Lifeworld

Loss of muscle mass is associated with aging. It is also associated with the metabolic syndrome, together with excessive body fat gain. It is safe to assume that having low muscle and high fat mass, at the same time, is undesirable.

The extreme opposite of that, achievable though natural means, would be to have as much muscle as possible and as low body fat as possible. People who achieve that extreme often look a bit like “buff skeletons”.

This post assumes that increasing muscle mass through strength training and proper nutrition is healthy. It looks into body fat levels, specifically how low body fat would have to be for health to be maximized.

I am happy to acknowledge that quite often I am working on other things and then become interested in a topic that is brought up by Richard Nikoley, and discussed by his readers (I am one of them). This post is a good example of that.

Obesity and the diseases of civilization

Obesity is strongly associated with the diseases of civilization, of which the prototypical example is perhaps type 2 diabetes. So much so that sometimes the impression one gets is that without first becoming obese, one cannot develop any of the diseases of civilization.

But this is not really true. For example, diabetes type 1 is also one of the diseases of civilization, and it often strikes thin people. Diabetes type 1 results from the destruction of the beta cells in the pancreas by a person’s own immune system. The beta cells in the pancreas produce insulin, which regulates blood glucose levels.

Still, obesity is undeniably a major risk factor for the diseases of civilization. It seems reasonable to want to move away from it. But how much? How lean should one be to be as healthy as possible? Given the ubiquity of U-curve relationships among health variables, there should be a limit below which health starts deteriorating.

Is the level of body fat of the gentleman on the photo below (from: ufcbettingtoday.com) low enough? His name is Fedor; more on him below. I tend to admire people who excel in narrow fields, be they intellectual or sport-related, even if I do not do anything remotely similar in my spare time. I admire Fedor.


Let us look at some research and anecdotal evidence to see if we can answer the question above.

The buff skeleton look is often perceived as somewhat unattractive

Being in the minority is not being wrong, but should make one think. Like Richard Nikoley’s, my own perception of the physique of men and women is that, the leaner they are, the better; as long as they also have a reasonable amount of muscle. That is, in my mind, the look of a stage-ready competitive natural bodybuilder is close to the healthiest look possible.

The majority’s opinion, however, seems different, at least anecdotally. The majority of women that I hear or read voicing their opinions on this matter seem to find the “buff skeleton” look somewhat unattractive, compared with a more average fit or athletic look. The same seems to be true for perceptions of males about females.

A little side note. From an evolutionary perspective, perceptions of ancestral women about men must have been much more important than perceptions of ancestral men about women. The reason is that the ancestral women were the ones applying sexual selection pressures in our ancestral past.

For the sake of discussion, let us define the buff skeleton look as one of a reasonably muscular person with a very low body fat percentage; pretty much only essential fat. That would be 10-13 percent for women, and 5-8 percent for men.

The average fit look would be 21-24 percent for women, and 14-17 percent for men. Somewhere in between, would be what we could call the athletic look, namely 14-20 percent for women, and 6-13 percent for men. These levels are exactly the ones posted on this Wikipedia article on body fat percentages, at the time of writing.

From an evolutionary perspective, attractiveness to members of the opposite sex should be correlated with health. Unless we are talking about a costly trait used in sexual selection by our ancestors; something analogous to the male peacock’s train.

But costly traits are usually ornamental, and are often perceived as attractive even in exaggerated forms. What prevents male peacock trains from becoming the size of a mountain is that they also impair survival. Otherwise they would keep growing. The peahens find them sexy.

Being ripped is not always associated with better athletic performance

Then there is the argument that if you carried some extra fat around the waist, then you would not be able to fight, hunt etc. as effectively as you could if you were living 500,000 years ago. Evolution does not “like” that, so it is an unnatural and maladaptive state achieved by modern humans.

Well, certainly the sport of mixed martial arts (MMA) is not the best point of comparison for Paleolithic life, but it is not such a bad model either. Look at this photo of Fedor Emelianenko (on the left, clearly not so lean) next to Andrei Arlovski (fairly lean). Fedor is also the one on the photo at the beginning of this post.

Fedor weighed about 220 lbs at 6’; Arlovski 250 lbs at 6’4’’. In fact, Arlovski is one of the leanest and most muscular MMA heavyweights, and also one of the most highly ranked. Now look at Fedor in action (see this YouTube video), including what happened when Fedor fought Arlovski, at around the 4:28 mark. Fedor won by knockout.

