Sunday, November 20, 2011

The argument for a SANE diet

This is the second in a series of commentaries on the ideas promoted in Jonathan Bailor's book "The Smarter Science of Slim."

This one presents my own spin on his argument for a SANE diet as an effective long term strategy for counteracting the trend toward obesity and obesity-related chronic illness.

In addition to recommendations for brief, infrequent, high intensity exercise to counter insulin resistance and reset metabolism, Bailor promotes what he calls a SANE diet. This is an acronym for satiety, "aggression", nutrition, and efficiency. Rather than duplicate his explanation, I'll just summarize by saying this refers to the quality of food rather than the quanitity, and takes a number of different quality factors into consideration. This note is intended to present my version of the argument for a mixed collection of quality factors in an anti-obesity strategy.

1. Human biology tends to regulate its body weight in a very narrow range for long periods under a wide range of natural and ancestral environments.

I came to understand this well over a decade ago and in my opinion the evidence base for it has grown rather than being seriously questioned in any significant way. This model does have a potentially misleading aspect to it in practice. Many people seem to assume that a body weight set point means different people are predisposed to different body weights. That is only partly true. The set point model does not assume a fixed value, it assumes that we tend to regulate our weight within a narrow range for long periods of time. It is obvious that the body fat set point changes over time, otherwise creeping obesity simply wouldn't happen. The issue is not whether the set point can change, but whether (and how) we change it in the other direction. The forces on it appear to be asymmetric.

My 1998 article on body fat regulation, showing the weak understanding I had at that point of the specifics but I think accurately depicting the concept and showing its historical origins and scientific rationale.

There have also been a number of helpful popular press articles expanding on the dynamic set point concept and its relation to weight loss plateau.

Obesity expert Arya Sharma discusses the set point concept and a unique theory of how it works.

2. Increasingly throughout the contemporary world, a combination of global economic drivers and local environments has created conditions that defeat the biology of weight regulation and cause body weight to creep upwards, resulting in an "obesity epidemic."

A recent Lancet special issue on obesity gave a summary of the current perspective on factors in obesity.

3. Clinical studies suggest a role for dietary glycaemic index (GI) in bodyweight regulation and diabetes risk.

There are a number of lines of evidence leading to the conclusion that glycemic index plays a central role in weight regulation through glucose homeostasis. I singled out this article because it also describes why some of the implications of that conclusion are controversial.

4. The effect of lowering GI is a dynamic change to metabolism, not a static linear dropping of weight because the body adapts to the loss of energy in order to maintain its set point. Static models of calories in vs. calories out do not take the effects of metabolism into consideration and therefore do not accurately predict weight loss.

Even though glycemic load is an important factor in obesity, we can't just cut out starches and sugars without making any other change and expect to keep losing weight. We will tend to compensate in other ways because of the significance of metabolism in weight regulation. As a result it is now considered essential to consider metabolism in predictions of weight loss rather than just calorie balance.

5. Solely manipulating GI in isolation has a diminishing return over time in weight loss because the reduction of calorie intake tends to slow metabolism and because of changes in potentially confounding dietary factors such as fiber content, protein content, palatability, and energy density.

This is a continuation of the previous claim, based on the evidence gathered from trying to control weight solely by reducing glycemic load.

6. CONCLUSION: An individual nutrition strategy that replaces high GI foods by taking energy density, palatability, fiber, protein, energy density, ad other factors into account can more successfully use a reduction in glycemic index to control body fat by improving fat metabolism, slowing or stopping the accumulation of insulin resistance, and reversing the upward creeping of the body fat set point..

None of that is particularly surprising scientifically as far as I know. The set point model of weight control has been standard in both human and animal research for a long time, it is not at all controversial among obesity and physiology researchers. You simply have to take metabolism into account when considering how the body absorbs, utilizes, and catabolizes nutrients and energy. You can't just assume that everything we take in minus some estimate of what we are "burning" is going to be an accurate model of body weight fluctuation.

The part where there is still room for argument is the specific causal sequence, and that has some additional implications. There's an old conundrum in psychology research: "do we cry because we are sad, or are we sad because we cry?" The answer seems intuitively obvious but it turns out that both causal models are partly right because there is a feedback look from our behavior to the way we feel.

There is a similar conundrum in obesity research. Do we get fat because we eat too much and don't move enough, or do we eat more and move less because of the effects of obesity. Again it turns out that both capture part of what is really going on. We do gain weight when we eat more and move less, at least in the short term before our metabolism starts to regulate our weight back to normal. But the thing that causes our weight to more permanently creep upward is the changes to our metabolism over time. And those hormonal and cellular changes make us less good at burning fat and better at absorbing it, changing our body fat set point over time.

Todd I. Stark
Nov 20,2011

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