Haidut's Summary Of PUFA

jaa

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Late to reply :bag:

And no, cardiolipin with 4 units of linoleic acid (18:2) is the most common form of cardiolipin in the human body. It is particularly concentrated in the heart.

The proof that 18:2 is absolutely necessary in a healthy human heart is found by examining the case of Barth's Syndrome, which is a genetic disorder that causes Heart Cardiolipin to be altered -- Barth syndrome - Wikipedia

Studies like this show the alteration, in which there is a loss of cardiolipin with 18:2, in favour of cardiolipin with 18:1 -- Bloodspot Assay Using HPLC–Tandem Mass Spectrometry for Detection of Barth Syndrome | Clinical Chemistry

The result are all the diseases of the heart and subsequent functionality in the humans born with this defect, which is very much fatal.

Dave Valentine (author of 'Human Longevity') has this to say:

The major molecular species of CL in cardiac cells is (18:2)4-CL, in which linoleic acid (18:2) occupies all four acyl positions. In Barth’s syndrome the trend is that the 18:2 chains are replaced with more saturated fatty acids, including 18:1.

Studies of Barth’s syndrome establish the essential role of cardiolipin in energy transduction in human mitochondria. CL is primarily located in the inner membrane but is distributed in both leaflets

The universality, localization, amounts, and structure of CL suggest multiple beneficial roles, including formation of supramolecular complexes enhancing energy efficiency as well as appropriate membrane motion and permeability.

These benefits are balanced against risks associated with membrane integrity and oxidative stability.
The risks that are mentioned are very clear -- Influence of cardiolipin remodeling on mitochondrial respiratory function in the heart

That last study shows that excess Delta-6 desaturase activity, presumably causing more unsaturated fatty acids in the heart, is directly harmful. That is, once you get cardiolipin that is unsaturated beyond the 2 double bonds in 18:2, peroxidative stress outweighs any benefit of better energetics.

This is very clearly a case of the body having to balance the fast and furious needs of a very active tissue like the Heart, while trying to minimise the downsides. It is clear that without these PUFA on cardiolipin, the heart fails to function, and it is clear that more than the required unsaturation causes damage over time.

Balance is key.

Are you wary of mitolipin for this reason? Or am I making the wrong connection?
 

tyw

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@tyw @haidut
Per @tca300, highly stress resistant animals have been bred in EFAD environments. If their cardiolipin contains PUFA, it must be Mead acid. Do you believe that Mead acid is inappropriate for the formation of cardiolipin, if indeed it is always necessary for cardiolipin to contain unsaturated lipids?

I think a bio-energetic explanation of tissue specific polyunsaturation is less mystical. Those tissues which tend to accumulate more PUFA, probably have more PUFA laden blood pumped into them during stress. The stress will produce fatigue, amplified by PUFA, from which highly active tissues are unlikely to fully recover. The fatigue produced and the time necessary to recover from it will tend to increase as an organism accumulates PUFA in fat stores. By the same mechanism by which global aging proceeds, more highly active tissues will hereby locally age. The consequent tendency to partial freezing (the partial rigor mortis of ATP depletion) of the tissues probably induces the incorporation of PUFA in structural components in order to produce an excitatory melting effect, much as such fats do in organisms which metabolise at lower temperatures, such as salmon or plant seeds. Just as plants need PUFA to produce excitatory activity at low temperatures, so might fatigued muscles. I would like to be more differentiated than a plant however, and therefore try to avoid fatiguing activities.

Barth syndrome involves much more than cardiolipin unsaturation, including global lack of cardiolipin, which is found in many of the PUFA-mediated degenerative disorders, and therefore does not seem to be a conclusive case that linoleic acid is necessary for cardiolipin to function correctly. In fact, this paper (Influence of cardiolipin remodeling on mitochondrial respiratory function in the heart) which you cite concludes with:

"Unexpectedly, we also found evidence for impaired assembly of mitochondrial proteins and strikingly, reduced synthesis and/or utilization of CoA, which may reflect direct or compensatory effects of altered cardiolipin metabolism on mitochondria. This suggests that perhaps it is impairment of the
tafazzin-mediated CL remodeling process itself, not the resulting change in cardiolipin composition, which causes the mitochondrial respiratory dysfunction in Barth syndrome." (p.g. 78).


"Cardiolipin Remodelling" refers to the unsaturation of cardiolipin associated fatty acids after cardiolipin is initially made. It is this step that is compromised, which then leads to a defective cardiolipin molecule that cannot be properly incorporated into membranes.

The steps of remodelling always follow (Valentine quotes):
  • Cardiolipin synthetase located specifically in mitochondria joins two phospholipids together through their head groups, generating a relatively saturated species of cardiolipin.

