In light of recent comments suggesting I'm barking up the wrong tree with my concerns over free fatty acids, I decided to bump this July 2010 post. I think it is an excellent review. The rest of the post remains unchanged.
Introduction
Since ancient times the search for causes of diabetes was related to the sweetness of urine and other body fluids. In England, Thomas Willis (1621–1675) was among the first to taste the urine of diabetic patients and declare that “its sweet taste was imbued with honey sugar” with the supposition that it was derived from blood. This finding led to the addition of “mellitus” to the word diabetes.
We should reconsider whether the definition of diabetes as mellitus is justified. The traditional emphasis on the insulin-glucose axis with respect to examining glucose tolerance, although diagnostically useful does not explain the basic pathophysiological mechanisms operating in diabetes. The glucose-insulin axis has been overemphasised, while alterations in the insulin to non-esterified fatty acid (NEFA) ratio and metabolism received much less attention both as diabetes derangement and as diagnostic potential. Perhaps this is partly due to the fact that the techniques for glucose measurements have been considerably simplified for home use, whereas the measurement of NEFA and triglycerides is still encumbered with relative difficulties, being more expensive and time consuming.
This article discusses what happens to post prandial (after eating) NEFA levels in normal, insulin resistant, obese and diabetic people. My research seems to point to the conclusion that elevated circulating NEFA precedes the development of IR and diabetes and is therefore likely the cause of these. Hyperinsulinemia may well be protective in that insulin controls the release of NEFA from adipose tissue, and VLC diets have been shown to blunt insulin's protective role and increase NEFA levels. I think this should give pause to those on VLC diets who are obese, insulin resistant and or diabetic.
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