Both Fedor and Arlovski are heavyweights; which means that they do not have to “make weight”. That is, they do not have to lose weight to abide by the regulations of their weight category. Since both are professional MMA fighters, among the very best in the world, the weight at which they compete is generally the weight that is associated with their best performance.

Fedor was practically unbeaten until recently, even though he faced a very high level of competition. Before Fedor there was another professional fighter that many thought was from Russia, and who ruled the MMA heavyweight scene for a while. His name is Igor Vovchanchyn, and he is from the Ukraine. At 5’8’’ and 230 lbs in his prime, he was a bit chubby. This YouTube video shows him in action; and it is brutal.

A BMI of about 25 seems to be the healthiest for long-term survival

Then we have this post by Stargazey, a blogger who likes science. Toward the end the post she discusses a study suggesting that a body mass index (BMI) of about 25 seems to be the healthiest for long-term survival. That BMI is between normal weight and overweight. The study suggests that both being underweight or obese is unhealthy, in terms of long-term survival.

The BMI is calculated as an individual’s body weight divided by the square of the individual’s height. A limitation of its use here is that the BMI is a more reliable proxy for body fat percentage for women than for men, and can be particularly misleading when applied to muscular men.

The traditional Okinawans are not super lean

The traditional Okinawans (here is a good YouTube video) are the longest living people in the world. Yet, they are not super lean, not even close. They are not obese either. The traditional Okinawans are those who kept to their traditional diet and lifestyle, which seems to be less and less common these days.

There are better videos on the web that could be used to illustrate this point. Some even showing shirtless traditional karate instructors and students from Okinawa, which I had seen before but could not find again. Nearly all of those karate instructors and students were a bit chubby, but not obese. By the way, karate was invented in Okinawa.

The fact that the traditional Okinawans are not ripped does not mean that the level of fat that is healthy for them is also healthy for someone with a different genetic makeup. It is important to remember that the traditional Okinawans share a common ancestry.

What does this all mean?

Some speculation below, but before that let me tell this: as counterintuitive as it may sound, excessive abdominal fat may be associated with higher insulin sensitivity in some cases. This post discusses a study in which the members of a treatment group were more insulin sensitive than the members of a control group, even though the former were much fatter; particularly in terms of abdominal fat.

It is possible that the buff skeleton look is often perceived as somewhat unattractive because of cultural reasons, and that it is associated with the healthiest state for humans. However, it seems a bit unlikely that this applies as a general rule to everybody.

Another possibility, which appears to be more reasonable, is that the buff skeleton look is healthy for some, and not for others. After all, body fat percentage, like fat distribution, seems to be strongly influenced by our genes. We can adapt in ways that go against genetic pressures, but that may be costly in some cases.

There is a great deal of genetic variation in the human species, and much of it may be due to relatively recent evolutionary pressures.

Life is not that simple!

References

Buss, D.M. (1995). The evolution of desire: Strategies of human mating. New York, NY: Basic Books.

Cartwright, J. (2000). Evolution and human behavior: Darwinian perspectives on human nature. Cambridge, MA: The MIT Press.

Miller, G.F. (2000). The mating mind: How sexual choice shaped the evolution of human nature. New York, NY: Doubleday.

Zahavi, A. & Zahavi, A. (1997). The Handicap Principle: A missing piece of Darwin’s puzzle. Oxford, England: Oxford University Press.

When it comes to losing fat and maintaining muscle, at the same time, there are no shortcuts. The process generally has to be slow to be healthy. When one loses a lot of weight in a few days, most of what is being lost is water, followed by carbohydrates. (Carbohydrates are stored as liver and muscle glycogen.) Smaller amounts of fat and protein are also lost. The figure below, from Wilmore et al. (2007), shows the weights in grams of stored water, carbohydrates (glycogen), fat, and protein lost during a 30-day water fast.


On the first few days of the fast a massive amount of water is lost, even though drinking water is allowed in this type of fast. A significant amount of glycogen is lost as well. This is no surprise. About 2.6 g of water are lost for each 1 g of glycogen lost. That is, water is stored by the body proportionally to the amount of glycogen stored. People who do strength training on a regular basis tend to store more glycogen, particular in muscle tissue; this is a compensatory adaptation. Those folks also tend to store more water.

Not many people will try a 30-day fast. Still, the figure above has implications for almost everybody.

