Only Dietary Fat, Not Protein Or Sugar (sucrose), Drives Obesity

Discussion in 'Scientific Studies' started by haidut, Jul 23, 2018.

  1. haidut

    haidut Member

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    This is a recent study that confirms another controversial one I posted on the forum more than a year ago.
    https://raypeatforum.com/community/...diet-healthier-than-caloric-restriction.6909/

    The newer study also had some unexpected findings. For example, increasing protein level in the diet did NOT increase satiety, and did not lead to weight loss. In fact, when dietary fat was higher than 20% of calories increasing protein levels led to increased weight. Some of that weight was lean mass but a lot of it was adipose tissue as well. At fat levels below 20%, varying protein levels up to 30% of calories had no effect on weight.
    The good news is that varying dietary sucrose also did NOT lead to weight gain - neither fat nor lean tissue. Even more interestingly, unlike protein, combining sugar with fat did NOT lead to weight gain even though the fat level was quite high - 41.7% of calories. Unfortunately, the study only looked at diets of up to 30% sucrose, which may be well-below the level of sucrose consumed by Peatarians or the general public for that matter. It would have been nice to see results from up to 60% sucrose. Still, the study is quite clear that official guidelines are mistaken in suggesting that sugar is leading to the obesity epidemic currently observed. It is all about the fat, they say. The study has a nice infographic at the beginning, which I am posting here because I think it illustrates quite nicely the results.

    https://www.cell.com/cell-metabolism/fulltext/S1550-4131(18)30392-9
    graphical_abstract.png

    New study finds that fat consumption is the only cause of weight gain | News | The University of Aberdeen
    "...Professor John Speakman, who led the study, said: “The result of this enormous study was unequivocal – the only thing that made the mice get fat was eating more fat in their diets. “Carbohydrates including up to 30% of calories coming from sugar had no effect. Combining sugar with fat had no more impact than fat alone. There was no evidence that low protein (down to 5%) stimulated greater intake, suggesting there is no protein target. These effects of dietary fat seemed to be because uniquely fat in the diet stimulated the reward centres in the brain, stimulating greater intake. “A clear limitation of this study is that it is based on mice rather than humans. However, mice have lots of similarities to humans in their physiology and metabolism, and we are never going to do studies where the diets of humans are controlled in the same way for such long periods. So the evidence it provides is a good clue to what the effects of different diets are likely to be in humans.”
     
  2. boxers

    boxers Member

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    Brilliant.. thank you for this
     
  3. Liubo

    Liubo Member

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    From the studies I've seen, lots of protein should have an effect kind of like niacin's, lowering NEFA and keeping it stored. This is the only study I have bookmarked right now but I'm sure there are more that say the same thing. Of course, I love when handsome men confirm my amateur research. @haidut
     
  4. OP
    haidut

    haidut Member

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    Well, thanks ;-)
    Protein increases insulin release at least as effectively as starch/glucose and sometimes even more. So, I am not surprised that combined with high fat diet it increased adiposity. However, in a lower fat diet I think it would lead to weight loss since it is thermogenic and lowers serotonin in the brain.
     
  5. CLASH

    CLASH Member

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    I dont think that this is entirely applicable to humans. Based on anatomical and physiologic differences in the GI tract between mice and humans I would say that humans are more geared towards eating fat whereas mice are not. The mouse small intestine has significantly less surface area and an enlarged cecum/ colon hypothesized to be specialized for fermentation. Whereas the human small intestine has many times greater surface area in the small intestine and a significantly smaller cecum and colon proportionally. These functions signify, atleast to me, a focus on absorption of nutrients in humans, while in mice a focus on fermentation. This article is a good refernce on the anatomical/ physiologic differences:
    How informative is the mouse for human gut microbiota research?