  • The second stage involves a remodeling process that adds increasing levels of unsaturated chains to cardiolipin.

    Specificity mechanisms ensure that the molecular species (18:2)4-CL is the most abundant of the highly polyunsaturated molecular species of CL in human mitochondria

    The presence of DHA and other HUFAs in CL suggests that the second stage of CL biosynthesis is far more active in mice than in humans.

This is what the paper is referring to, and not a lack of potential to make and transport cardiolipin. What happens is a reduced concentration of cardiolipin, most likely because of the lack of ability. It is the inability of the body to make (18:2)4-CL that causes the lack of cardiolipin in the tissues that need it.

This is supported by the data that adding Linoleic acid to Barth's Syndrome Fibroblasts restores their function -- Linoleic acid supplemention of Barth syndrome fibroblasts restores cardiolipin levels

It also remains true that the most abundant form of cardiolipin in the Human body contains 4 molecules of the PUFA Linoleic acid.

- This paper shows normative cardiolipin composition. (18:2)4-CL dominates -- Cardiolipin is a normal component of human plasma lipoproteins

Sidenote: Mead Acid is 20:3 -- ie: more peroxidisable than 18:2. This is not a good thing, and 18:2 on Cardiolipin is what is observed to be the preferred fatty acid.​

- http://www.heartlungcirc.org/article/S1443-9506(11)00526-9/abstract

- Once you add more unsaturated fatty acids (DHA in this case), things go bad -- Dietary docosahexaenoic Acid (22:6) incorporates into cardiolipin at the expense of linoleic Acid (18:2): analysis and potential implications. - PubMed - NCBI

-----

I have shown why the comparison to other animals with Essential Fatty Acid Deficiency / PUFA depletion are not comparable to humans at all.

Different species use PUFA differently -- they are not comparable.

- Mice will make tons of PUFA in their liver when you put them on a fast ....
- Humans need to concentrate more DHA than mice in their brains, and cannot make PUFA above 2-double-bonds in the liver.
- Whales will have tons of MUFA, but little PUFA, despite eating enough PUFA to kill any other animal.

These are not comparable; different organisms will react with different endogenous mechanisms when faced with deficiency or excess; We must not compare different organism with different endogenous regulation capacities.

Sidenote: also, one needs to make sure that any testing on essential fatty acid deficiency was done on normal animals, and not gnobiotic / germ-free animals.
Now a quote from Dr Valentine:

The DHA content of membranes of heart cells in mice is about 10 to 15 percent of total fatty acids compared to about one-tenth this level of DHA in human cardiac cells.

ie: a "PUFA-deficient" mice probably has the same tissue PUFA concentrations as a normal PUFA eating human ... Humans are designed to be low-PUFA dependent creatures, unlike mice. They are not comparable; mice are live at a higher rate of peroxidation (compared to Humans) no matter what diet they eat. Likewise, Birds and Bats live at lower rates of peroxidation (compared to Humans) no matter diet they eat.

The only metric worth comparing is the likelihood of membrane Peroxidation, which as we will see below, is dependent on much more than just gross PUFA amount.

All this is said against the backdrop that PUFAs are obviously used in Humans and many animals, and does not necessarily contribute to Peroxidative damage. The way these PUFAs are regulated in membranes are done precisely to ensure that their peroxidation is avoided as much as possible, while their function of accelerating reaction rate is maximised.

In Humans, there are many adaptations to prevent oxidation of PUFAs in the brain. Specifically:

- large chunks of myelinated axons to reduce O2 concentration to as low as possible (enough for O2 the high-O2-affinity Cyt C Oxidase to work, but not enough for peroxidation of PUFA)
- dependency on low-O2 dependent lactate metabolism
- exclusion of PUFAs away from the high oxygen demanding gray matter
- very tight regulation of PUFAs entering the brain (eg: MsfD2A only allows a very specific form of sn-2 DHA phospholipid to enter the brain)
- and probably many more factors ....

NOTE: and yet PUFAs are obviously necessary in a power-hungry tissues like the brain and heart. This isn't about fatigue, but rather about maintaining a constant flow of energy. This is where it seems the innately disruptive capacity of PUFAs are exploited for high efficiency activity in such tissues (and only such tissues, with lots of security protocols put in place).​

Mice (and almost any other animal) are either absent or present-with-very-poor-versions these adaptations. Again, not comparable.

Similarly, we humans likely do not have the adaptations that Birds do. These birds regulate concentrate a lot more PUFA compared to humans in their muscles, and yet do not suffer the consequences of peroxidation for whatever reason. They have somehow managed to hack the ability to use PUFA for their very obvious performance-enhancing capabilities, but without much of the downsides.

