Showing posts with label diseases of civilization. Show all posts
Showing posts with label diseases of civilization. Show all posts

Thursday, December 2, 2010

How lean should one be?

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.

Saturday, May 15, 2010

Intermittent fasting as a form of liberation

I have been doing a lot of reading over the years on isolated hunter-gatherer populations; see three references at the end of this post, all superb sources (Chagnon’s book on the Yanomamo, in particular, is an absolute page turner). I also take every opportunity I have to talk with anthropologists and other researchers who have had field experience with hunter-gatherer groups. Even yesterday I was talking to a researcher who spent many years living among isolated native Brazilian groups in the Amazon.

Maybe I have been reading too much into those descriptions, but it seems to me that one distinctive feature of many adults in hunter-gatherer populations, when compared with adults in urban populations, is that the hunter-gatherers are a lot less obsessed with food.

Interestingly, this seems to be a common characteristic of physically active children. They want to play, and eating is often an afterthought, an interruption of play. Sedentary children, who play indoors, can and often want to eat while they play.

Perhaps adult hunter-gatherers are more like physically active children than adults in modern urban societies. Maybe this is one of the reasons why adult hunter-gatherers have much less body fat. Take a look at the photo below (click to enlarge), from Wikipedia. It was reportedly taken in 1939, and shows three Australian aboriginals.


Hunter-gatherers do not have supermarkets, and active children need food to grow healthy. Adult urbanites have easy access to an abundance of food in supermarkets, and they do not need food to grow, at least not vertically.

Still, adult hunter-gatherers and children who are physically active are generally much less concerned about food than adults in modern urban societies.

It seems illogical, a bit like a mental disorder of some sort that has been plaguing adults in modern urban societies. A mental disorder that contributes to making them obese.

Modern urbanites are constantly worried about food. And also about material possessions, bills, taxes etc. They want to accumulate as much wealth as their personal circumstances allow them, so that they can retire and pay for medical expenses. They must worry about paying for their children’s education. Food is one of their many worries; for many it is the biggest of them all. Too much food makes you fat, too little makes you lose muscle (not really true, but a widespread belief).

Generally speaking, intermittent fasting is very good for human health. Humans seem to have evolved to be episodic eaters, being in the fasted state most of the time. This is perhaps why intermittent fasting significantly reduces levels of inflammation markers, promotes the recycling of “messed up” proteins (e.g., glycated proteins), and increases leptin and insulin sensitivity. It is something natural. I am talking about fasting 24 h at a time (or a bit more, but not much more than that), with plenty of water but no calories. Even skipping a meal now and then, when you are busy with other things, is a form of intermittent fasting.

Now, the idea that our hominid ancestors were starving most of the time does not make a lot of sense, at least not when we think about Homo sapiens, as opposed to earlier ancestors (e.g., the Australopithecines). Even archaic Homo sapiens, dating back to 500 thousand years ago, were probably too smart to be constantly starving. Moreover, the African savannas, where Homo sapiens emerged, were not the type of environment where a smart and social species would be hungry for too long.

Yet, intermittent fasting probably happened frequently among our Homo sapiens ancestors, for the same reason that it happens among hunter-gatherers and active children today. My guess is that, by and large, our ancestors were simply not too worried about food. They ate it because they were hungry, probably at regular times – as most hunter-gatherers do. They skipped meals from time to time.

They certainly did not eat to increase their metabolism, raise their thyroid hormone levels, or have a balanced macronutrient intake.

There were no doubt special occasions when people gathered for a meal as a social activity, but probably the focus was on the social activity, and secondarily on the food.

Of course, they did not have doughnuts around, or foods engineered to make people addicted to them. That probably made things a little easier.

Successful body fat loss through intermittent fasting requires a change in mindset.

References:

Boaz, N.T., & Almquist, A.J. (2001). Biological anthropology: A synthetic approach to human evolution. Upper Saddle River, NJ: Prentice Hall.

Chagnon, N.A. (1977). Yanomamo: The fierce people. New York, NY: Holt, Rinehart and Winston.

Price, W.A. (2008). Nutrition and physical degeneration. La Mesa, CA: Price-Pottenger Nutrition Foundation.

Tuesday, March 30, 2010

Adiponectin supplementation: Body fat loss

Adiponectin is a hormone exclusively secreted by body fat. This hormone has been recently gaining attention from researchers because of some of its functions. Two important ones are the regulation of glucose and fat metabolism.

