PUFAs Role On Skin

[Agent207]

I found this extract of the book "Lipids and Skin Health" from biochemist and skin researcher, Apostolos Pappas

This books is serious stuff, sadly its so expensive to buy and read it; but sure it provides very deep insightful knowledge on skin metabolism.


I think dietary pufas have functional use in some amounts, but the "pufa depletion" idea may not always be the way to go. Just like iron, we need a minimum level to avoid anemia, but to minimize storage accumulation too. PUFA may be the same, specially LA. The concept of cutting PUFAs in modern occidental diets is obviously a must in terms of health; but trying to deplete cutting it too drastically is another thing.

Maybe the ideal is to prevent it to accumulate it but not at the cost of reducing it that much, the same as iron. Skin health -the whole organ- is one of the best and most importants mirror of health.

PUFA's in breast milk (LA accounting for 90% of it) averages 12% (which matches that of the skin) of total fatty acids. Why not take that as reference? Sure cutting PUFAs all the possible has some benefits, specially for overweight people (+20% bf) with high pufa storage; but trade-offs too looking at epidermis layers innate composition.

But for a lean person, being around 10% bf, woulnd't be prudent to stick closer to the breast milk ratio? Before you answer I will refresh two famous quotes:

1. "We don't know a millionth of one percent about anything." - Thomas A. Edison.
2. "Don't put all your eggs in one basket." - Ancient proverb.

 

[Blossom]

There is some good discussion on Lipofuscin in this recent thread,
"Unsaturated Fats Linked To Longer Healthier Life" - Harvard Gazette

 

[tyw]

Good find

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First, if people could get 12% PUFA as a percentage of total fatty acids, even by serum tests, they are close to the "depletion" levels seen in animals, as well as in the case of William Brown (I think he reached just about 10% total serum lipids as PUFA). Most people today I see tested get serum levels at 30% or more PUFA.

We don't know whether serum lipids reflect actual storage levels, but the point being that most people have high PUFA levels.

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The next point is that percentage PUFA intakes do not reflect storage and use characteristics.

During breast feeding and the fast growth that accompanies it, that sort of PUFA percentage is fine -- absolute amounts need to accumulate proportionately in order for healthy growth.

This should not be compared to a fully-grown adult, and perhaps not even to a child or teenager -- in all these cases, that amount of PUFA causes accumulation in excess of what is "essential". Note that 12% of total fat in say a low fat 20%-of-calories 2,000kcal diet, is 5.3g of PUFA, if that were a 35% fat diet (more common in the general population), that's 9.3g of PUFA. More likely than not, even this amount is too much.

Percentages are not as useful when dealing with compounds like PUFA which are needed in small amounts. We should look at absolute amounts. Saying something like "limit PUFA to 5g a day" is probably a more useful heuristic.

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Next, PUFA composition in skin can and will vary according to many factors.

EPA and other PUFAs seem to be a double-edged sword -- if controlled by enzymes, are able to be used for defence against UV damage, and if not controlled, become harmful themselves:

- Photoprotective and anti-skin-aging effects of eicosapentaenoic acid in human skin in vivo
- Eicosapentaenoic acid inhibits UV-induced MMP-1 expression in human dermal fibroblasts
- Metabolism of polyunsaturated fatty acids by skin epidermal enzymes: generation of antiinflammatory and antiproliferative metabolites

Heheh, skin lipids kill bacteria -- Bactericidal Activity of the Human Skin Fatty Acid cis-6-Hexadecanoic Acid on Staphylococcus aureus

Again, we see tight endogenous regulation of where PUFAs goes, and what is done with them. I've talked about endogenous regulation a lot -- Some Thoughts On Avocadoes

Eating excessive PUFA is, by definition, either a direction dys-regulation of PUFA (too much supply) or at best, putting additional pressure to keep those PUFAs in check.

On the flip side, under-eating PUFA, puts pressure on the body to synthesise PUFAs when it needs to.

Which one should you pick? I think the evidence supports the idea that over-eating PUFA, and having it accumulate in dangerous amounts, is the far more dangerous route to take. More practical IMO is to always try and under-eat PUFA, which in all but the most extreme cases, will net you 3-5g of PUFA a day anyway (which is more than enough to meet requirements).

