Insulin Wars V: Dr. Richard Feinman
Jimmy Moore asked an array of people in LC circles for their thoughts HERE
The subject of this installment is Dr. Richard Feinman, infamous to me for his mangling of thermodynamics.
In any case, Feinman focuses on the relationship between insulin its suppression of hormone sensitive lipase, HSL, the enzyme responsible for lipolysis in our fat cells and release of free fatty acids (NEFA/FFA). This one really caught my eye because he evokes the following study by Hernandez et.al. that I have previously come across, demonstrating a similar effect of low-carb diets releasing NEFA that I blogged on HERE discussing the following study: Acute exposure to long-chain fatty acids impairs α2-adrenergic receptor-mediated antilipolysis in human adipose tissue.
Carbohydrate is the major stimulus for insulin secretion and carbohydrate restriction will lower insulin secretion and, as he says, the reduction in insulin will relieve the inhibition of hormone sensitive lipase so that fat will be mobilized and there will be an increase in fatty acids due to fat breakdown.
Feinman joins a long list of LC advocates focusing on only one "side" of the Fatty Acid/Triglyceride cycle. Yes, low insulin levels do lead to "fat breakdown", but the released FFA's have not left our bodies. Now either they are taken up by cells and ultimately "burnt" (oxidized), or they are "recycled" back into triglycerides, either taken back up by our adipose tissue or stored in lipid droplets in ectopic (non-adipose) tissues. Lipolysis is not fat burning.
So here is an example where chronic insulin is reduced from Hernandez, et al. comparing low carbohydrate diets (“high fat” in their paper) and high carbohydrate diets in healthy obese adults. The figure clearly shows the decrease in insulin and corresponding increase in circulating fatty acids. Notice how the release of fatty acids is exactly out of phase with the insulin. The meal comes at a low point in the insulin levels and as the insulin starts to go up, free fatty acids starts to go down as the breakdown of fat is inhibited by insulin.
Unfortunately the full text of that paper is not available for us to see the figure he's referring to, but I've highlighted before that NEFA is still released following a large carby/fatty meal. Nobody is arguing against insulin's suppressive role in this phenomenon.
This is from Eckel’s lab and the title of the paper is “Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet” which is not accurate; it is really the failure to suppress the response to dietary fat.
Oh, I don't know about that. Let's look at the abstract:
The purpose of this study was to compare the effect of a low-carbohydrate diet (≤20 g/d) with a high-carbohydrate diet (55% of total energy intake) on fasting and hourly metabolic variables during active weight loss.
Healthy, obese adults ( = 32; 22 women, 10 men) were randomly assigned to receive either a carbohydrate-restricted diet [High Fat; mean ± SD body mass index (BMI; in kg/m2): 35.8 ± 2.9] or a calorie-restricted, low-fat diet (High Carb; BMI: 36.7 ± 4.6) for 6 wk. A 24-h in-patient feeding study was performed at baseline and after 6 wk. Glucose, insulin, free fatty acids (FFAs), and triglycerides were measured hourly during meals, at regimented times. Remnant lipoprotein cholesterol was measured every 4 h.
Patients lost a similar amount of weight in both groups ( = 0.57). There was an absence of any diet treatment effect between groups on fasting triglycerides or on remnant lipoprotein cholesterol, which was the main outcome. Fasting insulin decreased ( = 0.03), and both fasting ( = 0.040) and 24-h FFAs ( < 0.0001) increased within the High Fat group. Twenty-four-hour insulin decreased ( < 0.05 for both groups). Fasting LDL cholesterol decreased in the High Carb group only ( = 0.003). In both groups, the differences in fasting and 24-h FFAs at 6 wk were significantly correlated with the change in LDL cholesterol (fasting FFA: = 0.41, = 0.02; 24-h FFA: = 0.52, = 0.002).
Weight loss was similar between diets, but only the high-fat diet increased LDL-cholesterol concentrations. This effect was related to the lack of suppression of both fasting and 24-h FFAs.
Fasting and 24-h FFA levels are regulated by the Triglyceride/FFA cycle and release from adipose tissue. Dietary fat is transported in bundled triglyceride form (chylomicrons), it contributes very little to 24-h FFA exposure and not at all to fasting levels. So I would say the authors properly entitled their research paper. Feinman continues:
This is not surprising given that there is much more fat in the low carbohydrate diet and the additional release of free fatty acids is a good thing on a weight loss diet. It means that you are losing fat.
Umm no and no. I've blogged extensively regarding the deleterious effects of elevated NEFA. Indeed, elevated fasting FFA levels is one of the factors considered in characterizing the metabolic syndrome and diabetes. Excessive circulating NEFA is as deleterious as hyperglycemia if not more. This paper shows that low carbohydrate diets, as I've feared, exacerbates this prong of MetS and diabetes during weight loss. Greater release of FFA's is not a good thing unless accompanied by increased oxidation of said FFA's. You are only "losing fat" if the FFA's are subsequently oxidized, otherwise you're just inducing insulin resistance, ectopic lipid accumulation, etc. It also can't be ignored, as Feinman does, that despite greater lipolysis and release of FFA's, the two groups lost a similar amount of weight.
The paper is also written as if this were a new effect rather than his particular eisegesis of a phenomenon that is in all the textbooks. So, there is no question that a low carbohydrate diet reduces insulin and lipolysis is increased.
Actually I've not seen weight loss comparison studies that compare the two dietary effects on NEFA levels. 24-h insulin decreased in both groups.
In any case, it has become clear to me that insulin plays a protective role by preventing excessive release of fatty acids from their proper storage depots, as stated in my above linked study.