Monday, August 29, 2011

Men who are skinny-fat: There are quite a few of them

The graph below (from Wikipedia) plots body fat percentage (BF) against body mass index (BMI) for men. The data is a bit old: 1994. The top-left quadrant refers to men with BF greater than 25 percent and BMI lower than 25. A man with a BF greater than 25 has crossed into obese territory, even though a BMI lower than 25 would suggest that he is not even overweight. These folks are what we could call skinny-fat men.


The data is from the National Health and Nutrition Examination Survey (NHANES), so it is from the USA only. Interesting that even though this data is from 1994, we already could find quite a few men with more than 25 percent BF and a BMI of around 20. One example of this would be a man who is 5’11’’, weighing 145 lbs, and who would be technically obese!

About 8 percent of the entire sample of men used as a basis for the plot fell into the area defined by the top-left quadrant – the skinny-fat men. (That quadrant is one in which the BMI measure is quite deceiving; another is the bottom-right quadrant.) Most of us would be tempted to conclude that all of these men were sick or on the path to becoming so. But we do not know this for sure. On the standard American diet, I think it is a reasonably good guess that these skinny-fat men would not fare very well.

What is most interesting for me regarding this data, which definitely has some measurement error built in (e.g., zero BF), is that it suggests that the percentage of skinny-fat men in the general population is surprisingly high. (And this seems to be the case for women as well.) Almost too high to characterize being skinny-fat as a disease per se, much less a genetic disease. Genetic diseases tend to be rarer.

In populations under significant natural selection pressure, which does not include modern humans living in developed countries, genetic diseases tend to be wiped out by evolution. (The unfortunate reality is that modern medicine helps these diseases spread, although quite slowly.)  Moreover, the prevalence of diabetes in the population was not as high as 8 percent in 1994, and is not that high today either; although it tends to be concentrated in some areas and cluster with obesity as defined based on both BF and BMI.

And again, who knows, maybe these folks (the skinny-fat men) were not even the least healthy in the whole sample, as one may be tempted to conclude.

Maybe being skinny-fat is a trait, passed on across generations, not a disease. Maybe such a trait was useful at some point in the not so distant past to some of our ancestors, but leads to degenerative diseases in the context of a typical Western diet. Long-living Asians with low BMI tend to gravitate more toward the skinny-fat quadrant than many of their non-Asian counterparts. That is, long-living Asians generally tend have higher BF percentage at the same BMI (see a discussion about the Okinawans on this post).

Evolution is a deceptively simple process, which can lead to very odd results.

This “trait-not-disease” idea may sound like semantics, but it has major implications. It would mean that many of the folks who are currently seen as diseased or disease-prone, are in fact simply “different”. At a point in time in our past, under a unique set of circumstances, they might have been the ones who would have survived. The ones who would have been perceived as healthier than average.

Monday, August 15, 2011

Book review: Sugar Nation

Jeff O’Connell is the Editor-in-Chief for Bodybuilding.com, a former executive writer for Men’s Health, and former Editor-in-Chief of Muscle & Fitness. He is also the author of a few bestselling books on fitness.

(Source: Bodybuilding.com)

It is obvious that Jeff is someone who can write, and this comes across very clearly in his new book, Sugar Nation.

Now, with a title like this, Sugar Nation, I was expecting a book discussing trends of sugar consumption in the USA, and the related trends in various degenerative diseases. So when I started reading the book I was slightly put off by what seemed to be a book about a very personal journey, written in the first person by the author.

Yet, after reading it for a while I was hooked, and literally could not put the book down. Jeff has managed to write something of a page-turner, combining a harrowing personal account with carefully researched scientific information, about a relatively rare form of type 2 diabetes.

Jeff has a genetic propensity to insulin resistance, just like his father did. What makes Jeff’s case a little unusual is that Jeff is thin, and apparently has difficulty gaining weight. The most common type of diabetes is type 2, and most of those who develop type 2 diabetes do so via the metabolic syndrome. Typically this involves becoming obese or overweight before getting diagnosed as a diabetic.