Elevated levels of adiponectin are associated with increased insulin sensitivity, and increased fat catabolism (i.e., fat burning). And these associations appear to be causal. That is, adiponectin levels do not seem to be only markers, but causes of increased insulin sensitivity and fat catabolism.

In other words, an increase in circulating adiponectin seems to lead to increased insulin sensitivity and increased fat catabolism. Insulin sensitivity is the opposite of insulin resistance. The latter is a precursor to diabetes type 2, and is associated with elevated fasting and postprandial (i.e., after a meal) glucose levels.

Adiponectin also seems to work closely with leptin, another hormone implicated in a number of diseases of civilization. It appears that adiponecting and leptin modulate each other’s secretion and effects in metabolic processes.

So what do we do to increase our levels of circulating adiponectin?

Well, apparently there is only one guaranteed way, and that is to lose body fat!

Adiponectin is unique among hormones secreted by body fat in that it increases as body fat decreases. Other important body fat hormones, such as leptin, decrease with body fat loss.

The figure below (from: Poppitt et al., 2008) shows a graph where adiponectin levels are plotted against body mass index (BMI). BMI is strongly correlated with body fat percentage.

As you can see from the figure above adiponectin levels more than double when BMI goes from 26 to 20. One does not need to be obese to take advantage of this effect, and to benefit from having increased adiponectin levels.

The linear (Pearson) correlation between BMI and adiponectin levels is indicated as a high 0.551. The fluctuations around the line (the "line" looks more like a quasi-linear curve obtained through quadratic regression), which are why the correlation is not 1, are probably due chiefly to two factors:

    - BMI is not a very precise measure of body fat. A very muscular person will have a high BMI and low body fat. That person will consequently have much higher adiponectin levels than an obese person with equal BMI.

    - Adiponectin levels are naturally higher in women than in men. This is another point in favor of adiponectin, as women have always been the evolutionary bottleneck among our Paleolithic ancestors.

Now you know why doctors prescribe weight loss to patients with diabetes type 2.

And, when we look at various hunter-gatherer groups that were apparently free of diseases of civilization prior to westernization, there are only a few common denominators. Diet was not one of them, as Weston Price and others have shown us, at least not in the sense of what they included in their diet.

One of the few common denominators was arguably the fact that those hunter-gatherers typically had relatively low levels of body fat; an almost universal feature among non-westernized hunter-gatherers.

Reference:

Poppitt, S.D. et al. (2008). Postprandial response of adiponectin, interleukin-6, tumor necrosis factor-α, and C-reactive protein to a high-fat dietary load. Nutrition, 24(4), 322-329.

Saturday, February 6, 2010

Vitamin D levels: Sunlight, age, and toxicity

Calcidiol is a pre-hormone that is produced based on vitamin D3 in the liver. Blood concentration of calcidiol is considered to be a reliable indicator of vitamin D status. In the research literature, calcidiol is usually referred to as 25-Hydroxyvitamin or 25(OH)D. Calcidiol is converted in the kidneys into calcitriol, which is the active form of vitamin D.

The table below (from: Vieth, 1999; full reference at the end of this post; click on it to enlarge), shows the average blood vitamin D levels of people living or working in sun-rich environments. To convert from nmol/L to ng/mL, divide by 2.496. For example, 100 nmol/L = 100 / 2.496 ng/mL = 40.1 ng/mL. At the time of this writing, Vieth (1999) had 692 citations on Google Scholar, and probably more than that on Web of Science. This article has had, and continues having, a high impact among researchers.


The maximum average level of blood (or serum) vitamin D shown in the table is 163 nmol/L (65 ng/mL). Given that the human body produces vitamin D naturally from sunlight, it is reasonable to assume that those blood vitamin D levels are not yet at the toxic range. In fact, one of the individuals, a farmer in Puerto Rico, had a level of 225 nmol/L (90 ng/mL). That individual had no signs of toxicity.

Several studies show that pre-sunburn full-body exposure to sunlight is equivalent to an oral vitamin D intake of approximately 250 µg (10,000 IU).

In spite of claims to the contrary, vitamin D production based on sunlight does not cease after 40 years of age or so. Studies reviewed by Vieth suggest that among the elderly (i.e., those aged 65 or above) pre-sunburn full-body exposure to sunlight is equivalent to an oral vitamin D intake of 218 µg (8,700 IU).

