakicic JM, Clark K, Coleman E, Donnelly JE, Foreyt J, Melanson E, Volek J, Volpe SL: American College of Sports Medicine position stand. Appropriate intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2001, 33: 2145-2156.

2. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK: American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2009, 41: 459-471.

3. Coker RH, Williams RH, Kortebein PM, Sullivan DH, Evans WJ: Influence of Exercise Intensity on Abdominal Fat and Adiponectin in Elderly Adults. Metab Syndr Relat Disord 2009.

4. Segerstrom AB, Glans F, Eriksson KF, Holmback AM, Groop L, Thorsson O, Wollmer P: Impact of exercise intensity and duration on insulin sensitivity in women with T2D. Eur J Intern Med 2010, 21: 404-408.

5. Ciolac EG, Bocchi EA, Bortolotto LA, Carvalho VO, Greve JM, Guimaraes GV: Effects of high-intensity aerobic interval training vs. moderate exercise on hemodynamic, metabolic and neuro-humoral abnormalities of young normotensive women at high familial risk for hypertension. Hypertens Res 2010, 33: 836-843.

6. Grediagin A, Cody M, Rupp J, Benardot D, Shern R: Exercise intensity does not effect body composition change in untrained, moderately overfat women. J Am Diet Assoc 1995, 95: 661-665.

7. Irving BA, Davis CK, Brock DW, Weltman JY, Swift D, Barrett EJ, Gaesser GA, Weltman A: Effect of Exercise Training Intensity on Abdominal Visceral Fat and Body Composition. Med Sci Sports Exerc 2008.

8. Bryner RW, Toffle RC, Ullrich IH, Yeater RA: The effects of exercise intensity on body composition, weight loss, and dietary composition in women. J Am Coll Nutr 1997, 16: 68-73.

9. Nicklas BJ, Wang X, You T, Lyles MF, Demons J, Easter L, Berry MJ, Lenchik L, Carr JJ: Effect of exercise intensity on abdominal fat loss during calorie restriction in overweight and obese postmenopausal women: a randomized, controlled trial. Am J Clin Nutr 2009, 89: 1043-1052.

10. Slentz CA, Duscha BD, Johnson JL, Ketchum K, Aiken LB, Samsa GP, Houmard JA, Bales CW, Kraus WE: Effects of the amount of exercise on body weight, body composition, and measures of central obesity: STRRIDE--a randomized controlled study. Arch Intern Med 2004, 164: 31-39.

11. Slentz CA, Tanner CJ, Bateman LA, Durheim MT, Huffman KM, Houmard JA, Kraus WE: Effects of exercise training intensity on pancreatic beta-cell function. Diabetes Care 2009, 32: 1807-1811.

12. Whyte LJ, Gill JM, Cathcart AJ: Effect of 2 weeks of sprint interval training on health-related outcomes in sedentary overweight/obese men. Metabolism 2010, 59: 1421-1428.

13. Chambliss HO: Exercise duration and intensity in a weight-loss program. Clin J Sport Med 2005, 15: 113-115.

14. Jakicic JM, Marcus BH, Gallagher KI, Napolitano M, Lang W: Effect of exercise duration and intensity on weight loss in overweight, sedentary women: a randomized trial. JAMA 2003, 290: 1323-1330.

Intermission - religion and science

2010-12-31T15:39:00.000+01:00

Some thoughts on the brink of a new year. An intermission in the exercise for fat loss rambling was at its place.

There are people in this world, quite a few people, who would let their children die in the hands of a holy man rather than have them live by the hands of a doctor. A holy man is trusted at the expense of logic and reason and without taking into account the human minds ability for imagination and self-deception. The doctor is disregarded because to the layperson he operates in a field as difficult to understand or more so than a religion with simple answers.

A holy man, be it priest, mullah, shaman or other is trusted because he is there, unlike the scientific paper(s) or the lines of reasoning that might, in the presence of sufficient schooling and training, convince people otherwise.

In the health store the poster tells us that the vitamin C supplements can cure our colds. It might be right even though Linus Pauling was made a laughing stock claiming so, but that’s not the point. The poster is there, unlike the scientific papers or biochemistry textbooks undermining the claim. It is there with bright colors, a friendly smile and a promise it would be so nice to believe in.

We humans are prone to base our beliefs and understandings on the closeness of the source of information. Of course we are. Education and religion show a negative correlation. In areas where education in increased religion is decreased. When the textbook is slammed on your desk with the incentive to learn its contents the information is there whether you want it or not. The availability of good information make the esoteric unnecessary. This is not to say that any religious person is less smart or wise than the atheist, the human brain is more complex than that.

As frustrating as it is to see religions firm grip on virtues I hold high like those of reason, logic and skepticism, it is also very understandable. The holy man is there.

When your doctor tells you to reduce your saturated fat intake he does so because the information that he relies on is there. It is there in the local medical journal and it is there in pharmaceutical statin commercials sent to him.

Albeit, closeness of information is not all it takes, but I believe it to help more than it may seem. The doctor is unlikely to being swayed just by being shown a meta-analysis from Kraus, by being told the story of Ancel Keys or by some of Ravnskovs marvelous statistics. Just as a devout christian is unlikely to cast away his beliefs when listening to the evolutionary biologist.

But, the presence of good information is likely to sow seeds of uncertainties. I know from my own experience that my present views are the product of constant drops of information leading to uncertainties not to be left unexplored.

When someone close lose weight by eating fat and the results are there and clear in my face the impact is stronger than simply having heard of a similar episode somewhere. Of course, we can train ourselves to be more or less open and skeptical and the training can reduce the effect of the distance of the information. But, before we are properly trained to investigate information for what it is, irrespective of its closeness, distance matters. The commercial poster beats the journal, and the priest beats the scientist by being there.

My conclusion and solution to all of this is to keep being up in peoples faces. Be there. Talk to the doctor and the priest and your friends, write a blog, write a letter and spread seeds of potential knowledge. Admit to it when proven wrong and yield when a better argument is presented, but don’t keep your knowledge to yourself.

What is the best exercise for fat loss? Part II

2010-12-29T17:11:00.000+01:00

Energy expenditure – does it count?

No current treatment for obesity reliably sustains weight loss, perhaps because compensatory metabolic processes resist the maintenance of the altered body weight.

Leibel, Rosenbaum and Hirsch 1995 [1]

The energy

For some background reading on energy, this might be of interest.

Most endurance exercise apparatus found in a gym are equipped with a calorie counter. By inputting your weight and height and measuring your heart rate the display will tell you how many calories (kilocalories) you’ve burned (Calorie is a measure of energy. The international standard is Joule, but this is largely ignored.). You can literally count the fat loss while exercising. Or can you?

Robert W. Jeffery and coworkers randomized 202 obese men and women to standard behavioral therapy with the goal of either expending 1000kcal/week of exercise or 2500kcal/week, for 18 weeks. The actual reported energy expenditure for kilocalories per week at 18 months was 1629 and 2317 for the 1000- and 2500-kcal/week groups, respectively. At 6 months, there were no differences for weight loss between the groups, despite a reported difference in weekly energy expenditure of 562kcal. Reported energy intake was similar between groups. At 18 months the high PA (physical activity) group showed significantly more weight loss than the low PA group, 8.8kg vs 6.7kg. Now that’s a lot of extra exercise for a mere 2kg extra weight lost over 18 months [2].

All participants in the Jeffery study were instructed to reduce daily energy intake to 1000–1500 cal depending on initial body weight and to consume less than 20% of energy as fat. In addition they attended weekly group sessions for 6 months and one session per month thereafter. That is a lot of effort, exercise and starvation for 7-9kg of weight loss in 1.5years. It should also be mentioned that unlike the low PA group the high PA group were instructed weekly by trained exercise coaches and the participants in the high PA group were given 3$ for each week that they achieved or exceeded the energy expenditure goal of 2500 kcal/wk during the last 6 months of active intervention. Imagine the cost of treating overweight this way.

The authors of course concluded that when it comes to weight loss, more exercise is better and Donnelly [3] uses the study to conclude similarly – more is indeed better. However the study shows how there is little association between the amount of energy spent and consequent weight loss.

Many studies have showed that adding exercise to an energy restricted diet does not cause a greater weight loss [4-6] . If you are still a believer in the energy in energy out dogma this should have you worried. The truth is that expending more energy often does not lead to greater weight loss.

Leanne M. Redman [7] reported that one study [8] showed an 80% increased weight loss with exercise. Participants in the study were put on a National Cholesterol Education Program (NCEP) diet or the same diet with exercise (brisk walking or jogging 3 times a week). What Redman forgot to mention was that the exercise group also reported a 550 kJ/day smaller energy intake compared to the diet group.

