Refute Anti Peat Paper? (Unsaturated Cell Membranes Good)

[Fredvanpeat]

I am new here but I have been reading forum and some of ray’s articles for a while and it’s really interesting stuff that I have been trying to apply to my own health. I enjoy trying to visualize things like a cell membrane. I read and bought into ray’s ideas of pufas not being good and membrane rigidity being good through saturated fats.

Anyways, found a scientific article on cell membranes in diabetes that concludes the opposite of rays ideas on saturated and unsaturated fats and how they affect health specifically in this case insulin resistance. It’s an interesting read but it is obviously quite contrary to peat. I am not skilled in biology or research or dissecting studies. @haidut @Such_Saturation anyone can you explain why this paper is wrong? Lipid Composition of Cell Membranes and Its Relevance in Type 2 Diabetes Mellitus

It seems to think that it is clear cut that the greater the unsaturation of the membrane the more insulin sensitive the membrane due to ease of integrating GLUT into membrane because of more flexibility. Therefore more glucose transport. It kind of makes sense through the proposed mechanism but obviously contradicts peat. Unless maybe it is just mufa and not pufa but I think they mention certain pufa. Still they say the more saturation the more diabetes.

 

[Fredvanpeat]

Going to try and revive post one last time and tag some of the knowledgeable people I’ve noticed on here. Apologies if you don’t want to be tagged or respond. @Amazoniac @Hans @paymanz @haidut

here is study again on membrane saturation:
Lipid Composition of Cell Membranes and Its Relevance in Type 2 Diabetes Mellitus

Why is it wrong?

 

[JKX]

Diabetes, scleroderma, oils and hormones

I dont think necessarily wrong, I think the key phrase is unsaturation increases glucose by insulin dependent glucose transporters.

They have set out to prove a mechanism and appear to have done so. Whether it is relatable to diabetes depends on your view of insulin.

I think the mainstream view of insulin clashes with Rays view. The study may demonstrate an increase of insulin sensitivity from unsaturated fats, but whether this is desirable remains debateable. The assumption that diabetes is purely insulin response related is also questionable I think.

Cells in children appear predominantly saturated. Yet their response to a high carb meal is completely different to most adults. A high carb meal will usually not provoke a high insulin response in a child.

As unsaturation increases, insulin response also appears to increase, probably as a response to clear glucose from the blood. What if we were to look at the problem in terms of non-insulin dependent glucose transport/ use?

 

[Fredvanpeat]

Thanks for the reply @JKX

Actually in the paper linked it they mention insulin independent glucose transport multiple times through the glucose transporters (GLUTs) other than GLUT4 which is insulin dependent. This paper is one of the few in my limited and basic research I have seen that mentions non insulin mediated glucose uptake that they refer to as glucose effectiveness. They go on to say that both insulin sensitivity characterized as GLUT4 insulin dependent glucose uptake (glucose effectiveness) and insulin independent glucose uptake (glucose effectiveness) can be explained by the same underlying biological mechanism of increased membrane rigidity due to increased saturated phospholipids in membrane and decreased unsaturated phospholipids.

They say the increased membrane rigidity doesn’t allow for the translocation of GLUT4 into the membrane which happens once insulin interacts with the cell. GLUT4 being correctly anchored in the membrane is then directly for the insulin mediated glucose uptake of cells. Basically the saturated cell membrane can’t make enough room in the membrane for the transporter GLUT4 and the same goes for the rest of the GLUTs (non insulin dependent glucose transporters) which need to be inserted into the membrane.

From what I understand ray peat and @haidut believe this membrane rigidity through saturated fatty acids and exclusion of PUFA is a good thing because of a lack of too much unorganized water in the cell and permeability of the cell. Whereas this author and other attached studies he quotes claim that unsaturation of the cell membrane is a great thing for insulin dependent and insulin independent glucose uptake.

Later in the article they do however mention that they agree with ray’s and haidut’s ideas about diabetes with the liver being important in releasing too much fat into the blood but they say that causes the change in increased saturation of membranes which causes more diabetes because of less glucose uptake. This continues cycle of liver releasing more fatty acids.

Some interesting questions would be is there a direct relationship between dietary fat intake (saturated vs unsaturated fats) and membrane saturation composition or could more desaturase enzymes kick in to make healthy saturated fats unsaturated In membrane for better insulin sensitivity. Maybe there is a protective mechanism to increase membrane saturation to keep bad stuff like endotoxin out that could be damaging cell and mitochondria? Maybe it is a bad paper and a bad theory. Idk I’m still a noob in this stuff. But they do attach studies saying that healthier more insulin sensitive individuals had a higher degree of unsaturation. Maybe it is a spectrum where too rigid (saturated) of a cell is bad and too fluid (unsaturated) of a cell is bad.

