MS Tied To Glucose Deficiency Due To Endotoxin And Fat, Extra Glucose May Treat It

[Kartoffel]

I bet that if was the opposite you wouldn't mind entertaining the idea.

<Table: Fatty acids rank'd according to their propensity to do a competition with dextrose>

That might be true. If anecdotal evidence (that's what his observations are in the end) coincides with the rest of one's knowledge, it's easily accepted. However, I think I would accept criticism pointing out the weakness of the evidence in a case like this. I don't think it is very unreasonable of me to question the validity of his results considering that he is saying that high PUFA oils (ω-6) cure/are not detrimental for MS (unless we are to assume they all consumed olive oil).

I can't see your table. Maybe that's because my confirmation bias is affecting my senses

 

[Amazoniac]

That might be true. If anecdotal evidence (that's what his observations are in the end) coincides with the rest of one's knowledge, it's easily accepted. However, I think I would accept criticism pointing out the weakness of the evidence in a case like this. I don't think it is very unreasonable of me to question the validity of his results considering that he is saying that high PUFA oils (ω-6) cure/are not detrimental for MS (unless we are to assume they all consumed olive oil).

I can't see your table. Maybe that's because my confirmation bias is blinding my senses

You find it easier to accept that he spent his life on a worthless pursue than considering for a few minutes if there wasn't something to it?

Most of the benefits came from lipid restriction, but the oils might be useful through others means, such as providing concentrated calories, being slightly bactericidal during digestion, slowing down the uptake of glucose (to prevent the sharp peak) while not being as competing to its oxidation as the fats, and so on. People that gain fat more easily might be better at clearing the fatty acids from circulation in an inopportune time for their burning, which must be protective in case of Microsoft. Was is insulin resistance?

 

[Kartoffel]

You find it easier to accept that he spent his life on a worthless pursue than considering for a few minutes if there wasn't something to it?

Most of the benefits came from lipid restriction, but the oils might be useful through others means, such as providing concentrated calories, being slightly bactericidal during digestion, slowing down the uptake of glucose (to prevent the sharp peak) while not being as competing to its oxidation as the fats, and so on. People that gain fat more easily might be better at clearing the fatty acids from circulation in an inopportune time for their burning, which must be protective in case of Microsoft. Was is insulin resistance?

Many researchers have spent their lives on worthless pursuits, so there is no reason to simply accept something for that reason. I don't consider Herr Lustig a serious researchers simply because proving that sugar is evil is the work of his life. The bactericidal fatty acids are in the solid fats, not the liquid oils, they also slow down digestion and provide concentrated calories (the MCTs in Kokosöl would be the easiest to use for a sick person, and they interfer least with CHO oxidation) and why would they (the oils) be less competing when evidence tells us otherwise?
Anyways, to not drag Mr Swank through the mire too much, I think there is still something to his work. While he couldn't possibly measure the fat/oil - SFA/PUFA ratio of his patients over a period lasting two decades with the methods he used, it's still fair to assume that most adhered to a high-carb low-fat protocol. While this shouldn't be too surprising for any of us today it probably was more of a big deal at a time when carbs and insulin secretion where basically considered the same thing as guaranteed diabetes.

 

[Amazoniac]

Many researchers have spent their lives on worthless pursuits, so there is no reason to simply accept something for that reason. I don't consider Herr Lustig a serious researchers simply because proving that sugar is evil is the work of his life.

It wasn't leave it or take it, it was leave it or inspect what's up.

The bactericidal fatty acids are in the solid fats, not the liquid oils, they also slow down digestion and provide concentrated calories (the MCTs in Kokosöl would be the easiest to use for a sick person, and they interfer least with CHO oxidation)

You missed the point. The only condition was the last part, regarding being less competing in the short-term, leaving him the option to either increase or not the oils. The guy was unsure about the positive effects, but was certain about the oils being neutral, therefore why more?

why would they (the oils) be less competing when evidence tells us otherwise?

I'm not aware of these, but I'm willing to change my cerebra.

 

[Kartoffel]

You missed the point. The only condition was the last part, regarding being less competing in the short-term, leaving him the option to either increase or not the oils. The guy was unsure about the positive effects, but was certain about the oils being neutral, therefore why more?

Again, I don't see how or why an unsaturated oil would be less competing in the short or long term.

I'm not aware of these, but I'm willing to change my cerebra.

Dietary polyunsaturated fats suppress the high-sucrose-induced increase of rat liver pyruvate dehydrogenase levels. - PubMed - NCBI

Adaptive changes in total pyruvate dehydrogenase activity in lipogenic tissues of rats fed high-sucrose or high-fat diets. - PubMed - NCBI

 

[Amazoniac]

Again, I don't see how or why an unsaturated oil would be less competing in the short or long term.