McTiernan and co workers [9] randomized 202 men and women (sedentary/unfit persons, 40 to 75 years old) to control or an exercise intervention for 12 months. The exercise intervention was facility- and home-based moderate-to-vigorous intensity aerobic activity, 60 min per day, 6 days per week. Mean exercise time was 370 min per week for men and 295min per week for women. At 12 months exercise had resulted in 1.9kg and 3kg reduction in fat mass in women and men respectively. As mentioned in my previous post, it is difficult to account for all the variables in a study. Although the participants were asked not to change their diet, the researcher has only poor data on the participants’ diet.

You might argue that the above study shows positive results, showing how exercise effectively reduces weight and hinders weight gain. However, exercising for 60min per day for an entire year only to lose 3kg of fat, do not strike me as great results. Clearly the energy expended through exercise should have resulted in a larger weight loss according to the leading energy in - energy out dogma.

Joseph A. Houmard [10] and colleagues randomized 154 sedentary, overweight/obese subjects to either control or an exercise group for 6 months: 1) low-volume/moderate intensity group [~12 miles walking/week at 40–55% peak O2 consumption], 2) low-volume/high-intensity group (~12 miles jogging/week at 65–80% VO2 peak), and 3) high-volume/high-intensity group (~20 miles jogging/wk at 65–80% VO2 peak). At six months the low-volume/moderate intensity group had lost 0.8kg of body mass. The low-volume/high-intensity group lost 0,6kg of body mass, while the high-volume/high-intensity group which expended the most energy exercising, lost a whopping 1,8kg of body mass.

The fairies in the back of my garden were thrilled.

Back to Leanne M. Redman at Pennington Biomedical Research Center. Although she is convinced that the human body can be considered equal to a closed system where energy in and energy out is easy to measure and control and is the only thing worth measuring, she has done some very fine research. With her colleagues she did a study where 36 overweight, but otherwise healthy people were randomized to either control (healthy weight maintenance diet), caloric restriction (25% reduction in energy intake), or calorie restriction plus exercise (12.5% reduction in energy intake and 12.5% increase in exercise energy expenditure) for 6 months. After three months weight had declined by 7.4% for calorie restriction only and 5.8% for calorie restriction plus exercise. At six months the numbers were 10.4% and 10.1%, respectively. So the weight loss was equal using two different strategies and calculated energy deficit was equal. However, for men in the diet group fat loss accounted for roughly 64% of the weight lost and 68% in the exercise group. For women, fat loss accounted for 75% of total weight lost in the diet group and 85% in the exercise group.

There was a substantial loss of non fat tissue regardless of method, but the loss of different tissues also indicates different amounts of energy lost.

In 2002, Jeff Volek and co workers [11] put 12 overweight women and 10 overweight men on a low fat/low calorie diet and made them exercise four to five times a week. The goal was to reduce weight by 5kg in eight weeks. The women in the trial lost 4.3+3.4kg. But only 58% of this was fat mass. Percentage body fat went from 44.2 to 43.2. After eight weeks the women were just as fat. Had all the weight lost been fat, body fat percentage would have dropped to 41.8 – a much more reasonable drop. Imagine these women losing weight like this outside of a study setting, eating less and exercising – perhaps watching the calorie counter on the treadmill. They would probably have been thrilled to lose 0.5kg of weight each week.

Robert Ross [12] randomized 52 obese men to control, weight loss by diet alone, weight loss by exercise alone or exercise with stable body weight. Participants in the diet-induced weight loss group were asked to reduce daily intake by 700kcal during the treatment period to achieve a weekly weight loss of approximately 0.6kg. To lose the same amount of weight, participants in the exercise-induced weight loss group were asked to maintain a pre study isocaloric diet for the duration of the treatment period and to perform exercise that expended 700 kcal/d. Participants assigned to exercise without weight loss were asked to maintain body weight and to consume enough calories to compensate for the 700 kcal of energy expended during the daily exercise sessions.

The average weight loss was similar for both the diet-induced weight loss group (7.4 kg) and the exercise-induced weight loss group (7.6 kg). And the caveat? Calculated daily energy deficit (Doubly Labeled Water 14 Days during Weeks 6 to 7) was -663kcal in the diet group and -1039kcal in the exercise group. And although the participants in the exercise group were to not change their diet, they were instructed to follow official dietary guidelines. In addition the total fat loss in the diet group was 4.8kg and 6.1kg in the exercise group.

I could go on showing exercise studies that does not support the view that energy expenditure and intake is something we can control and should base exercise on – that we can calculate fat lost by exercise. Weight loss is vastly different between studies that are aiming for similar energy deficits. It is likely that the type of exercise is a confounding factor, as well as individual differences and lots of other hard to control for variables. My point is, if researchers struggle this hard to calculate fat loss and to use energy expenditure and intake as guidelines in weight loss, how is regular Joe to cope with the same task?

In “Exercise for overweight or obesity”, a Cochrane Database Systematic Review from 2006, the authors found that “When compared with no treatment, exercise resulted in small weight losses across studies.” The actual mean weight lost with exercise was 0.5 to 4.0kg. In the conclusion come the rather sad statements:

“The results of this review support the use of exercise as a weight loss intervention, particularly when combined with dietary change. Exercise is associated with improved cardiovascular disease risk factors even if no weight is lost.”

Meaning that, exercise is good for you, even though you probably won’t lose any weight.

In “A dose-response relation between aerobic exercise and visceral fat reduction: systematic review of clinical trials,” Ohkawara [13] and co workers found that there is a correlation between visceral fat loss and amount of energy expended exercising. But, the correlation was only present in subgroup analyses and nonexistent if people with metabolic-related disorders were included. Once again those with metabolic dysfunction ruin the perfect stats, and once again it seems that in those that need it the most, exercise don’t yield the expected results.

Robert Ross also did a dose-response review, in 2001. He found a dose response relationship between exercise and weight loss only in short term studies (less than 26 weeks), and not in long term studies [14].

Although there is a positive dose response correlation between exercise and weight loss (fat loss) in subgroups of people we still cannot assume that the correlation exists because more energy expended causes more weight loss. Exercise may cause a shift in the metabolism that make us less hungry and make us compensate less for the energy expended. The effect may also be unrelated to the amount of energy expended. As mentioned, there are a lot of variables at play here. Often when energy expenditure is upped it is through higher intensity exercise. Any difference between low and high energy expenditure might just as well be because of different intensities.

You will have a difficult time finding solid data showing a strong correlation between energy expended during exercise and consequent fat loss. More exercise and more energy demanding exercise does not necessarily give better long term results. (it often does not) Because of this, when we want to find the exercise type that is best for weight loss, we should base our decision on factors other than energy expenditure.

The question is what factors?

I’ll let Katarina Melzer at Geneva University Hospital have the last word on this subject:

“Increased energy expenditure due to short-term PA is not immediately compensated for by changes in energy intake. Once moderate to intense PA is performed regularly and on the long-term basis, however, a distinction has to be drawn between lean and obese subjects. While the lean show a tendency to balance the extra PA energy expenditure by adapting their energy intake accordingly within a period, of about 3 days, the obese, probably due to their excess energy storage, do not show such a compensatory mechanisms.” [15]

Next: Exercise intensity

References

1. Leibel RL, Rosenbaum M, Hirsch J: Changes in energy expenditure resulting from altered body weight. N Engl J Med 1995, 332: 621-628.

2. Jeffery RW, Wing RR, Sherwood NE, Tate DF: Physical activity and weight loss: does prescribing higher physical activity goals improve outcome? Am J Clin Nutr 2003, 78: 684-689.

3. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK: American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2009, 41: 459-471.

4. Nieman DC, Brock DW, Butterworth D, Utter AC, Nieman CC: Reducing diet and/or exercise training decreases the lipid and lipoprotein risk factors of moderately obese women. J Am Coll Nutr 2002, 21: 344-350.

5. Cox KL, Burke V, Morton AR, Beilin LJ, Puddey IB: The independent and combined effects of 16 weeks of vigorous exercise and energy restriction on body mass and composition in free-living overweight men--a randomized controlled trial. Metabolism 2003, 52: 107-115.

6. Dengel DR, Galecki AT, Hagberg JM, Pratley RE: The independent and combined effects of weight loss and aerobic exercise on blood pressure and oral glucose tolerance in older men. Am J Hypertens 1998, 11: 1405-1412.

7. Redman LM, Heilbronn LK, Martin CK, Alfonso A, Smith SR, Ravussin E: Effect of calorie restriction with or without exercise on body composition and fat distribution. J Clin Endocrinol Metab 2007, 92: 865-872.

8. Wood PD, Stefanick ML, Williams PT, Haskell WL: The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. N Engl J Med 1991, 325: 461-466.

