HOW DO SOM CULTURES STAY LEAN WHILE STILL CONSUMING HIGH AMOUNTS OF CARBOHYDRATES By Peter Attia, MD For the sake of this discussion, let’s ignore the fact that the “historically” lean countries (e.g., France, Italy, Japan) are catching up to our levels of obesity and metabolic syndrome, especially in certain affluent subsets. After all, we did get a 40 year head start on how to eat poorly. So, let’s ask the question this way: How does the average person living in, say, Japan stay leaner and healthier than the average American while still consuming >70% of their caloric intake in the form of carbohydrates? I don’t claim to know the answer this question, but I’ve got a few ideas. ************************* MY IDEAS While there is a considerable range of variation in dietary starch intake among human populations, a distinction can be made between “high-starch” populations for which starchy food resources comprise a substantial portion of the diet, and the small fraction of “low-starch” populations with traditional diets that incorporate relatively few starchy foods. Such diets instead emphasize proteinaceous resources (e.g., meats and blood) and simple saccharides (e.g., from fruit, honey and milk). Recent study found that mean diploid AMY1 copy number is greater in high-starch populations. Strikingly, the proportion of individuals from the combined high-starch sample with at least 6 AMY1 copies (70%) was nearly 2 times greater than that for low-starch populations (37%). To visualize the allele-specific number and orientation of AMY1 gene copies, the authors performed high-resolution fluorescence in situ hybridization on stretched DNA fibers (fiber FISH); these results were consistent with diploid AMY1 copy number estimates from our qPCR experiments. Read more: ncbi.nlm.nih.gov/pmc/articles/PMC2377015/ Personally I think, that increased risk of obesity in persons with low amylase can be explained by a reduced responsiveness of the islet B-cells to incretins. Incretins are insulinotropic factors of the gut released by nutrients and stimulating insulin secretion in physiological concentrations in the presence of elevated blood glucose levels. The incretin effect refers to the phenomenon of oral glucose eliciting a higher insulin response than intravenous glucose at identical plasma glucose profiles. It is conveyed by the two insulinotropic incretin hormones: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Type 2 diabetes mellitus (T2DM) has been shown to be characterised by an almost abolished incretin effect. The incretin effect was shown to be affected in subjects who had impaired glucose tolerance and who were therefore at high risk for developing type 2 diabetes. This observation could imply a primary role for the reduced incretin effect in type 2 diabetes, but on the other hand, the finding could also represent an early consequence of the chronic mild hyperglycemia of impaired glucose tolerance. However, recent study suggests that reduced incretin effect in type 2 diabetes is a consequence of the diabetic state rather than a primary event leading to type 2 diabetes. (medscape/viewarticle/562484_4) Nevertheless primary role of reduced increting effect due to low amylase cannot be excluded. This assumption is supported by the fact, that proper assimilation of nutrients stimulates secretion of GIP and GLP.1. (ncbi.nlm.nih.gov/pubmed/20591345) Importantly, there is also evidence that genetic variants may influence the incretin effect and possibly also the responsiveness to incretin-based therapy in some patients. (care.diabetesjournals.org/content/34/Supplement_2/S251.full)
Posted on: Sun, 13 Jul 2014 10:22:34 +0000
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