Dietary polyunsaturated fats suppress the high-sucrose-induced increase of rat liver pyruvate dehydrogenase levels. - PubMed - NCBI

Adaptive changes in total pyruvate dehydrogenase activity in lipogenic tissues of rats fed high-sucrose or high-fat diets. - PubMed - NCBI

There's no way that you received the notification for my reply, read it, responded the first part, searched for the experiments, read both as well and posted all in less than 10 min; unless you had them already saved. But then I'm not sure what you mean by those links because they were after lipid synthesis, not dextrose oxidation in varied tissues. They even mentioned that lipogenic potential is correlated with the enzyme activity, so compare the groups again from this point of view.

What's your alternative interpretation for these transient effects?
- How The Sugar Industry Shifted Blame To Fat

↳ Hyperlipid: Protons (38) and ultra low fat once more
- Hyperlipid: Protons: Physiological insulin resistance addendum​

- How The Sugar Industry Shifted Blame To Fat
- People With The Lowest Overall Mortality Are Overweight

 

[Kartoffel]

There's no way that you received the notification for my reply, read it, responded the first part, searched for the experiments, read both as well and posted all in less than 10 min; unless you had them already saved. But then I'm not sure what you mean by those links because they were after lipid synthesis, not dextrose oxidation in varied tissues. They even mentioned that lipogenic potential is correlated with the enzyme activity, so compare for example 10% fish oil with 10% butter groups.

What's your alternative interpretation for these?
- How The Sugar Industry Shifted Blame To Fat

↳ Hyperlipid: Protons (38) and ultra low fat once more
- Hyperlipid: Protons: Physiological insulin resistance addendum​

- How The Sugar Industry Shifted Blame To Fat
- People With The Lowest Overall Mortality Are Overweight

Yes, I already had those studies and didn't need to look for them. As for the rest of the material - I already read those posts by tyw and the articles by Peter from Hyperlipid. While his theoretical musings are interesting, I don't think they have much to do with reality, and if we take his recommendations to heart, we should all eat high-fat diets.

In the first post you linked to, tyw mentions a reference saying: "Cooper et al. found that 80–100% of dietary 18:1 was oxidized within 24 h of feeding the labeled meal, while 10–25% of dietary 16:0 was oxidized over the same time frame [51]." If you read it, you might think: "wow, it's true oleic acid is the preferred fatty acid for oxidation and palmitic acid will just make you fat and insulin resistant." However, if you read the paper a little further, and don't pull this one study out of context, things appear to be a little more nuanced. This is from a summary paper, and this follows after tyw's passage:

Using this method, Cooper et al. found that 80–100% of dietary 18:1 was oxidized within 24 h of feeding the labeled meal, while 10–25% of dietary 16:0 was oxidized over the same time frame [51]. Similarly, greater oleate oxidation has been observed in overweight, post-menopausal women [52].[Now, this is the part he left out] Contradictory studies exist that show lower whole-body fat oxidation on a MUFA-rich diet compared to a diet rich in trans-fatty acids [53] and no difference in fat oxidation rates on MUFA- vs. SFA-rich diets [54]. Thus, although the beneficial effects of oleate on meal fatty acid oxidation are controversial, the data represent a promising area of research. As shown in Table 1 overall, the order of preference for oxidation appears to be PUFA>MUFA>SFA. A secondary hierarchy may exist between fatty acids within the same class of saturation; for example, shorter chain saturated fatty acids may be oxidized to a greater extent than longer chain fatty acids [47,55], but significant differences in oxidation between fatty acids of different chain lengths are not consistent across studies [56]. However, within a high-fat diet, the fatty acid composition of the diet seems to play less of a factor than quantity of fat [51,55].
​

I don't think these tracer studies are very useful for various reasons, and they often conflict with real life situations (just as Peters theoretical ideas). Some long chain SFA appear to circulate around longer, but @haidut has posted many a study showing why that is likely to be beneficial. The central question is still, if fatty acids interfere with glucose oxidation, and I think what you are hinting at is that SFA do, while PUFA don't because they supposedly increase insulin sensitivity or get burned more quickly. Study below seems to show the opposite. PUFA increase fatty acid oxidation, and that interferes with the oxidation of Traubenzucker.

I think the evidence seems to suggest this: If you want to promote CHO oxidation over fat oxidation, eating a moderate amount of saturated fat is better than eating whatever quantity of PUFA, as it increases free fatty acids, fat oxidation, and interferes with CHO oxidation.