=====

The point of all this discussion is to present a more balanced view of the PUFA. They are absolutely necessary in certain quantities. The quantities that are required are determined by each individual of a particular species based on endogenously regulated mechanisms.

From a practical standpoint, relying on such uncertain theory, and attempting PUFA depletion, can lead to contra-indications in certain people whom do not have well functioning endogenous PUFA regulation.

This is not a recommendation to try an extreme PUFA depletion diet, nor is it a recommendation to avoid said extreme diet. It is simply a precautionary measure against believing that a PUFA depleted state is always a good thing, when it clearly is racked with so much uncertainty. Pursuing an extreme PUFA depleted state when real world results are poor is a losing strategy.

.....
 
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Drareg

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Ray Peats articles all provide a balanced view on PUFA, people really need to read them.
These threads are arguments against forum members behaviour and not Peat. There is no refutation of Peat in any of these threads.

Ray Peat on pufa depletion if people can't be bothered with his articles.


Below are quotes from his articles on PUFA,there are a lot more like this.
"Over the years, it has become evident that the polyunsaturated fats are not very compatible with a high rate of metabolism, though they are necessary for organisms that live at low temperatures and metabolize slowly, such as fish and vegetables. The saturated fats solidify at low temperature; beef fat is very stiff at refrigerator temperature, and in a fat fish, such stiffness would be lethal."
"Even some hibernating rodents can stay alive with their body tissues close to the freezing point, and their stored fats have to be unsaturated. When their diet doesn't allow them to store enough polyunsaturated fat, they fail to go into hibernation. This is probably a clue to some of the general biological effects of the PUFA."
"Birds' mitochondrial fats are much less polyunsaturated than those of mammals, and birds' metabolic rates are much higher, and they live much longer than mammals of a similar size."
"But the people who claim that they are absolutely, rather than conditionally, essential, base their argument on the idea that they are needed for the formation of prostaglandins and cell membranes. The fact that cells can replicate in fat free conditions shows that the argument from membranes is unfounded. The argument from prostaglandins is more complex, but has no firmer foundation.

Peats views on PUFA are very well balanced,I'm sure those on here who have read his articles wil agree,he is again been quoted out of context.
If we don't try think creatively when we view research on animals and how it might apply to humans we will suffer the same problems as many rigid reductionists do.
 

Strongbad

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Feb 12, 2015
Messages
291
"Cardiolipin Remodelling" refers to the unsaturation of cardiolipin associated fatty acids after cardiolipin is initially made. It is this step that is compromised, which then leads to a defective cardiolipin molecule that cannot be properly incorporated into membranes.

The steps of remodelling always follow (Valentine quotes):
  • Cardiolipin synthetase located specifically in mitochondria joins two phospholipids together through their head groups, generating a relatively saturated species of cardiolipin.

  • The second stage involves a remodeling process that adds increasing levels of unsaturated chains to cardiolipin.

    Specificity mechanisms ensure that the molecular species (18:2)4-CL is the most abundant of the highly polyunsaturated molecular species of CL in human mitochondria

    The presence of DHA and other HUFAs in CL suggests that the second stage of CL biosynthesis is far more active in mice than in humans.

This is what the paper is referring to, and not a lack of potential to make and transport cardiolipin. What happens is a reduced concentration of cardiolipin, most likely because of the lack of ability. It is the inability of the body to make (18:2)4-CL that causes the lack of cardiolipin in the tissues that need it.

This is supported by the data that adding Linoleic acid to Barth's Syndrome Fibroblasts restores their function -- Linoleic acid supplemention of Barth syndrome fibroblasts restores cardiolipin levels

It also remains true that the most abundant form of cardiolipin in the Human body contains 4 molecules of the PUFA Linoleic acid.

- This paper shows normative cardiolipin composition. (18:2)4-CL dominates -- Cardiolipin is a normal component of human plasma lipoproteins

Sidenote: Mead Acid is 20:3 -- ie: more peroxidisable than 18:2. This is not a good thing, and 18:2 on Cardiolipin is what is observed to be the preferred fatty acid.​

- http://www.heartlungcirc.org/article/S1443-9506(11)00526-9/abstract

- Once you add more unsaturated fatty acids (DHA in this case), things go bad -- Dietary docosahexaenoic Acid (22:6) incorporates into cardiolipin at the expense of linoleic Acid (18:2): analysis and potential implications. - PubMed - NCBI

-----

I have shown why the comparison to other animals with Essential Fatty Acid Deficiency / PUFA depletion are not comparable to humans at all.

Different species use PUFA differently -- they are not comparable.