In fact, in a thin person who is insulin resistant it seems that body fat cells become resistant to the normal actions of insulin much sooner than in the obese. This essentially means that they start rejecting fat. This is a problem, because fat should either be stored in fat cells (adipocytes) or used for energy; as opposed to being deposited in other tissues or remaining in circulation. Apparently this makes it even more difficult for them to control glucose levels once insulin resistance sets in; there is no “cushion”, so to speak.

Still, Jeff appears to believe that his case was that of a skinny-fat person, where body fat percentage is a lot higher than expected based on a low body mass index, and where excess visceral fat is a main culprit. In fact, Jeff seems to think that most cases of thin folks who developed type 2 diabetes are like this, as they follow the metabolic syndrome progression pattern. Fasting triglycerides go up and HDL cholesterol goes down, among other things, but in a skinny-fat body.

Somewhat predictably, what Jeff found out is that, in his case, adopting a low carbohydrate diet made an enormous difference. In fact, it made the difference between having a fairly normal life versus constantly suffering through hypoglycemic episodes. And, at the stage in which Jeff caught the problem, he did not have to avoid all natural carbohydrate-rich foods, not even things like apples. (He had to control portions though.) It is the refined carbohydrate-rich foods that were the problem for him.

I must say that I disagree with a few of the statements in the book. For example, the author seems to believe that excess saturated fat and salt may be quite unhealthy. I think that foods rich in refined carbohydrates and sugars are much more of a problem; cut them out and often excess saturated fat and salt either cease to be a problem, or become healthy. Jeff doesn’t seem to think that excess omega-6 fats can also cause diabetes; I believe the opposite to be true, via a pro-inflammatory path.

Still, this is a great book on so many levels. Jeff meticulously records his experience dealing with doctors, most of whom seem to be clueless as to what to do to prevent the damage that is caused by abnormally high glucose levels. This happens even though diabetes is those doctors’ main area of expertise. He talks about himself with complete abandon, and manages to mix that up with quite a lot of relevant research on diabetes. He gives us an insider’s view of the professional bodybuilding culture, including its use of insulin injections. His description of the Amish is very interesting and somewhat surprising.

For these reasons and a few others, I think this is a great book, and highly recommend it!

Monday, August 8, 2011

Potassium deficiency in low carbohydrate dieting: High protein and fat alternatives that do not involve supplementation

It is often pointed out, at least anecdotally, that potassium deficiency is common among low carbohydrate dieters. Potassium deficiency can lead to a number of unpleasant symptoms and health problems. This micronutrient is present in small quantities in meat and seafood; main sources are plant foods.

A while ago this has gotten me thinking and asking myself: what about isolated hunter-gatherers that seem to have thrived consuming mostly carnivorous diets with little potassium, such as various Native American tribes?

Another thought came to mind, which is that animal protein seems to be associated with increased bone mineralization, even when calcium intake is low. That seems to be due to animal protein being associated with increased absorption of calcium and other minerals that make up bone tissue.

Maybe animal protein intake is also associated with increased potassium absorption. If this is true, what could be the possible mechanism?

As it turns out, there is one possible and somewhat surprising connection, insulin seems to promote cell uptake of potassium. This is an argument made many years ago by Clausen and Kohn, and further discussed more recently by Benziane and Chibalin. See also this recent commentary by Clausen.

Protein is the only macronutrient that normally causes transient insulin elevation without any glucose response. And the insulin response to protein is nowhere near that associated with refined carbohydrate-rich foods. It is much lower, analogous to the response to natural carbohydrate-rich foods.

A very low carbohydrate diet with more animal protein, and less fat, would induce insulin responses after meals, possibly helping with the absorption of potassium, even if potassium intake were rather limited. Primarily carnivorous diets, like those of some traditional Native American groups, would fit the bill.

Also, a low carbohydrate diet with emphasis on fat, but that was not so low in carbohydrates from certain sources, would probably achieve the same effect. This latter sounds like Kwaśniewski’s Optimal Diet, where people are encouraged to eat a lot more fat than protein, but also a small amount of carbohydrates (e.g., 50-100 g/d) from things like potatoes.

Kwaśniewski’s suggestions may sound counterintuitive sometimes. But, as it turns out, potatoes are good sources of potassium. One potato may not be a lot, but that potato will also increase insulin levels, bringing potassium intake up at the cell level.