I would say that Georgi Dinkov is up there with the greatest of the great
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@yerrag
I think you are correct about the shying away from the topic of fat metabolism, but I think this has to do with a lack of good answers in the research on this subject. I think Ray liked to focus on subjects that he had certainty or at least relative certainty on. If you read his articles, it is very difficult to disagree with any of his claims as he was very careful in his wording and direction. When it comes to fat metabolism, there are a few things that are clear and a few things that are not so clear. The clear answers are
-stress hormones increase lypolysis
-human fat stores tend to be a higher percentage unsaturated(perhaps intentionally to slow down metabolism in times of famine)
-polyunsaturated fats interfere with glucose metabolism and slow down metabolism
-saturated fats inhibit lypolysis while polyunsaturated fats increase itThe less clear answers/questions:
-is saturated fats interference with glucose metabolism dose/time dependent and what are the doses and time where interference happens
-does saturated fats interference with glucose metabolism matter? Or does increased blood sugar stability and decreased lypolysis outweigh these issues?
-what percentage of fat metabolism in mitchondria is ideal?I think the reason researchers shy away from these questions is that there aren’t really good answers out there. Ray knew that small amounts of saturated fat could stimulate metabolism through competitive inhibition of circulating polyunsaturates. He knew that mitochondrial glucose metabolism was ideal. He knew that lypolysis tended to release polyunsaturated fatty acids into circulation. Until he was certain of other aspects of fat metabolism, I don’t think he wanted to be boxed into a corner that he couldn’t defend with certainty. And I don’t think there is a lot of certainty out there in the research.
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@rayshit said in I would say that Georgi Dinkov is up there with the greatest of the great:
@ThinPicking @Vasi1311 @yerrag you three against me in a ring, 10 minutes, and it's over with yall's cockiness. dinkov's science stinks. mostly animal studies and poorly interpreted at that (same goes for ray sheet albeit slightly more sophisticated)
So good for you to finally realize people won't put with you with your coarse language intended to troll. Trolling is all you are doing, nothing else. You can't bring anyone to your side because all you do is bitch like a cry baby. Why are you even here? Do you want to learn something? Or do you have something of substance to share? If not, stop wasting your time and ours.
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@jamsey said in I would say that Georgi Dinkov is up there with the greatest of the great:
@yerrag
I think you are correct about the shying away from the topic of fat metabolism, but I think this has to do with a lack of good answers in the research on this subject. I think Ray liked to focus on subjects that he had certainty or at least relative certainty on. If you read his articles, it is very difficult to disagree with any of his claims as he was very careful in his wording and direction. When it comes to fat metabolism, there are a few things that are clear and a few things that are not so clear. The clear answers are
-stress hormones increase lypolysis
-human fat stores tend to be a higher percentage unsaturated(perhaps intentionally to slow down metabolism in times of famine)
-polyunsaturated fats interfere with glucose metabolism and slow down metabolismIt seems clear to me that you have read Ray a lot to understand his message and that he was still sorting out a few missing pieces to make his overall picture of inter-relationships more robust and coherent. I agree with all of the above conclusions you gathered about what has been more certain.
It still has been empirically-based and hard to explain on the why side of it, for some aspects of it. Like on why PUFAs and not SFAs interfere with glucose metabolism. As I went at least 4 years cold turkey on PUFAs and saw its fruits in turning around my blood sugar stability, my improved metabolism, and my increased imperviousness to allergies and respiratory infections.
Pre-Peat I subscribed to the metabolic typing principles of William Donald Kelley, which was even more empirically-based but valid just the same. Even though I was baffled in trying to understand the mechanism involved that explained why I am a certain metabolic type (fast metabolic), with the idea that people are disposed to be one of four general metabolic types and that there were food and supplements that would be helpful for each type in order to eventually become a balanced type, which is ideal. All Kelley would say is that we are affected or defined by our autonomic nervous system in its parasympathetic and sympathetic. Stated that way, I knew this was an explanation to end all further questions. All I could make of it is an "ohhh..." in the same way I would bow and bend my knee to the understanding (or mystery) of quantum physics.
