The Carbohydrate-Insulin Model of Obesity

(Bacon is a many-splendoured thing) #21

Interesting article. Apparently, I never lost 60 pounds, because as I increased my fat intake, all my body did was burn the fat I was eating, and not my body fat. So all my 42-inch trousers that I could barely button spontaneously stretched themselves into being loose enough to fall off, I guess, and my scale simultaneously decided to get progressively more erroneous in a manner that only mimicked weight loss. Fascinating!

#22

I agree with that 100% with everything you said.

When I’m block fasting my BG stays below 70. When I’m eating LC, my morning glucose is 85-100. Combining fasting with eating moderately low carb has worked brilliantly for me. I would not have achieved the results (in body comp or cellular healing) as quickly via a VLC diet. Carb tolerance depends on the degree of one’s metabolic derangement, and those are probably the people who gain the most benefit from a fasting regime.

(Alec) #23

C’mon Paul, get with the programme, you know by now what we do is physically impossible, and therefore it did not happen. We are delusional. We were really this healthy all along, and we only thought we were overweight and suffering from T2D. It was all in the mind.

(Bacon is a many-splendoured thing) #24

Dr, Fung weighs in:

(Bacon is a many-splendoured thing) #25

Funny, that’s not what the voices are telling me! :rofl: :rofl:

(Alec) #26

Oh boy, if you have not read this, you must. It is brilliant. I love Jason Fung!! His conclusion:

“The facts alone, without any spin would be this. A ketogenic diet, independent of calories, causes fat loss and causes an increase (or at least the stabilization) in EE. That’s the facts. And I love it. Because I can use these facts to help heal patients and save lives.”

BTW, EE = energy expenditure.

Interesting that this is from 2016, and Hall’s most recent paper (referenced above) was published a few days ago.

Now, my opinion is this: having read all this, I believe Dr Fung. Therefore I am tended to believe that Hall is desperately battling to save his reputation. And he needs to keep publishing evidence to support his previous work and conclusions. As Dr Fung clearly points out, this is confirmation bias, and is bad when you are pretending to be a scientist.

Echoes of a certain Mr Keys, anyone?

(Todd Allen) #27

Kevin Hall also authored the hit piece on David Ludwig’s paper which I linked to in my comment on the backlash starting. I had some issues with the hit piece such as Hall’s claim of high serum triglycerides refuting the idea that insulin can reduce available energy driving hunger and obesity. Hall ought to know that triglycerides in the blood aren’t readily useable when insulin is high. Insulin inhibits hormone sensitive lipase which is needed to strip a fatty acid off the glycerol back bone, the first step of burning a triglyceride. Anyway it is good to see Fung take a swing at Hall and hopefully others will land some punches too.

#28

Yeah there seems to be a lot of varying viewpoints…

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(TJ Borden) #29

Hmmm… in the model above of eating protein, is it possible the insulin isn’t as damaging because it doesn’t have the carbs available to grab for storage?

Also, we know that protein is only half as insulinogenic as carbohydrates, so it’s possible that insulin sensitivity could still increase with the absence of carbs.

Of course anytime a comparison is made with someone that is super lean, it’s probably reasonable to guess they aren’t insulin resistant.

I don’t know, just a couple thoughts. I’m not strong on the biochemistry.

#30

Yes, I am not sure either. Many conflicting viewpoints…just thought it was interesting that T.N. seems to be refuting it, too (unless I read it wrong).

(Bacon is a many-splendoured thing) #31

Hall has been making these points since some time in 2015, when he presented the preliminary results (called, I believe a “poster” presentation) at a conference. The study was formally published in 2016, which was when Dr. Fung wrote his piece. Dr. Mike Eades published a couple of blog posts about Kevin Hall in 2015 and 2016, as well.

(Doug) #32

Dr. Fung’s response is good. The study was just a beginning, ‘pilot’ project where there originally was to be a later, longer study. (I think NuSi did do some later stuff.) One big problem with what Hall wrote about was that it was only 4 weeks on the low-carb keto diet. I know studies are expensive, but I say let the people get truly fat-adapted - that’s going to make a big difference.

(Alec) #33

Abso-bloody-lutely!! How can anyone who knows anything in this field think they are doing science by looking at 4 weeks of data. Everyone knows you are not fat adapted by then. How is it the scientific researchers seem to not know anything about the area they are researching?? I am astonished by their ignorance. To publish serious science in such a flawed construct… it gives scientific research a bad name.

(Doug) #34

Yes indeed, Alec. There was a lack of communication, at the least - not everybody agreed on the methods and procedures. Moreover, it does seem like Kevin Hall had an agenda in his interpretation. I would say, "Okay, if you want to disprove the carbohydrate-insulin thesis, then at least address it in its entirety - including the necessary time for fat-adaptation and declining insulin levels. We’re all interested in the science, so let’s give the science time to work."

#35

I’m not sure what to make of Hall. He strikes me as obtuse.

Based on my limited reading of his “rebuttal” to CIM, it seems he avoids addressing one of its most interesting assertions: that calories shunted to fat storage are unavailable for energy, leading to a larger energy deficit, increased hunger, reduced metabolism, higher cortisol, etc.