​

Polyunsaturated: Saturated ratio of diet fat influences energy substrate utilization in the human
Peter J.H.Jones

Abstract
In order to examine the effect of dietary long chain fatty acid composition on energy substrate utilization, basal metabolism rate (BMR) and the thermogenic effect of food (TEF) were measured in eight subjects consuming diets varying only in diet fat polyunsaturated: saturated (P:S) ratio. Subjects consumed the low P:S (0.241 ± 0.02) and high P:S (1.65 ± 0.28) ratio diets for seven days using a crossover design. Fat and carbohydrate oxidation during BMT and TEF over 230 minutes after a breakfast meal were determined on days 1 and 7 of each diet period using open circuit respiratory gas exchange. On day 7, BMR respiratory quotient was reduced (P < .05) for the low P:S (0.826 ± 0.005) compared with high P:S (0.853 ± 0.014) ratio diet, resulting in an increased basal fat oxidation rate with low P:S (0.074 ± 0.006 g/min) compared with high P:S (0.059 ± 0.008 g/min) ratio diet feeding. The cumulative contribution of fat oxidation to TEF on day 7 was lower (P < .01) for the low P:S (1.35 ± 1.6 g) compared with high P:S (6.49 ± 0.8 g) ratio diets. This was paralleled by opposite differences (P < .05) in the contribution of carbohydrate oxidation to TEF (21.0 ± 3.0 g and 13.1 ± 3.4 g, respectively, for each diet treatment). On day 1 in subjects switching from either home and alternate test diets, and on day 7, caloric expenditure of TEF after low P:S was not statistically lower compared to the high P:S ratio diet. On day 1 subjects switching from the alternate diet showed a significant decrease (P < .05) in total fat oxidation of TEF after low P:S (13.5 ± 2.4 g) compared to high P:S (17.9 ± 1.6 g) ratio diets. These findings suggest that the long chain fatty acid composition of dietary fat modulates the oxidation of fat and carbohydrate acutely after meal feeding and after chronic feeding.

Edit: This study from tyw's summary paper also shows that cream as compared to olive oil increases CHO oxidation.

Sci-Hub | The acute effects of olive oil v. cream on postprandial thermogenesis and substrate oxidation in postmenopausal women. British Journal of Nutrition, 91(02), 245 | 10.1079/BJN20031047

I have gone through the mechanics many times on this forum, and regardless of whether we are talking about high Free Fatty Acids inhibiting glucose uptake (this is the Randle Effect, and is applicable to all tissues except the liver, brain, and heart), or if we are talking about Peter's mechanic of saturated fat causing mitochondrial insulin resistance via decreased membrane potential / delta-psi ...... it can be said that both the availability of Saturated fat reduces the potential ability for cells in the body to use glucose.

I would argue that this central statement by tyw regarding fatty acids and glucose oxidation is wrong. The evidence simply suggests otherwise, if you go beyond 24h tracer studies of fatty acid oxidation and Peter's FADH2 concept. PUFA promote fatty acid oxidation and free fatty acids in the blood, nearly every study shows that. Therefore I don't really understand how tyw arrives at his conclusions regarding the Randle cycle in this paragraph.

 

[Amazoniac]

Yes, I already had those studies and didn't need to look for them. As for the rest of the material - I already read those posts by tyw and the articles by Peter from Hyperlipid. While his theoretical musings are interesting, I don't think they have much to do with reality, and if we take his recommendations to heart, we should all eat high-fat diets.

In the first post you linked to, tyw mentions a reference saying: "Cooper et al. found that 80–100% of dietary 18:1 was oxidized within 24 h of feeding the labeled meal, while 10–25% of dietary 16:0 was oxidized over the same time frame [51]." If you read it, you might think: "wow, it's true oleic acid is the preferred fatty acid for oxidation and palmitic acid will just make you fat and insulin resistant." However, if you read the paper a little further, and don't pull this one study out of context, things appear to be a little more nuanced. This is from a summary paper, and this follows after tyw's passage:

Using this method, Cooper et al. found that 80–100% of dietary 18:1 was oxidized within 24 h of feeding the labeled meal, while 10–25% of dietary 16:0 was oxidized over the same time frame [51]. Similarly, greater oleate oxidation has been observed in overweight, post-menopausal women [52].[Now, this is the part he left out] Contradictory studies exist that show lower whole-body fat oxidation on a MUFA-rich diet compared to a diet rich in trans-fatty acids [53] and no difference in fat oxidation rates on MUFA- vs. SFA-rich diets [54]. Thus, although the beneficial effects of oleate on meal fatty acid oxidation are controversial, the data represent a promising area of research. As shown in Table 1 overall, the order of preference for oxidation appears to be PUFA>MUFA>SFA. A secondary hierarchy may exist between fatty acids within the same class of saturation; for example, shorter chain saturated fatty acids may be oxidized to a greater extent than longer chain fatty acids [47,55], but significant differences in oxidation between fatty acids of different chain lengths are not consistent across studies [56]. However, within a high-fat diet, the fatty acid composition of the diet seems to play less of a factor than quantity of fat [51,55].
​

I don't think these tracer studies are very useful for various reasons, and they often conflict with real life situations (just as Peters theoretical ideas). Some long chain SFA appear to circulate around longer, but @haidut has posted many a study showing why that is likely to be beneficial. The central question is still, if fatty acids interfere with glucose oxidation, and I think what you are hinting at is that SFA do, while PUFA don't because they supposedly increase insulin sensitivity or get burned more quickly. Study below seems to show the opposite. PUFA increase fatty acid oxidation, and that interferes with the oxidation of Traubenzucker.