9. McTiernan A, Sorensen B, Irwin ML, Morgan A, Yasui Y, Rudolph RE, Surawicz C, Lampe JW, Lampe PD, Ayub K, Potter JD: Exercise effect on weight and body fat in men and women. Obesity (Silver Spring) 2007, 15: 1496-1512.

10. Houmard JA, Tanner CJ, Slentz CA, Duscha BD, McCartney JS, Kraus WE: Effect of the volume and intensity of exercise training on insulin sensitivity. J Appl Physiol 2004, 96: 101-106.

11. Volek JS, Gomez AL, Love DM, Weyers AM, Hesslink R, Jr., Wise JA, Kraemer WJ: Effects of an 8-week weight-loss program on cardiovascular disease risk factors and regional body composition. Eur J Clin Nutr 2002, 56: 585-592.

12. Ross R, Dagnone D, Jones PJ, Smith H, Paddags A, Hudson R, Janssen I: Reduction in obesity and related comorbid conditions after diet-induced weight loss or exercise-induced weight loss in men. A randomized, controlled trial. Ann Intern Med 2000, 133: 92-103.

13. Ohkawara K, Tanaka S, Miyachi M, Ishikawa-Takata K, Tabata I: A dose-response relation between aerobic exercise and visceral fat reduction: systematic review of clinical trials. Int J Obes (Lond) 2007, 31: 1786-1797.

14. Ross R, Janssen I: Physical activity, total and regional obesity: dose-response considerations. Med Sci Sports Exerc 2001, 33: S521-S527.

15. Melzer K, Kayser B, Saris WH, Pichard C: Effects of physical activity on food intake. Clin Nutr 2005, 24: 885-895.

What is the best exercise for fat loss?

2010-12-20T17:50:00.000+01:00

You’d think this question was easy to answer after studying exercise and health for many years. You’d think I would know. I would think I would know, but when asking myself the question recently, it struck me that I didn’t. I can make a calculated guess, but I should know.

What sort of exercise would you recommend for an overweight person wanting to lose weight? Cardio, strength, plyometrics, combos? What about sets, repetitions, load, restitution and what about energy expenditure? Different exercise forms give different stimuli and affect different tissues, so it is likely that some forms of exercise are to be preferred to others. But which?

In "the Biggest Loser," overweight people are pushed through extreme exercise to lose weight

The Science

Let’s look at the basic science as an introduction.

If I was to give an overweight person exercise advice based on a superficial glance at the scientific literature, the advice would be, “Don’t exercise. It doesn’t work”. Exercise trials are usualy ineffective unless accompanied by a dietary intervention.

A 1995 meta-analysis [1] concluded that:.

“Aerobic exercise causes a modest loss in weight without dieting. Exercise provides some conservation of FFM [fat free mass] during weight loss by dieting, probably in part by maintaining glycogen and water.”

When the John E. Fogarty International Center at the National Institutes of Health sponsored two conferences that dealt with obesity as a public health problem, there was controversy surrounding the question of cause and effect and they concluded: “The importance of exercise in weight control is less than might be believed, because increases in energy expenditure due to exercise also tend to increase food consumption, and it is not possible to predict whether the increased caloric output will be outweighed by the greater food intake.”

A recently published study showed how overweight women put to exercise regularly, unconsciously compensated for the increased activity level by being less active when not exercising [2]. Based on my own experience with sports, I don’t find this odd at all.

Joseph E. Donnelly from the University of Kansas was the lead author of the American College of Sports Medicine position stand on “Appropriate Physical Activity Intervention Strategies for Weight Loss and Prevention of Weight” from 2009 [3].

On the question of whether physical activity will prevent weight gain they give it evidence category A. Evidence category A is in the words of NHLBI "Evidence is from endpoints of well-designed RCTs (or trials that depart only minimally from randomization) that provide a consistent pattern of findings in the population for which the recommendation is made. Category A therefore requires substantial numbers of studies involving substantial numbers of participants."

Trouble is, there are no studies that can point to exercise being the cause of weight not gained. It’s all based on the much observed inverse relationship between body weight and physical activity level. It is based on two factors co appearing i.e. leanness and exercise, but we do not have any data suggesting that the exercise is the cause of the leanness. Evidence category A anyone?

On the question of whether physical activity will prevent weight regain after weight loss they gave it an evidence category B. Evidence category B is defined thusly: “Evidence is from endpoints of intervention studies that include only a limited number of RCTs, post hoc or subgroup analysis of RCTs, or meta-analysis of RCTs. In general, Category B pertains when few randomized trials exist, they are small in size, and the trial results are somewhat inconsistent, or the trials were undertaken in a population that differs from the target population of the recommendation.”

Donnely et al refer to the 2000 systematic review by Finnish researchers Mikael Fogelholm and Katriina T. Kukkonen-Harjula [4]. This review concluded that “…the role of prescribed physical activity in prevention of weight gain remains modest.” Much of the blame is placed with study participants who showed poor adherence to exercise programs.

Joseph E. Donnelly

But Donnelly and colleagues agrees that physical activity is a poor strategy for weight loss and writes: "Few studies with sedentary overweight or obese individuals using PA as the only intervention result in >3% decreases of baseline weight. Therefore, most individuals who require substantial weight loss may need additional interventions (i.e., energy restriction) to meet their weight loss needs."

As Gary Taubes pointed out in The scientist and the stairmaster: "Rare is the person who decides the time has come to lose weight and doesn’t also decide perhaps it’s time to eat fewer sweets, drink less beer, switch to diet soda, and maybe curtail the kind of carb-rich snacks—the potato chips and the candy bars—that might be singularly responsible for driving up their insulin and so their fat."

Even the ultimate tome of complete gibberish, the report by the World Cancer Research Fund: “Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective” (http://www.dietandcancerreport.org/) gets at least something right and writes: “Eventually, food intake will increase to compensate for the exercise-induced energy loss, although the degree of compensation may vary greatly between individuals.”

The report from WCRF gives us several references in support of their argument that physical activity reduces the risk of obesity, but a closer look at the references reveals that more of the references go against the conclusion than are in support and none of the studies can show anything but correlation.

A new analysis in JAMA that notes an association between physical activity and weight gain start off with saying: “Data supporting physical activity guidelines to prevent long-term weight gain are sparse, particularly during the period when the highest risk of weight gain occurs.”

Another quite recent prospective cohort study involving 34 079 healthy US women (Women’s Health Study) found that among women consuming a usual diet, physical activity was associated with less weight gain only among women whose BMI was lower than 25, suggesting that if you’re already fat physical activity does not help. The study authors wrote: “…once overweight, it may be too late because physical activity—at least, at levels carried out by study participants—was not associated with less weight gain.”[5]

It is not hard to paint a bleak picture of the role of exercise in weight loss and weight loss maintenance. However, I still remain convinced that exercise is and should be a cornerstone in obesity treatment.

The trouble with exercise interventions is the same as is the subject of Gary Taubes recent blog post. The trouble is controlling for variables. If overweight people are included in an exercise intervention, it is very likely that they will also be more health conscientious when it comes to other lifestyle factors. When interventions that include both diet and exercise approaches are carried out, the researchers will try to control for the effect of different variables by doing multivariate analyses. But the analyses cannot and do not say anything about causation. Do people exercise because they are losing weight or are they losing weight because they exercise?

The fact that exercise recommendations are based on the correlation between exercise and weight loss and the fact that no study can point to a definitive causal link, does not mean that that causal link is not there. It does not make it less likely that exercise do cause weight loss and prevent weight gain. It just means we have to be careful when interpreting and to be open to new information.

The reporting of mean weight loss may also be deceiving. Boutcher and Dunn writes: “The results of exercise programmes designed to reduce body fat are disappointing. However, the reporting of weight loss as mean values disguises those individuals who do lose significant amounts of fat.”[6] Again, weight loss in those who actually do lose weight when exercising might be caused by many things, but it might also be caused by exercise. In addition, there is the trouble with reporting only weight loss, and not body composition.

Despite the lack of support from many scientific trials there are physiological mechanisms that make it likely that physical activity can prevent or protect against weight gain. There are also many risk factors related to the metabolic syndrome that are improved, seemingly by exercise alone – and if so, why should not fat mass be improved? The above mechanisms are the ones we have to efficiently address if we are to use physical activity as a weight loss tool. In addition many clues may in fact be hidden in articles whose conclusions does not favor exercise.

I will break this subject into several posts. Next posts theme: does the amount of energy expended during exercise affect the amount of fat mass lost?

References

1. Garrow JS, Summerbell CD: Meta-analysis: effect of exercise, with or without dieting, on the body composition of overweight subjects. Eur J Clin Nutr 1995, 49: 1-10.

