Interesting study results: "After six months, the people on the Atkins diet had lost an average of 31 pounds, compared with 20 pounds on the AHA diet, and more people stuck with the Atkins regimen. Total cholesterol fell slightly in both groups. However, those on the Atkins diet had an 11% increase in HDL, the good cholesterol, and a 49% drop in triglycerides. On the AHA diet, HDL was unchanged, and triglycerides dropped 22%. High triglycerides may raise the risk of heart disease. While the volunteers' total amounts of LDL, the bad cholesterol, did not change much on either diet, there was evidence that it had shifted to a form that may be less likely to clog the arteries." http://www.usatoday.com/news/health/2002-11-18-adkins_x.htm
The article totally underplays the significance of this outcome. LDL and total cholesterol are correlated with CVD and other diseases of civilization (DOC), but only sometimes, and in some populations. However, high triglycerides, high blood pressure, low HDL, and glucose intolerance is metabolic syndrome - these are unquestionable precursors to CVD and DOC. If you can break this profile, you are getting well and preventing damage to your body. The 'bad' cholesterol it turns out is only 'bad' in one of several forms - small, dense LDL (this is latest thinking but not proved; still, just as proved as the diet-heart hypothesis). Small dense LDL are lipoproteins result as an end stage product of VLDL (very low density - because they are filled with fat). When on a high carb diet, the body converts a lot of the sugar to tryglycerides (TG) in the liver. VLDL are created to shunt the TG around the body. As VLDL deposit their stores of TG, and become less full, they become 'small, dense LDL' and are easily oxidized. The current theory is the small dense LDL goes to the site of arterial injury as a repair team (cholesterol is not water soluable so is critical to cell structure), but instead gets 'stuck' to the artery through oxidation. The artery gets "rust" instead of repair. Now there's an even greater need for repair, and the construction of a plaque has begun. There are other mal-adaptive reactions to high blood sugars - AGE (advanced glycation end products) which also contribute to atherosclerosis by binding the artery protein together, preventing arterial expansion/flexibility. Small dense LDLs are very susceptible to glycation. The best way to reduce AGE - reduce blood sugar levels (intermittent fasting is one way to do this). TGs, thus small dense LDLs, plus AGEs are reduced through carb restriction.
This process of small, dense LDL creation is one of the elements of Metabolic Syndrome (also called Syndrome X). Metabolic syndrome is interrupted through carb restriction. It seems there is a subset of folks who cannot toerate high saturated fat levels, but a larger subset, much larger, than cannot tolerate chronicly high carb intake (100g/day being 'high'). Metabolic syndrome is the most likely driver of the DOC. In contrast with the 'diet-heart' hypothesis that began its most recent lifespan with Ancel Keys, the metabolic syndrome model is not controverted by any intervention study of which I'm aware, and is consistent with all observed criteria for reducing chronic diseases from Alzheimer's to CVD. Metabolic syndrome is also avoidable. Keep carb intake to 50-100g per day, and measure the results via blood pressure, triglycerides, HDL levels, and glucose tolerance. Adjust carb levels as necessary.
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