I think the evidence seems to suggest this: If you want to promote CHO oxidation over fat oxidation, eating a moderate amount of saturated fat is better than eating whatever quantity of PUFA, as it increases free fatty acids, fat oxidation, and interferes with CHO oxidation.

​

Polyunsaturated: Saturated ratio of diet fat influences energy substrate utilization in the human
Peter J.H.Jones

Abstract
In order to examine the effect of dietary long chain fatty acid composition on energy substrate utilization, basal metabolism rate (BMR) and the thermogenic effect of food (TEF) were measured in eight subjects consuming diets varying only in diet fat polyunsaturated: saturated (P:S) ratio. Subjects consumed the low P:S (0.241 ± 0.02) and high P:S (1.65 ± 0.28) ratio diets for seven days using a crossover design. Fat and carbohydrate oxidation during BMT and TEF over 230 minutes after a breakfast meal were determined on days 1 and 7 of each diet period using open circuit respiratory gas exchange. On day 7, BMR respiratory quotient was reduced (P < .05) for the low P:S (0.826 ± 0.005) compared with high P:S (0.853 ± 0.014) ratio diet, resulting in an increased basal fat oxidation rate with low P:S (0.074 ± 0.006 g/min) compared with high P:S (0.059 ± 0.008 g/min) ratio diet feeding. The cumulative contribution of fat oxidation to TEF on day 7 was lower (P < .01) for the low P:S (1.35 ± 1.6 g) compared with high P:S (6.49 ± 0.8 g) ratio diets. This was paralleled by opposite differences (P < .05) in the contribution of carbohydrate oxidation to TEF (21.0 ± 3.0 g and 13.1 ± 3.4 g, respectively, for each diet treatment). On day 1 in subjects switching from either home and alternate test diets, and on day 7, caloric expenditure of TEF after low P:S was not statistically lower compared to the high P:S ratio diet. On day 1 subjects switching from the alternate diet showed a significant decrease (P < .05) in total fat oxidation of TEF after low P:S (13.5 ± 2.4 g) compared to high P:S (17.9 ± 1.6 g) ratio diets. These findings suggest that the long chain fatty acid composition of dietary fat modulates the oxidation of fat and carbohydrate acutely after meal feeding and after chronic feeding.

Edit: This study from tyw's summary paper also shows that cream as compared to olive oil increases CHO oxidation.

Sci-Hub | The acute effects of olive oil v. cream on postprandial thermogenesis and substrate oxidation in postmenopausal women. British Journal of Nutrition, 91(02), 245 | 10.1079/BJN20031047



I would argue that this central statement by tyw regarding fatty acids and glucose oxidation is wrong. The evidence simply suggests otherwise, if you go beyond 24h tracer studies of fatty acid oxidation and Peter's FADH2 concept. PUFA promote fatty acid oxidation and free fatty acids in the blood, nearly every study shows that. Therefore I don't really understand how tyw arrives at his conclusions regarding the Randle cycle in this paragraph.

Both of them were acknowledging that PUFAs are harmful, so it's not an encouragement for their consumption.

Now you're making good points that are relevant for the discussion, the experiment is more reliable than speculations, so I have to change my mind about it.

Have you found different experiments agreeing that polyunsaturated fats are more readily metabolized than saturated? The other Pedro in the publication above and in 'Whole body oxidation of dietary fatty acids: Implications for energy utilization' suggests that there's "preferential portal transport and hepatic oxidation" with the polyunsaturated fats. Was is Swank assuming there's some truth to his odservations?