“Scientists” who dodge the central and most interesting aspect of a hypothesis, but instead resort to misdirection and obfuscation have an agenda - Hide The Salami.

(karen) #36

The weight-loss mimicking diet. :grin:

(Crow T. Robot) #37

The problem with the carbohydrate-insulin hypothesis (or ‘model’ per Ludwig) is that there’s no exact definition of what it is and therefore, what is being debated and what isn’t. I would say that high insulin inhibiting lypolysis and low insulin promoting it is nothing more than basic endocrinology, and not really a theory at all. However, plenty of people still dispute that it has anything to do with the obesity problem, and that at the end of the day, it’s still just about calories. IMO, this is where the trouble lies.

This is what Jason Fung effectively pushes back on in his blog post addressing the Kevin Hall pilot study. I’m not sure that Fung is really defending the CIH, though, as much as simply insulin versus CRaP.

I believe Gary Taubes popularized the CIH with ‘Good Calories, Bad Calories’. When people like Stephen Guyenet and Keven Hall dispute the CIH, they are disputing Taubes’ interpretation and to some extent things Atkins claimed as well. Someone correct me, but Taubes interpretation in GCBC is that high carbohydrates cause obesity. High carb diets increase insulin levels and extra glucose from the carbs are converted to fat via de novo lipogenesis, leading to obesity. Again, please correct me if I am misreading his position.

The problem is that most stored fat is dietary fat (this has been tested and demonstrated), showing that de novo lipogenesis is not really a factor in obesity. Also, it’s been shown that a starch/sugar only diet causes weight loss, in spite of being insulinogenic. So, when people say the CIH is “dead”, I take that to mean that it’s simply an incomplete model of obesity. By itself, it doesn’t explain the whole problem. Of course, when people like Hall (and to a lesser extent Guyenet) say it’s “dead”, they mean Taubes/Atkins is wrong and should be disregarded, which of course is not only silly, it’s unscientific.

(Todd Allen) #38

I think Taubes position is a little more nuanced; sugar is a primary driver of obesity, other carbs probably contribute but there are people who remain thin on high sugar / high carb diets.

(Bacon is a many-splendoured thing) #39

Forgive a few small corrections, please: As I understand it, the extra glucose is converted to fatty acids, which are then stored in adipose tissue as triglycerides, and the process of de novo lipogenesis is part of the ethanol/fructose pathway in the liver and is the result of dealing with an excess of either substance, hence fatty liver disease from too much alcohol or from too much sugar (sucrose = 1 glucose + 1 fructose) or high-fructose corn syrup ( = 45% glucose, 55% fructose). My reading of Taubes is that he shares that understanding.

This explains the fact that de novo lipogenesis is not a factor in visible obesity. You appear, however, to be overlooking the fact that it is relevant to visceral adiposity, which can remain hidden and indicates a high risk for metabolic disease (remember the medical term “TOFI” = “thin on the outside, fat on the inside”). A starchy diet can cause weight loss, but only if it is low in sugar. Moreover, for the record, a “starch/sugar only” diet is impossible; the human body requires a certain minimum intake of protein (which must include an adequate supply of the 9 essential amino acids) and a certain minimum intake of fat (which must include an adequate supply of the 2 essential fatty acids).

There are popluations, such as the Japanese in the 1960’s, who remained thin on a high carbohydrate diet, but the key, in Taubes’s view, was the level of sugar intake per capita. In The Case Against Sugar, Taubes states that Japan in the 1960’s was eating the same amount of sugar as America in the 1860’s, and that the incidence of diabetes and obesity in 1960’s Japan was comparable to that in America in the 1860’s, just before the diabetes epidemic began in the U.S. Now that Japan is consuming an amount of sugar comparable to U.S. consumption, the incidence of diabetes and obesity there is comparable to the incidence in the U.S.

Remember that Keys’ own data in the Seven Country study showed a very strong correlation between sugar consumption and cardiovascular disease in all 22 countries that he studied (including Japan), but he decided that this correlation was irrelevant, and so he focused his report on only the 7 countries out of the 22 that appeared to support his hypothesis about fat and cardiovascular disease.

(Crow T. Robot) #40

I think it is more nuanced now, but I was mostly referring to GCBC.

Not at all, I appreciate the corrections – that’s how we get to the truth. I definitely agree about the visceral fat.

I was mainly stating what I think to be the main reason some people consider the CIH “dead” (or one aspect of it, at least).

My opinion is that obesity is caused by overeating a combination of starch/sugar along with fat. The elevated insulin and glucose ensures that all the dietary fat gets stored, and the glucose gets pushed into the cells as glycogen or around the organs as fat, leaving very little energy for use, leading to feelings of hunger and deprivation within a short time, and subsequent snacking and overeating. I still feel that carbs are the problem for the reasons you state: fats and proteins are essential and, in the absence of carbs, are very difficult to overeat and don’t wreck your liver.

Someone who eats nothing but starch/sugar will likely also lose weight (e.g. the Potato Diet), but will also get very malnourished and sick.