- Mice will make tons of PUFA in their liver when you put them on a fast ....
- Humans need to concentrate more DHA than mice in their brains, and cannot make PUFA above 2-double-bonds in the liver.
- Whales will have tons of MUFA, but little PUFA, despite eating enough PUFA to kill any other animal.

These are not comparable; different organisms will react with different endogenous mechanisms when faced with deficiency or excess; We must not compare different organism with different endogenous regulation capacities.

Sidenote: also, one needs to make sure that any testing on essential fatty acid deficiency was done on normal animals, and not gnobiotic / germ-free animals.
Now a quote from Dr Valentine:

The DHA content of membranes of heart cells in mice is about 10 to 15 percent of total fatty acids compared to about one-tenth this level of DHA in human cardiac cells.

ie: a "PUFA-deficient" mice probably has the same tissue PUFA concentrations as a normal PUFA eating human ... Humans are designed to be low-PUFA dependent creatures, unlike mice. They are not comparable; mice are live at a higher rate of peroxidation (compared to Humans) no matter what diet they eat. Likewise, Birds and Bats live at lower rates of peroxidation (compared to Humans) no matter diet they eat.

The only metric worth comparing is the likelihood of membrane Peroxidation, which as we will see below, is dependent on much more than just gross PUFA amount.

All this is said against the backdrop that PUFAs are obviously used in Humans and many animals, and does not necessarily contribute to Peroxidative damage. The way these PUFAs are regulated in membranes are done precisely to ensure that their peroxidation is avoided as much as possible, while their function of accelerating reaction rate is maximised.

In Humans, there are many adaptations to prevent oxidation of PUFAs in the brain. Specifically:

- large chunks of myelinated axons to reduce O2 concentration to as low as possible (enough for O2 the high-O2-affinity Cyt C Oxidase to work, but not enough for peroxidation of PUFA)
- dependency on low-O2 dependent lactate metabolism
- exclusion of PUFAs away from the high oxygen demanding gray matter
- very tight regulation of PUFAs entering the brain (eg: MsfD2A only allows a very specific form of sn-2 DHA phospholipid to enter the brain)
- and probably many more factors ....

NOTE: and yet PUFAs are obviously necessary in a power-hungry tissues like the brain and heart. This isn't about fatigue, but rather about maintaining a constant flow of energy. This is where it seems the innately disruptive capacity of PUFAs are exploited for high efficiency activity in such tissues (and only such tissues, with lots of security protocols put in place).​

Mice (and almost any other animal) are either absent or present-with-very-poor-versions these adaptations. Again, not comparable.

Similarly, we humans likely do not have the adaptations that Birds do. These birds regulate concentrate a lot more PUFA compared to humans in their muscles, and yet do not suffer the consequences of peroxidation for whatever reason. They have somehow managed to hack the ability to use PUFA for their very obvious performance-enhancing capabilities, but without much of the downsides.

=====

The point of all this discussion is to present a more balanced view of the PUFA. They are absolutely necessary in certain quantities. The quantities that are required are determined by each individual of a particular species based on endogenously regulated mechanisms.

From a practical standpoint, relying on such uncertain theory, and attempting PUFA depletion, can lead to contra-indications in certain people whom do not have well functioning endogenous PUFA regulation.

This is not a recommendation to try an extreme PUFA depletion diet, nor is it a recommendation to avoid said extreme diet. It is simply a precautionary measure against believing that a PUFA depleted state is always a good thing, when it clearly is racked with so much uncertainty. Pursuing an extreme PUFA depleted state when real world results are poor is a losing strategy.

.....

Great post @tyw ! I read lots of your past posts and how you debunked many of the community's interpretation of Peat.

Peat says PUFA is bad, so people think let's deplete PUFA!
Peat says sugar is good, so people think let's eat tons of sugar!
Peat drinks lots of coffee, so people think let's drink lots of coffee!
Peat says undernourishment is bad, so people think let's eat a lot!
Peat says good thing about milk, so people think let's drink tons of milk!

Yet you debunked all of those things on your previous posts with precision and extreme details. I love it! I like it that you take the moderate, conservative approach to things rather than interpreting things and take them to the extreme.

All of your posts should be sticky and be on the *Must Read* category. Seriously, you're the Hall of Fame poster of this forum.
 
T

tca300

Guest
Me ~ " My diet of fruit, lowfat milk, occasional liver, gelatin, and hydrogenated coconut oil is very satisfying and makes me feel so good I have no desire to eat other foods. So are you saying we cant deplete our bodies of PUFA even if we keep it super low chronically?

Ray Peat's Answer ~ " That’s the sort of diet that will do it."

