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  #1   ^
Old Mon, Jul-09-18, 06:29
teaser's Avatar
teaser teaser is offline
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Default crapping on the insulin hypothesis

http://sci-hub.tw/10.1001/jamainternmed.2018.2920


Woo has been doing some criticism of this Kevin Hall, Rudy Liebel, Stephan Guyanet critique of low carb claims. I yoinked the title for this thread from label for the link for the paper.

http://itsthewooo.blogspot.com/2018...a-and-risk.html

Her latest post addresses failure of insulin to correlate with weight gain. She goes into more detail, but anybody familiar with the idea of a personal "fat threshold" beyond which insulin resistance/type II diabetes are liable to develop should see the problem. Once a person's adipose tissue grows to the point where it's hitting against their personal potential for fat growth, fat trapping is compromised. Fat starts to accumulate where it shouldn't, in the liver, pancreas and visceral area. Insulin resistance increases, insulin levels increase. This may serve to push subcutaneous fat to grow a little further, but since they're near their potential growth, the insulin isn't as effective. Some type II's will get to the point where they're losing weight, if they don't take insulin--they may be still producing enough insulin to be hyperinsulinemic, but due to insulin resistance, no longer enough to avoid losing calories in the urine etc.
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  #2   ^
Old Mon, Jul-09-18, 07:40
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GRB5111 GRB5111 is offline
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The bias of Kevin Hall is puzzling, as he's going to engineer his "studies" and references of other "studies" seemingly to suit his hypothesis. A combination of ego and irreverence that, unfortunately, many who call themselves scientists today exhibit in many other fields. I've gotten to the point where I no longer care to spend the time identifying the holes in these arguments, because there is no intellectual exchange here with a willingness to acknowledge flaws in studies to refute the original hypothesis. This is a true scientific approach that has been left by the wayside in our quest for fame, money, and credibility.
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  #3   ^
Old Mon, Jul-09-18, 08:16
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
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It's pretty crazy that there's an argument whether the subcutaneous fat tissue or the brain ultimately regulates the metabolism. It's like asking a plant whether it would rather have sunshine or water. Without the liver the pancreas can't regulate blood glucose. And vice versa. I think Woo's best point is that insulin causing fattening is a direct observation. It might take more insulin to fatten one person up than another, but you can get there.

The question of postprandial insulin and getting fatter is another thing, the meal that raises insulin the most--is there something about it that is decreasing insulin sensitivity? If it is--where? Muscle, fat, liver? What about Dr. Fung's contention that time spent with elevated insulin matters, as opposed to just peak insulin or even total insulin under the curve? We know fructose plus fat is fattening, neither nutrient is very insulinogenic on its own.

There is also the simple observation that when things are working right, the oxidative hierarchy dictates that carbohydrate, since we can only store so much glucose as glycogen, at some point must cause a decrease in oxidation of fat, whatever the insulin levels might be that facilitate that. There are a lot of studies showing that if the respiratory quotient is higher than the food quotient, people are likely to get fatter. RQ is a measure of fat vs carb oxidation, a high quotient means more energy is produced vs. oxygen use, since carbohydrate has some anaerobic energy production, it has a higher RQ, food quotient is the RQ that would result if what you oxidized was exactly what you ate.

During the low fat heyday researchers interpreted RQ/FQ mismatches as an inability for the body to switch to burning fat in response to a fat load. Of course low carbers can and do turn this around and say, fat oxidation is pretty much the default, so take the carbs out of the picture. I think both are sort of right--once you're already overeating a carbohydrate meal/diet, adding fat past a certain point for essential fat/vitamin needs really doesn't improve things.
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  #4   ^
Old Mon, Jul-09-18, 08:59
M Levac M Levac is offline
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Kevin Hall is an idjit, I've said it before. It feels like a response to Ludwig's "special commentary": http://forum.lowcarber.org/showthread.php?t=480690 but they're published same date, so instead Ima say both Ludwig's and Hall's were produced way before publish date, and Hall was given access to Ludwig's for the purpose of an appropriate counter, ya know, to give the impression of a neutral view from JAMA.
Quote:
However, this CM of obesity is a strawman that is inconsistent with the current state of obesity science because it omits the known neuroendocrine mechanisms that regulate energy homeostasis. Weight loss and obesity prevention are not simply a matter of willpower, and any accurate model of obesity must include the known physiological processes that resist weight loss and promote weight gain.

No, it's a concise description of the CICO hypothesis as understood by most who believe in that stuff. "Not simply" implies it's also that, so that's agreement. But here it means it's mostly that. That last phrase certainly comes from Guyenet (the leptin guy), cuz Hall can't make heads or tails of anything more complex than eat less move more. Now for the main idiocy.

"resist weight loss and promote weight gain"

Within the realm of physiology and all that stuff, obesity is merely one possible effect among many, not a primary function or anything like that. Therefore, characterizing obesity as function of phenomena which "resist weight loss and promote weight gain" fails to illustrate, and dare I say acknowledge, this realm of physiology. To wit, diabetes type 1, where phenomena resist weight gain and promote weight loss, which by virtue of being complete opposite, should be eminently pertinent to the question of obesity. Yet diabetes type 1 is merely one of many evidence that instruct us into the depth of the physiology of obesity.
Quote:
It therefore seems unlikely that insulin signaling in adipocytes is the primary locus of control in common obesity pathogenesis, although it may be an important determinant of body fat distribution.