One implication is that if you use a bioimpedance scale to measure your body fat, you can bet that it will give you fairly misleading results if your glycogen stores are depleted. Your body fat percentage will be overestimated, because water and glycogen are lean body mass. This will happen with low carbohydrate dieters who regularly engage in intense physical exercise, aerobic or anaerobic. The physical exercise will deplete glycogen stores, which will typically not be fully replenished due to the low intake of carbohydrates.

Light endurance exercise (e.g., walking) is normally easier to maintain with a depleted “glycogen tank” than strength training, because light endurance exercise relies heavily on fat oxidation. It uses glycogen, but more slowly. Strength training, on the other hand, relies much more heavily on glycogen while it is being conducted (significant fat oxidation occurs after the exercise session), and is difficult to do effectively with a depleted “glycogen tank”.

Strength training practitioners often will feel fatigued, and will probably be unable to generate supercompensation, if their “glycogen tank” is constantly depleted. Still, compensatory adaptation can work its “magic” if one persists, and lead to long term adaptations that make athletes rely much more heavily on fat than the average person as a fuel for strength training and other types of anaerobic exercise. Some people seem to be naturally more likely to achieve this type of compensatory adaptation; others may never do so, no matter how hard they try.

Another implication is that you should not worry about short-term weight variations if your focus is on losing body fat. Losing stored water and glycogen may give you an illusion of body fat loss, but it will be only that – an illusion. You may recall this post, where body fat loss coupled with muscle gain led to some weight gain and yet to a much improved body composition. That is, the participants ended up leaner, even though they also weighed more.

The figure above also gives us some hints as to what happens with very low carbohydrate dieting (i.e., daily consumption of less than 20 grams of carbohydrates); at least at the beginning, before long term compensatory adaptation. This type of dieting mimics fasting as far as glycogen depletion is concerned, especially if protein intake is low, and has many positive short term health benefits. The depletion is not as quick as in a fast because a high fat and/or protein diet promotes higher rates of fat/protein oxidation and ketosis than fasting, which spare glycogen. (Yes, dietary fat spares glycogen. It also spares muscle tissue.) Still, the related loss of stored water is analogous to that of fasting, over a slightly longer period. The result is a marked weight loss at the beginning of the diet. This is an illusion as far as body fat loss is concerned.

Dietary protein cannot be used directly for glycogenesis; i.e., for replenishing glycogen stores. Dietary protein must first be used to generate glucose, through a process called gluconeogenesis. The glucose is then used for liver and muscle glycogenesis, among other things. This process is less efficient than glycogenesis based on carbohydrate sources (particularly carbohydrate sources that combine fructose and glucose), which is why for quite a few people (but not all) it is difficult to replenish glycogen stores and stimulate muscle growth on very low carbohydrate diets.

Glycogen depletion appears to be very healthy, but most of the empirical evidence seems to suggest that it is the depletion that creates a hormonal mix that is particularly health-promoting, not being permanently in the depleted state. In this sense, the extent of the glycogen depletion that is happening should be positively associated with the health benefits. And significant glycogen depletion can only happen if glycogen stores are at least half full to start with.

Reference

Wilmore, J.H., Costill, D.L., & Kenney, W.L. (2007). Physiology of sport and exercise. Champaign, IL: Human Kinetics.

The degree of nonexercise activity thermogenesis (NEAT) seems to a major factor influencing the amount of fat gained or lost by an individual. It also seems to be strongly influenced by genetics, because NEAT is largely due to involuntary activities like fidgeting.

But why should this be?

The degree to which different individuals will develop diseases of civilization in response to consumption of refined carbohydrate-rich foods can also be seen as influenced by genetics. After all, there are many people who eat those foods and are thin and healthy, and that appears to be in part a family trait. But whether we consume those products or not is largely within our control.

So, it is quite possible that NEAT is influenced by genetics, but the fact that NEAT is low in so many people should be a red flag. In the same way that the fact that so many people who eat refined carbohydrate-rich foods are obese should be a red flag. Moreover, modern isolated hunter-gatherers tend to have low levels of body fat. Given the importance of NEAT for body fat regulation, it is not unreasonable to assume that NEAT is elevated in hunter-gatherers, compared to modern urbanites. Hunter-gatherers live more like our Paleolithic ancestors than modern urbanites.

