Saturated Fats (SFA) Increase Glucose Oxidation While PUFA Decrease It

[Hugh Johnson]

What do you think the best weapons against negative emotional experiences are, if a person cannot currently find a way out of them?

Feel them fully. You could tap them away or something but the gold is found only by experiencing them.

 

[cyclops]

Sugar. Reduced breathing exercises. Thyroid.

Feel them fully. You could tap them away or something but the gold is found only by experiencing them.

Good Advices. Will implement.

 

[Waremu]

But that seems not to be the case. Most fats in our adipose tissue are oleic acid, followed by variou saturated fatty acids, while PUFA are something between 10-25% depending on dietary intake. And there are animal studies suggesting that the body prefers to quickly oxidize linoleic acid (18:2) in particular while barely storing any. When you feed rats cocoa fat or olive oil for 8 weeks, they quickly store a lot of it as triglycerol in the muscle. On the other hand, safflower oil doesn't increase it, at all. Hence, at least muscle cells seem to prefer storing SFA while burning PUFA when activated/stressed.

Differential effects of saturated versus unsaturated dietary fatty acids on weight gain and myocellular lipid profiles in mice

I have been looking into this more, lately. Thanks for showing this. So it seems, if adipose tissue is not mostly PUFA that has accumulated, that Ray Peat is wrong on that, and that adipose tissue is on average around 10-25%, do you still agree that the 10-25% PUFA is still more than enough or all that is needed to cause problems due to it's biochemical structural nature of being bad for mitochondria, etc.? (Maybe kind of like how if you pour a teaspoon of a toxic poison into a gallon of water, the toxic liquid chemical doesn't have to be equal to the volume of the gallon of the water to do damage due to it's toxic potency, so maybe the 10-25% PUFA in adipose tissue is all that is needed to be considered 'high' or cause problems in the body?). Is your only disagreement that adipose tissues aren't fully saturated with PUFA?

From what I gathered from email changes with Peat from others, Peat seems to say that in a slight caloric deficit PUFA will likely be burned than stored but in caloric surplus PUFA will likely be stored, to some degree, and as fat stories increase, the PUFA content increases. But haven't seen much on this in relation to studies.

 

[cyclops]

Ray Peat is wrong on that

impossible.

 

[Kartoffel]

Is your only disagreement that adipose tissues aren't fully saturated with PUFA?

I don't think Peat ever claimed that. He said that PUFA continue to accumulate with age and with increasing amounts in the diet. I actually think that PUFA might accumulate to a slighter greater proportion than what you have in your diet (especially 18:2 linoleic acid), but I think the studies that I have seen do not support his claim that they are preferably stored in very large quantities.

 

[Mauritio]

I did some PUFA depletion with good results but all this seem to be unnecessary. Now I believe orlistate and supplement some SFA topicaly is the way to avoid extremely restricting diets and deplete PUFA painlessly.

Can you elaborate on how that should work ?

 

[methylenewhite]

Can you elaborate on how that should work ?

Using general diet guidelines posted here you gonna get low fat diet. Orlistate will take care about remaining fats turning you pufa depletion diet from extremely restricting to tolerable or even enjoyable depending on your food choices. SFA topicaly, bypassing orlistate, to ease pufa depletion symtoms and protect from unavoidable damage made by liberated PUFA. There is a lot of information about topical SFA applications on this forum.

 

[methylenewhite]

I don't think Peat ever claimed that. He said that PUFA continue to accumulate with age and with increasing amounts in the diet. I actually think that PUFA might accumulate to a slighter greater proportion than what you have in your diet (especially 18:2 linoleic acid), but I think the studies that I have seen do not support his claim that they are preferably stored in very large quantities.

I believe that fats accumulation and the whole fat metabolism is genetically/environmentally determinated and may vary widely.

 

[Wagner83]

Dietary Fatty Acids Alter Lipid Profiles and Induce Myocardial Dysfunction without Causing Metabolic Disorders in Mice

 

[haidut]

Dietary Fatty Acids Alter Lipid Profiles and Induce Myocardial Dysfunction without Causing Metabolic Disorders in Mice

Not sure how this is related to the thread topic. Also, consider this statement in the abstract.
"...Long-term intake of dietary long-chain SFA differentially affected the fatty acid composition in cardiac phospholipids. All long-chain SFA diets increased the levels of arachidonic acid and total SFA in cardiac phospholipids. The preferential incorporation of individual SFA into the cardiac phospholipid fraction was dependent on the dietary SFA species. Cardiac ceramide content was elevated in all mice fed long-chain SFA diets, while cardiac hypertrophy was only presented in mice fed HMD or HPD. We have demonstrated that the intake of long-chain SFA species differentially alters cardiac lipid profiles and induces cardiac dysfunction, without causing remarkable metabolic disorders."