It was with reading Peat that I found much of the answers, after much reading of him scattered all throughout his newsletters and interviews. And it mattered which part of the timeline I was reading from. As Ray was still learning while he was writing, but not in the way some health experts do by winging it and making things up. We only know that as his views would change over time, but we can only know that by reading and following him. He realizes this flux as well, and he cautions us to not simply trust his word, but to also do our own research and to be critical.
More and more, I understand this as part of the discovery process. There are answers, and there are definitive answers, and some that open up more questions than answers.
-saturated fats inhibit lypolysis while polyunsaturated fats increase it
I am unsure about this. As even poultry and pigs plump up on PUFAs, and if PUFAs increase lipolysis, shouldn't the chickens be lean eating PUFAs?
That observation applies to human.
As well as my pets. Koi and cats. My koi and cats eat fish (raw for koi and cooked for cats) and mature coconut flesh ( finely chopped for koi and grated for cats) and they don't get plump and cute (show koi are plump and not healthy) and plump cats seem like an accident waiting to happen.
The less clear answers/questions:
-is saturated fats interference with glucose metabolism dose/time dependent and what are the doses and time where interference happens
-does saturated fats interference with glucose metabolism matter? Or does increased blood sugar stability and decreased lypolysis outweigh these issues?I don't agree with the basic premise behind these questions though. As I doubt SFAs interfere with glucose metabolism when fatty oxidation remain relatively small compared to sugar mitochondrial oxidation. I believe it even moderates the rate of glucose metabolism to keep blood sugar levels more stable and stay within limits that avoid excess insulin secretion from high blood sugar and an adrenalin/cortisol response from low blood sugar.
As to the last question, Blood sugar stability does not have to come together with decreased lipolysis If you just consider insulin as a an inhibitor of lipolysis, and consider also that insulin secretion and levels are increased when blood sugar is high (not a feature of blood sugar stability), you would see that as blood sugar becomes more stable, insulin levels are lower, and lipolysis is less inhibited. This means with blood sugar stability comes more lipolysis. I believe this provides more substrate for fatty acid oxidation to go along with good mitochondrial sugar oxidation. Tempered though by FAO being under the shadows of sugar oxidation.
-what percentage of fat metabolism in mitchondria is ideal?
In a recent interview with Mercola posted by @DavidPS , Haidut said FAO would not interfere so much with mitochondrial sugar metabolism as long as it is a third of sugar metabolism. I may have paraphrased a bit.
I think the reason researchers shy away from these questions is that there aren’t really good answers out there. Ray knew that small amounts of saturated fat could stimulate metabolism through competitive inhibition of circulating polyunsaturates. He knew that mitochondrial glucose metabolism was ideal. He knew that lypolysis tended to release polyunsaturated fatty acids into circulation. Until he was certain of other aspects of fat metabolism, I don’t think he wanted to be boxed into a corner that he couldn’t defend with certainty. And I don’t think there is a lot of certainty out there in the research.
I agree. I am that way, and you are that way as well, when we prefer not throwing something out we would later have to take back.
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@rayshit said in I would say that Georgi Dinkov is up there with the greatest of the great:
@ThinPicking @Vasi1311 @yerrag you three against me in a ring, 10 minutes, and it's over with yall's cockiness. dinkov's science stinks. mostly animal studies and poorly interpreted at that (same goes for ray sheet albeit slightly more sophisticated)
You're an idiot.
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@yerrag I was looking for something else but I thin that this discussion you may find interesting https://raypeatforum.com/community/threads/pregnenolone-for-obesity-and-insulin-resistance.6902/
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Thanks for sharing. That exchange generally establishes the kinda allergic attitude of RPF towards fat regardless of whether it's SFA or PUFA, where both lipolysis and fatty acid oxidation has to be zero. I had that disposition as well, but looking back it made little sense. If we don't move away from that position these days and put some qualifications and nuance to it, it would not be helpful as it now looks to be an ideological position.
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@yerrag
yep but for quite some time everything on most of the subjects is extreme and looks like more to abuse which troubles me ...