Me ~ " How many grams of PUFA per day do you think is safe? I have heard that you recommend keeping them under 4 grams per day, but I haven't heard or read anything from you about how much your personally get or recommend."

Ray Peat's Answer ~ " I think I manage to keep mine below 1.5 most of the time; I have switched from regular coconut oil to fully hydrogenated.

Ray Peat ~ " I think it’s good to keep the total PUFA as low as possible, but two tablespoons of butter per day would be o.k.
@Strongbad @Drareg
 
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T

tca300

Guest
" At birth, the baby's mitochondria contain a phospholipid, cardiolipin, containing palmitic acid, but as the baby eats foods containing polyunsaturated fatty acids, the palmitic acid in cardiolipin is replaced by the unsaturated fats. " http://raypeat.com/articles/aging/aspirin-brain-cancer.shtml

"Palmitic acid, which is a major component of the cardiolipin which regulates the main respiratory enzyme, becomes displaced by polyunsaturated fats as aging progresses." Mitochondria and mortality

" The crucial mitochondrial respiratory enzyme, cytochrome c oxidase, declines with aging (Paradies, et al., 1997), as the lipid cardiolipin declines, and the enzyme's activity can be restored to the level of young animals by adding cardiolipin. The composition of cardiolipin changes with aging, "specifically an increase in highly unsaturated fatty acids."
(Lee, et al., 2006). " Fats, functions and malfunctions.

"These toxic oils are sometimes called the "essential fatty acids" or "vitamin F," but this concept of the oils as essential nutrients was clearly disproved over 50 years ago." Unsaturated Vegetable Oils: Toxic

" On a typical diet, tissues progressively accumulate linoleic acid, and this alters the structure of mitochondrial cardiolipin, which governs the response of the mitochondrial enzymes to the thyroid hormone. This process is especially evident in the female liver. In the “autoimmune” diseases, such as lupus, there are typically antibodies to cardiolipin, as if the body were trying to reject its own tissues, which have been altered by the storage of linoleic acid. The altered mitochondrial function, which is involved in so many symptoms, can become part of a vicious circle, with endotoxin and estrogen having central roles, once the stage has been set by the combination of diet, stress, and toxins." Food-junk and some mystery ailments: Fatigue, Alzheimer's, Colitis, Immunodeficiency. Carrageenan

"When animals are made “deficient” in all the exogenous polyunsaturated fatty acids, linoleic and arachidonic acid as well as linolenic and DHA, they become remarkably resistant to all sorts of stress and toxins." Aging Eyes, Infant Eyes, and Excitable Tissues

"Cytochrome oxidase is one of the enzymes damaged by stress and by blue light, and activated or restored by red light, thyroid, and progesterone. It's a copper enzyme, so it's likely to be damaged by excess iron. It is most active when it is associated with a mitochondrial lipid, cardiolipin, that contains saturated palmitic acid; the substitution of polyunsaturated fats lowers its activity. Mitochonrial function in general by the unsaturated fats, especially arachidonic acid and DHA." Aging Eyes, Infant Eyes, and Excitable Tissues
 
T

tca300

Guest
@Drareg The title of that video is misleading, and only pertains to people consuming a " moderate amount " of fat from butter and or regular coconut oil, as Ray said in the video. People keeping pufa very low by eating a truly low fat diet, or eating a normal amount of fat that is from hydrogenated coconut oil can become "deficient" in the Polyunsaturated fatty acids.
 

tyw

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Cairns, Australia
@tca300 Points noted.

I think I've already covered why some unsaturation in Cardiolipin good, but more than that some unsaturation is horrible. The case to be made here isn't "avoid PUFA at all costs". It is "ensure that endogenous cardiolipin regulation systems are functioning well". The HUFAs (highly unsaturated fatty acids) in cardiolipin are obviously bad, and I have provided references to show the chaos that this causes.

In that vein, I will argue that some level of PUFA is absolutely essential in the context of Humans. Whether it be DHA in the retina, or linoleic acid in cardiolipin.

However, practically speaking, the rule of thumb is always going to be "avoid PUFA". I would say that most diets are going to net you some degree of PUFA no matter what happens ....

Let's take anything other that the most extreme diets, which we know from practical experience on this forum, that not everyone can do ... I myself can survive on truly fat deficient diets (like <5g fat a day), but this is not something that most people can handle.

So let's take an average person eating only 2,000 kcal a day, which is not a very high calorie diet. Let's make that diet 20% fat, which is bordering on the low side, but definitely not super low fat. That's 2000 * 0.2 / 9 = 44 grams of fat.

Let's say you get all this fat from butter. Butter is 3% Linoleic acid, and 1% alpha-Linoleic acid (and 24% oleic acid BTW). That is 44 * 0.04 = 1.76 grams of PUFA. This calculation obviously scales to all forms of dairy fat.