--
Believe it or not, this bizarre passage is from Koch:

"The Eskimos rarely develop cancer. The largest part of their diet is fat and this contains full quantity of unsaturated fatty acid. The lesson to be taken from these facts is that the fats sold for the kitchen and table today, that do not become rancid, are of no help to the health of the body. The preparation of a fat so it will not become rancid is to saturate the unsaturated groups with hydrogen. Generally a nickel catalyst is used. But that makes no difference, perhaps. The destruction of the double bonds in the fatty acid greatly lowers its chance to undergo autoxidation and thus to induce the oxidation of toxins or aid its own oxidation for the production of energy. Everyone should pay particular attention to this, for when the fat is reduced so as to not be able to form peroxides and no longer tastes rancid in consequence, it is difficult to burn in the body and will pile on in undesired places. But worst of all, it is bad for the complexion. Since the auto-oxidations that natural un-saturated fatty acids are intended to produce in germ toxins are no longer possible in Spry and Crisco, so the germs that injure the skin have no such health factor to contend with and can mar the complexion with a much freer hand. Adding oxygen to become the peroxide makes the fat rancid. Therefore, one must buy fats that are not rancid yet, but can come so on exposure to air. It is the process of becoming rancid that is the change that is helpful; not the rancid fat. Thus in the body, the taking up of oxygen to become a peroxide induces other unsaturated atomic groups that are unable to do so themselves to take up oxygen and to become burned also. So it is not only the fat you buy that we are considering, but fats in other foods as well as germ and metabolic toxins that un-saturated fats help to get rid of and convert into energy."​

 

[Kartoffel]

Have you found different experiments agreeing that polyunsaturated fats are more readily metabolized than saturated? The other Pedro in the publication above and in 'Whole body oxidation of dietary fatty acids: Implications for energy utilization' suggests that there's "preferential portal transport and hepatic oxidation" with the polyunsaturated fats. Was is Swank assuming there's some truth to his odservations?

There are many studies demonstrating these effects. You just have to snowball through some of the references to find more. I didn't cite the studies right away because I thought this point was accepted, canonical knowledge in this forum. It's one of Peat's main points that PUFA interfere with CHO oxidation while SFA don't. He presses this claim in several articles and interviews.

Believe it or not, this bizarre passage is from Koch:

"The Eskimos rarely develop cancer. The largest part of their diet is fat and this contains full quantity of unsaturated fatty acid. The lesson to be taken from these facts is that the fats sold for the kitchen and table today, that do not become rancid, are of no help to the health of the body. The preparation of a fat so it will not become rancid is to saturate the unsaturated groups with hydrogen. Generally a nickel catalyst is used. But that makes no difference, perhaps. The destruction of the double bonds in the fatty acid greatly lowers its chance to undergo autoxidation and thus to induce the oxidation of toxins or aid its own oxidation for the production of energy. Everyone should pay particular attention to this, for when the fat is reduced so as to not be able to form peroxides and no longer tastes rancid in consequence, it is difficult to burn in the body and will pile on in undesired places. But worst of all, it is bad for the complexion. Since the auto-oxidations that natural un-saturated fatty acids are intended to produce in germ toxins are no longer possible in Spry and Crisco, so the germs that injure the skin have no such health factor to contend with and can mar the complexion with a much freer hand. Adding oxygen to become the peroxide makes the fat rancid. Therefore, one must buy fats that are not rancid yet, but can come so on exposure to air. It is the process of becoming rancid that is the change that is helpful; not the rancid fat. Thus in the body, the taking up of oxygen to become a peroxide induces other unsaturated atomic groups that are unable to do so themselves to take up oxygen and to become burned also. So it is not only the fat you buy that we are considering, but fats in other foods as well as germ and metabolic toxins that un-saturated fats help to get rid of and convert into energy."

I find his points fairly unconvincing. I'm not sure how much cancer the Eskimos get, but they are protected by several other factors in their diet such as a high intake of fat soluble vitamins and thyroid, and they seem to age rapidly, which is undoubtedly also due to the conditions of their environment. Peat has talked about the people trying to copy the high PUFA diet of the Eskimos just to find their sperm content go to zero. But his point that the freshness of PUFA might speed up their oxidation, and reduce the accumulation of the toxic byproducts of their oxidation, might be worth looking into.
Nevertheless, there are many traditional cultures that eat a "full quanitity" of saturated fat such as the Masai, Tokelauans, various Melanesian&Polynesian tribes, etc. and I don't think they get more cancer than the Eskimos

 

[Amazoniac]

There are many studies demonstrating these effects. You just have to snowball through some of the references to find more. I didn't cite the studies right away because I thought this point was accepted, canonical knowledge in this forum. It's one of Peat's main points that PUFA interfere with CHO oxidation while SFA don't. He presses this claim in several articles and interviews.

Most of Raj's work against PUFA is on tissue accumulation or when they is liberated as free fatty acids from storage. Given that lipids are metabolized differently after a meal, there could be nuances (offel, 2019) to explain unexpected effects. Yes, palmitic acid gives you wings and makes you immortal, but if it was all clear without sublebelties, questions of this sort would never pop up.