True genetic diseases, caused by recent harmful mutations, are usually rare. If low NEAT were truly a genetic “disease”, those with low NEAT should be a small minority. That is not the case. It is more likely that the low NEAT that we see in modern urbanites is due to a maladaptation of our Stone Age body to modern life, in the same way that our Stone Age body is maladapted to the consumption of foods rich in refined grains and seeds.

What could have increased NEAT among our Paleolithic ancestors, and among modern isolated hunter-gatherers?

One thing that comes to mind is lack of comfortable furniture, particularly comfortable chairs (photo below from: prlog.org). It is quite possible that our Paleolithic ancestors invented some rudimentary forms of furniture, but they would have been much less comfortable than modern furniture used in most offices and homes. The padding of comfy office chairs is not very easy to replicate with stones, leaves, wood, or even animal hides. You need engineering to design it; you need industry to produce that kind of thing.


I have been doing a little experiment with myself, where I do things that force me to sit tall and stand while working in my office, instead of sitting back and “relaxing”. Things like putting a pillow on the chair so that I cannot rest my back on it, or placing my computer on an elevated surface so that I am forced to work while standing up. I tend to move a lot more when I do those things, and the movement is largely involuntary. These are small but constant movements, a bit like fidgeting. (It would be interesting to tape myself and actually quantify the amount of movement.)

It seems that one can induce an increase in NEAT, which is largely due to involuntary activities, by doing some voluntary things like placing a pillow on a chair or working while standing up.

Is it possible that the unnaturalness of comfy furniture, and particularly of comfy chairs, is contributing (together with other factors) to not only making us fat but also having low-back problems?

Both obesity and low-back problems are widespread among modern urbanites. Yet, from an evolutionary perspective, they should not be. They likely impaired survival success among our ancestors, and thus impaired their reproductive success. Evolution “gets angry” at these things; over time it wipes them out. In my reading of studies of hunter-gatherers, I don’t recall a single instance in which obesity and low-back problems were described as being widespread.

Ballor et al. (1996) conducted a classic and interesting study on body composition changes induced by aerobic and strength training. This study gets cited a lot, but apparently for the wrong reasons. One of these reasons can be gleaned from this sentence in the abstract:

    “During the exercise training period, the aerobic training group … had a significant … reduction in body weight … as compared with the [strength] training group ...”

That is, one of the key conclusions of this study was that aerobic training was more effective than strength training as far as weight loss is concerned. (The authors refer to the strength training group as the “weight training group”.)

Prior to starting the exercise programs, the 18 participants had lost a significant amount of weight through dieting, for a period of 11 weeks. The authors do not provide details on the diet, other than that it was based on “healthy” food choices. What this means exactly I am not sure, but my guess is that it was probably not particularly high or low in carbs/fat, included a reasonable amount of protein, and led to a caloric deficit.

The participants were older adults (mean age of 61; range, 56 to 70), who were also obese (mean body fat of 45 percent), but otherwise healthy. They managed to lose an average of 9 kg (about 20 lbs) during that 11-week period.

Following the weight loss period, the participants were randomly assigned to either a 12-week aerobic training (four men, five women) or weight training (four men, five women) exercise program. They exercised 3 days per week. These were whole-body workouts, with emphasis on compound (i.e., multiple-muscle) exercises. The figure below shows what actually happened with the participants.


As you can see, the strength training group (WT) gained about 1.5 kg of lean mass, lost 1.2 kg of fat, and thus gained some weight. The aerobic training group (AT) lost about 0.6 kg of lean mass and 1.8 kg of fat, and thus lost some weight.

Which group fared better? In terms of body composition changes, clearly the strength training group fared better. But my guess is that the participants in the strength training group did not like seeing their weight going up after losing a significant amount of weight through dieting. (An analysis of the possible psychological effects of this would be interesting; a discussion for another blog post.)

The changes in the aerobic training group were predictable, and were the result of compensatory adaptation. Their bodies changed to become better adapted to aerobic exercise, for which a lot of lean mass is a burden, as is a lot of fat mass.

So, essentially the participants in the strength training group lost fat and gained muscle at the same time. The authors say that the participants generally stuck with their weight-loss diet during the 12-week exercise period, but not a very strict away. It is reasonable to conclude that this induced a mild caloric deficit in the participants.

Exercise probably induced hunger, and possibly a caloric surplus on exercise days. If that happened, the caloric deficit must have occurred on non-exercise days. Without some caloric deficit there would not have been fat loss, as extra calories are stored as fat.