    Furthermore the more I read it, the more it seems that endotoxin is the main driver of obesity, weight gain and general inflammation (in conjunction with PUFA of course). There are many posts on this forum discussing endotoxin and inflammation. So what I think you have happening here with the mice is the fat that they are ingesting is disrupting thier bacterial populations and carrying endotoxin to thier livers as thier small intestine is not as focused on absorption as it is fermentation. Whereas with humans it seems that saturated fat is actually protective of the small intestine by encouraging bile flow (1), protecting the liver (2), being anti-bacterial itself (3) and carrying endotoxin out of the lumen of the intestine to be detoxified by the liver (4). Not too mention, I think that the fat may help to spare glucose for the nervous system. Also, It seems that many animals including gorillas and cows actually eat a high fat diet due to the production and utilization of short chain fatty acids in the colon and rumen. As a personal aside when I went low fat in a peat fashion I was having adrenaline rushes multiple times a day, however when I added a decent amount of fat back into my diet the adrenaline rushes decreased significantly.
    I think feeding high fat diets to rats is akin to feeding high grain diets to cows; they can eat it but its not thier optimal food source and the overtime it will make them sick. I don’t think this is the case, atleast from my perspective right now, assuming the fat is saturated (maybe monounsaturated) in humans. Although, I do recognize the issues with fats like the oleamide issue brought up by @Travis and the accumulation of PUFA as well as randle effect brought up by Peat. I’m open to differing views though, I’d really like to figure this out.

    (1) How bile acids confer gut mucosal protection against bacteria

    (2)/ (4)
    Dietary fat sources differentially modulate intestinal barrier and hepatic inflammation in alcohol-induced liver injury in rats. - PubMed - NCBI

    (3) INFLUENCE OF TRACE AMOUNTS OF FATTY ACIDS ON THE GROWTH OF MICROORGANISMS
     
  6. Travis

    Travis Member

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    Oleic acid is fun issue to consider, but I think there are more dangerous fatty acids. I believe that free oils do absorb quicker than lipids in their natural matrix, and something like olive oil could increase brain oleic acid while olives would not. Although most attention is given to the larger lipoproteins and chylomicrons, a person could suppose there are smaller micelles circulating in the blood. @haidut had posted data detailing how oleic acid micelles had been found in the brains of Alzheimer's cases, so perhaps free oils are persorbed as sub-chylomicron micelles and 'beeline' straight for the brain‽ A few days ago I had made garlic oil—i.e. olive oil + microplaned garlic—and it had made me feel so odd that I had entertained the notion that allicin-containing oleic acid micelles had literally traveled to my brain. Assuming this actually occurs it would probably depend on the density of the lipid, with lower-density unsaturated fatty acids perhaps posing a greater risk. Saturated fatty acids also have a greater propensity for traveling to the liver beforehand for incorporation into lipoproteins, while unsaturated fatty acids immediately form chylomicrons and bypass the liver. The average lipoprotein is approximately ¹⁄₂ protein while chylomicrons are mostly lipid. More of the fatty acids found in their natural matrix could be liberated at a later timepoint and hence be destined for the liver, via the portal vein, while the 'free oils' such as olive- and flaxseed- could be rapidly chylomicron'ed in the duodenum or might even be persorbed as smaller micelles. . .
     
  7. michael94

    michael94 Member

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    A few years ago I brought up chylomicrons to a doctor because of issues I was having with fat to see if he had anything to hypothesize... Wish you were the doctor back then instead of him, would have been a worthwhile visit.

    I have oregano "infused" olive oil that Ive yet to open
     
  8. Travis

    Travis Member

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    Well: you probably had interrupted his reverie about how his tailor had 'borked' the custom lambskin cover destined for his oversize BigBertha™ golf club, and chylomicron talk is not conducive to that particular problem.
    Watch out! Olive oil does have between 5–15% linoleic acid, so perhaps it should be consumed in small bits. I only use a few drops every now and then, and usually go for the whole-coconut and the occasional goat cheese fatty acids. Moreover, thymol looks like it could be a dopamine antagonist (lol). . . [‽]
     
  9. fradon

    fradon Member

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    here's a video showing the various degrees insulin raises when combined with protein and fat. START AT 35 MINUTE MARK

     
  10. Fractality

    Fractality Member

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    How do people lose weight on high fat and moderate/high protein diets then? Is it because of elevated cortisol levels?
     
  11. rei

    rei Member

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    Because people are not rats. Amazing how every rat finding is immediately taken as confirmation for same in human, often mangled through some "correcting" formula to find "equivalent" dose.
     
