EFA Linoleic Acid?

Luna

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Patients following a fat free or diet with MCT oil as the only fat source for any length of time may need to supplement essential fatty acids (EFA) and fat soluble vitamins. Essential fatty acid deficiency (EFAD) can begin to occur within as little as five days without provision (16). MCT oil contains negligible, if any, EFA (Mead Johnson’s = 29% C8, 67% C10 and < 4% greater than C10) (http://www.meadjohnson.com/products/hcp-adult-med/mctoil.html). EFA cannot be produced by the body and must be received in the diet. Linoleic acid is the primary EFA. Linolenic acid and arachadonic acid are other associated fatty acids that can be produced by the body in the presence of adequate linoleic acid. EFAD can result in skin lesions, eczema, impaired wound healing, thrombocytopenia, and growth problems. EFA needs can be met by providing approximately 2%–4% of total caloric intake (approximately 40–80 kcal) of essential fatty acids per day for a 2000-calorie diet. Linoleic
acid is found in vegetable oils, especially those made from safflower, sunflower or corn oil. For EFA content of selected vegetable oils see Table 6. It may be possible to replace EFA by topical application of EFA, however, if this is to be continued for a significant length of time, EFA status should be monitored (17).

It seems at least in the opinion of that article, that EFA plays a role in the body. That the intake of linoleic acid is necessary.

I wonder what Ray Peat and Peatarians have to say about that?
 

tyw

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(a) Amounts of EFAs required are so low that almost any diet above say 15% fat intake will provide enough of them. The only exception if you are truly hardcore, and only eat hydrogenated coconut oil -- all other natural fat sources will contain some form of PUFA.

(b) There is research supporting the idea that adipocytes in the body can and will make all the EFAs the body needs -- De novo lipogenesis in the differentiating human adipocyte can provide all fatty acids necessary for maturation

IMO, dietary PUFAs of any form are truly unessential when endogenous pathways are working well. How to determine that "endogenous pathways are working well" is a different story, and I do not have a generic answer for that.

....
 

charlie

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Morning Star

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Shouldn't such a "deficiency" come about only in those who completely PUFA depleted, which
even under a strict regimen PUFA avoidance should take several years. The vast, vast majority of individuals would have kilos of the precious EFA sequestered away in their ample bodyfat. I'd doubt the essentially of the stuff if the body weren't able to tap into it's reserves in periods of scarcity. And considering the requirements being absolutely minuscule, and these fats so pervasive in the food supply, such a condition would only arise in a laboratory, or the diet of some Ray Peat zealots.
 
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(a) Amounts of EFAs required are so low that almost any diet above say 15% fat intake will provide enough of them. The only exception if you are truly hardcore, and only eat hydrogenated coconut oil -- all other natural fat sources will contain some form of PUFA.

(b) There is research supporting the idea that adipocytes in the body can and will make all the EFAs the body needs -- De novo lipogenesis in the differentiating human adipocyte can provide all fatty acids necessary for maturation

IMO, dietary PUFAs of any form are truly unessential when endogenous pathways are working well. How to determine that "endogenous pathways are working well" is a different story, and I do not have a generic answer for that.

....

Yas. It's impossible to become fatty acid deficient, even if you believe there are no EFA's, which I do. If you have adipose tissue, you have fatty acids. If you've burned through all of your adipose tissue and you have none left and you enter starvation then yes, then you'll be fatty acid deficient. We can make all of the saturated fats like palmitate and stearate and we can also desaturate stearic acid to make oleic acid and our own series of polyunsaturates. So we make our own olive oil inside ourselves.

"We make fats from sugar, starch, and amino acids. Even the brain has enzymes to make new fats." -RP
 

paymanz

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if EFAs are absolutely unessential then what is the explanation for symptoms carnivore animals such as cats get when their diet are devoid of Arachidonic acid ?
Ray peat said:
I think people have extrapolated ideas from EFAD rats to cats, without recognizing that carnivores have higher metabolic rates and nutritional needs, so that the mistakes of the Burrs are even easier to make.