- The Great Fish Oil Experiment

"Although fish oils rapidly destroy vitamin E in the body, some of them, especially the liver oils, can provide useful vitamins, A and D. In studies comparing fish oil diets with standard diets, these nutrients, as well as any toxins besides fatty acids (Huang, et al., 1997; Miyazaki, et al., 1998) in either type of oil, should be taken into account, but they seldom are.

Despite the nutritional value of those vitamins, fish oils are generally much more immunosuppressive than the seed oils, and the early effects of fish oil on the "immune system" include the suppression of prostaglandin synthesis, because the more highly unsaturated long chain fats interfere with the conversion of linoleic acid into arachidonic acid and prostaglandins. The prostaglandins are so problematic that their suppression is helpful, whether the inhibition is caused by aspirin or vitamin E, or by fish oil."​

I find his points fairly unconvincing. I'm not sure how much cancer the Eskimos get, but they are protected by several other factors in their diet such as a high intake of fat soluble vitamins and thyroid, and they seem to age rapidly, which is undoubtedly also due to the conditions of their environment. Peat has talked about the people trying to copy the high PUFA diet of the Eskimos just to find their sperm content go to zero. But his point that the freshness of PUFA might speed up their oxidation, and reduce the accumulation of the toxic byproducts of their oxidation, might be worth looking into.
Nevertheless, there are many traditional cultures that eat a "full quanitity" of saturated fat such as the Masai, Tokelauans, various Melanesian&Polynesian tribes, etc. and I don't think they get more cancer than the Eskimos

It's the idea of oxidative stress to restore normal functioning.

 

[Kartoffel]

Yes, palmitic acid gives you wings and makes you immortal, but if it was all clear without sublebelties, questions of this sort would never pop up.

What question are you referring to specifically? There wasn't any that immediately struck me as fitting our discussion. I don't think that saturated fats like palmitate have any magical, curative properties, I think of them and oleic acid as the neutral fats that do no harm and don't interfere with glucose too much.
Just out of curiosity, what kind of fat do you use for cooking, frying, etc? - in case you're not on a Tsimane diet right now. Have you secretly experimented with the forbidden oils and noticed any positive effects?

 

[Amazoniac]

What question are you referring to specifically? There wasn't any that immediately struck me as fitting our discussion. I don't think that saturated fats like palmitate have any magical, curative properties, I think of them and oleic acid as the neutral fats that do no harm and don't interfere with glucose too much.
Just out of curiosity, what kind of fat do you use for cooking, frying, etc? - in case you're not on a Tsimane diet right now. Have you secretly experimented with the forbidden oils and noticed any positive effects?

Topical thyroid for male pattern baldness.
Safflower oil is my go-to the choice. I consume it to punish myself since there are no positives and gives me acne for a couple of days.

Roy has some curious images throughout his material, but it got me a little concerned to find one of his experiments published by the American Hearty Association.

 

[Kelj]

Interestingly, this is known in eating disorder recovery.
This letter, addressed to doctors by the Eating Disoder Institute says:

Dear Doctor: Your patient has an eating disorder.

"before you get tripped up with all the common misdiagnoses (PCOS, IBS, anemia, MS, hypothyroidism (both antibody-driven and not), and etc.), here are some data to help you rule in or out the causative impact of an eating disorder:"

"Fatigue, anemia, depression, hypothyroidism and neuropathies all represent various ways in which the body catabolizes itself to release energy from living cells into the blood stream and suppresses all non-essential biological functions to stay alive as long as possible when faced with an ongoing energy deficit. If you treat these symptoms in the absence of getting the patient to re-energize with enough food to rectify the energy deficit, then you will be pushing the living system and overriding its inherent life-saving energy usage reduction mechanisms. 13"

It is always helpful to see another study exposing the ways our sick obsession to limit energy intake, especially from carbs, is harming us.

 

[nbznj]

We live in a world where people push crazy caloric restriction strategies and fear carbs like never before. Oh well. I think that less calories work if carbs are kept high. That’s what Swank and the current plant based doctors are doing. They seem to do more good than harm. I feel extremely good on a 70% carb diet. Others go up to 80%. 50% or less means humongous amounts of proteins and fats and I see negative effects within days, no more morning erections, less energy at the gym, subpar skin etc. I don’t know how people do it, I guess they don’t know any better.

I don’t think that the Inuits are a good example for anyone who isn’t living in a super cold and hostile environment. Their TDEE is sky high. Same goes for the Masai. They don’t have cancer and don’t die from heart attacks because they’re probably not overeating, even though they consume those (non industrial) foods

 

[CLASH]

@Amazoniac
@Kartoffel
Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse - ScienceDirect

“Diet and disease - The Israeli paradox: Possible dangers of a high omega-6 polyunsaturated fatty acid diet”
https://www.researchgate.net/public..._high_omega-6_polyunsaturated_fatty_acid_diet


I think the tracer studies are relatively useless, especially if the broader context is brought into play. Overtime PUFA reliably seem to induce insulin resistance, heart disease and cancer in humans. There is little evidence supporting the long term consumption of PUFA, except a minor benefit of fish oil protecting against an excess of omega 6; still overall a shitty place to be in physiologically.