  12. Travis

    Travis Member

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    Rat melatonin research is especially dubious if extrapolated to humans because they're nocturnal.
     
  13. Terma

    Terma Member

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    Oh god, that statement.

    Amino acids are the major inducer of satiety. Especially lysine, but also leucine, arginine, glutamate, taurine may all be major players, depending on which study you read:
    The Satiating Secret of Arginine, Lysine and Glutamic Acid. Plus: Things You May Not Know About These Aminos - SuppVersity: Nutrition and Exercise Science for Everyone

    Ghrelin, leptin, insulin, orexin, agouti peptide, neuropeptide Y control satiety, via a mechanism that was thought to be related to mTor activation in the hypothalamus ( Single Rapamycin Administration Induces Prolonged Downward Shift in Defended Body Weight in Rats ) but I read different things about that and left off.
     
  14. Terma

    Terma Member

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    Agreed.
     
  15. Terma

    Terma Member

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    Yes, thank you.

    Rodents are a starting point but I wish they would just stop killing rodents for macronutrient studies involving carbs and protein like this (ratios and requirements). This is last decade stuff at this point. You can compare SFA with PUFA on them but I wouldn't take it past that.
     
  16. bzmazu

    bzmazu Member

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    low carb... keto...
     
  17. theLaw

    theLaw Member

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    Bump @haidut

    I'm curious about this as well. Thanks!:D
     
  18. RobertJM

    RobertJM Member

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    I’m currently experimenting with a much lower carb and higher fat diet, and I immediately lost 7 pounds. A huge amount. My belly has flattened out completely. And I feel better. The experience alone has taught me that I don’t need to go crazy with carbs. More = doesn’t equal better. But then, I’ve spent the last four years PUFA restricting, so maybe I’m in a position to do this without turning into a car crash (poor temps, etc). My temps are really good.
     
  19. benaoao

    benaoao Member

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    I think that this title is misleading. It’s the bad combination of carbs and fats that drive obesity.

    This is explained properly here:

    Hyperlipid: Protons (38) and ultra low fat once more

    (Keep in mind this is a low carb blog, so his bias is real)

    In my opinion the worst scenario is either this:

    I don’t really understand why SFAs are that much worse than unsaturated fatty acids though. I’d need a better explanation than this:

    @Travis @haidut and whoever is better than I am at biochemistry - thoughts much welcome.
     
  20. yerrag

    yerrag Member

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    Yes. This means the body uses fat for energy. The blood glucose stays steady. No carbs eaten means no glucose enters the bloodstream, and glucose does not accumulate to cause blood sugar to increase to a point where insulin is released. Insulin release causes blood sugar to come down, often to a point where one would feel hungry again, and he would eat again. The frequent need to eat would mean increased calorie consumption, and increased consumption only leads to more blood sugar being converted to fats from the insulin response of high blood sugar.

    But glucose isn't supposed to accumulate in the blood when the body metabolizes sugar well. When you can metabolize sugar well, you don't get obese easily. Glucose entering the bloodstream doesn't get to accumulate causing blood sugar to rise to where insulin is secreted. Glucose is readily metabolized by the body, and this keeps blood sugar from getting too high. An insulin response is avoided, an eventual low blood sugar condition (from insulin response) is avoided, and with normal blood sugar levels, one isn't feeling the need to eat again.

    For people that don't metabolize sugar well because of the presence of fatty acids in the blood blocking sugar from being metabolized, they would see the immediate benefit of a ketogenic diet. They would lose weight because they don't experience the sugar highs and lows that cause them to eat more, and they also don't experience the frequent conversion of sugar to fats because they don't experience high blood sugar that triggers insulin to convert blood sugar to fat.

    Meanwhile, fat is used to produce energy using beta-0xidation. Beta oxidation is less efficient than oxidative metabolism, where glucose is used. But it also produces carbon dioxide as a by-product. Not only is it less efficient, but it also creates an acid load by producing keto acids. Since the liver and kidneys have to work more to maintain acid-base balance, there is waste of energy inherent in burning fat.
     
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