Response to Insulin Series Part 2

On to part 2 of the insulin series articles, which can be found here.

In the beginning of this article, we are reminded of the trials that showed dietary protein to be a potent effector for insulin secretion (though, as I said in my critique, all of the protein meals contained significant carbohydrate and so you have equivocal results). Thus, Krieger states that insulin spikes are normal and healthy. I do not disagree that spikes are normal and healthy, provided they are transient and intermittent. Insulin is secreted in pulses as the pancreas continually assesses the amount of circulating blood sugar. Every 5 minutes or so we get another insulin dose in response to a meal until blood sugar returns to normal. In people with impaired insulin sensitivity and glucose tolerance, the insulin response is dulled (not enough) and chronic high blood sugar becomes a problem, necessitating possible insulin injections.What leads to this state of poor insulin sensitivity and glucose tolerance is repeated high insulin spiking. Your brain and pancreas “remember” the glucose load from previous meals, and anticipate the next meal by stimulating higher insulin release. A diet high in carbohydrates leads to high blood sugar and thus high insulin response, and so the body becomes routinely inundated with insulin, thus making it resistant.

Now Krieger introduces the effects of a drug called Exenatide (BYETTA), which restores the insulin response in glucose intolerant and type II diabetic people. The figures he shows illustrate the effectiveness of the drug at reintroducing the rapid phase insulin response to a meal. Then he notes that the people who take BYETTA in these studies supposedly lose weight, and concludes therefore that the rapid phase insulin spike is conducive to weight loss. This conclusion is wrong. What he fails to mention is the entirety of the effects of BYETTA. From their website (here), you can learn that BYETTA does a few important things to aid with glucose tolerance. Most importantly, it slows down the time it takes for dietary glucose to be absorbed into the blood stream. This means there is less glucose to deal with in the blood. BYETTA also stimulates the pancreas to release insulin and then stops the signal once the blood sugar is back low again. Essentially, BYETTA reinstates the normal phase insulin response, but also controls the rate at which glucose is absorbed, so there is no need for high insulin in the first place. BYETTA is recommended for diabetics who are taking insulin injections. Thus, prior to using the BYETTA, these people likely had to inject large doses of insulin (since their pancreas wasn’t producing or releasing any) in response to a meal. So, Krieger misleads the reader into thinking that these people had low insulin response and were fat and sick, and then suddenly they take this drug that reinstates a high insulin response and they lose weight, so low and behold, insulin helps you lose weight and keep you healthy. No, not at all. These people were sick and likely injecting large doses of insulin prior to BYETTA, and then once they go on the drug, they have decreased blood glucose per meal (lower absorption rate) AND the drug helps their body release insulin in normal pulses as it should, and the pulses are probably lower than they would previously have had to inject.

So to reiterate, insulin did not help these people lose weight. Reinstating insulin sensitivity did. The blood glucose control and lower absorption necessitated overall less insulin release than they were injecting. Controlling blood glucose was done by using a drug, but it can also be done by reducing carbohydrate consumption. This is all right in the charts Krieger posted (with no reference by the way). Not surprisingly, the “post-prandial plasma glucose” is lower in the subjects injected with BYETTA, but yet Krieger wants to credit all of the beneficial effects to the fact that their insulin response was restored. Once again we have confirmation bias and a failure to see all the variables at play.

The next little blurb continues with how BYETTA mimics glucagon-like peptide-1 (GLP-1) who’s role is to stimulate insulin. Really though, once you understand the interplay between glucagon and insulin, this paragraph is completely inconsequential. Glucagon is inhibited by insulin, but insulin is stimulated by glucagon. When you eat a meal, you insulin goes up, and glucagon is temporarily inhibited. As insulin lowers, glucagon expresses a bit more to make sure blood sugar doesn’t drop too low. If too much glucagon is present, insulin will increase a little once again. This back and forth ensures stable blood glucose levels. BYETTA, again, works to restore some of the original healthy function of the body’s metabolism. I don’t think there is any argument that a healthy metabolism (one that releases insulin even!) stabilizes weight and promotes proper hunger management.Perhaps the satiation factor comes because the body is actually receiving its nutrients thanks to proper insulin spiking? Yes. That is, after all, one of the main roles of insulin. We need this hormone, it lets us put meat on our bones and put the energy in our cells where it needs to be. Not surprised at all. I think we can move on.