Again with this out-of-realm idea that obesity somehow is some primary thing. Three things to that. Gender hormones testosterone and estrogen, insulin-induced lipohypertrophy, and muffin top. Gender hormones are well-known to determine fat distribution in a specific gender. For example, women have more fat around the legs and waist, while men have less fat there but more above the waist. Insulin-induced lipohypertrophy certainly makes it look like insulin will determine fat distribution, but only because when a diabetic type 1 injects insulin in the same spot for years, this insulin causes local fat tissue to grow independently from the rest of fat mass, i.e. fat lumps. Muffin top is a typical fat distribution where more fat grows around the waist than elsewhere. In this case, there's two things going on at once. First, there's the physical restraint (in this case, very tight jeans) where when we exert a physical force on a body part for years, this part will be shaped accordingly and there's ample evidence of that. Second, this particular fat mass has grown because of something, and it's very very very improbable that the cause is simply that we eat too much or move too little. Instead, we can invoke insulin-induced lipohypertrophy, where the bulk of insulin is taken in or responded to by tissue closer to site of production and degradation, the pancreas and the liver respectively. I thought of reserving this phenomenon to women, but we've know for eons about mens' love handles. In humans, insulin does not perform any task of distribution whatsoever, except within the carbs-insulin hypothesis where it distributes fuel between lean and fat tissues (when there's too much or a problem with sensivity/resistance of various tissues, i.e. obesity), or where it fails to distribute any fuel to any tissue (when there's none of it, i.e. diabetes type 1, where insulin sensivitity of all tissues is described as "exquisite").
Quote:
For example, a central tenet of the CIM is that low energy availability of circulating fuels is the proximal cause of increased energy intake leading to obesity. However, individuals with obesity have normal or elevated levels of circulating fuels, including free fatty acids (FFA) and glucose, and their adipose tissue releases more total FFA and glycerol. Furthermore, the energy availability calculations used by Ludwig and Ebbeling did not include plasma triglycerides, which are a major contributor to circulating chemical energy, are typically increased by higher carbohydrate diets, and are often elevated in obesity.

I did say Ludwig was out of his element with the mechanistic and logic stuff. Well, when you're out of it, this is the responses you get to that. Let's see anyways. This phrase: "plasma triglycerides, which are a major contributor to circulating chemical energy". Witin context, it seems to mean instead, or at least imply "available chemical energy". Triglycerides is not a form of available energy, it's a form of energy storage. The bloodstream can't possibly be deemed a storage medium of any kind. But more to the point, if the energy present is in the stored form, it simply cannot be used by any tissue, unlike fatty acids, glucose, ketones, etc, unless this stored energy is first converted to its usable form, like glycogen/glucose, triglycerides/fatty acids, etc. As a result of not being usable by any tissue, any of that energy can't be included in any calculation about total available energy, so while Ludwig is out of his element, it seems he got something right when he omitted triglycerides in his calculations for total available energy. Also, I posit here that any and all biological molecules are inherently signaling molecules to some degree, including triglycerides. If this is true, it could be that when triglycerides hit something, this something then responds appropriately. If, for example, the something is not a storage organ, it will signal that it's receiving storage stuff, but can't take it in, so send something else instead, something it can actually take in and use.
Quote:
Nevertheless, hypoglycemia can be a powerful stimulus for food intake in the context of aberrent or exogenous insulin delivery.

Say the hell what?!? Diabetes type 1 contadicts every single word of that phrase, including "in", "for" and "a". Three symptoms always present in diabetes type 1: Hyperphagia, hyperglycemia, and hypoinsulinemia. The instant we inject insulin in that person, all three of these symptoms disappear simultaneously. And, within the hypothesis of CICO (or CM as named by Hall and Guyenet), paradoxically, fat tissue mass increases.

And they put their names on that crap?

Ima ignore everything that comes from Hall and Guyenet from this point forward until the end of universe.
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  #5   ^
Old Mon, Jul-09-18, 10:04
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Ms Arielle Ms Arielle is offline
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Plan: atkins, carnivore 2023
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Of all the researchers that I have personally met--a big ego is evident immediately. A rare noteable few are humble.
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  #6   ^
Old Mon, Jul-09-18, 13:36
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BillyHW BillyHW is offline
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Plan: Keto + IF
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Quote:
Originally Posted by Ms Arielle
Of all the researchers that I have personally met--a big ego is evident immediately. A rare noteable few are humble.


Yep, despite their claims to be open-minded and going where the evidence takes them, nobody is less likely to change their minds than a scientist.
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  #7   ^
Old Tue, Jul-10-18, 06:16
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Susky2 Susky2 is offline
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Plan: Keto-ish
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Quote:
Originally Posted by BillyHW
Yep, despite their claims to be open-minded and going where the evidence takes them, nobody is less likely to change their minds than a scientist.


Great...now I have to clean coffee off of my keyboard.
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  #8   ^
Old Mon, Jul-16-18, 18:17
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Valtor Valtor is offline
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In all honesty, I found Stephan Guyenet's book, The Hungry Brain, to be seriously interesting.

Anyone else here has read it ?

Patrick
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