2. Manthou E, Gill JM, Wright A, Malkova D: Behavioural Compensatory Adjustments to Exercise Training In Overweight Women. Med Sci Sports Exerc 2009.

3. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK: American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2009, 41: 459-471.

4. Fogelholm M, Kukkonen-Harjula K: Does physical activity prevent weight gain--a systematic review. Obes Rev 2000, 1: 95-111.

5. Lee IM, Djousse L, Sesso HD, Wang L, Buring JE: Physical activity and weight gain prevention. JAMA 2010, 303: 1173-1179.

6. Boutcher SH, Dunn SL: Factors that may impede the weight loss response to exercise-based interventions. Obes Rev 2009, 10: 671-680.

Play

2010-12-10T20:41:00.000+01:00

Let’s face it, we are social animals. Being forced to solitary living is considered a punishment and rightly so. As social animals we play, both as young and as adults. Play builds social skills, it makes sure our neurons are properly connected and it builds and protects our body.

With ever growing focus on lifestyle and health comes ever new approaches to living healthy. Health is not just diet or exercise, it’s a lifestyle. The Paleo diet, which focuses on a natural human diet based on evolutionary and anthropologic data, seems to be here for good. And with paleo dieting came paleo living. Paleo living seem to fill a void, a longing for something less urban, something real.

Erwan Le Corre at MovNat writes: “The 'zoo' is a modern, global and growing phenomenon generated by the powerful combination of social conventions, technological environment and commercial pressures. Increasingly disconnected from the natural world and their true nature, zoo humans are suffering physically, mentally and spiritually.”

I believe he is correct and I believe that all around us we can see the results of people fighting it.

Many new exercise trends focus on natural movements or movement patterns. The appeal to our primordial needs sell. Not only do natural movements sell and appeal, but so does natural surroundings to move in. No doubt our urban surroundings can be depressing and alienating. The walls are hard and unforgiving if met with force, the ground we walk upon equally so.

Undoubtedly, the human animal is not well adapted to asphalt and steel living. We can smash our skulls open simply by falling from an upright position, and in an urban surrounding we often place our heads far higher than our bodies’ height. In other words, we brake easily and surrounding ourselves with metal and concrete might not be the best of ideas. We all like things soft. Of course we don’t feel good.

An innate urge to move, suppressed

That, to the right is me, teaching local kids how to do a so called wall flip. I teach them Parkour, or at least I am there supervising while they run around.

When a group of human youngsters, like those in my group, are given space to play in, equipment to play with and a few examples to follow, their behavior is strikingly similar to most other large group living mammals. It is a natural movement pattern utilizing all the movements of the body. They’re rolling, vaulting, climbing, jumping, crawling, falling, running, sliding and so on. Play will cause such diverse movement patterns because it is not stylized. The movements become natural because they’re dictated by biomechanical efficiency or the acute pleasure of doing that move.

Those advocating exercise in the nature tells us to throw away our shoes, leap into the forest, find a log and toss it about. There is nothing natural about running on a rubber clad stationary treadmill followed by sitting in various contraptions pushing and pulling on metal and plastic. And the repetitiveness of it all might damage both our motivation and bodies.

Because going to the gym does not appeal much to our more primitive needs or our mammalian instincts (except perhaps that it serves as a location for mating rituals where males swill strut like a Blue Bird of Paradise and the females assess the potential, or vice versa), it will easily make us bored. For many, it will feel meaningless and unfulfilling and the risk is high that any joy of exercising will be replaced by the joy of getting positive results at the expense of any personal pleasure of moving.

Getting results is an external (extrinsic) motivation often directed at body weight, size, shape or function. These goals are to be reached in time and exercise is only a means to reach that goal. This motivation differs a lot from an internal (intrinsic) motivation, one that comes from the joy of exercising in itself and which is thus instantly rewarding.

It does not require a very large step back and a bigger perspective gained for the tragicomic situation of fitness studio exercise to become apparent.

Most social animals will to my knowledge play mostly as younglings, and play will gradually constitute smaller part of the day. It is the same with us humans. When we are young we are allowed to play, encouraged even to move with no apparent meaning or goals other than the share joy of moving. As we age, physical activity is gradually stylized, systematized and organized. We join sports, often competition sports where the main goal is performance. And we no longer call it play – it is far too serious to be called play.

So when we are young we play, but when we grow up we have to call is exercise and we often do it even when we don’t want to.

This lack of play in modern forms of physical activity goes very well with our mechanistic view of the human body. Focus should be on fat burning, muscle growth, body sculpting, VO2max, lactate threshold and all the rest. We no longer exercise the body, we exercise tissues.

The countermeasures
When our Parkour training starts, in no way do I have to tell the kids to start exercising or to motivate them to start. I have to hold them back. I have to hold them back so I don’t suddenly find one of them hanging under the roof without something soft to land on. There is an inherent drive to play in us, so strong it is hard to control and it is most obvious in the young. And why should we control it? In these sessions no one lies down doing sit-ups to get six pack abs. They roll, run, climb, hang, crawl and within minutes have activated most of the skeletal muscles in the body.

It’s like letting your dog run and play with other dogs – when it is play time there is no stopping the playful instinct. Mark Sisson knows the importance of play and advises us to go on imaginary hunts for joggers. I’m sure it’s good advise although I am somewhat afraid that one can easily get carried away and suddenly find oneself sitting on top of a panic-stricken jogger, heart racing with pure adrenaline joy.

No motivation for exercise is all intrinsic or extrinsic. Even if we really enjoy the exercise in itself we most often have external goals driving us. The problems occur when the scale gradually tips in favour of external rewards.

In no way am I suggesting that we are not playing. There is lots of play out there and all is not stylized and boring.

I believe that many of the smaller physical activity trends have emerged because of a lack of play in traditional sports. Skateboarding is a prime example. In the beginning of skateboarding it was all just for fun. No rules, no competitions, just the board, the wheels, your shoes and your body.

Snowboard is an equal example from winter sports. Unlike most forms of skiing it was all for fun. No rules. Just play. In the water the board to play with can be a surfboard, wakeboard or any other floating device.

Play does not, however, exclude competition. One of the fastest growing sports in the US is Ultimate Frisbee. It is a playful activity indeed. Frisbee golf is also great fun and even more fun with some competition (even better with a cold beer halfway in).

Many such exercise trends have emerged and seems to me to be emerging in increasing numbers. The trend is great and YouTube is overflowing with examples of skilled people exercising for the fun of it.

An interesting aspect with some of these new play-based exercise trends, is that they have in them something other than the activity itself and something other than results and play. It is not about our bodies, but our surroundings. When the traceur (Parkour performer) (or a skateboarder for that matter) is running around in the city he is taking back his alienating surroundings. He is making the concrete jungle* his jungle. We are being estranged by our very homes, we don’t feel good and we don’t much want to move when everything is so bloody hard. But where the average person sees a wall and a blocked path the traceur sees a challenge. If our surroundings are hard then we’ll be soft.

There is no need to take of your shoes and look for the nearest forest. It is not our surroundings that that make us behave naturally. Although it may help, we do not need trees or grass to stimulate play and natural behavior. An alien watching chimps play in the forest and kids playing in the urban jungle would have a hard time differentiating the species. One covered in hair, the other by fabric.

You can take the human out of nature, but you cannot take nature out of the human. Any ground is our playground.

*Urban jungle is perhaps not a good term. A city is nothing like a jungle. Humans evolved living in small groups, small enough for an individual to properly know all other individuals of that very group. A city may be comprised of hundreds of thousands and even millions of people. The only way for an individual to retain his mental health is to form small subgroups (tribes) and to consider everybody else part of the background. So one major reason to seek forest exercise is to avoid the social overkill of city living. To take a break – to be distracted. And distraction is indeed one of the most important reasons why physical exercise makes us feel good.

The Human Animal

2010-12-03T19:15:00.001+01:00

When I grew up I loved watching nature shows on TV (and I still do). My dad is a science teacher and used to tape all the good shows. I especially remember David Attenborough coming closer to animal life than anyone I had ever seen. The Velvet Claw made a big impression as did The Living Planet.

I also remember well another show hosted by Desmond Morris, called The Human Animal. I remember how his most famous book, The naked ape was always part of the bookshelf at home and I watched the show over and over.

For some reason I started thinking about this great TV show and found it’s available online. One episode in particular is very interesting. Morris looks at feeding behavior and the evolution of it. How the fruit eating forest ape became the meat eating plains ape, the nutritional value of insects, earth eating and much, much more. He also argues that humans are not very well adapted to savannah living and that human ancestors might have gone from forest living to becoming an “aquatic ape”.

Great show and recommended viewing here.

