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Most nutritionists like to cherry pick studies that support their cause (even when they're low quality observational studies) and attack studies that oppose it.
by spion 9y ago
Most nutritionists like to cherry pick studies that support their cause (even when they're low quality observational studies) and attack studies that oppose it. Michael Greger (the author of nutritionfacts) is quite the typical example (don't get me wrong, Gary Taubes has done that too in the "opposing" camp)
The most likely theory I've seen is:
1. We have a certain amount of genetic propensity for higher-than-necessary insulin secretion
2. How we develop that propensity is still unknown (!).
Gary Taubes likes the sugar hypothesis (i.e. something about fructose metabolism in the liver causes the system's self-regulation to fail) but thats mostly supported by observational studies - the mechanics aren't clear at all.
Michael Greger likes the lipid hypothesis (fat inhibits muscle ability to absorb carbohydrates i.e. causes insulin resistance) but that doesn't explain why the liver continues to produce tons of fat despite its insulin receptors being clogged.
Jason Fung likes the overflow hypotheis (as the muscles get fuller of glycogen, they're less able to store blood glucose, which means more insulin is needed to do it - however the liver isn't resistant and insulin upregulates its fat production) - but that doesn't fully explain how there are people who do lots of heavy physical activity yet remain obese and insulin resistant.
Its possible that any subset of the above could be a cause if excessive enough - high GI carbs to raise the blood sugar, fat to slow sugar absorption and lack of exercise to keep your muscle cells overfilled with glycogen all contribute to high insulin secretion, together.
3. Insulin definitely regulates fat accumulation in fat cells. No doubt about it - more insulin means less fat released by fat cells and more carbs converted to fats by the liver and stored in fat cells. Insulin also blocks leptin which signals our brain that we're full, so we feel hungrier.
4. Keto and fasting definitely work in that they remove the primary reason for insulin to secrete. You can't have raised insulin secretion if you don't have a lot of sugars in your blood to start with.
5. Its possible that vegans (on average) also remove the secondary reason for insulin to over-secrete, whatever that is. Keep in mind that vegans on average are more mindful about having a healthy lifestyle, so it could be any number of things (correlation is not causation). But if veganism itself was the definite fix, we would expect to see no long-term vegans that are obese. Good averages to compare would be long-term vegans with long-term "ketoers"
Keep in mind, the mechanisms to prevent weight gain are very different from those needed to actually lose weight. The first one is about maintaining a stable homeostatic state while the second one is about deliberately causing a different non-homeostatic state.
- cageface 9y agohttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5466941/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5466941/ "Replacing carbohydrates (mainly refined starches and simple sugars) and saturated fats with monounsaturated and polyunsaturated fats lowered hemoglobin A1c and improved insulin resistance; polyunsaturated fats were also noted to improve insulin secretion. The authors concluded that in comparison to carbohydrates and saturated fats, monounsaturated and polyunsaturated fats had the most favorable effect on glycemia, insulin resistance, and secretion. In terms of foods, these findings support consumption of vegetable fats (e.g., nuts, avocados, olives) in place of animal fats and refined grains."
- spion 9y agoThats a great meta-analysis referenced there (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4951141/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4951141/), but the table of studies only contains baseline measures (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4951141/bin/pmed.1002087.s003.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4951141/bin/pme...) - I can't find the original non-aggregate data on the after-effect (benchmark) measurements of each of the analysed studies. One thing it seems to assume is that effects of carbohydrate reduction are linear, which might not be the case. The study analysed the effect of "replacing 5% energy from carbohydrate with SFA" and found it had no significant effect on fasting glucose - this might be true even if ketosis works perfectly, since on average the trials listed there are medium-to-high carb. It would be very useful if they also had listed a table with the individual study outcome data. Another thing that seems weird is that they deem an increase in insulin secretion capacity as good. Increasing insulin secretion capacity and insulin sensitivity will lower blood glucose, but at the expense of increased obesity - the blood sugar is going somewhere and its either the muscles or fat. So it seems to me that in T2D the increase of secretion capacity only postpones the problem. Ideally what you want is the (fasting) insulin levels to drop while maintaining the same or somewhat lower blood glucose.
- ericschmidt 9y agoYou've severely mischaracterized Jason Fung's work. >but that doesn't fully explain how there are people who do lots of heavy physical activity yet remain obese and insulin resistant. The only reason "that doesn't fully explain [x]" is because you've mischaracterized Fung's work in the first place. He discusses a great deal more than what you deem "the overflow hypothesis." And his model does fully explain why there are people who do a ton of physical excercise and are still obese — it's because they eat in such a way that it raises their insulin. I seriously don't even think you've read Fungs work and you're just seizing the opportunity to present your little pet theory, because in reality Fung has a far more developed and rational model of human biology than you've just articulated.