Br J Nutr. 1981 Jul;46(1):93-6.
Essential fatty acid deficiency and evidence for arachidonate synthesis in the
cat.
Sinclair AJ, Slattery W, McLean JG, Monger EA.
1. There is controversy regarding the capacity of the cat to convert 18: 2 omega
6 to 20: 4 omega 6 and the ability of the essential fatty acid (EFA)-deficient
cat to produce 20: 3 omega 9. 2. This paper reports the isolation and
identification of 20: 3 omega 9 from kidney phospholipids of EFA-deficient cats.
3. The results suggest that the cat is capable of limited synthesis of 20: 4
omega 6 using a delta 5- and delta 8-desaturase.
from ray's reply i assume that he believe arachidonic acid is essential , then how it can possible PUFAs being absolutely non essential?!

on practical level its not matter, we get very small amount even if avoid oils and nuts,etc, and thats enough.but i hope ray really clarify on this subject!

there is so many studies on infants using skimmed milk and they get symptoms.
Error encountered - PubMed - NCBI
 

tyw

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from ray's reply i assume that he believe arachidonic acid is essential , then how it can possible PUFAs being absolutely non essential?!

on practical level its not matter, we get very small amount even if avoid oils and nuts,etc, and thats enough.but i hope ray really clarify on this subject!

there is so many studies on infants using skimmed milk and they get symptoms.
Error encountered - PubMed - NCBI

See figure 2 of the study I cited -- De novo lipogenesis in the differentiating human adipocyte can provide all fatty acids necessary for maturation

And @Westside PUFAs ;) , we can not just "make our own olive oil", but you can clearly see fatty acid 20:4 (Arichidonic acid) being made in significant amounts. All PUFAs could be made by Adipocytes in that study (either the PUFA directly was observed in the adipocytes, or a precursor for a PUFA was made -- eg: even DHA precursors were made in the adipocytes)

----

What constitutes a good diet for an infant is different from what constitutes a good diet for anyone other than an infant. We can speculate on why this is, though it probably has to do with the rapid rate of brain growth, and thus a rapid need for cholesterol and other lipid synthesis for the nervous system.

Obviously the brain uses some degree of PUFAs for signalling. I have speculated that this is due to the cholesterol exclusion behaviour of PUFAs, which would allow the brain to control how quickly and where cholesterol moves in the brain.

Regardless, there is some degree of PUFA requirement for the brain, and during the first 3-5 years of rapid brain growth with corresponding underdevelopment of the rest of the body, endogenous PUFA synthesis is not optimal.

So how much PUFA is needed? Well, if you assume breast milk to have the optimal ratios -- Docosahexaenoic and arachidonic acid concentrations in human breast milk worldwide

The mean (±SD) concentration of DHA in breast milk (by wt) is 0.32 ± 0.22% (range: 0.06–1.4%) and that of AA is 0.47 ± 0.13% (range: 0.24–1.0%), which indicates that the DHA concentration in breast milk is lower than and more variable than that of AA.​

Another study -- A study on lipid content and fatty acid of breast milk and its association with mother’s diet composition

The content of fat was 2.17 ± 1.22 g/100 ml breast milk. Arachidonic acid (AA, 20:4n-6) and docosohexaanoic acid DHA (22:6n-3) made 0.8 ± 0.4% and 0.3 ± 0.2% of total fatty acids. Although the AA/DHA ratio in our study is suitable, but the content of DHA is nearly low.​

Which is roughly the same as the previous study.

We are still talking very low amounts of PUFA in the diet on the order of 1% PUFA of TOTAL FATTY ACIDS. ie: if you eat 50g of fat a day (which is a significant amount), that's like 0.5g to 1g of these so called "essential" AA and DHA.

Infants probably need some fat, but if anything, it's going to be the saturated fats -- all of Long-chain SFA, Medium Chain SFA, and Short Chain SFA, are are found abundantly in breast milk, and we assume that Natural pressure has given rise to a decently optimal breast milk composition after all these years of evolution.


----

Therefore .... Nope, explicit dietary PUFA consumption considered unnecessary at best, and harmful at worst.

Anything other than a completely fat-free diet will provide more than enough PUFA for anyone other than an infant (This sort of diet is almost impossible without it being fully processed to remove all the fat).


....
 
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paymanz

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thanks @tyw

it is very interesting,that study and its citations.