What if…

2010-11-20T20:49:00.000+01:00

“And then, one Thursday, nearly two thousand years after one man had been nailed to a tree for saying how great it would be to be nice to people for a change, a girl sitting on her own in a small cafe in Rickmansworth suddenly realized what it was that had been going wrong all this time, and she finally knew how the world could be made a good and happy place. This time it was right, it would work, and no one would have to get nailed to anything. Sadly, however, before she could get to a phone to tell anyone about it, a terrible stupid catastrophe occurred, and the idea was lost forever.”

Douglas Adams

What if there was one way to lose weight that was the correct way. One way that would always work. In the name of moderation, let’s say a method that works 90% of the time – there will always be the odd case of Prader-Willi or some strange genetic disorder that screws up the perfect statistics. So let’s say 90% and round it up.

So, a way to lose weight that always works. Let us also say that this method already exists and that it has been around for ages, and although many know about it few know it is the right one.

Let us also imagine that there are two main foundations to the method. One is the reduction of inflammation, in which the intake of easily digestible carbohydrates and the intake of omega 6 fatty acids amongst other factors play important roles. The other foundation is the increase of lipolysis (getting the body to burn its own excessively stored energy instead of asking for external energy), because weight loss and fat burning are two parts of the same. In increasing lipolysis the reduction of insulin and glucose levels are of paramount importance. Doing so requires the reduction of easily digestible carbohydrates.

Now let us say that this method i.e. eating mostly animal products, supplementing with vegetables and taking in copious amounts of non omega 6 fats and no refined carbohydrates, always works. But we don’t know it, because too few of us are looking at the details, and to many are focusing on the entire weight loss “package.”

In weight loss studies the participants lose weight by utilizing different approaches, but no approach ever has a 100% success rate. All participant may lose some weight, but some lose more than others and some often nothing at all. But no matter the method, lost weight often returns quickly. These results have led many researchers to think weight loss in it self is futile. It has led some to reason it is all due to lack of willpower.

But might the results fool us?

Imagine you start following the Atkins diet. You lose lots of weight during the first weeks. But then you start feeling unwell. You get tired, light headed and you get headaches and your stamina is not what it used to be.

So you decide to increase your intake of carbohydrates. The symptoms disappear and in a short while the lost weight has returned. From that moment on you proclaim that you have tried everything from Ornish to Atkins, but nothing worked for you.

But let’s say one of the many weight loss regimes you tried actually was the right one. That “this time it was right, it would work” but “a terrible stupid catastrophe occurred, and the idea was lost forever.”

You forgot to put salt on your food.

Salt is important when you restrict your carbohydrate intake and you often have to increase your salt intake with carbohydrate restriction, not decrease it as many does.

Such a simple, stupid little thing could separate success and failure. It could deprive you of the chance to finally get it right.

There are many less significant factors that can easily mess thing up despite us having the foundational principles right and thus make the whole strategy seem futile. Salt is one, stress another. Too little sunlight or even to little carbohydrates are yet others.

Imagine that the right way is already here, but we are blinded by our search for quick fixes, inability to deduct or simply our lack of knowledge.

When I first learned of carbohydrate restriction it all sounded so easy. I thought everybody could lose weight if only they were taught the basic principles – the foundations. I’ve changed my mind now. Not getting professional help could be what keeps you from finally getting to the truth.

The great tragedy of it all is that most weight loss strategies will be unsuccessful most of the time and you will not know if your unsuccessful attempts are because the basic principles are wrong or if you got them right, but a minor detail was out of whack.

Like talking to a brick wall

2010-11-16T15:25:00.000+01:00

To disagree only as much as the evidence permits
Jamie Scott, the Primal Muse hit a brick wall recently. Metaphorically speaking, of course. The wall’s embodiment was a narrow minded and rude purveyor of what to the untrained eye might look like science.

Scientific disagreements are fascinating because science as a “reality exploring tool” does not or rather should not actually have disagreements. That is, at least not in the “difference of opinion” definition. This is because the data and methods are what they are and leave little room for personal interpretation. A scientific disagreement, I believe, is more often a refusal or a failure to agree in which personal opinion has no other part but to cause the actual refusal.

- The evidence does not support recommendations to reduce intake of saturated fat to avoid or treat heart disease.
- I disagree.
- …?

Are scientific disagreements simply the result of insufficient knowledge?

I am hoping to start earning myself a ph.d. in the near future. As often, funding is sparse and getting scientific studies up and running is a tedious process. In the process there are many professors and wise men and women to meet with. Sometimes when talking to the very people who are in charge of educating the nation’s finest in the fields of health and nutrition I find that I disagree strongly with some of the things they have to say.

Although, I feel disagree is not the proper wording. To me, disagree implies a matter of opinion when what it really is, is a matter of facts. Sometimes I know with certainty that the person across the table is wrong. We don’t disagree, this is a conflict. There are contradictory statements and at least one statement is wrong.

I find myself thinking that “…boy this person hasn’t done his homework!” But rarely is the moment a good moment to air my disagreement (and thus being in an open conflict) out loud even if in the most humble manner. These are the very people whom I am thoroughly dependent upon to climb my way up the ladder of knowledge, steadily ascending towards a decent job and paycheck. A disagreement must wait and make way for a smile and a nod.

I know how this may sound, and let me make a small defensive note. I am in no way attempting to put myself above these very skilled and experienced people. In no way do I like the feeling of knowing something that my adversary obviously has gotten wrong or should know.

The thing is, it only takes one small fact which one person possesses and the other do not to make a conflict. The conflict isn’t based on a disagreement of opinion, but on a lack of knowledge. The lack of knowledge is regardless of the total amount of knowledge the conflicting parties may possess.

However, when experiencing those tongue biting moments I wonder. I’ve been taught how scientific paradigms rarely change and when doing so it is often because new blood comes in and old blood goes out of the particular scientific community. I’ve been told that one of the reasons why scientist rarely change their mind and leading hypotheses is because they are humans, subject to the same mentality as the rest of us and as we know, the rest of us don’t like being wrong.

But how often really, are scientists exposed to hypothesis-slaying data or information and still manage to shield their belief and change the premises in a most acrobatic manner? How often really, is the ego to blame and how often is the disagreement caused simply by a lack of knowledge?

More and more often I am inclined to think the latter most likely. Being no expert on the human psyche I find it very odd if so many people would intentionally lie and deceive for personal gains and to save face.

Now, I am not trying to excuse people like the Muse’s brick wall. As scientists, it is their responsibility to be updated or to at least to know when they are not. A lack of knowledge may cause conflicts but the cause of insufficient knowledge often seems consciously self imposed – an unwillingness to seek out the correct, important or “alternative” information.

So paradigms linger on and disproven hypotheses remain because some people don't bother to read a book. How many keepers of the saturated fat – heart disease dogma do you think has chosen not to read Colpo, Kendrick or Ravnskov and dismissed the literature simply from reading the title of the books? My guess is many, and so the conflict remains.

The occasional twat knowing he’s wrong, but unwilling to admit it is the exception and not the rule.

Many, if not most of these people are good people, and for the time being, acting as protector of the hill and are thus prone to fall into defensive mode. But, they are acting in the belief that they are in fact doing good – spreading and accumulating knowledge – being the horsemen of science and reason. How delusional we can be.

It is a misconception that every conflict has to parties, as it is a misconception that one of the parties comprising the conflict must be right and the other wrong. It only takes one.

And sadly it the world of conflicts, when rational arguments bounce off like the sun's rays in a mirror blinding you in return, the only remaining alternatives are surrender or full-on battle.

Come on guys, you’re smarter than this

2010-11-09T20:30:00.000+01:00

Just because a wording, written or spoken is simplified to better communicate the message at hand, it does not mean we should think simple thoughts.

When I tell my pupils that sugar makes us fat (the word fat can be replaced by sick with no consequences for the argument), they look at their bottle of coke, then down at their skinny teenager body and say, “Oh yeah! I drink a lot of soda, but I’m not fat”

I can excuse and understand the response because I know a 14 year old has too little experience in logic thought. They are on a constant pubertal high and struggles to imagine consequences beyond those of tomorrow. And they are always out to get you and prove you wrong.

Patiently, I can explain to the teenager that “…all that sugar is going to make you fat, but not instantly. Not now, but in time.” “Sugar make us fat,” does not mean “Taste sugar and expand immediately.”

I find it more difficult to excuse the adult population who has a longer track record in being exposed to logic and who are consistently being reminded of the complexities of life.

Life gets more complicated after puberty. Black and white turn into shades of grey. Not because life itself changes, but because we gradually see the complexities. Fortunately, life also gets less confusing with age, but that’s a different matter.

The Twinkie professor is losing weight while eating junk. Does this prove that junk food is not to blame for obesity and lifestyle disease? No, of course not. You are smarter than that.