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Next, skin is one of many tissues. PUFA requirements will vary according to tissue.

The highest PUFA requirements will be found in the neuroectoderm class of tissues, of which skin is part of (as well as the nervous system). PUFA requirements from such tissue cannot be compared to the likely lower requirement of all other types of tissue, which form the predominant mass of the body.

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Finally, as an aside, 10% body fat is really low , most "lean people" are not at that level. I'm probably just above 10% body fat (got DXA'd at 13% when I was 75kg, now about 70kg).

I'd agree that at lower body fat percentages, excess PUFA becomes less of an issue, but the potential is still there.

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[Agent207]

Thanks, I had already read it. Lipofuscin is one of the multiple factors on skin health. Estrogen+iron+pufa. But as I mention, I dont see much sense on extremely cutting estrogen, iron and pufa all the way down. Aside of individual needs and circumstances, a minimum healthy levels of them is desirable to keep homeostasis.

Even if cutting more pufas is achievable, I wouldn't want a faster thyroid at the expense of degraded skin quality. Every path has trade-offs, Im just debating for the ideal balance, and that going to anyone of the extremes won't take us to get the best of it.

 

[Agent207]

Very good points tyw.

I get at breast feeding, pufas accumulate at a lower rate or none at all. So in a similar scenario that 12% nature choice would be ok, right? Well, I try to see beyond the "growing baby non-accumulating" vs. "adult acumulating" status. I guess there will be various degrees of pufa accumulating states, depending on individual and circumstancial variables. They won't accumulate at the same rate ie. two twins, one being an overfed sedentary person, the other an active one eating at the edge of his caloric expense -both eating the same macros-; or one having better thyroid output than the other... shouldn't we take those factors into account?

Maybe wee should look at first instance to mimic and pursue that ideal "baby non-accumulating status" scenario as much as possible and within our capabilities (keeping proper metabolic rate, healthy thyroid, liver...etc) and then adjusting with pufa % modulation accordingly, as a background measure; but being conscious of this measure to be more of a secondary "patch" just to protect the former but not being free of sides like probably impairing epidermis optimal lipid composition.


Also keep in mind babys get from breast mill 12% pufas of total fatty acids, but fat for them constitutes 50-60% of their total calorie intake. Just that will be double the number in absolute amounts comparing with a person having same 12%pufa from fat, but with his fat accounting for 25% of his calorie intake (in base to their weight).

 

[Such_Saturation]

Lol, I've eaten in the milligrams of PUFA a day for multiple weeks and I'm still here to tell the tale.

 

[tyw]

@Agent207 Yes, the vastly different needs and diets of a baby is why I don't like a direct comparison to their diet.

Whether we like it or not, the brain is the highest DHA turnover tissue, and the brain (and other nervous system tissue) is growing at the fastest rate in babies. It makes sense that this is the time of greatest PUFA need.

The high fat diet with significant sugars is also probably what is needed to support the energetics of that growth -- breastfed babies should have high levels of serum free fatty acids with high levels of ketones, and some simple sugars which do not mess with ketosis to the same extent as glucose.

Again, this is a stage where glucose need is going to be low -- skeletal muscle need is basically none, sugars constantly topped off any carbohydrate need, etc ....

And as such, it is not really comparable to what a fully grown human needs.

That said, as an aside, I said there should be a focus on absolute values.

Well, turns out that if you look at DHA, babies would get anywhere from 100mg to 270mg through breastfeeding -- Docosahexaenoic Acid (DHA) . IMO, this is not too far off what I recommended in that article for adults, which is a DHA flux of around 100mg as well.

Pregnant mothers though, I think can benefit from 200mg a day. And for the DHA nuts in my previous community , No, this doesn't mean "eat seafood like mad". It means, "eat a 6oz piece of salmon once a week" -- 5oz about 150g, and 150g of salmon would have anywhere from 1,000 to 1,500mg of DHA. This plus some eggs through the week is enough PUFA.​

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I agree that a biologic system would ideally match the required PUFA flux, for their given environmental conditions and internal state of health.

