Saturday, June 29, 2013

The Nutrition Debate #121: “Behavior Change is Incredibly Difficult.”


That’s a conclusion of Jason Vassy’s piece in “Personalized Medicine” that came up recently on a Medscape alert. He was referring to the outcome of two recent trials that examined whether genotype information was helpful in motivating health behavior changes in a population that was genetically susceptible to Type 2 diabetes. It was “hoped” that knowledge of one’s genetic susceptibility might be a “clinically useful tool” in targeting “primary prevention strategies before the onset of certain diseases.” Sadly, he concluded that “At present, however, genetic testing for T2D risk likely does not improve preventive health behaviors in today’s diabetogenic environment.” Quelle surprise!

If you are interested in genetic testing for Type 2 diabetes susceptibility, however, there were some tidbits to glean from this article, to wit: “At least 65 genetic loci contribute to T2D risk. Of these, rs790316 in the TCF7L2 gene is associated with the greatest risk: each copy of the T allele carries an odds ratio for T2D of 1.39. The effect sizes of most other T2D loci are generally much smaller (odds ratios typically ranging from 1.05 to 1.15).” This is, of course, all “Greek” to me, but it is worth noting that some people argue that you should ignore almost any study with an odds ratio under 2.

Vassy hastens to point out, though, that “This (greater susceptibility to T2D risk) contrasts with the much larger effect-sizes of family history: T2D in one or both parents multiplies one’s risk by up to two- and six-fold, respectively.” He does not point out, though, that the association with family history goes far beyond genetics or ethnicity; it includes diet, economics, cultural practices, and many other environmental factors generally too complex to reliably isolate in even large epidemiological studies. Alas, he finally concludes, “Genotype risk scores that combine multiple T2D-associated loci significantly predict the future risk of T2D, but they may not improve traditional T2D prediction models consisting of routine risk factors such as family history, BMI, and fasting glucose.”

Behavior change, however, was the hoped-for outcome of these two studies and this author’s commentary. They were all disappointed but, I suspect, not surprised. The medical establishment has come to expect failure. Vassy expresses that outcome succinctly: “These results will not surprise clinicians, whose efforts at counseling patients for weight loss and improvement in diet and exercise habits often fail.” The implication is it’s the patient’s fault. The patient is deemed “non-compliant” with the “prescription” because, they say empathetically “behavior change is incredibly difficult.”

It never seems to occur to the practitioner that that expected outcome failed to materialize because it was a failed protocol – the wrong prescription to treat the cause of the syndrome (see #9, "Metabolic Syndrome," here for the indications), of which obesity is merely a symptom, not the cause. A large percentage of the world’s peoples are apparently genetically predisposed and therefore susceptible to this scourge. It is the outcome of eating a Westernized diet. We become fat not because we eat too much fat and cholesterol (and are too sedentary), but because we (who are susceptible) eat too many sugars and processed carbohydrates. Our metabolism becomes deranged (“disregulated”) – in other words “broken.” We make and store fat as a consequence of eating sugars, processed carbs and fat. The body uses the sugars and processed carbs for energy and stores the fat for the inevitable famine that it is designed to expect and be prepared for. The trouble is the famine never comes. We live in a world with an overabundance of relatively cheap carbohydrates in the form of manufactured and processed foods. This is in contrast to the animal-based dietary of protein and fat, plus seasonal whole foods (including unprocessed carbohydrates) our ancestors ate. Instead, we now graze on processed carbohydrates all day long as though we lived in a veritable corn-utopia©, which, in fact, we do.

Our body is an exquisitely designed system that works flawlessly until or unless we mess with it. Even then, it works against even our best efforts to subvert its protective mechanisms. It will until it “breaks” or unless we learn how to work with it. If we eat Low Carb or Very Low Carb, and just two or three small meals a day of moderate protein/high fat over an 8 or 10 hour period, and then fast for 16 or 14 hours, we will be living much the way our ancestors did. The outcomes of this Way of Eating are weight loss for most, high energy levels, improved health markers (even before weight loss), well being, and longevity.
This “prescription” doesn’t occur to our health care providers. Their “hopes” are still pinned on weight loss, and their protocol is still a balanced diet, with less saturated fat and dietary cholesterol, and more exercise. That this bias is assumed and built into the two studies and the commentary of Vassy’s piece is self-evident: “Overall, participants did not change their dietary fat intake or exercise habits over the study period, although most already had ‘good’ habits at baseline.” Then, “However, receiving a higher genetic risk estimate for obesity was associated with greater fat intake and lower exercise scores…” Thus, these changes in diet and energy expenditure, the universally prescribed standard lifestyle modification program, did not work to reduce T2D risk. Behavior change is incredibly difficult, when it is the wrong lifestyle modification. The right one, VLC, is simple. Outcome: Weight loss and improved health, without hunger.

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