Sunlight-induced vitamin D production does seem to decrease with age, but not dramatically.

Post-sunburn sunlight exposure does not increase vitamin D production. Since each person is different, a good rule of thumb to estimate the number of minutes of sunlight exposure needed to maximize vitamin D production is the number of minutes preceding sunburn. For a light-skinned person, this can be as little as 7 minutes.

Vitamin D accumulation in the body follows a battery-like pattern, increasing and decreasing gradually. The figure below, from Vieth’s article, shows the gradual increase in blood vitamin D concentrations following the start of daily supplementation. This suggests that levels start to plateau at around 1 month, with higher levels reaching a plateau after 2 months.


While sunlight exposure does not lead to toxic levels of vitamin D, oral intake may. Below is a figure, also from Vieth’s article, that plots blood levels of vitamin D against oral intake amounts. The X’s indicate points at which intoxication symptoms were observed. While typically intoxication starts at the 50,000 IU intake level, one individual displayed signs of intoxication at 10,000 IU. That individual received a megadose that was supposed to provide vitamin D for an extended period of time.


Non-toxic levels of 10,000 IU are achieved naturally through sunlight exposure. This applies to modern humans and probably our Paleolithic ancestors. Yet, modern humans normally limit their sun exposure and intake of vitamin D to levels (400 IU) that are only effective to avoid osteomalacia, the softening of the bones due to poor mineralization.

Very likely the natural production of 10,000 IU based on sunlight was adaptive in our evolutionary past, and also necessary for good health today. This is consistent with the many reports of diseases associated with chronic vitamin D deficiency, even at levels that avoid osteomalacia. Among those diseases are: hypertension, tuberculosis, various types of cancer, gingivitis, multiple sclerosis, chronic inflammation, seasonal affective disorder, and premature senescence.

Reference:

Reinhold Vieth (May 1999). Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. American Journal of Clinical Nutrition, Vol. 69, No. 5, 842-856.

Sunday, January 31, 2010

Vitamin D deficiency, seasonal depression, and diseases of civilization

George Hamilton admits that he has been addicted to sunbathing for much of his life. The photo below (from: phoenix.fanster.com), shows him at the age of about 70. In spite of possibly too much sun exposure, he looks young for his age, in remarkably good health, and free from skin cancer. How come? Maybe his secret is vitamin D.


Vitamin D is a fat-soluble pro-hormone; not actually a vitamin, technically speaking. That is, it is a substance that is a precursor to hormones, which are known as calcipherol hormones (calcidiol and calcitriols). The hormones synthesized by the human body from vitamin D have a number of functions. One of these functions is the regulation of calcium in the bloodstream via the parathyroid glands.

The biological design of humans suggests that we are meant to obtain most of our vitamin D from sunlight exposure. Vitamin D is produced from cholesterol as the skin is exposed to sunlight. This is one of the many reasons (see here for more) why cholesterol is very important for human health.

Seasonal depression is a sign of vitamin D deficiency. This often occurs during the winter, when sun exposure is significantly decreased, a phenomenon known as seasonal affective disorder (SAD). This alone is a cause of many other health problems, as depression (even if it is seasonal) may lead to obesity, injury due to accidents, and even suicide.

For most individuals, as little as 10 minutes of sunlight exposure generates many times the recommended daily value of vitamin D (400 IU), whereas a typical westernized diet yields about 100 IU. The recommended 400 IU (1 IU = 25 ng) is believed by many researchers to be too low, and levels of 1,000 IU or more to be advisable. The upper limit for optimal health seems to be around 10,000 IU. It is unlikely that this upper limit can be exceeded due to sunlight exposure, as noted below.

Cod liver oil is a good source of vitamin D, with one tablespoon providing approximately 1,360 IU. Certain oily fish species are also good sources; examples are herring, salmon and sardines. For optimal vitamin and mineral intake and absorption, it is a good idea to eat these fish whole. (See here for a post on eating sardines whole.)

Periodic sun exposure (e.g., every few days) has a similar effect to daily exposure, because vitamin D has a half-life of about 25 days. That is, without any use by the body, it would take approximately 25 days for vitamin D levels to fall to half of their maximum levels.

