A mouse eats an average of 3g food per day so max case was 600 IU per day ? What's the equivalent for a human ? Value seems very low.

@Vapid-Bobcat said in Why is the epidemiological literature overwhelmingly in favor of PUFAs?: In pretty much every retrospective, cohort study or RCT I happen to take a look at, higher PUFA consumption, especially linoleic acid, almost always leads to better outcomes than lower PUFA consumption. @Vapid-Bobcat I suspect that there are ulterior motives. But then, I've become pretty cynical. Sometimes animal research performed for the preservation of an industry (and making $) provides better designed studies and interesting results that can be extrapolated to humans in general ways. Thiamine Deficiency M74 Developed in Salmon (Salmo salar) Stocks in Two Baltic Sea Areas after the Hatching of Large Year-Classes of Two Clupeid Species—Detected by Fatty Acid Signature Analysis "Fatty fish that feed on fatty marine prey fish are prone to suffer from thiamine deficiency [1,13] because the requirement for thiamine increases with the increase in the diet’s energy content [14] and because thiamine is depleted as a consequence of lipid peroxidation [14,15,16]." "In fish with a high tissue concentration of n−3 PUFAs, thiamine can be depleted during the pre-spawning fast so that the eggs do not provide enough thiamine for the yolk-sac fry (free embryos or eleutheroembryos [23]) to develop. Thiamine deficiency, therefore, primarily affects yolk-sac fry [8,24,25], which must survive on yolk nutrients from hatching to the alevin stage, i.e., the stage when the hatched fry start external feeding [23]. As THIAM is a reserve form of thiamine, its concentration of the different thiamine components in eggs varies most, depending on the female’s thiamine status [8]. The thiamine deficiency of the offspring of fish can, therefore, be predicted from the THIAM concentration of the eggs [8,26]. At worst, thiamine deficiency can be seen as weakness and loss of equilibrium in brood fish before spawning, and they may die before spawning [8,27,28,29]." also: Changes in thiamine concentrations, fatty acid composition, and some other lipid-related biochemical indices in Baltic Sea Atlantic salmon (Salmo salar) during the spawning run and pre-spawning fasting also: Fatty acid signatures connect thiamine deficiency with the diet of the Atlantic salmon (Salmo salar) feeding in the Baltic Sea "Thiamine is an essential micronutrient, which has a central role in energy metabolism (Lonsdale 2006) and also a linkage to fatty acid (FA) metabolism. Moreover, thiamine serves as an antioxidant (Lukienko et al. 2000; Gibson and Zhang 2002). Fish need to obtain thiamine from their diet (Niimi et al. 1997), and the requirement for it depends on the energy density of the food (Woodward 1994). As the net energy value of lipids is more than double that of proteins (Kriketos et al. 2000), the need for thiamine largely depends on the lipid content of prey fish." -end pastes- I think that each of these studies confirm Ray Peat's work regarding fats. The added wrinkle is the connection to thiamine deficiency. Thiamine deficiency is implicated in many of today's chronic diseases, including coronary heart disease, diabetes, and the dementias.

Profiling of faecal water and urine metabolites among Papua New Guinea highlanders believed to be adapted to low protein intake [image: 1707871068742-25efe6d1-dc8d-4cd0-9770-1acf096fc89b-image.png] Role of urea in intestinal barrier dysfunction and disruption of epithelial tight junction in CKD "The rise in urea concentration in the intra-cellular and extra-cellular fluid compartments results in its heavy influx into the gastro-intestinal tract (7). Within the intestinal lumen urea is hydrolyzed by microbial urease forming large quantities of ammonia [CO(NH2)2 +H2O → CO2+2NH3] which is readily converted to ammonium hydroxide [NH3 + H2O → NH4OH] (8,9). Ammonium hydroxide, in turn, leads to a modest rise in the luminal fluid's pH, causes mucosal irritation and promotes enterocolitis [10,11]. Based on these observations we hypothesize that ammonium hydroxide generated from hydrolysis of urea by microbial urease in the intestinal lumen of uremic patients may contribute to the epithelial barrier dysfunction and erosion of the TJ protein constituents." "The present study revealed that at clinically-relevant concentrations, urea significantly lowered the TER [Transepithelial Electrical Resistance] in the tight junction-forming polarized human colonic epithelial cell monolayer in vitro. The effect of urea was dramatically amplified by urease which was used to simulate the effect of urease-possessing microbial species in the colon. These observations illustrate the potential contribution of influx of urea into the intestinal tract in the pathogenesis of the uremia-induced intestinal barrier dysfunction in the uremic patients. The observed fall in the TER was accompanied by and was largely due to the urea-concentration-dependent depletion of occludin, claudin 1, and ZO1 which are the key protein constituents of the epithelial TJ. The erosive effect of urea on the measured TJ proteins was greatly intensified in the presence of urease leading to near complete depletion of ZO1 and occludin and severe reduction in claudin 1 abundance." "As noted above, accumulation of urea in the intra- and extra-cellular fluid compartments in patients and animals with advanced CKD results in its heavy influx into the gastro-intestinal tract via passive diffusion and incorporation in the glandular secretions (7–9). As noted earlier within the intestinal lumen urea is hydrolyzed spontaneously and by microbial urease forming large quantities of ammonia [8,9]. Ammonia is, in turn, converted to ammonium hydroxide which is a caustic base capable of causing cytotoxicity and tissue damage. Recent studies conducted by our group have shown marked changes in the composition of microbial flora in humans and animals with advanced CKD [21]. Five of the 10 microbial families which were most abundant in the CKD patients possessed functional urease [2,21]. Thus massive influx of urea into the gastrointestinal tract together with the dominance of urease-possessing bacteria in the uremic individuals, work in concert to promote formation of ammonia and ammonium hydroxide in the intestinal tract [8,9]. This can account for the dramatic impairment of the barrier function and destruction of TJ apparatus observed in the present in vitro experiments designed to simulate the effect of uremia in vivo."