- Sugar may cause diabetes.
- But many people eat high sugar diets, and do not get diabetic…
- So?

Sugar still causes diabetes. Stop thinking in absolutes. You can be smarter than that. Never mind the fact that I said “may”. We are complex organisms. Our genes differ in type and expression. We live in different environments and we feel different feelings. When too many factors coincide, sugar causes diabetes. I did not say always.

Eating a low carb diet will make most overweight people lose weight. The fact that your friend heard of a person not losing weight on a low carb diet, does not mean carbohydrate restriction is not an effective weight loss tool. Stop for a while and think. You should be smarter than that.

- Overweight may be caused by a too large intake of carbohydrates.
- But what about all those skinny Asians on a high rice diet?
- What about them?

Carbohydrates may still cause overweight and may still be the single most important factor in developing overweight. We are complex beings in a complex world. When too many factors coincide, carbohydrates will make you fat. An insufficient amount of factors have coincided in the people you are referring to. Stop thinking in absolutes. Be smarter than that.

- Grains make us sick.
- But most people here eat lots of grains and many are not sick.
- So?

Most people do not know how great they can feel, how good their heath can be. Just because you don’t consider yourself sick, does not mean your health couldn’t be much better.

Your recurring headaches, your stiff joints in the morning, your inability to concentrate, falling asleep on the couch when you get home from work, your mood swings and all the rest of those small symptoms you notice every day, but never consider to be anything but the normal state, are all signs of something being wrong. It is possible to feel great most of the time. You just haven’t experienced it yet or have forgotten Grains may be to blame for the fact that we no longer know how good we can feel as humans.

The black swan disproves the hypothesis claiming all swans to be white. Or so we are told. But the one fat person eating a low carb diet does not prove that carbohydrate restriction is not a very effective weight loss tool. It proves nothing. Stop thinking in absolutes. You need to be smarter than this.

Poppers swan example is perhaps not the best example for everyday use. If you knew there were no black swans yet encountered one during your walk by the water, you’d look for the punk with the spray can.

If most data indicate easily digestible carbohydrates as the primary cause of overweight and you see people that over time live on diets high in easily digestible carbs, yet remain lean, look for the punk with the spray can. Look for the confounding factors. There are many. The hypothesis remains.

The most horrible examples of a juvenile mind stuck in a body that has been pushed through a scientific education are found in the riders of the thermodynamic approach to weight management – those claiming overweight is caused by a too high energy intake. Those that tell you to count your calories and to calculate your energy expenditure despite the fact that they themselves have never bothered about energy in or out yet still stay perfectly thin.

In these people, the bell that should have gone off in the back of the mind is malfunctioning. Perhaps because of a lack of animal products in the diet. Perhaps because of the grains. No matter the cause, the result is an inability to see the gargantuan crack in their own wall of logic.

Stop thinking like a teenager. You have to be smarter than that.

The Twinkie professor has proven nothing and no headline has ever given you all the information you need to refute a theory.

Smoking causes lung cancer. The observation that your grandmother smoked all her life without getting cancer and dying of old age at 100 years, is not refutation material.

Jumping out of a plane without a parachute will kill you. There might have been people who have survived even this, but jumping out of a plane without a parachute will kill you. Just as grains make you sick and smoking gives you lung cancer.

The troublesome issue at hand is largely rhetoric in nature. Our constant efforts at trying to be skeptic, open minded and to prove others wrong result in alarmingly silly discussions. If each and every utterance should consider all related and relevant factors, our language will no longer be suited for communication.

“Carbohydrates may make you fat” is a better wording than, “carbohydrates may, in time, if ingested in high insulin raising form, and if ingested in the face of full glycogen stores, especially if ingested in a low nutritious form such as corns or in combination with a high omega 6 diet, and if ingested in periods of stress and in an individual whose genes make him or her susceptible to endoplasmatic reticulum stress and insulin resistance, make you fat.”

The first wording is no less correct because of its inferior word count and the sentence does not mean carbohydrates will always and under any circumstance inflate you beyond recognition upon touching your tongue. The second wording elaborates and describes very normal circumstances.

The first wording is not an absolute and if you consider it so, it is because you think in absolutes. Stop doing that. It only makes things worse.

Remember, media wants you to think in absolutes. A story considering all the factors will only appeal to the scientist and will not appear in your newspaper. This will confuse you, as the media will through using absolutes constantly contradict itself. One day carbs are good, the next day they will kill you. Stop and think. For the sake of sound minds everywhere, you must be smarter than this.

A closer look at adiponectin

2010-10-14T18:36:00.000+02:00

Whether insulin or leptin or adiponectin or PPAR gamma or NF KB or a bajillion cytokines are the proximate mediators of obesity or atherosclerosis is hardly the point, is it?

Kurt G. Harris MD

Although biochemistry can be marvelously exiting we must not lose sight of the bigger picture. It is increasingly unlikely that any one tiny substance is going to be our savior.

Still, adiponectin would be a good candidate. Adiponectin is indeed popular these days. If you type it in Pubmed you get about 7150 hits of which a whopping 4800 of these are from after 2006

Leptin is adiponectins evil twin brother
Whereas leptin is considered a pro inflammatory substance which may contribute to the development and progression of autoimmune responses, adiponectin seem to act as an anti-inflammatory factor. If your adiponectin level is low, you want to increase it. Leptin is generally high in obesity and lifestyle diseases while adiponectin is low. In vitro studies indicate that leptin promotes human breast cancer cell proliferation while adiponectin exhibits anti-proliferative actions.

Despite being produced almost exclusively by the fat tissue (lymphocytes also produce it) obese persons usually have low adiponectin levels. Expression of the mRNA responsible for the production of adiponectin is significantly decreased in the adipose tissue of obese mice and humans, which may explain why this occurs.

Adiponectin has showed numerous inverse correlations with weight, BMI, insulin, glucose, HOMA, atherogenic lipid profiles, cancers, liver disease, and dementia and so on. In short, adiponectin seems to positively correlate with anything positive.

Adiponectin itself may be antiatherosclerotic, as it acts as an endogenous antithrombotic factor and inhibits macrophage activation and foam cell accumulation, both being critical cytologic elements of atheromas. Stroke, coronary heart disease, steatohepatitis, insulin resistance, nonalcoholic fatty liver disease, and a wide array of cancers have been associated with decreased adiponectin levels.

Wozniak et al 2009

Serum adiponectin concentrations are inversely associated with obesity, insulin resistance and type 2 diabetes in rodents and humans, whereas increased serum adiponectin concentrations are associated with improved insulin sensitivity.

If you are overweight with good insulin sensitivity it means your fat tissue is doing its job, that there is minimal endoplasmatic reticulum stress, minimal inflammation and that you probably have a high adiponectin level.

Morrison et al (2010) examined 108 obese girls of who 31 was identified with having paradoxically high adiponectin levels. In these 108 obese girls, adiponectin levels at age 16 years independently predicted HDL level (positive) and waist circumference (negative), insulin level (negative), and glucose (negative) at age 23. Paradoxically high adiponectin levels at age 16 was a negative independent predictor for waist circumference, HOMA-IR and for the components of the metabolic syndrome at age 23.

Adiponectin and rodents
Most of what we know about adiponectin is from rodent studies. T. Yamauchi and colleagues showed that decreased expression of adiponectin correlates with insulin resistance in mouse models of altered insulin sensitivity. They propose that adiponectin decreases insulin resistance by increasing fatty acid oxidation and thus decreasing triglyceride content in muscle and liver in the obese mice. In lipoatrophic insulin resistant mice the resistance was completely reversed by administering a combination of physiological doses of adiponectin and leptin. When administered separately the resistance was only partially improved. The results from these trials are of course interesting and important, but the authors naturally concluded that “...adiponectin might provide a novel treatment modality for insulin resistance and type 2 diabetes,” thus missing the bigger picture by a mile.

In normal mice adiponectin administration has been shown to improve insulin sensitivity and lower glucose levels.

The insulin sensitizer agonist with the marvelous name of peroxisome proliferator-activated receptor-gamma (PPARg) stimulates adiponectin production in fat tissue. Adiponectin is thought to be part of this agonist's mechanism for lowering circulating fatty acids and increasing fat oxidation. The increase in insulin sensitivity by adiponectin might be simply from the increased fatty acid oxidation ameliorating fat cell overload.

Additionally, adiponectin has a direct effect on glucose uptake in skeletal muscle and adipose tissue and may increase the glucose transporter (GLUT4) translocation to the plasma membrane. Interestingly, pro-inflammatory cytokines, such as TNF-α and IL-6 are potent inhibitors of adiponectin gene expression or protein secretion.