Beef tallow, is similarly about 4% PUFA. Non-fully-hydrogenated Coconut oil is similarly about 4% PUFA.

One egg => 1 gram of PUFA.

Grass fed Beef has more PUFA than grain fed beef (see Table 2) -- A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef

Now, scale that up to say a 2500kcal diet that is 30% fat (which is a moderate amount of fat, which some people seem to need). That's 2500 * 0.3 / 9 = 83 grams of fat. Again, if everything were from "high saturated fat sources" like beef or butter, thats still 83 * 0.04 = 3.32 grams of PUFA.

----

The point here being that any nutritious diet with a normal amount of fat found in regular food will almost by default contain some degree of PUFA beyond what Peat supposedly recommends.

This just isn't consistent with some of the other ideas that Peat puts out, and which are good ideas for most people .... like eating a little bit of seafood and organ meats and eggs, all of which will push PUFA beyond this limit.

Then, if taken with the advice of trying to "eat more", the chances of any amount of PUFA in the body to accumulate will increase. This is simple biomechanics, whereby carbs (and alcohol) will always be preferentially oxidised before fat, leading to that fat being stored away and mobilised as needed.

Sidenote: I do not know where this idea came from. My impression of Peat was always "eat until you are not hungry" / "use hunger as a guide as to how much to eat".​

Personally, given the reality of these constraints, and given all the mechanics I have discussed in previous posts, I am not militant about the whole idea of reducing PUFA intake to as close to nothing as possible. It is clear that excess dietary PUFA intake is bad, and also clear that deficiency in dietary PUFA intake forces endogenous PUFA regulation mechanisms into effect. Both extremes require endogenous response by the body, which will try to seek the balance that it wants.

Restricting dietary PUFA to zero is,
(a) very difficult,
(b) obviously leads to some issues in many people over the long run,
(c) not guaranteed to actually lead to a PUFA depleted state (as measured by mitochondrial PUFA concentrations, of which human studies are basically non-existent, and whereby animal studies don't hold much weight for reasons I've discussed),
(d) there is still doubt about whether a PUFA depleted state is beneficial for Humans in particular (see my comments about species-specificity).

And again, I will remind people that a "no fat diet" done when in a state where there is excess fat to lose is simply a normalisation to baseline healthy levels. I will guarantee that all of these people with fat to lose have a significant amount of PUFA stored in that fat, and thus are "eating some PUFA" by using that fat for fuel. It is then important to recognise that any success of short term no fat dieting cannot be extrapolated to the period of weight maintenance after that fat is lost.

-----

@Strongbad and @Liubo thanks for the nice comments ;)

But despite the analysis that is displayed in my posts, I view all of this as pure entertainment .... :pompous:. I am fond of the warning, "Far too many people study the truth in order to avoid it".

I will assert that Life is never lived well if left up to conscious analyses and debating over Platonic ideals of theory. Practical measures call for practical experimentation, and self directed Authority to make decisions that are optimised for oneself in particular.

Almost always, practical conclusions are reached through some inexplicable creative process that is never understood by trying to "think harder" about the supposed problem. More likely it is a large set of heuristics (whether conscious or unconscious attained and activated), that steer the individual towards better decision making.

Therefore, should someone be militant about reducing PUFA as much as possible, with the potential tradeoff of eating less "PUFA containing but nutrient dense" foods like Eggs, Organ Meats, and Seafood? This is up to the individual to experiment and decide ....

I personally happen to take the "reduce PUFA" leaning more often than not, but that is just me, and I have no idea how I came to that conclusion .... and have no idea how that will change into the future.​

I'd still encourage absorbing as much information as possible, but I also like the attitude: "Take what you like and leave the rest ... come back for seconds if you happen to like the first taste ;) "

At the end of the day, the only thing I am concerned about is that the health decisions I make for myself are my own, and not something that "X person said I should do". And never will I think: "Oh noes! I am not following X person's recommendations :oops:".

NOTE: this doesn't mean "don't obey your doctor's advice" :bag:. More like, "I obey you for the contracted period of time, in order to see who is wrong about me" .... Ultimately, we're on our own journey to fix our own health.​

.....
 