There are many self-help books and programs online whose main claim is to have a “revolutionary” prescription for concurrent fat loss and muscle gain – the “holy grail” of body composition change.

Well, it may be as simple as combining strength training with a mild caloric deficit, in the context of a nutritious diet focused on unprocessed foods.

Reference:

Ballor, D.L., Harvey-Berino, J.R., Ades, P.A., Cryan, J., & Calles-Escandon, J. (1996). Contrasting effects of resistance and aerobic training on body composition and metabolism after diet-induced weight loss. Metabolism, 45(2), 179-183.

The term “diabetes” is used to describe a wide range of diseases of glucose metabolism; diseases with a wide range of causes. The diseases include type 1 and type 2 diabetes, type 2 ketosis-prone diabetes (which I know exists thanks to Michael Barker’s blog), gestational diabetes, various MODY types, and various pancreatic disorders. The possible causes include genetic defects (or adaptations to very different past environments), autoimmune responses, exposure to environmental toxins, as well as viral and bacterial infections; in addition to obesity, and various other apparently unrelated factors, such as excessive growth hormone production.

Type 2 diabetes and the “tired pancreas” theory

Type 2 diabetes is the one most commonly associated with the metabolic syndrome, which is characterized by middle-age central obesity, and the “diseases of civilization” brought up by Neolithic inventions. Evidence is mounting that a Neolithic diet and lifestyle play a key role in the development of the metabolic syndrome. In terms of diet, major suspects are engineered foods rich in refined carbohydrates and refined sugars. In this context, one widely touted idea is that the constant insulin spikes caused by consumption of those foods lead the pancreas (figure below from Wikipedia) to get “tired” over time, losing its ability to produce insulin. The onset of insulin resistance mediates this effect.



Empirical evidence against the “tired pancreas” theory

This “tired pancreas” theory, which refers primarily to the insulin-secreting beta-cells in the pancreas, conflicts with a lot of empirical evidence. It is inconsistent with the existence of isolated semi/full hunter-gatherer groups (e.g., the Kitavans) that consume large amounts of natural (i.e., unrefined) foods rich in easily digestible carbohydrates from tubers and fruits, which cause insulin spikes. These groups are nevertheless generally free from type 2 diabetes. The “tired pancreas” theory conflicts with the existence of isolated groups in China and Japan (e.g., the Okinawans) whose diets also include a large proportion of natural foods rich in easily digestible carbohydrates, which cause insulin spikes. Yet these groups are generally free from type 2 diabetes.

Humboldt (1995), in his personal narrative of his journey to the “equinoctial regions of the new continent”, states on page 121 about the natives as a group that: "… between twenty and fifty years old, age is not indicate by wrinkling skin, white hair or body decrepitude [among natives]. When you enter a hut is hard to differentiate a father from son …" A large proportion of these natives’ diets included plenty of natural foods rich in easily digestible carbohydrates from tubers and fruits, which cause insulin spikes. Still, there was no sign of any condition that would suggest a prevalence of type 2 diabetes among them.

At this point it is important to note that the insulin spikes caused by natural carbohydrate-rich foods are much less pronounced than the ones caused by refined carbohydrate-rich foods. The reason is that there is a huge gap between the glycemic loads of natural and refined carbohydrate-rich foods, even though the glycemic indices may be quite similar in some cases. Natural carbohydrate-rich foods are not made mostly of carbohydrates. Even an Irish (or white) potato is 75 percent water.

More insulin may lead to abnormal fat metabolism in sedentary people

The more pronounced spikes may lead to abnormal fat metabolism because more body fat is force-stored than it would have been with the less pronounced spikes, and stored body fat is not released just as promptly as it should be to fuel muscle contractions and other metabolic processes. Typically this effect is a minor one on a daily basis, but adds up over time, leading to fairly unnatural patterns of fat metabolism in the long run. This is particularly true for those who lead sedentary lifestyles. As for obesity, nobody gets obese in one day. So the key problem with the more pronounced spikes may not be that the pancreas is getting “tired”, but that body fat metabolism is not normal, which in turn leads to abnormally high or low levels of important body fat-derived hormones (e.g., high levels of leptin and low levels of adiponectin).

One common characteristic of the groups mentioned above is absence of obesity, even though food is abundant and often physical activity is moderate to low. Repeat for emphasis: “… even though food is abundant and often physical activity is moderate to low”. Note that having low levels of activity is not the same as spending the whole day sitting down in a comfortable chair working on a computer. Obviously caloric intake and level of activity among these groups were/are not at the levels that would lead to obesity. How could that be possible? See this post for a possible explanation.