What are those amounts? We have no clue unfortunately .... and have no clue how to measure it .....

In wild animals, it's clear that they purposefully accumulate PUFA to become insulin resistant and slow their metabolism for the winter. In humans, it's clear that insulin sensitivity is decreased in winter time, which may account for "PUFA requirements" (I've written about this extensively elsewhere, let me know if I should post it here )

In any case, PUFA requirements can and will change according to many factors.

My approach has been to say, "The body can make PUFAs. Let it make what it needs". I do not know if that is the ideal path for everyone. Clearly it has worked for populations like the Okinawans and Kitavans, whom both live in sub-tropical or tropical locations with not much seasonal light variation.

Does this it apply to someone with heavy seasonal variation? My current bias is to say, "Yes, but don't sweat some small PUFA consumption of 5g a day".

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On another note, I did write recently about how organisms regulate the amount of PUFA on their mitochondria -- Some Thoughts On Avocadoes

The same would likely apply to the skin, whereby cells take in whatever PUFAs they need, when they need it.

In that regard, compounds like vitamin A and E play a role in regulating such PUFA distribution. I still need to do more research on that topic, and intend to write something up at some point (soon .....)

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[Agent207]

Whether we like it or not, the brain is the highest DHA turnover tissue, and the brain (and other nervous system tissue) is growing at the fastest rate in babies. It makes sense that this is the time of greatest PUFA need.

Hehe... you keep relying on dha to back your position. I agree on you with dha special need on babys brain (even though already formed), OK. But that still doesn't explain the ω-6 (mostly linoleic acid), which accounts for +80% of total pufas in breast milk.

Sure would it be great if you posted anything you consider related to this topic :)

 

[tyw]

Hehe... you keep relying on dha to back your position. I agree on you with dha special need on babys brain (even though already formed), OK. But that still doesn't explain the ω-6 (mostly linoleic acid), which accounts for +80% of total pufas in breast milk.

Sure would be great if you posted anything you consider related to this topic :)

Yes, since DHA seems to be all the rage these days, and has the most studies and plausible mechanisms to back it up.

It is not clear what the mechanism behind PUFAs are. Clearly there are some which are used as specific precursors, but the same generic observations that we see regardless of which PUFA is incorporated into cell membranes, is indicative that the mechanism of action is exactly the same, and that this mechanism is reliant on the C=C double bond. Hence the more double bonds, the greater the effect, and DHA is the PUFA with the most double bonds (6 bonds) that is most commonly available (there are other 6 C=C bond fats, but they are very rare).

It is also not clear whether or not an organism would "prefer all DHA if it could", or would it also need some of the lower double bond PUFAs.

Credit to Chris Masterjohn here, for the reminder that biology takes advantage of naturally occurring phenomena; it can't invent new mechanics. ie: The only reason we may see less high double bond count fats, is because they are more unstable to begin with, and are harder to make in the process (every additional double bond means more enzymatic machinery is needed).

Arachidonic Acid is often cited as being necessary as well. With 4 double bonds, it may well be "powerful enough" as a PUFA.

Again, at this point in time, I view all PUFAs as "C=C double bond carriers", and view their functional effects to only differ depending on the structure of that double bond structure, and in what orientations it can be exposed to.

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[tyw]

And another thing to remember is that infants do not handle the PUFAs present in breast milk the same way that even a child would.

I still do not think that it is accurate to using breast milk's fatty acid composition as a guideline for what adults should eat.

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The first question is to ask: What fatty acids do breast milk contain?

Answer: -- Human milk fatty acid composition from nine countries varies most in DHA. - PubMed - NCBI

PDF here: https://www.researchgate.net/profil...ost_in_DHA/links/56a8d0e808ae997e22be0165.pdf

(NOTE: percentages are of Total Fatty Acids)

Saturated fat content (Table 1) is very consistent -- 6% Stearic, 18-23% Palmitic, around 4-6% Mystiric, and then some small variation in the C12 and below

Monounsaturated fat content (Table 2) is almost entirely Oleic acid, and that varies a little more -- mostly in the 30-36%, but then Chile at 26% and the Phillipines at 21%

Interesting to note that the Phillipines is also where Linoleic acid is the lowest (8%), and the medium chain fats are the highest.