The portion that is highlighted is impossible unless the diets contained a significant amount of PUFA. Arachidonic acid cannot be synthesized from SFA. So, yet another study that somehow sneaked PUFA into the protocol and then blamed SFA.

 

[Waremu]

Not sure how this is related to the thread topic. Also, consider this statement in the abstract.
"...Long-term intake of dietary long-chain SFA differentially affected the fatty acid composition in cardiac phospholipids. All long-chain SFA diets increased the levels of arachidonic acid and total SFA in cardiac phospholipids. The preferential incorporation of individual SFA into the cardiac phospholipid fraction was dependent on the dietary SFA species. Cardiac ceramide content was elevated in all mice fed long-chain SFA diets, while cardiac hypertrophy was only presented in mice fed HMD or HPD. We have demonstrated that the intake of long-chain SFA species differentially alters cardiac lipid profiles and induces cardiac dysfunction, without causing remarkable metabolic disorders."

The portion that is highlighted is impossible unless the diets contained a significant amount of PUFA. Arachidonic acid cannot be synthesized from SFA. So, yet another study that somehow sneaked PUFA into the protocol and then blamed SFA.

I noticed this as well and was scratching my head for a moment until it hit me. I have seen studies like this where they use conventional Lard (which has a good amount of PUFA) and label it as a SFA source, or add other PUFA sources to a mixture of SFA fat sources, but then blame the SFA. I am tempted to say it seems they deliberately manipulated this study to give these results to blame SFA because anyone with a background in basic biochemistry should know that arachidonic acid cannot be synthesized from SFA, according to our current understanding of the mammalian system. I personally think they knew what they were (deceptively) doing here (how could they not know this?).

 

[Wagner83]

Not sure how this is related to the thread topic.

"4. Discussion
The major findings of this study are that uptakes of all dietary long-chain SFA induced cardiac dysfunction, without causing significant changes in blood pressure, fasting blood glucose, glucose tolerance and insulin resistance in mice, suggesting that over-supply of individual SFA may compromise myocardial function by mechanisms independent of the majority of metabolic disorders."

I'll reply to the rest somewhere else.

 

[Cirion]

The major findings of this study are that uptakes of all dietary long-chain SFA induced cardiac dysfunction, without causing significant changes in blood pressure, fasting blood glucose, glucose tolerance and insulin resistance in mice, suggesting that over-supply of individual SFA may compromise myocardial function by mechanisms independent of the majority of metabolic disorders."

Well, the intake of long-chain SFA and medium-chain SFA is an important distinguishment too, no?

Medium-chain SFA's are more beneficial than long-chain from my understandings.

 

[Waremu]

One thing to consider though is that, even with a high intake of saturated fat, you can get a considerable amount of PUFA. While it is still a lower intake of PUFA compared to people who eat SAD, maybe it is still enough for things like cancer growth over time. So if there are studies (and I think I've seen a few on here) that do use pure saturated fat food sources with no added PUFA, it may be that there is enough AA (arachidonic) to be produced from even mostly saturated fat food sources that have some PUFA, hence the reason why Ray Peat recommends a lower fat diet since PUFA accumulates with age even on a higher saturated fatty acid diet. In fact, that is probably why Ray has said over the years that he eats low fat foods (skim/1% milk, very lean meat, etc.) with the only exception of hydrogenated coconut oil, to stay under his 1.5g daily PUFA threshold.

 

[haidut]

"4. Discussion
The major findings of this study are that uptakes of all dietary long-chain SFA induced cardiac dysfunction, without causing significant changes in blood pressure, fasting blood glucose, glucose tolerance and insulin resistance in mice, suggesting that over-supply of individual SFA may compromise myocardial function by mechanisms independent of the majority of metabolic disorders."

I'll reply to the rest somewhere else.

OK, I see. I guess since it discusses glucose tolerance it is related. I was thinking more along the lines of effects on PDH.

