4 Grams Of PUFA A Day Is Not A Threshold

[Mito]

It’s interesting that Paul Jaminet came to approximately the same “safe” amount of PUFA in the diet as Ray. Chapter 11 in the Perfect Health Diet titled “The Dangerous Fats: PUFA”, concludes that “We’ve found that for optimal health we want to minimize omega-6 fats, keeping them below 4% of energy and preferably near 2% of energy.”

Two percent of energy assuming a 2,000 calorie diet works out to 4.4 grams of PUFA.

 

[Wagner83]

[....]

[52] Requirement of Essential Fatty Acid for Mammary Tumorigenesis in the Rat

"Diets rich in fat are known to enhance the development of tumors in several rodent mammary cancer models. Most of the studies involve chemically induced mammary tumors in rats, although there are a number of reports which show that dietary fat is also capable of increasing the growth of both spontaneous and transplantable mammary tumors in mice. An excellent review of this subject by Welsch and Aylsworth (22) has appeared recently in the literature. In addition to quantity of fat, the type of fat has also been considered to be important."

"Carroll and Hopkins (3) demonstrated that diets containing 3% sunflower seed oil (polyunsaturated fat) and 17% beef tallow or coconut oil (saturated fats) enhanced tumorigenesis as much as did a diet containing 20% sunflower seed oil. [!] Rats on these diets developed twice as many tumors as those fed diets containing 20% of the saturated fats alone."

Replacing 3% of those 20% with sunny flowers of the seeds oils was enough to double the amount of tumors induced by a certain carcinogen. It is about 70% linoleic acid. When you replace it, you have 17% fat with 2% linoleic acid and 3% fat with 70% linoleic acid: now with 2.5%. A 20% sunny flower diet is one with 14% of linoleic acid.​

.[...]​

​

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.

Perhaps all of those things are related, in this study the saturated fats used were reliable (beef tallow, milk fat, cocoa butter and palm oil).

"The most abundant polyunsaturated fatty acids (PUFA) detected in the serum, arachidonic acid (20:4, AA), accumulated much more in serum lipids from mice fed HBD, HCD and HPD for 6 months, than those from mice fed CHD (p < 0.05 or p < 0.01). Interestingly, the levels of docosahexaenoic acid (22:6, DHA) were greatly lower in mice fed CHD for six months, compared with those fed CHD for three months (0.25 ± 0.06 versus 0.44 ± 0.06), while slight changes in DHA level in serum lipids were documented in other high dietary fat diets, when a comparison was made between medium (3 months) and long (6 months) feeding periods. This might suggest that long-term intake of medium-chain SFA led to elevated transformation of DHA to other metabolites."

 

[haidut]

​

Perhaps all of those things are related, in this study the saturated fats used were reliable (beef tallow, milk fat, cocoa butter and palm oil).

"The most abundant polyunsaturated fatty acids (PUFA) detected in the serum, arachidonic acid (20:4, AA), accumulated much more in serum lipids from mice fed HBD, HCD and HPD for 6 months, than those from mice fed CHD (p < 0.05 or p < 0.01). Interestingly, the levels of docosahexaenoic acid (22:6, DHA) were greatly lower in mice fed CHD for six months, compared with those fed CHD for three months (0.25 ± 0.06 versus 0.44 ± 0.06), while slight changes in DHA level in serum lipids were documented in other high dietary fat diets, when a comparison was made between medium (3 months) and long (6 months) feeding periods. This might suggest that long-term intake of medium-chain SFA led to elevated transformation of DHA to other metabolites."

Still, the only way for arachidonic acid to increase is to have it from the diet directly or as its precursor linoleic acid. SFA by themselves cannot cause that increase.

 

[lvysaur]

Still, the only way for arachidonic acid to increase is to have it from the diet directly or as its precursor linoleic acid. SFA by themselves cannot cause that increase.

They said SFA diet, so probably beef fat.

All animal fats have arachidonic acid, with the absolute singular exception of dairy fat. Anything else from an animal has PUFA.

 

[Rafael Lao Wai]

Beef fat has only 40 mg of arachidonic acid per 100 grams. How much of the ingested linoleic acid is transformed into arachidonic acid?

 

[Wagner83]

Still, the only way for arachidonic acid to increase is to have it from the diet directly or as its precursor linoleic acid. SFA by themselves cannot cause that increase.

I guess the question is: could the intake of large amount of sfa enhance the deleterious effects of small amounts of pufas ? Tyw tried to make sure to burn the ingested pufas right away rather than store them.