Interesting also that the researchers claim:

The levels of lauric and myristic acids were similar among all countries, with the exception of the Philippines.

The samples from the Philippines were obtained from women of low economic status; high milk levels of lauric and myristic acids suggest that the diet of these women was relatively high in carbohydrate and low in fat.

Insull et al. (27) compared milk composition of women receiving either a fat-free diet or an isocaloric diet containing 40% of calories as fat.

The lauric and myristic acid levels of milk in the group consuming the fat-free diet were much higher than levels in women consuming the fat containing diet. Studies of milk composition from women whose typical diet was low in fat agree with our finding that lauric and myristic acid levels are elevated (19,28,29).
​

Is this a good thing? For one, lauric acid and myristic acid are at worst, harmless fatty acids, and at best, good metabolic substrate with other potential effects (look up the many effects of lauric acid for example)​

Once you reach PUFA content (Table 3), the variation becomes huge .... I've highlighted Linoleic acid, since it is the most unpredictable -- both in terms of presence, as well as in terms of use patterns after consumption (will get to this).

In any case, this is an extreme variation, and there is no way to pull out what the "best Linoleic acid" intake is.

More likely is the idea that biology is chasing the effects of Linoleic Acid -- ie: it's further conversion to the higher carbon fatty acids (which incidentally, are not directly used in metabolism, but almost seemed to be designed to be delayed in the queue, and potentially stored for signalling purposes. Look up peroxisome beta-oxidation and chain length limitations).

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Even among babies, we find that newborns do not even handle that Linoleic acid well, excreting up to 30% of it -- Pediatric Research - Variation in [U-13C] [alpha] Linolenic Acid Absorption, [beta]-oxidation and Conversion to Docosahexaenoic Acid in the Pre-Term Infant Fed a DHA-Enriched Formula

This inefficiently gets rapidly diminished with age. The question is, "Why?". It is because the infants are now starting to gain the necessary desaturase ability to convert that Linoleic Acid to other, likely more useful forms?

What is clear is that Linoleic Acid in and of itself is not the likely endpoint. I personally think that the Arichidonic Acid (22:4n-6) is the desired endpoint, and if so, this shows a very clear bias in biology toward endogenous regulation of PUFA levels.

The large variation in mother's breast milk PUFA content is also likely indicative that the mother's body is "trying to tune the PUFA dose" to whatever it thinks the baby needs best in that environment. Again, more endogenous regulation.

IMO, in adults -- whom have the ability to both synthesize PUFAs, and elongate them as needed -- the diet should bias the dealings of PUFAs to be as much endogenously regulated as needed.

(This is of course assuming enough nutrient availability, which I think is a good assumption for areas where famine isn't a problem).

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[schultz]

Breast milk fatty acid composition varies with diet and fat depots. If breast milk is considered to have 12% of its fat as PUFA, this is just an average amount correlating with an average societal intake and storage. @tyw showed some variation between different cultures in the post above.

There are a few papers dating from around the 1950's, where they could control the womans diet heavily in a hospital ward and thus control the composition of the breast milk. I'm not sure they would do these sorts of experiments now-a-days with women... from my perspective it's abusive considering the amount of corn oil they were giving them. The poor baby! Anyway, here is a study done on a single female showing such variation.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC293173/pdf/jcinvest00328-0179.pdf

The study gave different amounts of fat for a different amounts of time to the woman. So 40% of the diet was lard between days 12-18 postpartum with maintenance calories set at 2,750, days 19-26 were a 0% fat diet with calories set at 3,750, days 27-33 were a 0% fat diet with below maintenance calories set at 1,838, days 34-43 were 3,750 calories with 70% of the diet as corn oil, days 44-48 were 2,938 with corn oil as 70% of the diet and days 49-52 were 2,938 calories with corn oil set as 40% of the diet.

Using the 2 extremes, during the overfeeding low fat period the PUFA in the breast milk dropped to around 2.5% and during the 70% corn oil high calorie period the PUFA rose to around 45% of the fat in the breast milk.