Excessive body fat gain, lipotoxicity, and type 2 diabetes

There are a few theories that implicate the interaction of abnormal fat metabolism with other factors (e.g., genetic factors) in the development of type 2 diabetes. Empirical evidence suggests that this is a reasonable direction of causality. One of these theories is the theory of lipotoxicity.

Several articles have discussed the theory of lipotoxicity. The article by Unger & Zhou (2001) is a widely cited one. The theory seems to be widely based on the comparative study of various genotypes found in rats. Nevertheless, there is mounting evidence suggesting that the underlying mechanisms may be similar in humans. In a nutshell, this theory proposes the following steps in the development of type 2 diabetes:

    (1) Abnormal fat mass gain leads to an abnormal increase in fat-derived hormones, of which leptin is singled out by the theory. Some people seem to be more susceptible than others in this respect, with lower triggering thresholds of fat mass gain. (What leads to exaggerated fat mass gains? The theory does not go into much detail here, but empirical evidence from other studies suggests that major culprits are refined grains and seeds, as well as refined sugars; other major culprits seem to be trans fats, and vegetable oils rich in linoleic acid.)

    (2) Resistance to fat-derived hormones sets in. Again, leptin resistance is singled out as the key here. (This is a bit simplistic. Other fat-derived hormones, like adiponectin, seem to clearly interact with leptin.) Since leptin regulates fatty acid metabolism, the theory argues, leptin resistance is hypothesized to impair fatty acid metabolism.

    (3) Impaired fat metabolism causes fatty acids to “spill over” to tissues other than fat cells, and also causes an abnormal increase in a substance called ceramide in those tissues. These include tissues in the pancreas that house beta-cells, which secrete insulin. In short, body fat should be stored in fat cells (adipocytes), not outside them.

    (4) Initially fatty acid “spill over” to beta-cells enlarges them and makes them become overactive, leading to excessive insulin production in response to carbohydrate-rich foods, and also to insulin resistance. This is the pre-diabetic phase where hypoglycemic episodes happen a few hours following the consumption of carbohydrate-rich foods. Once this stage is reached, several natural carbohydrate-rich foods also become a problem (e.g., potatoes and bananas), in addition to refined carbohydrate-rich foods.

    (5) Abnormal levels of ceramide induce beta-cell apoptosis in the pancreas. This is essentially “death by suicide” of beta cells in the pancreas. What follows is full-blown type 2 diabetes. Insulin production is impaired, leading to very elevated blood glucose levels following the consumption of carbohydrate-rich foods, even if they are unprocessed.

It is widely known that type 2 diabetics have impaired glucose metabolism. What is not so widely known is that usually they also have impaired fatty acid metabolism. For example, consumption of the same fatty meal is likely to lead to significantly more elevated triglyceride levels in type 2 diabetics than non-diabetics, after several hours. This is consistent with the notion that leptin resistance precedes type 2 diabetes, and inconsistent with the “tired pancreas” theory.

Weak and strong points of the theory of lipotoxicity

A weakness of the theory of lipotoxicity is its strong lipophobic tone; at least in the articles that I have read. See, for example, this article by Roger H. Unger in the Journal of the American Medical Association. There is ample evidence that eating a lot of the ultra-demonized saturated fat, per se, is not what makes people obese or type 2 diabetic. Yet overconsumption of trans fats and vegetable oils rich in linoleic acid does seem to be linked with obesity and type 2 diabetes. (So does the consumption of refined grains and seeds, and refined sugars.) The theory of lipotoxicity does not seem to make these distinctions.

In defense of the theory of lipotoxicity, it does not argue that there cannot be thin diabetics. Many type 1 diabetics are thin. Type 2 diabetics can also be thin, even though that is much less common. In certain individuals, the threshold of body fat gain that will precipitate lipotoxicity may be quite low. In others, the same amount of body fat gain (or more) may in fact increase their insulin sensitivity under certain circumstances – e.g., when growth hormone levels are abnormally low.

Autoimmune disorders, perhaps induced by environmental toxins, or toxins found in certain refined foods, may cause the immune system to attack the beta-cells in the pancreas. This may lead to type 1 diabetes if all beta cells are destroyed, or something that can easily be diagnosed as type 2 (or type 1.5) diabetes if only a portion of the cells are destroyed, in a way that does not involve lipotoxicity.

