Except that not all of us are hyperinsulinemic, you could hear Dr Lustig, after an impressive talk about the relationship between the insulin and leptin in a body weight management, asking a question at 37:28:

Then you hear that we (as a population) have doubled or tripled our insulin levels than we had 35 years ago.
I will cut this short: The favorite reason of Dr Lustig is that the fructose intake causes insulin resistance. That fructose does not drive insulin response as high as glucose does, he leaves out. In this respect the glucose was pronounced by him as good because insulin and glucose act on the brain as appetite suppressants. Well, while this does not quite go together for me with his talk earlier in this video that the high insulin blocks leptin and promotes food intake, I am not going to elaborate on this because it also must have some explanation and I may look at it a bit closer in the future. I only know from my research on ghrelin and appetite that glucose and insulin truly suppress the appetite.
For now I would like to highlight and remind to you the trends in the nutrients intake for the past 40 years and you tell me which correlated with the elevated insulin levels not only for the 30 years (prior 2000), when the sugar (and fat) consumption was on a minor rise in comparison to the flour and starches, but also since 2000 when the sugar consumption started to go down and something else in the American diet went up. Both USDA and NHANES data agree on these trends, the difference was only in the figures of absolute amounts.

So where did the insulin come from? Fructose in sugar? Or rather processed carbohydrates based on glucose? I bet. How the fat fits in this?
Well, you could read elsewhere how the overeating and a low physical activity at the same time make muscles insulin blind. That means when the muscles are constantly supplied with energy molecules (glucose and fat), but do not burn the energy they have in their cells, they cannot take anymore. It is the same mechanism as Dr Lustig pictures for the fructose and liver, except the liver does not need insulin to take up fructose and also glucose.
So, when the energy molecules such as fats and glucose are not taken into the muscles, which have insulin dependent receptors for glucose uptake, these energy molecules keep circulating in blood and the pancreas tries to clear the glucose somewhere by increased production of insulin. And here you have an elevated glucose and also insulin. This is a pre-diabetic state.
The role of fructose in the development of insulin resistance is more sophisticated and not as straightforward as the simple mechanism of a constant positive energy balance. Several studies examining this role of fructose had reported the link only after they fed the participants huge amounts of fructose (some as high as 30% of their total energy intake or even on top of their energy requirements - again causing a positive energy balance). You also may find it interesting that the participants were also not allowed to be physically active more than about 3 hours a WEEK. They were basically sedentary. Any wonders why the metabolic issues were reported for these poor folks?
These studies did not reflect the free-living humans who consume sugars or HFCS that contain approximately equal amounts of fructose and glucose and their fructose intake is not as high on average. Some individuals do manage to drink liters and liters of soft drinks per day but again: they are already obese. A 60 kg person has no chance to gulp down this amount of soft drinks and to manage to eat those 3000 or more kcal per day as many overweight or obese people do. The athletes are an exception.
I am aware that many folks will try to dismiss my arguments and stick with Dr Lustig as a much more qualified professional than I am. Fine. But read this:

The IR refers to insulin resistance and NAFLD means non-alcohol fatty liver disease - the one which Dr Lustig links with only the fructose consumption. You can find this text in the review published back in 2005.This piece of paper practically debunks Dr Lustig metabolic cascade he repeatedly presented and you could also hear it here at 10:45 minute. He says that it is the fatty liver that triggers the insulin resistance in the whole body, the paper says (as I suggested earlier) that firstly the muscles will become insulin resistant and then it will affect the liver.
I have asked a research community about what they think of the liver induced whole body insulin resistance. One of them (M. Constantine Samaan from McMaster University) replied:
"...muscle also has a fat compartment [extramyocellular] that grows with obesity and attracts immune cells that activate the inflammatory response and cause local inflammation and insulin resistance."He also wrote:
"...skeletal muscle, which forms 40% of body mass and takes up to 75% of postprandial glucose, is an important organ to consider."This was in connection with the previous quotation and my query about a possible cause of body insulin resistance. So here you can see the disagreement in the scientific community - at least between the researchers and Dr Lustig.
So, the positive energy balance not only leads to increased concentrations of plasma glucose and then insulin, it even contributes to the insulin resistance in muscles, responsible for three quarters of glucose uptake in the body. And this glucose uptake is insulin dependent, unlike for the liver which does not need insulin to take glucose in.
And regarding those 20% of obese people who were pronounced as metabolically 'normal' by Dr Lustig, they were probably more physically active so they did not express the usual negative effect of comfortable lifestyle in abundance. Genes also play role in this, or the environmental pollution, or, as I recently heard - the use of psychiatric medication, which is quite frequent in the U.S.. But that does not mean the obesity is not a problem. It is. People do not normally become obese without a positive energy balance.
No comments:
Post a Comment