So the 12% you're referring to is not some set amount of PUFA in the milk, it's simply related to diet and fat stores. Not only that but the study showed that PUFA can vary between the left and right breast even!

Another thing the study showed was that during times of underfeeding, the body will pull more fat from storage, so the composition will reflect that, and during times of abundance the body will use what it's given instead of relying on fat stores.

 

[Amazoniac]

Agent's main point is simple (and wise): if you restrict some nutrient for too long - regardless if it's detrimental even in small amounts - you'll probably start to adapt to its scarcity by better retention over time, which is something unwanted in the case of PUFA.
His question is not how much is too much, but how much is too little..

 

[tyw]

Agent's main point is simple (and wise): if you restrict some nutrient for too long - regardless if it's detrimental even in small amounts - you'll probably start to adapt to its scarcity by better retention over time, which is something unwanted in the case of PUFA.
His question is not how much is too much, but how much is too little..

I think that was well answered . Note that my answer is obviously based on personal interpretation, but I've explained the rationale above.

Agree with @schultz , that the PUFA content of basically every component the organism will vary with input.

There doesn't seem to any "over-compensation" of PUFAs just because of it being low in the diet. Neither is there any "over-eager storage" after not eating PUFA for a long time, and then suddenly putting it back in.

There are environmental factors which will cause the organism to try and make more PUFAs. The most studied factor is cold exposure, in which everything from bacteria to humans tend to accumulate PUFAs on membranes upon chronic exposure to such environments.

This environmental adaptation is independent of dietary input -- the organism will try and upregulate machinery needed to store and/or build PUFAs under such environmental conditions, regardless of how much PUFA they eat. Eating more PUFA simply accelerates the storage process, which is a survival advantage when dealing with this sort of environmental stress.

I've made my opinion clear that almost any whole-food dietary input is considered too much given today's modern human environment.

Any lack of PUFA can likely be made up for with endogenous synthesis. Even then, I doubt that any whole food diet will lead to a true lack of PUFA (even the very low fat diets).

The only exception are infants, whom do not have the ability to regulate PUFA well. In that case, they should be breast fed.

Note: what to do if the infant isn't breast fed? Dunno. And the recommendations and nuances are too difficult to ascertain. I do think that infants will benefit from a higher fat diet that mimics the high fat content of breast milk, but that is a whole separate discussion.​

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[Drareg]

I think that was well answered . Note that my answer is obviously based on personal interpretation, but I've explained the rationale above.

Agree with @schultz , that the PUFA content of basically every component the organism will vary with input.

There doesn't seem to any "over-compensation" of PUFAs just because of it being low in the diet. Neither is there any "over-eager storage" after not eating PUFA for a long time, and then suddenly putting it back in.

There are environmental factors which will cause the organism to try and make more PUFAs. The most studied factor is cold exposure, in which everything from bacteria to humans tend to accumulate PUFAs on membranes upon chronic exposure to such environments.

This environmental adaptation is independent of dietary input -- the organism will try and upregulate machinery needed to store and/or build PUFAs under such environmental conditions, regardless of how much PUFA they eat. Eating more PUFA simply accelerates the storage process, which is a survival advantage when dealing with this sort of environmental stress.

I've made my opinion clear that almost any whole-food dietary input is considered too much given today's modern human environment.

Any lack of PUFA can likely be made up for with endogenous synthesis. Even then, I doubt that any whole food diet will lead to a true lack of PUFA (even the very low fat diets).

The only exception are infants, whom do not have the ability to regulate PUFA well. In that case, they should be breast fed.

Note: what to do if the infant isn't breast fed? Dunno. And the recommendations and nuances are too difficult to ascertain. I do think that infants will benefit from a higher fat diet that mimics the high fat content of breast milk, but that is a whole separate discussion.​

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At what age does the child like metabolism become somewhat ideal as Peat mentions?

Could it not be construed as the infant being in a form of protective coma of sorts, going in and out for food? The PUFA assist this? A coma does not reduce metabolic rate or temps?
The cause of coma can vary.
Some smaller animals regularly wake for food in hibernation,smaller animals with higher heart rates, I'm not sure if research was done on smaller animals to deduce if they are hibernating with lower body temps and rates or is it more coma?