High fat feeding of rats/ mice is not the same as high fat feeding of humans. Theyre entire digestive physiology and methods for nutrient aquisition are very different from humans. Theres a reason they have an expanded cecum and we have a “vestigal” appendix. Sucrose and fats make mice fat. Theyre digestive physiology is meant for fermentation primarily, not absorption. I dont think thier livers are set up to absorb/ utilize these energy dense substrates as ours are. Our expanded small intestine and the function of our livers are set up to absorb dense sources of calories, fats, proteins and carbs, we cannot physiologically rely on fermentation. When you see high fat diets causing dysbiosis in rat models its because the rats are having fats reach their cecum. For humans much of the fat, protein and carbs we eat is absorbed in the small intestine with proteins and carbs (unless your eating rat foods like many raw vegetables, whole grains, resistant starches, legumes, nuts and seeds). Since we do much of our studies with rats, it seems we (mainstream science) have adopted the idea of a rat diet being physiologically the best; its quite funny actually. I think rats/ mice may handle PUFA differently than we do as well.

Saturated fats and monounsaturated fats are neutral at worst and have many benefits at best. The only argument i see against them is a transient change in insulin sensitivity via randal cycle (that doesnt seem to really matter in my experience) and a transient increase in plasma endotoxin which is paradoxically (not really paradoxical tho if you actually look at the research and mechanisms) a benefit to the human body. Also, theres such a focus on the oxidation of substrate that people seem to forget fat serves many other functions besides being oxidized for fuel. Its funny when people come on this forum and eat super low fat diets and then complain of low cholesterol. Then people tell them the best way to raise cholesterol (becuase they heard peat say it, not because they took the time to read the research) is to eat more sugar despite the fact that said individual is already eating a ton of sugar. Then people talk about eating more fructose to raise cholesterol, which an excess of fructose will reliably do. However, its funny because excess fructose in relation to glucose increases cholesterol by increasing endotoxin (which upregulates cholesterol production as a protective measure since cholesterol binds endotoxin).

Low carb diets are problematic.
Low saturated/ monounsaturated fat diets are problematic.
Low protein diets are problematic.
Different people seem to do well with different ratios of macros, although protein seems to have a threshold while carbs and fats can be adjusted accordingly.
Its interesting to note though, that most large mammals have what would be considered high fat diets.

 

[GAF]

Dear Therapist: Your Client Has an Eating Disorder.

To reiterate, someone BMI 37 can be facing as severe an energy deficit due to an eating disorder as someone BMI 17. Weight does not correlate to health status.

Fat is not a storage unit; it’s an exceedingly complex hormone-producing organ in our bodies. The body has two methods of staying alive when we diet and generate energy deficits in our body: catabolism (destruction of all cells (not just fat cells) to release energy), and metabolic suppression (shut down of entire systems in the body to lower the demand for energy). The more efficient the metabolic clamping (which varies from one individual to the next) the more likely the body’s mass can even increase despite calorie restriction. Metabolic suppression is as damaging as catabolism

 

[GAF]

There is some phenomenal writing and insight on the The Eating Disorder Institute site.

Well worth the time to read.

 

[Amazoniac]

@Amazoniac
@Kartoffel
Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse - ScienceDirect

“Diet and disease - The Israeli paradox: Possible dangers of a high omega-6 polyunsaturated fatty acid diet”
https://www.researchgate.net/public..._high_omega-6_polyunsaturated_fatty_acid_diet


I think the tracer studies are relatively useless, especially if the broader context is brought into play. Overtime PUFA reliably seem to induce insulin resistance, heart disease and cancer in humans. There is little evidence supporting the long term consumption of PUFA, except a minor benefit of fish oil protecting against an excess of omega 6; still overall a shitty place to be in physiologically.

High fat feeding of rats/ mice is not the same as high fat feeding of humans. Theyre entire digestive physiology and methods for nutrient aquisition are very different from humans. Theres a reason they have an expanded cecum and we have a “vestigal” appendix. Sucrose and fats make mice fat. Theyre digestive physiology is meant for fermentation primarily, not absorption. I dont think thier livers are set up to absorb/ utilize these energy dense substrates as ours are. Our expanded small intestine and the function of our livers are set up to absorb dense sources of calories, fats, proteins and carbs, we cannot physiologically rely on fermentation. When you see high fat diets causing dysbiosis in rat models its because the rats are having fats reach their cecum. For humans much of the fat, protein and carbs we eat is absorbed in the small intestine with proteins and carbs (unless your eating rat foods like many raw vegetables, whole grains, resistant starches, legumes, nuts and seeds). Since we do much of our studies with rats, it seems we (mainstream science) have adopted the idea of a rat diet being physiologically the best; its quite funny actually. I think rats/ mice may handle PUFA differently than we do as well.