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haidut

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" At birth, the baby's mitochondria contain a phospholipid, cardiolipin, containing palmitic acid, but as the baby eats foods containing polyunsaturated fatty acids, the palmitic acid in cardiolipin is replaced by the unsaturated fats. " http://raypeat.com/articles/aging/aspirin-brain-cancer.shtml

"Palmitic acid, which is a major component of the cardiolipin which regulates the main respiratory enzyme, becomes displaced by polyunsaturated fats as aging progresses." Mitochondria and mortality

" The crucial mitochondrial respiratory enzyme, cytochrome c oxidase, declines with aging (Paradies, et al., 1997), as the lipid cardiolipin declines, and the enzyme's activity can be restored to the level of young animals by adding cardiolipin. The composition of cardiolipin changes with aging, "specifically an increase in highly unsaturated fatty acids."
(Lee, et al., 2006). " Fats, functions and malfunctions.

"These toxic oils are sometimes called the "essential fatty acids" or "vitamin F," but this concept of the oils as essential nutrients was clearly disproved over 50 years ago." Unsaturated Vegetable Oils: Toxic

" On a typical diet, tissues progressively accumulate linoleic acid, and this alters the structure of mitochondrial cardiolipin, which governs the response of the mitochondrial enzymes to the thyroid hormone. This process is especially evident in the female liver. In the “autoimmune” diseases, such as lupus, there are typically antibodies to cardiolipin, as if the body were trying to reject its own tissues, which have been altered by the storage of linoleic acid. The altered mitochondrial function, which is involved in so many symptoms, can become part of a vicious circle, with endotoxin and estrogen having central roles, once the stage has been set by the combination of diet, stress, and toxins." Food-junk and some mystery ailments: Fatigue, Alzheimer's, Colitis, Immunodeficiency. Carrageenan

"When animals are made “deficient” in all the exogenous polyunsaturated fatty acids, linoleic and arachidonic acid as well as linolenic and DHA, they become remarkably resistant to all sorts of stress and toxins." Aging Eyes, Infant Eyes, and Excitable Tissues

"Cytochrome oxidase is one of the enzymes damaged by stress and by blue light, and activated or restored by red light, thyroid, and progesterone. It's a copper enzyme, so it's likely to be damaged by excess iron. It is most active when it is associated with a mitochondrial lipid, cardiolipin, that contains saturated palmitic acid; the substitution of polyunsaturated fats lowers its activity. Mitochonrial function in general by the unsaturated fats, especially arachidonic acid and DHA." Aging Eyes, Infant Eyes, and Excitable Tissues

Thanks for this. I think it is pretty clear from Ray's writings on where stands on PUFA levels. I get accused of somehow ascribing to him extreme views when the man is pretty willing to say so directly in email or in his articles. I understand that we all have different views. But Peat's position on PUFA is pretty clear, especially on the depletion of body stores.
 
T

tca300

Guest
@tca300 Points noted.

I think I've already covered why some unsaturation in Cardiolipin good, but more than that some unsaturation is horrible. The case to be made here isn't "avoid PUFA at all costs". It is "ensure that endogenous cardiolipin regulation systems are functioning well". The HUFAs (highly unsaturated fatty acids) in cardiolipin are obviously bad, and I have provided references to show the chaos that this causes.

In that vein, I will argue that some level of PUFA is absolutely essential in the context of Humans. Whether it be DHA in the retina, or linoleic acid in cardiolipin.

However, practically speaking, the rule of thumb is always going to be "avoid PUFA". I would say that most diets are going to net you some degree of PUFA no matter what happens ....

Let's take anything other that the most extreme diets, which we know from practical experience on this forum, that not everyone can do ... I myself can survive on truly fat deficient diets (like <5g fat a day), but this is not something that most people can handle.

So let's take an average person eating only 2,000 kcal a day, which is not a very high calorie diet. Let's make that diet 20% fat, which is bordering on the low side, but definitely not super low fat. That's 2000 * 0.2 / 9 = 44 grams of fat.

Let's say you get all this fat from butter. Butter is 3% Linoleic acid, and 1% alpha-Linoleic acid (and 24% oleic acid BTW). That is 44 * 0.04 = 1.76 grams of PUFA. This calculation obviously scales to all forms of dairy fat.

Beef tallow, is similarly about 4% PUFA. Non-fully-hydrogenated Coconut oil is similarly about 4% PUFA.

One egg => 1 gram of PUFA.

Grass fed Beef has more PUFA than grain fed beef (see Table 2) -- A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef

Now, scale that up to say a 2500kcal diet that is 30% fat (which is a moderate amount of fat, which some people seem to need). That's 2500 * 0.3 / 9 = 83 grams of fat. Again, if everything were from "high saturated fat sources" like beef or butter, thats still 83 * 0.04 = 3.32 grams of PUFA.

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The point here being that any nutritious diet with a normal amount of fat found in regular food will almost by default contain some degree of PUFA beyond what Peat supposedly recommends.

This just isn't consistent with some of the other ideas that Peat puts out, and which are good ideas for most people .... like eating a little bit of seafood and organ meats and eggs, all of which will push PUFA beyond this limit.