What would be interesting is to observe the sleep/wake cycles and general behaviour of baby's not breast fed and on low PUFA in particular in modern times.

 

[Blossom]

gain the necessary desaturase ability to convert that Linoleic Acid to other, likely more useful forms?

Do you have any information on how (or even if) lacking the delta 6 desaturase enzyme would impact an adult?

 

[tyw]

First off, looking at infant PUFA requirements has not been something that I have done. This post is an attempt to make sense of more information .

I will address both posts simultaneously.

At what age does the child like metabolism become somewhat ideal as Peat mentions?

Could it not be construed as the infant being in a form of protective coma of sorts, going in and out for food? The PUFA assist this? A coma does not reduce metabolic rate or temps?
The cause of coma can vary.
Some smaller animals regularly wake for food in hibernation,smaller animals with higher heart rates, I'm not sure if research was done on smaller animals to deduce if they are hibernating with lower body temps and rates or is it more coma?

What would be interesting is to observe the sleep/wake cycles and general behaviour of baby's not breast fed and on low PUFA in particular in modern times.

Do you have any information on how (or even if) lacking the delta 6 desaturase enzyme would impact an adult?

I just this study, done on actual pre-term infants at very young ages (<1 month) -- Pediatric Research - The Very Low Birth Weight Premature Infant Is Capable of Synthesizing Arachidonic and Docosahexaenoic Acids from Linoleic and Linolenic Acids

It shows that there is some level of delta-6 desaturase activity going on in these infants, and that even this limited amount does actually produce significant absolute values of Arachidonic Acid (AA) and Docosahexaenoic Acid (DHA).

The researcher's conclude:

This observation suggests that the δ6 desaturation may not be a rate-limiting step in our patients.
​

But only after acknowledging that:

Several studies measuring plasma polyunsaturated FA levels indicate that the infants fed formulas devoid of LCP exhibit lower plasma levels than their human milk-fed counterparts (8).

Decreasing plasma LCP concentrations are also described in preterm infants fed their own mother's milk (28).

Whether this results from a complete inability by the small preterm infant to synthesize LCP (circulating LCP would then result from the recirculation of LCP acquired during fetal life) or whether the requirements are so high that the levels decrease despite active LCP synthesis was not known.​

Another interesting note:

Our data allow us to only estimate the amount of dietary LA and LNA converted into plasma phospholipid AA and DHA. We found that 6.05 ± 2.26% and 14.07 ± 4.20% of the total dose of[13C]LA and LNA were converted into plasma phospholipid AA and DHA, respectively.​

Which in my mind, is a very efficient conversion ratio .... Note that "LNA" is used here to refer to alpha-linolenic acid, and "LA" to refer to linoleic acid. In adults, usually we see low single digits conversion efficiencies (eg: 3.8% LNA to DHA in this study -- Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)? - PubMed - NCBI)

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If delta-6 desaturases are not the rate limiting step in infant PUFA elongation, then we need to look for other pathways. This paper suggests some potential alternative pathways -- Pediatric Research - Intermediates in Endogenous Synthesis of C22:6[omega]3 and C20:4[omega]6 by Term and Preterm Infants

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This will change my opinion on the mechanics of PUFA metabolism, and bring more uncertainty into play. We are seeing less reliance on the direct consumption of highly unsaturated fats like AA and DHA.

I think it is fair to say that it is part of healthy function to be able to regulate PUFA levels, and apparently even human infants can do this well.

NOTE: this doesn't change the fact that older infants can elongate PUFAs better than younger infants, nor that young infants excrete more PUFA. But the idea that young infants must rely on direct highly-unsaturated PUFA intake may not be true. ie: direct AA and DHA supplementation may not be absolutely essential.​

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While the inability to regulate PUFA is rare, it does exist

Here is a paper showing a 9-year-old patient who had a couple of skin disease conditions, and also had skin fibroblasts that did not exhibit delta-6 desaturase activity -- Identification of a fatty acid Δ6-desaturase deficiency in human skin fibroblasts

She improved upon direct supplementation of a combined AA and DHA supplement. It is cases like these where dietary consumption of PUFA is probably needed. I expect such cases to be rare.