The body responds to vitamin D intake in a "battery-like" manner, fully replenishing the battery over a certain amount of time. This could be achieved by moderate (pre-sunburn) and regular sunlight exposure over a period of 1 to 2 months for most people. Like most fat-soluble vitamins, vitamin D is stored in fat tissue, and slowly used by the body.

Whenever sun exposure is limited or sunlight scarce for long periods of time, supplementation may be needed. Excessive supplementation of vitamin D (i.e., significantly more than 10,000 IU per day) can cause serious problems, as the relationship between vitamin D levels and health complications follows a U curve pattern. These problems can be acute or chronic. In other words, too little vitamin D is bad for our health, and too much is also bad.

The figure below (click on it to enlarge), from Tuohimaa et al. (2009), shows two mice. The one on the left has a genetic mutation that leads to high levels of vitamin D-derived hormones in the blood. Both mice have about the same age, 8 months, but the mutant mouse shows marked signs of premature aging.


It is important to note that the skin wrinkles of the mice on the left have nothing to do with sun exposure; they are associated with excessive vitamin D-derived hormone levels in the body (hypervitaminosis D) and related effects. They are a sign of accelerated aging.

Production of vitamin D and related hormones based on sunlight exposure is tightly regulated by various physiological and biochemical mechanisms. Because of that, it seems to be impossible for someone to develop hypervitaminosis D due to sunlight exposure. This does NOT seem to be the case with vitamin D supplementation, which can cause hypervitaminosis D.

In addition to winter depression, chronic vitamin D deficiency is associated with an increased risk of the following chronic diseases: osteoporosis, cancer, diabetes, autoimmune disorders, hypertension, and atherosclerosis.

The fact that these diseases are also known as the diseases of civilization should not be surprising to anyone. Industrialization has led to a significant decrease in sunlight exposure. In cold weather, our Paleolithic ancestors would probably seek sunlight. That would be one of their main sources of warmth. In fact, one does not have to go back that far in time (100 years should be enough) to find much higher average levels of sunlight exposure than today.

Modern humans, particularly in urban environments, have artificial heating, artificial lighting, and warm clothes. There is little or no incentive for them to try to increase their skin's sunlight exposure in cold weather.

References:

W. Hoogendijk, A. Beekman, D. Deeg, P. Lips, B. Penninx. Depression is associated with decreased 25-hydroxyvitamin-D and increased parathyroid hormone levels in old age. European Psychiatry, Volume 24, Supplement 1, 2009, Page S317.

P. Tuohimaa, T. Keisala, A. Minasyan, J. Cachat, A. Kalueff. Vitamin D, nervous system and aging. Psychoneuroendocrinology, Volume 34, Supplement 1, December 2009, Pages S278-S286.

Saturday, January 30, 2010

Cancer patterns in Inuit populations: 1950-1997

Some types of cancer have traditionally been higher among the Inuit than in other populations, at least according to data from the 1950s, when a certain degree of westernization had already occurred. The incidence of the following types of cancer among the Inuit has been particularly high: nasopharynx, salivary gland, and oesophageal.

The high incidence of these “traditional” types of cancer among the Inuit is hypothesized to have a strong genetic basis. Nevertheless some also believe these cancers to be associated with practices that were arguably not common among the ancestral Inuit, such as preservation of fish and meat with salt.

Genetic markers in the present Inuit population show a shared Asian heritage, which is consistent with the higher incidence of similar types of cancer among Asians, particularly those consuming large amounts of salt-preserved foods. (The Inuit are believed to originate from East Asia, having crossed the Bering Strait about 5,000 years ago.)

The incidence of nasopharynx, salivary gland, and oesophageal cancer has been relatively stable among the Inuit from the 1950s on. More modern lifestyle-related cancers, on the other hand, have increased dramatically. Examples are cancers of the lung, colon, rectum, and female breast.

The figure below (click on it to enlarge), from Friborg & Melbye (2008), shows the incidence of more traditional and modern lifestyle-related cancers among Inuit males (top) and females (bottom).


Two main lifestyle changes are associated with this significant increase in modern lifestyle-related cancers. One is increased consumption of tobacco. The other, you guessed it, is a shift to refined carbohydrates, from animal protein and fat, as the main source of energy.

Reference:

Friborg, J.T., & Melbye, M. (2008). Cancer patterns in Inuit populations. The Lancet Oncology, 9(9), 892-900.