They said SFA diet, so probably beef fat.

All animal fats have arachidonic acid, with the absolute singular exception of dairy fat. Anything else from an animal has PUFA.

You can check the study, there were different groups, beef tallow, milk fat, cocoa..

Btw, I don't know how relevant those mice studies are for us and whether or not it's easy to extrapolate human concerns from them.

 

[lvysaur]

You can check the study, there were different groups, beef tallow, milk fat, cocoa..

This is extremely interesting, looking at table 1 of the study: Dietary Fatty Acids Alter Lipid Profiles and Induce Myocardial Dysfunction without Causing Metabolic Disorders in Mice.

3 months into the diet, beef tallow did not increase arachidonate levels that much.

6 months in, it did; but so did cocoa butter and palm oil. Cocoa butter is a highly saturated plant fat and should not have done that.

Could there be something about the chain length that affects how the triglyceride is processed? I could imagine something like: long fats > triglyceride gets absorbed differently, including the short fats > linoleic acid gets more converted to arachidonic.

 

[CLASH]

Perhaps mice werent meant to eat these types of fats and in these quantities. Perhaps based on thier GI tract thier diet was meant to have more of a fermentative function than an absorptive function...

 

[Waremu]

I guess the question is: could the intake of large amount of sfa enhance the deleterious effects of small amounts of pufas ? Tyw tried to make sure to burn the ingested pufas right away rather than store them.

You can check the study, there were different groups, beef tallow, milk fat, cocoa..

Btw, I don't know how relevant those mice studies are for us and whether or not it's easy to extrapolate human concerns from them.​

This is what I am thinking it is looking like from the study as well. I don't see how we could conclude anything else, since the only source of AA could be from the small amount of PUFA in the saturated fat foods. I have seen fairly recent email changes one person shared where Peat mentioned that he recommends a slight caloric deficit to ensure the PUFA consumed is burned, which seems to agree with what TYW said as well. And Peat made this recommendation in conjunction to an already very low PUFA diet. Ray mentioned that PUFA would accumulate with age at over 0.5 grams per day in a few email exchanges when asked. This is a very low threshold, so perhaps if we extrapolate that into this study where the PUFA even from saturated fat sources was enough to increase AA levels in mice, then perhaps it makes perfect sense why it was enough, given the low threshold, assuming their metabolism of PUFA is similar enough to ours. Makes sense to me why Ray switched to hydrogenated coconut oil, given the context. Palm oil was one of the fats which was used in the study, as mentioned, and Palm oil in considerable amounts actually has a pretty good amount of PUFA. The study says that the fat of the high fat group was around 20% of total calories. Well, in humans, 20% of calories coming from fat in the form of palm oil on a 2000 calorie diet would yield well over 4 grams of PUFA, and from cacoa butter, that would be well over 1 gram of PUFA. Even beef tallow would yield almost 2 grams PUFA. So this would seem to be in line with what Ray Peat says is enough to accumulate in the body with age, especially if it is consumed at even a slight caloric surplus. And one other things I thought of: mice have very short lifespans, so 3-6 months of PUFA accumulation like from the study, is years of PUFA accumulation equivalent in humans. So for that reason it may make a lot of sense why higher AA levels were seen 6 months in as opposed to 3 months in. Their metabolic rate perhaps slowed as it accumulated, leading to more accumulation by the sixth month in, which was already 25-50% of their lifespan. (I believe they typically live 1-2 years). Interestingly, this would be the human equivalent age range of 18-37 for a adult male in human years, which also so happens to be the general age range when, according to Ray Peat, enough PUFA has accumulated in the average westerner adult male to begin to dramatically start slowing down the metabolic rate with age, etc. All of this is just thinking off the top of my head as I glance over the study, so just some preliminary thoughts at the moment as I look continue looking at it.

 

[Amazoniac]

