Death by mediocrity

"Moderation is a fatal thing. Nothing succeeds like excess."

Oscar Wilde

One of the truly great obstacles on our path to optimal health is the solid belief in the golden mean or everything in moderation. Rarely have such an inadequate and useless thought been given so much undeserving acceptance.

The belief in a dietary golden mean seems based on lack of knowledge. But it is understandable that, when faced with the choice of two seemingly extremes, we choose a desirable mean. This thinking has probably saved many lives throughout history. But when it comes to diet, it is a poor guidance.

"I hear both carbs and fat are fattening, so I try to eat a little of both. Everything in moderation you know."

Yes, I know, but you are not making sense. Some sort of a cognitive dissonance is making you choose a bloody poor strategy.

Because the truth is that a strategy that seems like an extreme, might be your best choice, thus making all other choices poorer. Your notion of what is extreme, is likely not based on knowledge of the field.

This is all a matter of perspective. I, for example, consider a diet based on whole grains, with 60% of energy from carbs, fruit five times a day and as little saturated fat, cholesterol and red meat as possible, to be very extreme indeed. By others it is considered a safe choice or even an optimal choice.

But if grains affect you in a negative way, the belief that everything can be eaten in moderation, will lead to far greater negative health effects than that seemingly extreme no grain diet.

Disagreeing professionals confuse us. Who should we trust? In our despair we opt for a mean. Yet the desire for optimal is just as strong. Often, the golden mean is so far from the optimal, that the positive health effects honor us with their absence.

So, if disagreeing "experts" make you choose a middle way, know that you have not chosen the optimal way. And when the nutritionist or doctor advice you to eat everything in moderation, put your fingers in your ears and walk away.

Following general principles is a dangerous sport. General principles are just that, general. They don't always apply. When it comes to diet, "everything in moderation" is not a good guiding rule. Optimal diet is optimal diet, regardless of our preferences or feelings.

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

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

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

“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

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

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?

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.