The more research that’s published, the more evidence I seem to run into that indicates insulin resistance (and consequently obesity) seems to be related to oxidative stress and/or nutritional deficiencies. As I’ve pointed out before, one of the strange paradoxes that most theories generally can’t explain is why obesity often goes hand in hand with poor nutrition. That is, if obesity is caused solely by overeating, then we should see the lack of obesity in populations where food is scarce or nutrient poor. As several populations have shown us (most notably the Pima Indians), that isn’t always the case.
Several current theories say that obesity is actually caused by nutritional deficiencies, which would jive with the observations above. Several vitamins/minerals that have been implicated in insulin control include chromium, vitamin C, calcium, and more recently vitamin D.
The research around vitamin D and insulin resistance is actually fairly interesting. As most people are aware, vitamin D is primarily produced by the body as a response to sun exposure. Several working theories are implicating vitamin D deficiency as a central or possibly even primarily role in the development of type-II diabetes.
This theory actually makes a lot of sense to me. First, we know that many animals hibernate in the winter. Prior to hibernation, most animals gain weight (in fact, human weight’s vary as well, generally being higher in the winter and lower in the summer). If you believe that excess insulin causes the accumulation of fat (which most research supports), and that vitamin D has a role in controlling insulin production (which current research seems to indicate), then you can hypothesize that vitamin D levels directly influence weight storage by their affects on insulin levels.
One crucial logic point involves causality. Most of the current research tends to show that exercise, while it obviously makes you healthier, often doesn’t lead to any noticeable or long term weight loss — it generally leads to hunger. Diets can help you lower weight, but the reasons behind the loss aren’t entirely understood. If you’re a low-carb (i.e. low insulin) proponent, then reducing your food intake naturally lowers the insulin levels in your blood, which generally causes you to lose weight. If you’re a low-fat proponent, you’ll probably argue that the weight loss is directly related to a reduction in calories.
If you believe the low-carb camp (which a lot of the research supports), then people are not getting fat because they are eating too much, they are eating too much because they are getting fat (the casualty is reversed). That is, because obese people generally have hyperinsulinemia (high levels of insulin in the blood) and insulin causes fat to be stored in fat cells, obese people generally display a level of internal starvation (their muscle cells are literally starved for food because their fat cells are hoarding nutrients) and generally can’t satisfy their body’s demands for energy by eating. In this scenario, lethargy isn’t a cause of obesity, it’s an effect of it (due to the internal starvation).
With regards to vitamin D, the same can be said. Since most people have an increased exposure to sunshine in the summer months, the internal levels of vitamin D would go up. In that case, insulin levels would drop, and weight would naturally decrease. In the winter, when exposure to sunshine is reduced, vitamin D levels would drop, insulin would rise, and fat would be stored. So that bear who is stocking up on food for the winter — he’s not gaining weight because he’s eating more, he’s eating more because he’s gaining weight.
Obviously it’s just a hypothesis, but it jives with most of the current observations. Additional support to the theory can be found in several research reports, one of which reported “heart attacks peak in winter and decline in summer in temperate but not tropical latitudes,” which also lends credit to the idea that exposure to sunshine may ultimately influence insulin production.
Here’s one of the recent studies I was reading tonight:
Common obesity is associated with the metabolic syndrome and can be distinguished from secondary obesity and from rare forms of monogenic and polygenic obesity. The prevalence of common obesity has become a public health concern in many countries as phenomenological approaches to the understanding of obesity have failed to achieve any long term effect on prevention or treatment. There is evidence for a central control mechanism which maintains body-weight to a set-point by the regulation of energy intake and energy expenditure through homeostatic pathways. It is suggested in this paper that common obesity occurs when the set-point is raised and that accumulation of fat mass functions to increase body size. Larger body size confers a survival advantage in the cold ambient temperatures and food scarcity of the winter climate by reducing surface area to volume ratio and by providing an energy store in the form of fat mass. In addition, it is suggested that the phenotypic metabolic and physiological changes observed as the metabolic syndrome, including hypertension and insulin resistance, could result from a winter metabolism which increases thermogenic capacity. Common obesity and the metabolic syndrome may therefore result from an anomalous adaptive winter response. The stimulus for the winter response is proposed to be a fall in vitamin D. The synthesis of vitamin D is dependent upon the absorption of radiation in the ultraviolet-B range of sunlight. At ground level at mid-latitudes, UV-B radiation falls in the autumn and becomes negligible in winter. It has previously been proposed that vitamin D evolved in primitive organisms as a UV-B sensitive photoreceptor with the function of signaling changes in sunlight intensity. It is here proposed that a fall in vitamin D in the form of circulating calcidiol is the stimulus for the winter response, which consists of an accumulation of fat mass (obesity) and the induction of a winter metabolism (the metabolic syndrome). Vitamin D deficiency can account for the secular trends in the prevalence of obesity and for individual differences in its onset and severity. It may be possible to reverse the increasing prevalence of obesity by improving vitamin D status.
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