Saturated fats and monounsaturated fats are neutral at worst and have many benefits at best. The only argument i see against them is a transient change in insulin sensitivity via randal cycle (that doesnt seem to really matter in my experience) and a transient increase in plasma endotoxin which is paradoxically (not really paradoxical tho if you actually look at the research and mechanisms) a benefit to the human body. Also, theres such a focus on the oxidation of substrate that people seem to forget fat serves many other functions besides being oxidized for fuel. Its funny when people come on this forum and eat super low fat diets and then complain of low cholesterol. Then people tell them the best way to raise cholesterol (becuase they heard peat say it, not because they took the time to read the research) is to eat more sugar despite the fact that said individual is already eating a ton of sugar. Then people talk about eating more fructose to raise cholesterol, which an excess of fructose will reliably do. However, its funny because excess fructose in relation to glucose increases cholesterol by increasing endotoxin (which upregulates cholesterol production as a protective measure since cholesterol binds endotoxin).

Low carb diets are problematic.
Low saturated/ monounsaturated fat diets are problematic.
Low protein diets are problematic.
Different people seem to do well with different ratios of macros, although protein seems to have a threshold while carbs and fats can be adjusted accordingly.
Its interesting to note though, that most large mammals have what would be considered high fat diets.

Guru, those wered human experiments and the broader context was not into question, only immediate effects to explain the guy's odservation. Pedro III discussed some of the issues with labeling, but it applies to all of them. They was taken as free fatty acids yet must have reformed triglycerides during adsorption. Since it's a comparison between each, it should not be disconsider'd.

What I don't understand is Roy's comment that fatty aggregates with unsaturated fats predominating circulate easilier and tend not to clump. With two different fatty acids complexes of the same chain length, the one that's saturated should be compacter, take up less space and move around freelier; unless they form a block as he implies, but since they is centered in lipoproteids, I have no idea what he had in mind. The compactness is the opposite of the chaotic tail of our beloved DHA.
Raj has commented that saturation makes fats relativity less wasser-soluble.

 

[Kartoffel]

High fat feeding of rats/ mice is not the same as high fat feeding of humans. Theyre entire digestive physiology and methods for nutrient aquisition are very different from humans. Theres a reason they have an expanded cecum and we have a “vestigal” appendix. Sucrose and fats make mice fat.

I think even that is a wrong generalization. Rats have a very similar digestive physiology to ours in many regards, that's why we sacrifice them by the thousands in our experiments. Sucrose and fat make mice fat because of the way experiments are usually set up, and because they eat as much as they can. If you offer rats free access to saturated fat next to their usual diet, they will eat more and gain no or only slightly extra weight.

Long term highly saturated fat diet does not induce NASH in Wistar rats

Its interesting to note though, that most large mammals have what would be considered high fat diets.

Apes don't, and they are most similar to us. I think elephants don't get much fat either, and they are the only guys that have a bigger brain than humans.

 

[CLASH]

@Amazoniac
The mouse/ rat discussion was a seperate discusion from the tracer studies.

Perhaps it would be more reasonable to say, that I think the tracer studies are relatively useless from the perspective of the long term effects.

I’d have to go back and look at the studies showing the change in lipoprotein type and cholesterol to answer that, i’m not sure right now. I do know, atleast from what I read, that ray is indeed correct, the PUFA is more water soluble due to the unsaturated nature of the fatty tails.

@Kartoffel
There are similarities but there are also major differences. I think “very similar” is somewhat of a stretch. The relative small intestine size and cecum size is very different between rats and humans. I think this becomes apparent, specifically in the microbiome studies.

We sacrifice thousands of mice/ rats because they reproduce quickly, have shorter lifespans and are easy to manage. They have many differences from us that make them poor candidates for extrapolation to humans. For starters they are nocturnal...

I have seen studies where rats gain weight from higher fat diets, even with relatively decent set ups. I dont think this applies to humans very well.

Regardless of the finer points, i agree, the studies are often set up poorly or to extract a specific result. Everytime i read the composition of the rat/ mouse diet I face palm. High saturated fat diet= lard with supplemented corn oil wtf...

When accounting for fermentation in the bowels of both great apes and elephants, they do indeed have a high fat diet. Whales do as well, i.e. fermentation of chitin from krill.

Digestive wise, i think we are closer to pigs than apes.