In the early 2000 Matthias Blüher and colleagues produced a strain of the genetically engineered FIRKO mouse. This mouse lacks insulin receptors in the fat tissue. An inability to store energy in fat tissue and especially to take up glucose is normally very harmful. The FIRKO mice are immune to the dietary induced obesity used in other mice. However they live quite a lot longer than normal mice. Due to its genetic defect the FIRKO mouse have normal insulin sensitivity and normal glucose homeostasis. Despite its lean shape the FIRKO mouse also over express adiponectin. Transgenic mice lacking adiponectin on the other hand show impaired insulin sensitivity and an abnormal glucose homeostasis.

The over expression of adiponectin could be what saves the FIRKO mouse from the normally observed ill effects of adipocyte insulin resistance.

Intravenous injections of adiponectin in rodents have increased adiponectin in the cerebrospinal fluid which indicates brain transport. When injected directly into the brain adiponectin decrease body weight in rodents mainly by increasing energy expenditure.

The leptin deficient ob/ob mice respond particularly well to adiponectin injections both in brain and serum and shows increased thermogenesis, weight loss and reduction in serum glucose and lipid levels after injections.

One proposed mechanism for the coexistence of obesity and insulin resistance is endoplasmatic reticulum stress caused by the growing adipocytes. Obesity induces ER stress in mouse adipose tissue, which also correlates with reduced adiponectin levels. Suppressing ER stress increases adiponectin levels in 3T3-L1 adipocytes in vitro and alleviates diet induced adiponectin downregulation in mice.

Adiponectin, diet and weight loss
The best way to increase adiponectin is to lose weight as adiponectin increases in plasma with fat loss. Shai et al fond a significant increase in adiponectin level during both weight-loss and maintenance phases despite dissimilar macronutrient intakes.

Severely obese women has significant less fasting and postprandial (medium carb diet) adiponectin compared to lean women.

Sidika E Kasim-Karakas gave 22 healthy postmenopausal women a eucaloric low fat – high carb diet for 4 months followed by the same diet (15%fat) only energy restricted for 8 months. The researchers wondered whether energy restriction would modulate the inflammatory response to a high carb diet. The eucaloric diet decreased adiponectin from 16.3 to 14.2mg/L (P<0.05). The energy restricted diet increased adiponectin from 14.2 back to 16.3.

During the eucaloric phase, the low-fat – high carbohydrate diet exerted unfavorable effects on several inflammatory markers. The energy restricted low-fat – high-carbohydrate diet caused weight loss and affected inflammatory markers favorably thus indicating a protective role of energy restriction on the inflammatory effect of high carbohydrate feeding.

Pischon et al recently reported that in the 532 male participants of the Health Professionals Follow-Up Study, serum adiponectin concentrations correlated inversely with the glycemic load and positively with the total fat content of the diet.

Hypoadiponectinemia is as mentioned associated which the metabolic syndrome with all its components and also correlate with non alcoholic fatty liver disease (NAFLD). There is however much indicating that low GI diet in these conditions increases adiponectin level.

Keogh et al (2008) explains that adiponectin seem to only increase in the face of substantial but not moderate weight loss. Keogh et al found no effect of weight loss on adiponectin level either by a low carbohydrate or low fat diet. The weight loss was 6-7kg in 8 weeks. However Keogh had previously found an improvement in adiponectin after 12 months but not after 3 months, which suggests a delayed weight loss response on adiponectin.

Hivert et al looked at blood samples from the Nurses' Health Study. They found that in the women who did not develop diabetes, baseline levels of adiponectin were associated with significantly greater weight gain after adjusting for age, BMI, physical activity, diet, and other factors. The women in the highest quintile of adiponectin gained 3.18 kg compared to women in the lowest quintile who gained 0.80 kg over 4 years. There was no such association in the women who did develop diabetes. The finding might indicate that higher adiponectin production by adipocytes might be a sign of healthier adipose tissue with further capacity to store fat. This is supported by the finding that a good fat storing ability seems to protect against insulin resistance.

Weight reduction has been found to increase plasma adiponectin in both obese and diabetic patients. Exercise interventions of short duration that does not alter body weight or body fat does not change adiponectin levels. Layman et al (2005) found that an exercise regimen that reduced body fat increased adiponectin levels. The positive changes in adiponectin remained even when controlling for changes in body fat.

Other effects
In vitro studies suggest that adiponectin plays an important role in nitric oxide (NO) generation which is an important function for arterial elasticity. Impaired NO generation plays a role in endothelial dysfunction and atherosclerosis. Decreased plasma adiponectin correlates with impaired insulin-stimulated nitric oxide synthase activity in skeletal muscles and also severity of insulin resistance in people with type 2 diabetes. This finding may provide one link between reduced plasma adiponectin levels and accelerated atherosclerosis in type 2 diabetes.

Adiponectin also affects endothelial progenitor cells which play an important part in repairing damages to the vasculature. Adiponectin seem to inhibit EPC apoptosis in vitro.

A Japanese study found a correlation between cognitive impairment and adiponectin. Plasma adiponectin was significantly higher in people with mild cognitive impairment and people with Alzheimer’s disease compared to normal controls.

Smoking lowers adiponectin

As with many other biological substances adiponectin level varies with day and night and feeding/fasting. This lends caution to interpretation of adiponectin results.

Enough is better than too much – the only dietary guidelines you’ll ever need.

2010-10-12T14:18:00.000+02:00

Now that I’ve gotten your attention with an overly bold title I will still be so bold as to introduce the draft of my very own dietary guidelines.

The American Dietary Guidelines Advisory Committee (DGAC) has recently produced a draft for the new American dietary guidelines. The Norwegian government has been doing the same here at home. Both in the US as in Norway the guidelines are greatly criticized, most recently and publicly in this article by Hite and colleagues in the journal Nutrition.

I sent a mail with the article to the big chief working on the Norwegian guidelines. I got a "thank you", but I doubt it’ll make a big impact.

The draft for the new Norwegian guidelines is a 370 page document consisting of close to 140000 words. It’s a tome and although it is great fiction I doubt very many will have the stamina to read it in its entirety.

As I feel the new guidelines are not fit to wipe my ever whitening bottom, I decided to make my own guidelines.

They are, I claim, far more likely to reflect the truth and a far better choice if health is your concern. And best of all, my guidelines are only 360 words.

Nutritional guidelines should of course be temporary and modified in accordance with the development of scientifically produced knowledge. I would thus be grateful for any suggestions or additions that might contribute towards improving my guidelines.

It is of course of importance that the dietary guidelines are for the general public. Because of its audience the guidelines must be easily understandable and easy to follow in everyday life. No general guidelines like the official or those presented here should attempt to cover all aspects of health and all eventualities. We still need professionals to address individual health.

The guidelines

1. Relax
Don’t worry. Don’t worry about details, not even those pertaining to diet and lifestyle. If you focus too much on the details, your health will suffer and would indeed be better off with you not worrying about the details.

This is not strictly a dietary advice, but it's too bloody important to leave out.

2. Eat like humans are built to eat
Science tells us that humans can thrive with good health on quite a lot of different diets, but the diets which accompany good health have a few but important things in common. Here are the main aspects of a healthy diet:

Don’t eat too much grain

Grains or products made of grains should only be a small part of the diet, and wheat should probably be avoided all together.

Eat unprocessed foods

Most of the diet should be unprocessed foods; eat all sorts of animal and vegetable products but try to get most of it in unprocessed form. Now, processed is in itself not bad. Cheese is a processed food, but still a very fine food. While a sausage may be fine a steak is probably better in the long run. Processed foods that should be especially avoided are those with added sugars and starch, deep fried foods and those with added vegetable oils.

Eat fat

Eat plenty of fats but avoid plant oils rich in omega 6. Eat animal fats. Eat butter, not margarines.

Don’t eat sweet

Keep a low intake of added sweeteners in any form, natural and artificial. Sugars should be avoided most of the time.

3. Some of us need a little extra

If your body show symptoms of carbohydrate intolerance usually symptoms like weight gain and blood sugar fluctuations you should probably also reduce the total amount of carbohydrates in the diet.

Dietary supplements can make things even better. Extra vitamin D and long chain omega 3 fatty acids may benefit many of us. If you are an athlete, under lot of stress or in any other way are subject to stress physical or mental, supplements are more important and should be addressed by someone who knows what they're talking about.

There it is. Nutritional guidelines as three main advises and four distinct and concrete dietary guidelines all adding up to 360 words. Suggestions will be considered and may appear in the final version.

A scientist’s dilemma

2010-09-27T16:47:00.000+02:00

I would like to consider myself a scientist – or at the very least a man of science. I do science for a living, although admittedly I don’t actually know what science is.