 

[Wagner83]

One thing to consider though is that, even with a high intake of saturated fat, you can get a considerable amount of PUFA. While it is still a lower intake of PUFA compared to people who eat SAD, maybe it is still enough for things like cancer growth over time. So if there are studies (and I think I've seen a few on here) that do use pure saturated fat food sources with no added PUFA, it may be that there is enough AA (arachidonic) to be produced from even mostly saturated fat food sources that have some PUFA, hence the reason why Ray Peat recommends a lower fat diet since PUFA accumulates with age even on a higher saturated fatty acid diet. In fact, that is probably why Ray has said over the years that he eats low fat foods (skim/1% milk, very lean meat, etc.) with the only exception of hydrogenated coconut oil, to stay under his 1.5g daily PUFA threshold.

4 Grams Of PUFA A Day Is Not A Threshold

 

[Waremu]

4 Grams Of PUFA A Day Is Not A Threshold

Thank you for this. I'll check it out.

 

[methylenewhite]

The portion that is highlighted is impossible unless the diets contained a significant amount of PUFA. Arachidonic acid cannot be synthesized from SFA. So, yet another study that somehow sneaked PUFA into the protocol and then blamed SFA.

"4. Discussion
The major findings of this study are that uptakes of all dietary long-chain SFA induced cardiac dysfunction, without causing significant changes in blood pressure, fasting blood glucose, glucose tolerance and insulin resistance in mice, suggesting that over-supply of individual SFA may compromise myocardial function by mechanisms independent of the majority of metabolic disorders."

I'll reply to the rest somewhere else.

I noticed this as well and was scratching my head for a moment until it hit me. I have seen studies like this where they use conventional Lard (which has a good amount of PUFA) and label it as a SFA source, or add other PUFA sources to a mixture of SFA fat sources, but then blame the SFA. I am tempted to say it seems they deliberately manipulated this study to give these results to blame SFA because anyone with a background in basic biochemistry should know that arachidonic acid cannot be synthesized from SFA, according to our current understanding of the mammalian system. I personally think they knew what they were (deceptively) doing here (how could they not know this?).

In the study they claim usage of custom made rodent chow made by Harlan Laboratories. Harlan labs is called Envigo now, www.harlan.com is redirected to www.envigo.com. Here are links from custom made chow page from their website.
https://www.envigo.com/resources/data-sheets/09766.pdf <<<--- milkfat diet
https://www.envigo.com/resources/data-sheets/08500.pdf <<<--- hydrogeneted coconut oil diet

What we see down there? 30g per kg of soybean oil. And 5-23% pufa in any chow. And all these chows used in the study are called obesogenic by the manufacturer.
"Purified high fat diets used to induce obesity and obesity-related complications such as diabetes and metabolic syndrome typically have 40-60% of energy derived from fat. The diet tables below summarize relevant diet features for several Teklad custom research diets commonly used in rodent models."

And I suspect some linolenic acid content adjustment made by authors to prevent "efa deficiency" because the materials section states ~9.5% of linolenic content.

 

[haidut]

In the study they claim usage of custom made rodent chow made by Harlan Laboratories. Harlan labs is called Envigo now, www.harlan.com is redirected to www.envigo.com. Here are links from custom made chow page from their website.
https://www.envigo.com/resources/data-sheets/09766.pdf <<<--- milkfat diet
https://www.envigo.com/resources/data-sheets/08500.pdf <<<--- hydrogeneted coconut oil diet

What we see down there? 30g per kg of soybean oil. And 5-23% pufa in any chow. And all these chows used in the study are called obesogenic by the manufacturer.
"Purified high fat diets used to induce obesity and obesity-related complications such as diabetes and metabolic syndrome typically have 40-60% of energy derived from fat. The diet tables below summarize relevant diet features for several Teklad custom research diets commonly used in rodent models."

And I suspect some linolenic acid content adjustment made by authors to prevent "efa deficiency" because the materials section states ~9.5% of linolenic content.

Wow, just wow! No wonder so many of the studies report "conflicting" results. How about quite expected results given the diets commercially available for rodents. If the scientists are aware of these PUFA/SFA/MUFA ratios in diets and still calling them "SFA diets", this is criminal behavior and the authors should be reported for scientific misconduct. I have to check and see if there is a way to report studies for suspected misconduct and misrepresentations in the "matherials and methods" section.

 

[Rafael Lao Wai]

Damn, so it's true that most of value of a study is in the methods.