This is what I am thinking it is looking like from the study as well. I don't see how we could conclude anything else, since the only source of AA could be from the small amount of PUFA in the saturated fat foods. I have seen fairly recent email changes one person shared where Peat mentioned that he recommends a slight caloric deficit to ensure the PUFA consumed is burned, which seems to agree with what TYW said as well. And Peat made this recommendation in conjunction to an already very low PUFA diet. Ray mentioned that PUFA would accumulate with age at over 0.5 grams per day in a few email exchanges when asked. This is a very low threshold, so perhaps if we extrapolate that into this study where the PUFA even from saturated fat sources was enough to increase AA levels in mice, then perhaps it makes perfect sense why it was enough, given the low threshold, assuming their metabolism of PUFA is similar enough to ours. Makes sense to me why Ray switched to hydrogenated coconut oil, given the context. Palm oil was one of the fats which was used in the study, as mentioned, and Palm oil in considerable amounts actually has a pretty good amount of PUFA. The study says that the fat of the high fat group was around 20% of total calories. Well, in humans, 20% of calories coming from fat in the form of palm oil on a 2000 calorie diet would yield well over 4 grams of PUFA, and from cacoa butter, that would be well over 1 gram of PUFA. Even beef tallow would yield almost 2 grams PUFA. So this would seem to be in line with what Ray Peat says is enough to accumulate in the body with age, especially if it is consumed at even a slight caloric surplus. And one other things I thought of: mice have very short lifespans, so 3-6 months of PUFA accumulation like from the study, is years of PUFA accumulation equivalent in humans. So for that reason it may make a lot of sense why higher AA levels were seen 6 months in as opposed to 3 months in. Their metabolic rate perhaps slowed as it accumulated, leading to more accumulation by the sixth month in, which was already 25-50% of their lifespan. (I believe they typically live 1-2 years). Interestingly, this would be the human equivalent age range of 18-37 for a adult male in human years, which also so happens to be the general age range when, according to Ray Peat, enough PUFA has accumulated in the average westerner adult male to begin to dramatically start slowing down the metabolic rate with age, etc. All of this is just thinking off the top of my head as I glance over the study, so just some preliminary thoughts at the moment as I look continue looking at it.

Wagner wagnering with another great find. According to them:

"[..]we chose the total fat content of high SFA diets with 20% (w/w), or calculated as about 40% energy from fat, because they altered blood lipid profiles but did not change most vital metabolic profiles, including body weight, blood pressure level, fasting blood glucose level, insulin and glucose tolerance."

"Neutral lipids, which mostly consist of triglycerides in mammalian cells, represent tissue lipid storage; while phospholipids, the most abundant lipid class in biomembranes, influence membrane properties and function [14,25]."​

..and after 3 months it was worse than after 6, with the exception of palm oil.

It's interesting that they got different outcomes with diets that had a similar content of PUFA, but they all had 9.5% of their fat as linoleic acid. What kind of dairy fat, cocoa butter, and tallow contain this much? It's usually 3-4%. So the experiment is the fat in question with something else.

- Butterfat - Wikipedia
- Cocoa butter - Wikipedia
- Tallow - Wikipedia
- Palm oil - Wikipedia

 

[Waremu]

Wagner wagnering with another great find. According to them:

"[..]we chose the total fat content of high SFA diets with 20% (w/w), or calculated as about 40% energy from fat, because they altered blood lipid profiles but did not change most vital metabolic profiles, including body weight, blood pressure level, fasting blood glucose level, insulin and glucose tolerance."

"Neutral lipids, which mostly consist of triglycerides in mammalian cells, represent tissue lipid storage; while phospholipids, the most abundant lipid class in biomembranes, influence membrane properties and function [14,25]."​

..and after 3 months it was worse than after 6, with the exception of palm oil.

Okay, I must have missed that...so still then, the higher PUFA SFA food mice were the only ones which did worse progressively than the other SFA food mice. This makes sense since Palm oil has a much higher PUFA content than the other fats, which would still seem to agree with what Ray Said, that well into 25-50% of their life span, the higher PUFA fat mice did worse....especially if other PUFA fat sources were added in which would exacerbate the SFA to PUFA ratio effects in the Palm group.

It's interesting that they got different outcomes with diets that had a similar content of PUFA, but they all had 9.5% of their fat as linoleic acid. What kind of dairy fat, cocoa butter, and tallow contain this much? It's usually 3-4%. So the experiment is the fat in question with something else.

Yes, that does seem pretty high for SFA. So you think they added in other higher PUFA fat into the SFA sources? I don't see how else they could get those numbers using pure SFA.

 

[Wagner83]

It's interesting that they got different outcomes with diets that had a similar content of PUFA, but they all had 9.5% of their fat as linoleic acid. What kind of dairy fat, cocoa butter, and tallow contain this much? It's usually 3-4%. So the experiment is the fat in question with something else.

- Butterfat - Wikipedia
- Cocoa butter - Wikipedia
- Tallow - Wikipedia
- Palm oil - Wikipedia

Thanks I just noticed, it's hidden in a zip file which has to be downloaded. I have no idea, could it be that they just added the high fat on top of the chow?
I remember reading about PUFAs increasing fatty acid oxidation, so like I et alii said there's a question on whether or not there are particularly deleterious effects from combining pufas with sfas as the pufas ain't burned. I guess this is where slight calorie deficit, low body fat, some muscle mass and physical activity as well as spending time away from meals can help negate some of the effects.

