https://www.sciencedaily.com/releas...71019100957.htm



Two solutions. Thirty bananas a day/rice diet/juice fasting. Eat nothing but sugars, otherwise you're wasting calories on food that won't raise your brain glucose levels. Just kidding. Sort of. Or side step the issue, a low carb or ketogenic diet isn't going to raise your blood glucose much, so satiety must work a little differently.

Thinking back, trying to remember Dr. Fung's comments on insulin resistance, and the different kinds, liver specifically and wasn't there also brain insulin resistance? Meaning, glucose not being taken up by the brain tissue because of insulin resistance? Wouldn't that explain it? Given that these people were either obese or poorly controlled diabetics, IR is more or less assumed.

I would also wonder about inflammation, which could also be assumed in those two groups, being a factor.

There are studies where insulin administered to a mouse's brain is effective against obesity. For a while, "insulin is not obesogenic types" were very fond of this as evidence for their case. It's hard to say how bad an argument I think that is nicely. Systemic insulin has the whole body fighting over whatever glucose there is in the blood. Locally elevated insulin--you get those localized fat pads people can get when they inject insulin in the same spot for years on end. In the brain--you get a small area taking up a little more glucose. Massive insulin will starve the whole body of glucose. Local elevation of glucose just has local cells taking in more nutrients. It's the difference between starving the brain of nutrients, and increasing nutrition locally. So-called obesity researchers who write popular blogs sometimes skip the distinction. This is stupid. See? Hard to say it nicely.

Here's the full paper we're discussing here: https://insight.jci.org/articles/view/95913

On this forum, from experience, we know carbs cause obesity, i.e. carbohydrates stimulate insulin stimulate excess fat accumulation. We know this not from a hypothesis, but from direct observation and experiments.

In the paper we're discussing here, it says in the introduction "Glucose is the primary energy source for the brain, which consumes more glucose (~60% of total glucose-derived energy) than any other organ in the body (3).", but this directly opposes the facts we know about carbs and obesity and the effect of low-carb on all of it. Facts trump hypothesis. Facts win. Glucose is not the primary energy source for the brain.

In this paper, check Table 2, it's much more pertinent than anything else. See ghrelin and leptin. From personal experience, I promise that ghrelin is a very, very, very potent stimulator of hunger. Leptin opposes ghrelin, it shuts down hunger, causes satiety, and absolutely effective for leptin deficiency (doh!), but completely ineffective for leptin resistance (doh?). And check insulin too, it's ridiculously ridiculous high for T2DM subjects.

Now check Figure 3. It reminds me of the graphs from the 7 Country Study by Ancel Keys. Can't see any tendency at a glance, must be drawn on top based on statistics. Red flag. Too few subjects. Red flag. I could imagine they didn't have enough money for hundreds of subjects, but it was financed by Pfizer and Regeneron where there's literally tons of money for that kind of crap. Call me cynical.

I was about to write something smart, but the experiment and results are just too complicated for me, they don't fit what I know. I prefer simple to explain it all, like money from big pharma.

Ok, forget everything I wrote above. This is the only thing I need to know:

I dunno... glucose seems to be a primary fuel unless somebody's on a very strict ketogenic diet.



https://www.cambridge.org/core/jour...05D0A9F1C172A6A

22 grams of carbohydrate a day, 30 percent of calories as protein, the rest fat--only a 5 percent lower supply of glucose to the brain. Four times the ketone flux of people on the higher carb diet--but that's four times an extremely low contribution to energy that ketones provide on a high carb diet.

Never mind that it's 12 subjects 4 weeks. Instead, consider only this undeniable conclusion.

Dietary carbs is not necessary to feed the brain all the glucose it apparently needs.

Gut microbiome alterations in Alzheimer’s disease
https://www.nature.com/articles/s41598-017-13601-y

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Alterations in the composition of this complex ecosystem have been associated with the development of a variety of gastrointestinal and metabolic diseases including inflammatory bowel disease (IBD), obesity, diabetes, and insulin resistance10. More recently, the influence of gut microbiota on central nervous system function – often referred to as the gut-brain axis – has received significant attention, and alterations in the gut microbiome have been associated with neurological conditions including autism spectrum disorder, multiple sclerosis, and Parkinson’s disease11,12,13.
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