All responses welcome

 

[JKX]

Just wanted to say thanks. Your post lead me to reread a few of Ray's articles. I was in need of a refresh. I'm sure you'll be familiar with:
Membranes, plasma membranes, and surfaces

I also reread the study you posted. I think its good to bear in mind it is a literature review and there are lots of postulations within in it. Nothing is being proven, its just drawing conclusions from previous studies. So in that sense its only as good as the composition of the studies being used. It also seems a bit one sided to me. If you are going to produce a literature review, I think it makes sense to also consider studies with views in opposition to the theory being proposed.

I'm sure someone more knowledgeable will chime in. This has probably been discussed on the forum previously and I may have a search later.

Failing all that, You could always put the questions you raise to Dr Peat.

 

[catharsis]

Hey @Fredvanpeat, nice paper you posted.

I think it's important to engage Ray Peat's ideas very critically and actively if you want to integrate his ideas of the human biological system into your understanding and life. Mindless reading taught no one, right? (at least I hoped some of my college textbooks would somehow osmotically transmit their information to my consciousness before each exam)

The paper you posted argues that the increase in cell membrane fluidity increases the effectiveness and ease of integration of GLUT4 into the cellular membrane, I would argue that this is a moot point when it comes to saturated fats and diabetes. Ray, as far as I know, argues that insulin is not extremely needed for cellular glucose uptake and Type 2 Diabetes is actually caused by excess lipolysis and cortisol. This matches some of my reading that insulin is not needed for glucose uptake, how it only interacts with GLUT4, and how even insulin-deficient animals still have glucose uptake by cells (even increasing uptake due to hyperglycemia) [Sonksen & Sonksen 2000]

As for the relationship between saturated fats and insulin resistance, I believe this is just a correlation and not causation. De Novo Lipogenesis (DNL) predominately creates palmitic acid (if I remember correctly), and this could cause the elevated ratio of saturated fats in these studies. The study cited in "Lipid Composition of Cell Membranes..." in the discussion section to argue for saturated fats uses Gestational Diabetes Mellitus (GDM) as a model to show SFA's causative power in diabetes and insulin resistance. According to Ray, diabetes during pregnancy or high blood sugar normally results in extremely intelligent children. Doesn't seem too bad of a side-effect and PUFA is known to increase inflammation, estrogen, cortisol, and serotonin; all of which can increase FFAs and stress in the body, lowering proper glucose oxidation through Randle cycle and damaged organelles.

As for saturated fats and unsaturated fats in vivo, desaturase enzymes do exist and do synthesize unsaturated fats from saturated fats in the diet. Desaturase inhibitors, I believe, are being investigated for obesity treatment but I would argue that there would be more uses for these inhibitors. I am interested if there are any toxic effects (another reason why Mead Acid should be investigated!)

I would agree with @Hans, @haidut, or Peat's point of view that insulin does not really factor in cellular glucose uptake and it's more important for anabolic actions and its anti-lipolytic property and anti-gluconeogenesis property. There are also studies on how intranasal insulin can be used as a nootropic (@LostFalco if anyone remembers him). The only thing I am afraid of is possible pro-cancer pathways involving mTOR and IGF-1, and how they relate to insulin.

Hope this answers your questions...

 

[Elast1c]

I am new here but I have been reading forum and some of ray’s articles for a while and it’s really interesting stuff that I have been trying to apply to my own health. I enjoy trying to visualize things like a cell membrane. I read and bought into ray’s ideas of pufas not being good and membrane rigidity being good through saturated fats.

Anyways, found a scientific article on cell membranes in diabetes that concludes the opposite of rays ideas on saturated and unsaturated fats and how they affect health specifically in this case insulin resistance. It’s an interesting read but it is obviously quite contrary to peat. I am not skilled in biology or research or dissecting studies. @haidut @Such_Saturation anyone can you explain why this paper is wrong? Lipid Composition of Cell Membranes and Its Relevance in Type 2 Diabetes Mellitus

It seems to think that it is clear cut that the greater the unsaturation of the membrane the more insulin sensitive the membrane due to ease of integrating GLUT into membrane because of more flexibility. Therefore more glucose transport. It kind of makes sense through the proposed mechanism but obviously contradicts peat. Unless maybe it is just mufa and not pufa but I think they mention certain pufa. Still they say the more saturation the more diabetes.

would think it at least has to do with the membrane not being made of lipid to begin with and also having structure with affinity for water itself.

 

[GelatinGoblin]

Bump