Just one high-fat meal sets the perfect stage for heart disease
https://www.sciencedaily.com/releas...80329083259.htm
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Gosh, I hope I posted this before any of you ate any fat. :D Quote:
So, is this an investigation, or a demonstration? Fat is bad, we know this, here's this little "study" we did with an easily predictable outcome, in order to make the news and sway public opinion? They mention fatty diets hurting rodents long term, but the observation that there are high fat diets that don't hurt the animals isn't something to ignore. The question isn't "is fat harmful?" it's "under what conditions is fat harmful?" I would concede that a diet of sugary milk shakes might be worse for you than a diet of sugary cereal. I concede this with heavy cream on my breath. |
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Did the grain and dairy industry fund the study is the standard go-to question, but in addition, why is there not a control group eating ribeyes with butter on top? |
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The control I want is plain heavy cream. Also at least a week for people to adapt to eating this meal, the acute response to a food depends to large degree on habitual diet.
It's mentioned that these short term effects on red blood cells are mirrored in rodents on high fat diets long term. Well, the sort of fatty, sugary carby diet they're talking about is just the thing to elevate fasting triglycerides, maybe it's not surprising if that does the same thing to red blood cells as a large fat meal for somebody not accustomed to it. Jeff Volek has done some work looking at the blood triglyceride response to a similar high fat meal in people on high carb, low fat or low carb, high fat diets. In the low carb, high fat dieters, fat tolerance was much higher, blood triglycerides much lower at all time points. |
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Terrific talk by Nina. Thanks for the link. |
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Let's see, today we had panna cotta made with cream - no sugar. Tomorrow is ribeye & another serving of panna cotta - different flavor (I'm experimenting :yum: ). Somehow, I don't think the fat is going to effect me like a full-sugar milkshake would. I guess it's reports like this that make my doctor think I should be taking a statin. No thanks. My blood sugar likes my diet. So do my taste buds. It's funny - people think my diet is restrictive. But I eat SO much better than when I was eating high carb crap. |
I skimmed the paper. There's an interesting bit about free fatty acids. The LFM group saw a drop from about 109um/l to about 40um/l. Where are the FFAs going? Not in the blood, trigs stayed about the same. The FFAs must be going somewhere, I bet it's to fat tissue. In other words, that single low-fat meal made the guys fatter. Otherwise ain't nothin' to see here. The discussion paragraph says it all (parentheses and bold mine):
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If I can paraphrase. Fat is bad, it took a single milkshake to prove it. It's sciance, we are sciantists, you must believe us this time, cuz it's the truth full of acronyms and stuff. Ima paraphrase something else. The Bellevue all-meat trial lasted one year. Two men participated. They each ate about 230g (or about 3 of those milkshakes) of fat each day of that year, spread over several meals each day, for about 1,000 meals each total. Conclusion from those sciantists doin' the sciance: No observed adverse effect. Alright, here's how it's gonna go down for me. Either they just found out that fat is truly bad, or they just found out why the Bellevue all-meat trial didn't find nothin' bad, you know cuz of all those nasty acronyms and stuff. Some math. In this latest sciance, there's 10 subjects, half HFM so 5 milkshakes. In the Bellevue all-meat trial, there's two subjects, total ~2,000 meals. Quick calculus, we got 400x (or 1995+, if you prefer) meals that suggest fat is benign at worse. Let me put it another way. Somebody hits something with a hammer 5 times, somebody else hits something with a hammer 2,000 times, they completely disagree on the results, we gotta decide which guy is telling the truth. |
"Either they just found out that fat is truly bad, or they just found out why the Bellevue all-meat trial didn't find nothin' bad, you know cuz of all those nasty acronyms and stuff."
Isn't it interesting how it was "them" studying us and determining what the proper (diet, drug etc. you fill in the blank) and now we study "them" as well.. Fortunately, consciousness allows us to not 'always' be the victim. There's hope. |
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Not only benign results. Quote:
If there was a pill that would produce these results, it would be as hot as Viagra :lol: :lol: :lol: Quote:
Thank you, thank you, for bringing up panna cotta. This has set my mad scientist side into ecstasies -- what a versatile thing which combines some favorite stuff in fun ways. I even have the grass-fed gelatin! |
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I found the almond flavor needed something more - perhaps berries. I'll try that when the berries are in season - if winter ever ends. We still have snow. :( But the orange extract - marvelous! Let me know what you experiment with. :) |
I commiserate. We can still walk on the bay.
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https://www.ncbi.nlm.nih.gov/pubmed/19632695 Just the abstract, this is that Volek study showing less of a triglyceride response in people habituated to a low carb diet. Something that should be addressed in all milkshake of death studies (but probably won't be) going forward. |
So adaptation switches it around. Note how pp insulin gets cut in half for CRD (low-carb). Post-prandial insulin is special because normally the bulk gets sucked up by the liver before we can measure it at the arm. Since there was a big drop for the CRD group, it follows that the liver became very insulin sensitive.
My paradigm explains this by an increase in ketones, where ketones activate insulin receptors. There's little to no ketones in the LFD group, so there's no insulin receptor activation, hence the very small drop comparatively. Also, dietary fat activates the PPAR-a pathway in the liver, which then activates insulin-degrading enzyme, ultimately resulting in a greater capacity to degrade insulin once it hits the liver. After twelve weeks of adaptation to just these two mechanisms meal after meal, a single high-fat meal challenge is no longer a big deal. Since it's the same high-fat meal challenge for both groups, the insulin response from the pancreas should be the same too. But since there's both a greater capacity to receive insulin by the liver and greater capacity to degrade this insulin due to 12 weeks of high-fat meals, the insulin measured at the arm has already been cut in half by the liver compare to the LFD group. Besides dietary fat, I suspect fat-solubles, especially vitamin A since it's stored in the liver, play a central role in all this. Forgot. Why is it more kinda sorta steady-state for the LFD group? Simple. There's always more insulin everywhere. |
Yeah, I found a lower insulin response to the exact same meal interesting.
Insulin response to non-carbohydrate nutrients like fatty acids, amino acids and ketones is largely glucose dependent, so that's another thing. It would be interesting to see the same experiment, but looking at the effects of a lean protein meal under the two diets. |
[QUOTE=teaser]Yeah, I found a lower insulin response to the exact same meal interesting.
This article focuses mainly on a high protein (from Optimising Nutrition). If you don't know this group, the guy who runs it is an engineer whose wife has type 1 diabetes, as I remember. https://optimisingnutrition.com/201...nse-to-protein/ |
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