Nor does the theory of lipotoxicity predict that all those who become obese will develop type 2 diabetes. It only suggests that the probability will go up, particularly if other factors are present (e.g., genetic propensity). There are many people who are obese during most of their adult lives and never develop type 2 diabetes. On the other hand, some groups, like Hispanics, tend to develop type 2 diabetes more easily (often even before they reach the obese level). One only has to visit the South Texas region near the Rio Grande border to see this first hand.

What the theory proposes is a new way of understanding the development of type 2 diabetes; a way that seems to make more sense than the “tired pancreas” theory. The theory of lipitoxicity may not be entirely correct. For example, there may be other mechanisms associated with abnormal fat metabolism and consumption of Neolithic foods that cause beta-cell “suicide”, and that have nothing to do with lipotoxicity as proposed by the theory. (At least one fat-derived hormone, tumor necrosis factor-alpha, is associated with abnormal cell apoptosis when abnormally elevated. Levels of this hormone go up immediately after a meal rich in refined carbohydrates.) But the link that it proposes between obesity and type 2 diabetes seems to be right on target.

Implications and thoughts

Some implications and thoughts based on the discussion above are the following. Some are extrapolations based on the discussion in this post combined with those in other posts. At the time of this writing, there were 90 posts on this blog, in addition to many comments. See under "Labels" at the bottom-right area of this blog for a summary of topics addressed. It is hard to ignore things that were brought to light in previous posts.

    - Let us start with a big one: Avoiding natural carbohydrate-rich foods in the absence of compromised glucose metabolism is unnecessary. Those foods do not “tire” the pancreas significantly more than protein-rich foods do. While carbohydrates are not essential macronutrients, protein is. In the absence of carbohydrates, protein will be used by the body to produce glucose to supply the needs of the brain and red blood cells. Protein elicits an insulin response that is comparable to that of natural carbohydrate-rich foods on a gram-adjusted basis (but significantly lower than that of refined carbohydrate-rich foods, like doughnuts and bagels). Usually protein does not lead to a measurable glucose response because glucagon is secreted together with insulin in response to ingestion of protein, preventing hypoglycemia.

    - Abnormal fat gain should be used as a general measure of one’s likelihood of being “headed south” in terms of health. The “fitness” level for men and women shown on the table in this post seem like good targets for body fat percentage. The problem here, of course, is that this is not as easy as it sounds. Attempts at getting lean can lead to poor nutrition and/or starvation. These may make matters worse in some cases, leading to hormonal imbalances and uncontrollable hunger, which will eventually lead to obesity. Poor nutrition may also depress the immune system, making one susceptible to a viral or bacterial  infection that may end up leading to beta-cell destruction and diabetes. A better approach is to place emphasis on eating a variety of natural foods, which are nutritious and satiating, and avoiding refined ones, which are often addictive “empty calories”. Generally fat loss should be slow to be healthy and sustainable.

    - Finally, if glucose metabolism is compromised, one should avoid any foods in quantities that cause an abnormally elevated glucose or insulin response. All one needs is an inexpensive glucose meter to find out what those foods are. The following are indications of abnormally elevated glucose and insulin responses, respectively: an abnormally high glucose level 1 hour after a meal (postprandial hyperglycemia); and an abnormally low glucose level 2 to 4 hours after a meal (reactive hypoglycemia). What is abnormally high or low? Take a look at the peaks and troughs shown on the graph in this post; they should give you an idea. Some insulin resistant people using glucose meters will probably realize that they can still eat several natural carbohydrate-rich foods, but in small quantities, because those foods usually have a low glycemic load (even if their glycemic index is high).

Lucy was a vegetarian and Sapiens an omnivore. We apparently have not evolved to be pure carnivores, even though we can be if the circumstances require. But we absolutely have not evolved to eat many of the refined and industrialized foods available today, not even the ones marketed as “healthy”. Those foods do not make our pancreas “tired”. Among other things, they “mess up” fat metabolism, which may lead to type 2 diabetes through a complex process involving hormones secreted by body fat.

References

Humboldt, A.V. (1995). Personal narrative of a journey to the equinoctial regions of the new continent. New York, NY: Penguin Books.

Unger, R.H., & Zhou, Y.-T. (2001). Lipotoxicity of beta-cells in obesity and in other causes of fatty acid spillover. Diabetes, 50(1), S118-S121.