@AkJono ??

Here Peat talks about atropine / jimson weed, aka Datura stramonium, infamous for its hallucinogenic and intoxicating properties, but medicinal in this context: "...the medical standard for a long time was to use muscle relaxant like atropine or jimson weed to relax the duct out of the gallbladder and then take olive oil to stimulate the contraction" "But is there something, what did you say, Doc, you do before the gallbladder flush that is good to do to relax the muscles around the gallbladder? The jimson weed. It works like atropine, very similar chemical. And that 50 to 100 years ago was recognized as very effective and safe, but the atropine, partly because drug culture used it for entertainment, it lost a lot of its medical use [...] A piece of leaf the size of your thumbnail sometimes was enough" bioenergetic:life: 05.16.22 PEAT RAY

@Pillman Do you have any brand recommendations?

[image: 1707514329747-ad896bf0-2e4f-4a15-b8d3-617528f70bbe.jpeg] Dall-e attempting to make a chart on the benefits of aspirin.

@Amazoniac , Good catch. Thanks for the correction. I've edited my post (the 1st two bullets). I am a bit puzzled though why the authors in the OP study didn't use monomeric Si if they were looking for Si bioavailability. Perhaps, the concentrations of the Si polymer that they fed to the rats were low enough that they formed monomers...

extremely real, my skull and bone all became thicker when i first started peating.

@CurmudgeonApple They use same metabolic pathways and when combined they synergistic effect. Metformin + Berberine combination is superior to using only one medication.

@77sahara an important one is by b. a. houssay, who showed that a high saturated fat diet prevented diabetes in rats and a high pufa diet caused it. "In 1947, B. A. Houssay found that a diet based on sugar as a source of energy was more protective against diabetes than a diet based on lard, while the most protective diet was based on coconut oil. Lard reflects the pigs' diet, and is usually extremely unsaturated, especially since it became standard to fatten them on soybeans and corn. Essentially, his study seems to show that unsaturated (pork) fat permits diabetes to develop, sugar is slightly protective, and coconut oil is very protective against the form of diabetes caused by a poison." piorry and bud cured diabetics using large amounts of sugar in the 1800s. "Budd described another patient, a young man who had become too weak to work and who was losing weight at an extreme rate. Budd's prescription included 8 ounces of white sugar and 4 ounces of honey every day, and again, instead of increasing the amount of glucose in the urine, the amount decreased quickly as the patient began eating almost as much sugar as was being lost initially, and then as the loss of sugar in the urine decreased, the patient gained weight and recovered his strength." the hyperglycemia in diabetes is the liver overproducing glucose , not a build up of unused sugar. diabetics die quicker without sugar. "Since the first doctor noticed, hundreds of years ago, that the urine of a diabetic patient tasted sweet, it has been common to call the condition the sugar disease, or sugar diabetes, and since nothing was known about physiological chemistry, it was commonly believed that eating too much sugar had to be the cause, since the ability of the body to convert the protein in tissues into sugar wasn’t discovered until 1848, by Claude Bernard (who realized that diabetics lost more sugar than they took in). Even though patients continued to pass sugar in their urine until they died, despite the elimination of sugar from their diet, medical policy required that they be restrained to keep them from eating sugar. That prescientific medical belief, that eating sugar causes diabetes, is still held by a very large number, probably the majority, of physicians." insulin allows you to use the glucose but it also blocks the free fatty acids “Diabetes is caused by excess FFA floating in the blood, which blocks sugar oxidation as per the Randle cycle. Niacinamide lowers excess lipolysis/FFA and thus allows the cell to oxidize sugar again. Insulin also lowers FFA and also stimulates the glucose oxidation. This is why it is a therapy for diabetes. Diabetics have high FFA and glucose in the blood but the former part is almost never mentioned by doctors unless somebody ends up in ketoacidosis (driven by excess FFA) and even then the narrative is somehow still shifted to blame the "evil" sugar, while hyperglycemia is just a sign of high FFA.” -haidut https://raypeat.com/articles/articles/sugar-issues.shtml https://raypeat.com/articles/articles/glycemia.shtml https://raypeat.com/articles/articles/glucose-sucrose-diabetes.shtml https://raypeat.com/articles/articles/diabetes.shtml

@donovan all the studies for HPA seem to be on incipient decay, not progressed decay with destroyed enamel and tooth structure, so there’s no clear research I’ve found on the structure being re-formed through the introduction of enamel-like components. Possible that scientists just assume it isn’t possible so they haven’t studied it, although it seems plausible that if you can restrengthen existing enamel with calcium and phosphorus those same minerals will reform the structure itself.

UCP1 activation is also one of the pathways thought of that methionine restriction causes lifespan extension: [image: 1706873358448-67f2904f-dd47-446a-9824-509da944a385-image-resized.png] https://pubmed.ncbi.nlm.nih.gov/34263088/

Very nice find, thanks.