 

[johnwester130]

Thanks I just noticed, it's hidden in a zip file which has to be downloaded. I have no idea, could it be that they just added the high fat on top of the chow?
I remember reading about PUFAs increasing fatty acid oxidation, so like I et alii said there's a question on whether or not there are particularly deleterious effects from combining pufas with sfas as the pufas ain't burned. I guess this is where slight calorie deficit, low body fat, some muscle mass and physical activity as well as spending time away from meals can help negate some of the effects.

how much PUFA does the average Westerner eat ?

It must be about 40 grams a day ?

 

[Cirion]

how much PUFA does the average Westerner eat ?

It must be about 40 grams a day ?

which certainly explains the rapid aging syndrome we see nowadays plus almost everyone being overweight to obese nowadays at least in the West and even 20-30 somethings getting cancer now.

 

[Amazoniac]

Okay, I must have missed that...so still then, the higher PUFA SFA food mice were the only ones which did worse progressively than the other SFA food mice. This makes sense since Palm oil has a much higher PUFA content than the other fats, which would still seem to agree with what Ray Said, that well into 25-50% of their life span, the higher PUFA fat mice did worse....especially if other PUFA fat sources were added in which would exacerbate the SFA to PUFA ratio effects in the Palm group.



Yes, that does seem pretty high for SFA. So you think they added in other higher PUFA fat into the SFA sources? I don't see how else they could get those numbers using pure SFA.

The diets seemed evened for PUFA content, they might have used canola oil for that since the heart had high levels of fatty acid named erucic acid.

What was detrimental to the animals was not the ratio (tallow diet had a higher PUFA:SFA ratio than the palm diet for example), it was the type of fat in each diet. The MCT diet was the safest, but their 'medium' was skewed to the shorter chains.

Speaking of tyw, I remember him writing something about the selectiveness of tissues for their fat composition. This must be one of the reasons why the hearty lipid profile started to decrease in all diets (rather than increase, as expected). Some time ago I was doing a wonder if a diet rich in MCT (with more fats being burned for energy) could leave more PUFA unspaced and more prone to cause damage. Yeeet! This wasn't the case in Wagner's experiment:

Spoiler

I don't want to accuse without proof here but it appears to me that I was actually getting paid wonder that.

West of the sides mentioned that too much fat makes a harm, even if it's (long-chain) saturated: right once again.

Regarding Ivysaur's post, what can happen is that the shorter chain fats don't trigger bile release to the same extent as the longer ones, therefore less fat ends up being adsorbed. One way to counteract this is by ingesting plenty of calcium along to form Raj's insoluble soaps.

 

[Fractality]

Regarding Ivysaur's post, what can happen is that the shorter chain fats don't trigger bile release to the same extent as the longer ones, therefore less fat ends up being adsorbed. One way to counteract this is by ingesting plenty of calcium along to form Raj's insoluble soaps.

This would seem to help validate my near 2 qyarts a day of whole goat milk consumption.

 

[Gadsie]

"For example, rats fed lard or olive oil developed about the same number of tumors as those fed corn oil or soybean oil, although the latter oils are much more highly unsaturated"

Is this with comparable amounts? That would mean we need to avoid MUFA just as much as PUFA

 

[Rafael Lao Wai]

"For example, rats fed lard or olive oil developed about the same number of tumors as those fed corn oil or soybean oil, although the latter oils are much more highly unsaturated"

Is this with comparable amounts? That would mean we need to avoid MUFA just as much as PUFA

I think that's because both lard and olive oil have a very significant amount of PUFA( especially the lard). Olive oil is something like 10 to 15% PUFA. Lard nowadays is 20%+ PUFA and one study shultz posted mentioned that lard could be as high as 40% PUFA.

This quote from one of the studies in the OP is great: "Once the EFA requirement for optimal tumor expression is met, further enhancement of development would depend on the amount and not on the type of dietary fat."

Even though olive oil isn't crazy high in PUFA, it seems to have enough to be just as bad the vegetable oils, if you're using it to get a lot of calories.

I would think macadamia nut oil, which is very low in PUFA( around 3 %) but very high in MUFA( 80%), would have similar effects to beef tallow and coconut oil, with regards to carcinogenicity. Also, beef tallow itself has a lot of MUFA.