If you want mice studies, full deletion of the FADS2 gene responsible for delta 5 and 6 desaturase activity resulted in no metabolic nor longevity consequences, but rendered the mice sterile -- Δ6-Desaturase (FADS2) deficiency unveils the role of ω3- and ω6-polyunsaturated fatty acids

The mice could not make leukotrienes in white blood cells. I'd expect immune response to be impaired.

The mice could not heal induced thrombotic injury as quickly (twice as long bleeding times).

Dietary supplementation of AA, EPA, and DHA reversed some of the conditions (see section 'The fads2-null mutant is an auxotrophic mutant')

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Personally, I would expect similar effects in humans that completely lack this gene. More likely, we'll not see loss of gene activity, but will see some variation in the ability to synthesise PUFA -- Genetic variants of the FADS1 FADS2 gene cluster are associated with altered (n-6) and (n-3) essential fatty acids in plasma and erythrocyte phosph... - PubMed - NCBI

What this means for actual real-life humans I do not know, since there is no way to measure the degree of a lack of PUFA in a particular tissue. I want to say, "if you have a serious PUFA regulatory issue, you'd already be dead or seriously impaired", since this touches so many important functions, but do not know if that is true.

On a practical note, I do not see much harm with low dose PUFA consumption (like 3 eggs a day), and really don't think people should try and "optimise PUFA intake" unless there is a good reason to.

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Finally, I do not have much to say regarding the hibernation or coma state.

Clearly there are massive reductions in metabolic rate during hibernation -- https://www.une.edu.au/__data/assets/pdf_file/0013/32701/AnnuRevPhysiol04.pdf

See Table 1, we're talking at least 50% reduction, and in some cases up to 90+% reduction. This reduction is proportionate to the observed decrease in body temperature (with some of the listed animals dropping their body temp all the way down to the low single digits Celsius).

Induced coma definitely also reduces metabolic rate even further than a regular resting individual (maybe about -5% in this study) -- http://www.ncbi.nlm.nih.gov/pubmed/23963523


I do not think it is accurate to describe babies as being comatose by the actual medical definition . The discussion of coma state metabolism does not apply to a healthy infant.

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[paymanz]

so my question is that if babies have less ability to de novo fatty acid and also they have high need for fats during first years of growth..., then a mother who follows a restricted pufa intake can still provide enough PUFA to her babies?!!!

in some tribes of indian-africa traditionally they dont use pufa oils obviously but they know that in order to have healthy babies they should feed the mother with lot of butter oil-ghee.

i think for a breastfeeding mother having some egg yolks and butter is important to not risk the babies health.

 

[Blossom]

Thanks @tyw for the thorough explanation and links. I've been trying to find the answer to that question for years.

 

[Richiebogie]

For those new to this site, I don't think Ray Peat would agree with the above.

I believe Ray Peat sees omega 3, omega 6 as poisons in humans which we should minimise as much as possible, though not so much as to avoid nutritious foods like oysters and dairy.

Rather than talking of the body 'synthesizing' DHA, AA and EPA, Peat may think of these as toxic chemicals created by the unstable oils reacting haphazardly in the body.

He might say that finding them in the brain and skin is a sign of ageing and disease, not health.

He might consider a lot of the research linked to above as being funded by vested interests like the fish oil and seed industries.

 

[paymanz]

For those new to this site, I don't think Ray Peat would agree with the above.

I believe Ray Peat sees omega 3, omega 6 as poisons in humans which we should minimise as much as possible, though not so much as to avoid nutritious foods like oysters and dairy.

Rather than talking of the body 'synthesizing' DHA, AA and EPA, Peat may think of these as toxic chemicals created by the unstable oils reacting haphazardly in the body.

He might say that finding them in the brain and skin is a sign of ageing and disease, not health.

He might consider a lot of the research linked to above as being funded by vested interests like the fish oil and seed industries.

he doesnt say that clearly!

for example i asked him a question,have you seen his reply?! Ray Peat Email Advice Depository