Now I want to directly quote and point out a logical fallacy at play:

It is well established that rapid rises and falls in blood glucose can contribute to hunger.  Because rapid rises in blood glucose also cause rapid rises in insulin, people end up blaming insulin (and the effects of high glycemic carbohydrates on insulin) for the problem.

According to Krieger, we can blame hunger on blood glucose spikes rather than insulin spikes even though he freely admits that the two are directly tied to one another. Blood glucose spike induces an insulin spike, but oooh no it’s not the insulin people, nope, it’s the blood glucose. If A causes C by way of B, then does B have any relation to C? Of course. What sort of logic would conclude different?

We move on to some myth and fact type statements, the first about amylin, a co-secreted hormone with insulin that works to break down fat. I’m not sure how this whole bit fits in with supporting Krieger’s argument that insulin is “not the bad guy.” What I get out of this is that comparing a healthy metabolism where everything functions as it should to one where things aren’t responding or secreting properly means you can’t expect the same results. I think that’s quite obvious and really a better example of why insulin injections, overproduction, and insensitivity are dangerous. If damaging your insulin sensitivity also damages co-responders, then injecting with plain old insulin certainly isn’t going to reproduce a non-pathological state.

On to insulin and satiety again- insulin has two effects, as do many hormones, an acute and a chronic effect. An acute effect (immediate effect) of insulin in the brain is that it clears dopamine, a signal for the end of a meal. Chronically released insulin blunts the efficacy of the receptors, and the brain no longer responds. This is the same effect as would happen if you would knocked out the the insulin receptors, which they do to the mice in the study Krieger linked. When the brain can’t read the release of insulin, it can’t control the insulin secretion. Poor regulation and sensitivity to insulin interferes with the hormone, leptin, which is the actual hormone that signals satiety. Leptin resistance is a real and known cause of overeating. Robert Lustig did the first studies of leptin on obese children and adults and found that their ability to register satiation drastically affected their hunger and energy levels. As for the article that Krieger links, the researches really show that disrupted control of hypothalamic neuropeptide levels may contribute to the development of obesity, and that should come as no surprise. If the animal can’t read insulin levels, then it won’t properly produce insulin, which then interferes with leptin sensitivity, and the animal will think it’s starving and so overeats.

To conclude, I’ll just run through Krieger’s ending statements. They do run very circular. He essentially says two things at once. On the one hand, he acknowledges that control of blood sugar is important in controlling weight and preventing or aiding diabetes. However he says that this is not the same as controlling insulin. If blood sugar directly affects insulin release, then controlling one means you control the other. Insulin does matter and it is the effectiveness of the insulin response that keeps us healthy. You can’t acknowledge that and still maintain that insulin is a passive bystander in the whole thing. I also find this statement to be particularly ticklish on the logical fallacy detectors:

…but it is also evident from the fact that high protein diets have been found to help both diabetics and obese individuals, despite the fact that protein is a powerful stimulus of insulin secretion.

First, he never proved anything with high protein diets and insulin because they were convoluted with variables. We do know that protein stimulates insulin, however it does not stimulate near as powerful an effect on insulin as do carbohydrates. Second, to eat high quality protein, you typically have to consume fat. When you increase your fat and protein, what goes down? Carbohydrates. So all this literary fluff is actually just in agreement with eating low-carb.

His final statement is to eat low glycemic foods, high quality protein, fruits, vegetables, high fiber, low carbs, and whole foods over processed foods. This is great advice, this is exactly how I think we should eat for our entire lives. This type of diet keeps blood glucose low and therefore keeps insulin secretion low. Yes high blood glucose is dangerous, but so is its concurrent effect of chronically elevating insulin levels.

Responses

  1. […] second part to my insulin series response is up. Check it out here or just click on the Insulin article series tab and go to “part […]

  2. You are amazing.


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