When I talk to people about nutrition, whether in person or in front of a class, I make an attempt at presenting nutrition from what I believe to be a scientific standpoint.

But there invariably comes a point during my rambling monologues when the listeners who aren’t sleeping realize that my advice on nutrition is roughly the opposite of what everybody else say, the opposite of what their textbooks says and the opposite of what the government recommends.

“Eat fat,” I say, “preferably saturated fat. Butter is great. Avoid sugar and eat proteins. In fact, just make sure that most of what you are eating was also once eating something. Don’t eat grains, at least no wheat. If you don’t like seafood you might want to supplement with omega 3.” You get the picture.

At this point, a hovering hand usually catches my attention.

“Are you telling us the government is wrong?”

“Yes, that is correct,” I think to myself. But I don’t say it.

Instead I try my best at working around question and feeling very much like a greased up politician I effectively avoid the question by saying something about how scientific results are often disagreed upon, how it takes time to change scientific paradigms, how textbooks are slowly updated, how science is not immune to the ways of money and how even scientists rarely admit to being wrong even though the evidence calls for it.

But, what I would like to say is, “Yes, that is correct.” In fact, what I would like to say that it is hard to be more wrong than the official guidelines.

I dodge the question, because I know I will lose credibility by asserting myself. Claiming to possess a knowledge that has escaped most everybody but me will drive my audience away and luckily so. It is after all a sign of healthy skepticism in my audience.

If I succeed in getting across the message that even the government might get it wrong, there invariably is a follow-up question.

“Who then should we listen to?”

“Me,” I think.

But I don’t say it.

Instead I talk about how, if you really want to know the truth, if you really want to know about nutrition and health, you have to read. You have to read and study and accumulate your own knowledge. Only then can you make sensible decisions about whom to listen to.

If however, you don’t want to spend your time learning about nutrition and navigating the maze of confusing information, you’ve got three more or less sensible choices:

1. You can trust your experience and the experience of those around you. A lot can be learned from listening to the body, cleaning out the senses and having a keen eye for the obvious. Humans however, are prone to deceiving themselves.

2. Find any random person or organization that promote a dietary strategy and follow it. This strategy is commonly used in religion and judging by the number of religious people around, I would say it’s an easily followable approach.

3. Don’t give a crap and eat whatever you want to eat.

I hate that there are no better options. When asked about whom to trust I would like to give people a name. Preferably the government, as it should be their responsibility to make correct and important knowledge available to the public. But I can’t give a name. In truth, the only option for those who really seek the truth is to find it themselves.

And how bloody ineffective it all is. But as I claim that those who should be trusted can’t be trusted there is no way people will or should blindly trust me.

And who’s to blame for this sticky situation? Much of the blame lies with scientists; the very group of people I would like to consider myself a part of.

Scientists have disagreed far more than the evidence permits. They have been led by money, fame and feelings and are in general guilty of being just like ordinary humans.

I do not think nor hope that the day comes when I can teach a nutrition- and health approach that everybody agrees upon. After all, the progress of science rests entirely on disagreement. But it should be possible to agree about the important issues. It is possible, but agreement honors us with its absence. And in the meantime everything is so much more difficult than it has to be and the obvious question poses a dilemma where there should be none.

Exercise Zen

2010-09-10T20:26:00.006+02:00

“When I'm in this state everything is pure, vividly clear. I'm in a cocoon of concentration. And if I can put myself into that cocoon, I'm invincible. . . . I'm living fully in the present. I'm absolutely engaged, involved in what I'm doing. . . . It comes and it goes, and the pure fact that you are out on the first tee of a tournament and say, "I must concentrate today," is no good. It won't work.”

Tony Jacklin

For a good proportion of us humans, our body is nothing more than a way of getting the brain from A to B. We have become a brain transporter tool – a way of moving the “ego” around. Although this does not necessarily strike everybody as problematic, It very well can be.

It can limit our happiness.

iStockphoto

Not because you have to have a magazine cover body and put down miles on the treadmill to be happy.

I do not wish to be considered as one of those hyperactive, overly positive, too good looking individuals, often observed at any local gym, that truly believe they can change the world by getting everybody to exercise more and eating healthy. I don’t want everybody to be fit or thin – what a horrible thought and what a depressingly boring world it would be.

But, I would like people to be able to get the information they want and need so that they can do what they want with their bodies and their lives.

The reason why the body becoming a brain carrying tool can be problematic, is because the mind and the body are impossible to differentiate. It is problematic to talk of them as two separate things as it is equally problematic to consider them to be one (René Decartes is much to blame for our dualistic view of ourselves).

Just as our thoughts and feelings affect the functions of our body and the bodily milieu, our body greatly affects our thoughts, feelings and personality.

Our oversized human brain and the concomitant great ability to imagine situations, to plan ahead and to consider multiple situations and outcomes can be a curse. For example, I can sit in quiet surroundings with a body at rest and still have an overactive mind. Because I can picture possible future outcomes, I can stress myself silly and sick while being totally at rest. Adrenaline and cortisol can go up. My heart is beating faster and stronger, I start sweating and breathing heavily, all while sitting perfectly still.

Most tragic of all is that I can make my body respond like this by thinking of things to come that most likely will never happen. Let’s face it, as humans we are great at considering multiple future situations, but not necessarily any better at predicting the actual future to be. How often does a situation turn out to be exactly how you pictured it would be?

This stress can gradually destroy my body from the inside out. My cells function more poorly and are broken down to a greater degree. Stress is a catabolic state. While sitting perfectly still and wrenching my mind I am effectively weakening my own body.

We do not need to have a higher than normal heart rate to be stressed. Feeling bad is also stress. Depression seems to be as deteriorating as anxiety. Over time, feeling bad can reduce a body to ruins.

As negative thought patterns is detrimental to the body, a poor physical health and poorly functioning body can be detrimental to the mind. Luckily for us, both the body and the mind are ours to mold. Neither is unchangeable.

There are many reasons why being physically active can improve our mental health and well being. The secreting of hormones that increase our well being is one effect. A more effective vasculature, improved transportation potential and even the forming of new cells are other. There is also an anthropologic aspect worth considering. As humans, our bodies are made for (have involved into) activity and unless the body are given the stimuli it is made for, we will feel unfulfilled.

Last but not least, physical activity or exercise can give our minds much needed rest. Exercise is distraction for the mind.

While it is easy to fill the mind with multiple thoughts and feelings at rest, it is much harder to concentrate on multiple things while being active.

One of the greatest ways of giving the mind a rest is by giving the body the opposite. Once you step on a treadmill, jump on bike, go for a run/swim/walk or whatever, the body takes over. While intensity is gradually increasing, while the muscles work harder and harder, while you sweat more and the heart beats faster, there is no longer room for thoughts and feelings.

The body forces the mind to focus on one thing. The head is no longer filled with thoughts about annoying colleagues, what to eat for dinner, how to get a job, how to pay the loan or what to do with your life. The exercise forces the mind to let go of all of this and to simply focus.

Although I admittedly spend most of my time sitting on my ass, I do go out for the occasional exercise. In particular, I like jumping. I like landing too, but not nearly as much as I like jumping.

The wonderful thing about jumping is that it freaks the hell out my mind. The higher the fall and the bigger the challenge, the less my mind is involved. It is uninvolved not because of panic or fear, but because there is no room for thoughts. A difficult physical situation requires my body to do what it does best. To react to stimuli and to adjust quickly. There is no time for thinking.

Photo: Jon Lucas

This feeling is independent of activity type. Some people report that they get lost in the activity during a spinning class. With pounding hypnotic music, heart racing and lungs screaming they let the body take over and they become the cycling. You can lose your self in your Grok workout or when going for a quick walk.

A Japanese Zen Buddhist would probably call this “Mushin”- simply translated; “no mind.” A sport psychologist would probably call it flow or possibly runners high.

No matter the name it is given, giving the mind a break while making the body a little more fit is a wonderful experience - an experience in which, even for just a second, the line between the body and the activity is eliminated. Making a distinction between myself and the activity no longer make any sense. In this state I am the jump.

In fact, some of my most peaceful moments are in situations where my heart is racing and my muscles aching.

“If one puts his mind in the action of his opponent’s body, his mind will be taken by the action of his opponent’s body.
If he puts his mind in his opponent’s sword, his mind will be taken by that sword.
If he puts his mind in thoughts of his opponent's intention to strike him, his mind will be taken by thoughts of his opponent’s intention to strike him.
If he puts his mind in his own sword, his mind will be taken by his own sword.
If he puts his mind in his own intention of not being struck, his mind will be taken by his intention of not being struck.
If he puts his mind in the other man’s stance, his mind will be taken by the other man’s stance.
What this means is that there is no place to put the mind.”

Takuan Soho