tag:blogger.com,1999:blog-36840063.post3497533545777756728..comments2024-03-27T22:57:00.742+00:00Comments on Hyperlipid: Surwit diet and derivativesPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger8125tag:blogger.com,1999:blog-36840063.post-5337452905497080102021-08-31T21:18:43.399+00:002021-08-31T21:18:43.399+00:00Back looking at the Surwit diet. Even here, it'...Back looking at the Surwit diet. Even here, it's clearly the PUFA that is causing the obesity (more to follow on this!).<br /><br />But the question is: what is acting as a co-factor to accelerate the obesogenic quality of the PUFA?<br /><br />I'd wager it's not the trans fat in the hydrogenated coconut oil, which contains minute quantities (represented as zero).<br /><br />I'd wager it's the MCTs, which are like dietary ketones, blocking oxidative metabolism of the PUFA aldehydes...Tucker Goodrichhttps://www.blogger.com/profile/09455436946187786398noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-37778935882848295362020-05-08T06:28:50.553+00:002020-05-08T06:28:50.553+00:00Ha! These people are so superficial. PDK4 is upreg...Ha! These people are so superficial. PDK4 is upregulated in the liver of diabetics because that's how gene expression tries to protect you from the ministrations of the PUFAphiles. PDH complex probably down regulates because normal soybean oil is supplying a sh!tload of low FDAH2:NADH linoleic acid which means the supply of acetyl-CoA will be in excess of the cell's needs and getting more from pyruvate is not needed. So the liver uses PDK4 to avoid even more of a disaster than the cardiologists are pushing for...<br /><br />Just looking down at the ETC level.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-74172105305582433582020-05-07T15:25:36.903+00:002020-05-07T15:25:36.903+00:00"There is more to obesity than PUFA (gasp).&q..."There is more to obesity than PUFA (gasp)."<br /><br />Not so fast!<br /><br />I was of course curious to see what Surwit et al were up to here. They have a very fat-agnositic view of diet: fat is fat. He changes the formulation of his high-fat, high sucrose (HH) diet from F1850 to D12330 in 1992, but still uses the old studies as references for the new ones, despite switching from lard to hydrogenated coconut oil.<br /><br />Fat is fat.<br /><br />"...we used mice and precisely defined isocaloric diets to compare the metabolic effects of saturated fat from coconut oil, unsaturated fats from soybean oil and fructose. To our knowledge, this is the first study not only to compare the effects of these three dietary factors in mice, but also to perform genome-wide expression profiling and metabolomics analysis of livers from animals fed a soybean-oil enriched diet."<br /><br />Bingo: "Four isocaloric diets with 4.87 kcal/gm (5.56 kcal total) (Table 1) were formulated in conjunction with Research Diets, Inc. (New Brunswick, NJ). The diets are based on the Surwit diet..."<br /><br />1.2 kcal% (control) vs 2.2 kcal% vs 10 kcal% from LA.<br /><br />The title says it all:<br /><br />"Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver"<br /><br />She was subsequently hired to show that low-LA GMO soybean oil (Plenish) is less obesogenic than regular soybean oil. Which she did.<br /><br />Neat bit: "One of these genes, Pdk4, which was upregulated in SO-HFD livers, is known to inhibit the pyruvate dehydrogenase complex that links the TCA cycle with glucose and fatty acid metabolism. Repression of the pyruvate dehydrogenase complex shifts the balance towards gluconeogenesis which could result in hyperglycemia [76]. Consistent with our findings are reports that PDK4 expression is increased in diabetics [122] and that Pdk4-/- mice are resistant to HFD-induced hepatic steatosis and are more glucose tolerant [123,124]. Thus Pdk4 upregulation may be a contributing factor to both lipid accumulation in the liver and the development of diabetes and glucose ntolerance in SO-HFD mice."<br /><br />That could be a problem...<br /><br />Lots more interesting findings. Pity Surwit didn't have a more nuanced view of fat.<br /><br />(I was looking for some sort of explanation as to why he had switched from F1850 to D12330, and changed the fat used but still added soybean oil. Couldn't find it, Research Diets just mentions that he called them up and specified what became D12330.)Tucker Goodrichhttps://www.blogger.com/profile/09455436946187786398noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-86726033862714113912020-04-30T21:00:21.230+00:002020-04-30T21:00:21.230+00:00Oh, animals? No, not to my knowledge.
PeterOh, animals? No, not to my knowledge.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-81919750459636244112020-04-30T20:59:32.830+00:002020-04-30T20:59:32.830+00:00Anything issue with pathological insulin sensitivi...Anything issue with pathological insulin sensitivity might need profound hypo-insulinaemia to resolve. Just logically, zero carb might be more likely to help...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-22378894706459049532020-04-30T20:24:55.363+00:002020-04-30T20:24:55.363+00:00Thanks Peter. Lipedema is an odd disease, for sure...Thanks Peter. Lipedema is an odd disease, for sure. It's possible to have very little abdominal or visceral fat, but huge and painful fat distribution in legs. In my case, with many lipomas too. I am trying a PKD diet, with around 20% from carbs, but may have to reduce that further. After 6 months, it has made no difference to my BMI. Do animals ever get something like lipedema?Alternate Futurehttps://www.blogger.com/profile/17857871213929577642noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-15169443050014562392020-04-30T19:31:14.782+00:002020-04-30T19:31:14.782+00:00Just thinking logically, the decreased risk of DMT...Just thinking logically, the decreased risk of DMT2 would suggest an oddly distributed hypersensitivity to insulin. It also follows the distribution of fat loss of acquired lipodystrophe, though there is no suggestion that I can see of it being auto immune. You have to wonder whether going to something like the PKD might be effective. But I can see that the PKD without even a tenuous evidence base would be difficult. But people do try these things. I doubt anyone would have suggested carnivory for depression 20 years ago, so who knows?<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-21286974914842825792020-04-30T18:54:47.236+00:002020-04-30T18:54:47.236+00:00Hi Peter
Thank you for the nuanced take on insulin...Hi Peter<br />Thank you for the nuanced take on insulin and insulin resistance. I am trying hard to learn about the causes of obesity and the role of the different hormones. If you don't mind, I have a question for you about lipedema (this is a fat disorder, where fat is largely stored in the hips and thighs and is very resistant to dietary and exercise changes). Women with lipedema are generally not insulin resistant and for the same BMI, have a lower incidence of Type 2 diabetes. I think this ties in with your conclusion that the amount of insulin is the problem rather than the sensitivity to insulin. Thanks<br />Sarah Alternate Futurehttps://www.blogger.com/profile/17857871213929577642noreply@blogger.com