The expression of lipogenic enzymes, which are greater in the adipose tissue of lean people (9, 10), specifically, those with smaller adipocytes (5), relates inversely to obesity

from one of citations said:
De novo lipogenesis (DNL) is paradoxically up-regulated by its end product, saturated fatty acids (SAFAs)

they also mentioned saturated fatty acids/palmitic toxicity a few times!

--------------
Indeed, the lipogenic capacity of fetal human fat cells is high as the cells develop into mature adipocytes
but your explanation for infant's lower capacity of making pufa is still interesting.

-------------

other stuff was interesting for me is synthesis of 12:0 lauric acid in those tissues.

and biotin and b5 are among other things they included in the medium.

------------

and omega 7 fatty acids, it shows we make a lot of them,then i looked at nutrition data to see whats are best sources of it(palmitoleic acid) , and it was whale fat, a warm blooded aquatic animal!

this study and other ones by that team should change a lot of things in biology.peat never mentioned ability of human cell to produce pufa! he only talks about mead acid,and in this study the only thing they havent mentioned is mead acid.
 
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And @Westside PUFAs ;) , we can not just "make our own olive oil", but you can clearly see fatty acid 20:4 (Arichidonic acid) being made in significant amounts. All PUFAs could be made by Adipocytes in that study (either the PUFA directly was observed in the adipocytes, or a precursor for a PUFA was made -- eg: even DHA precursors were made in the adipocytes)

Olive oil is about 70% oleic acid. I was going off of what Peat said here at 3:03: Ray Peat on the myth of PUFA depletion and making our own fats
 

tyw

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thanks @tyw

it is very interesting,that study and its citations.

they also mentioned saturated fatty acids/palmitic toxicity a few times!

--------------

but your explanation for infant's lower capacity of making pufa is still interesting.

-------------

other stuff was interesting for me is synthesis of 12:0 lauric acid in those tissues.

and biotin and b5 are among other things they included in the medium.

------------

and omega 7 fatty acids, it shows we make a lot of them,then i looked at nutrition data to see whats are best sources of it(palmitoleic acid) , and it was whale fat, a warm blooded aquatic animal!

this study and other ones by that team should change a lot of things in biology.peat never mentioned ability of human cell to produce pufa! he only talks about mead acid,and in this study the only thing they havent mentioned is mead acid.

Regarding the statement: "they also mentioned saturated fatty acids/palmitic toxicity a few times!"

(a) This study is about DNL production of fatty acids. Focus should be placed on empirical results, and less so on researcher interpretations.

(b) Palmitate toxicity to a cell is a known fact.

You'll find many many papers about this, whereby you start to see insulin resistance at concentrations at even 0.05mM, with significant effects at 0.15mM to 0.2mM. A realistic physiological level on a ketogenic diet is probably around this 0.2mM mark.

"Toxicity" really sets in only in 2 cases:

- High glucose + High palmitate -- eg: 8.0mM glucose with 0.3mM palmitate, which is something that only happens in vitro, and in diabetics.

- Really high palmitate -- above 2.0mM, which should never ever happen in your body. At this concentration, you literally start to see morphological changes in the cell.


(c) This doesn't generalise to all saturated fats

-----

Regarding endogenous PUFA synthesis. Whether it be omega-7 fatty acids, Mead acid, .... whatever. The body can and will make it when needed. This assumes that:

(a) the pathways needed to produce these fatty acids are working
(b) we trust the body to make "Just Enough" PUFA according to what it needs.

Practical questions like "do I need to eat PUFA" revolve around those 2 assumptions.

You've heard @haidut 's example of PUFAs being used to prevent organ transplant rejection. PUFAs shut down the immune system really well, and this could be a conditionally beneficial fringe-case use.

Similarly, really unsaturated fats like DHA taken orally act to completely suppress and possibly lead to apoptosis of intestinal border cells and/or colonocytes. It's a horrible idea to take this if you're either healthy, or have a bacterial infection. It's not a horrible idea if you're battling serious colon cancer.

And of course, all of these are fringe cases where the person is already very unhealthy. Every unhealthy person is sick in a specific way -- specific treatment needs to be applied first in order to allow for energy addition strategies to work.

But for normal folk, I still contend that avoiding dietary PUFA completely is the best path.

....
 

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