Then, if taken with the advice of trying to "eat more", the chances of any amount of PUFA in the body to accumulate will increase. This is simple biomechanics, whereby carbs (and alcohol) will always be preferentially oxidised before fat, leading to that fat being stored away and mobilised as needed.

Sidenote: I do not know where this idea came from. My impression of Peat was always "eat until you are not hungry" / "use hunger as a guide as to how much to eat".​

Personally, given the reality of these constraints, and given all the mechanics I have discussed in previous posts, I am not militant about the whole idea of reducing PUFA intake to as close to nothing as possible. It is clear that excess dietary PUFA intake is bad, and also clear that deficiency in dietary PUFA intake forces endogenous PUFA regulation mechanisms into effect. Both extremes require endogenous response by the body, which will try to seek the balance that it wants.

Restricting dietary PUFA to zero is,
(a) very difficult,
(b) obviously leads to some issues in many people over the long run,
(c) not guaranteed to actually lead to a PUFA depleted state (as measured by mitochondrial PUFA concentrations, of which human studies are basically non-existent, and whereby animal studies don't hold much weight for reasons I've discussed),
(d) there is still doubt about whether a PUFA depleted state is beneficial for Humans in particular (see my comments about species-specificity).

And again, I will remind people that a "no fat diet" done when in a state where there is excess fat to lose is simply a normalisation to baseline healthy levels. I will guarantee that all of these people with fat to lose have a significant amount of PUFA stored in that fat, and thus are "eating some PUFA" by using that fat for fuel. It is then important to recognise that any success of short term no fat dieting cannot be extrapolated to the period of weight maintenance after that fat is lost.

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@Strongbad and @Liubo thanks for the nice comments ;)

But despite the analysis that is displayed in my posts, I view all of this as pure entertainment .... :pompous:. I am fond of the warning, "Far too many people study the truth in order to avoid it".

I will assert that Life is never lived well if left up to conscious analyses and debating over Platonic ideals of theory. Practical measures call for practical experimentation, and self directed Authority to make decisions that are optimised for oneself in particular.

Almost always, practical conclusions are reached through some inexplicable creative process that is never understood by trying to "think harder" about the supposed problem. More likely it is a large set of heuristics (whether conscious or unconscious attained and activated), that steer the individual towards better decision making.

Therefore, should someone be militant about reducing PUFA as much as possible, with the potential tradeoff of eating less "PUFA containing but nutrient dense" foods like Eggs, Organ Meats, and Seafood? This is up to the individual to experiment and decide ....

I personally happen to take the "reduce PUFA" leaning more often than not, but that is just me, and I have no idea how I came to that conclusion .... and have no idea how that will change into the future.​

I'd still encourage absorbing as much information as possible, but I also like the attitude: "Take what you like and leave the rest ... come back for seconds if you happen to like the first taste ;) "

At the end of the day, the only thing I am concerned about is that the health decisions I make for myself are my own, and not something that "X person said I should do". And never will I think: "Oh noes! I am not following X person's recommendations :oops:".

NOTE: this doesn't mean "don't obey your doctor's advice" :bag:. More like, "I obey you for the contracted period of time, in order to see who is wrong about me" .... Ultimately, we're on our own journey to fix our own health.​

.....
(a) very difficult - Nothing worth while in life is easy. I have been eating under 2 grams of pufa for a long time ( years ) its actually not that hard.
(b) obviously leads to some issues in many people over the long run. - No not obviously, hardly anybody has done it, and the ones who have get great results, like myself, haidut, and Ray.
(c) not guaranteed to actually lead to a PUFA depleted state (as measured by mitochondrial PUFA concentrations, of which human studies are basically non-existent, and whereby animal studies don't hold much weight for reasons I've discussed). - Just because there are lacking studies doesn't mean it cant be done, thats silly thinking imo. If everyone had that mentality in life nothing new would be proven or discovered, and our understanding of everything would immediately stay where it is and be stagnant, or if people thought your way in the beginning, we would know nothing about anything. What your saying could be true, but is highly unlikely based on the studies of other mammals, and a few human experiences. When doing something that has never been done before there is always uncertainty.
(d) there is still doubt about whether a PUFA depleted state is beneficial for Humans in particular (see my comments about species-specificity). - You have doubt... Ray doesnt have doubt and others who have stuck with a low pufa diet much much longer than you have no doubt.

It is then important to recognise that any success of short term no fat dieting cannot be extrapolated to the period of weight maintenance after that fat is lost
. - Nobody that im aware of who has eaten very low pufa for years eats a no fat diet. I get around 10% total fat but could get much more through hydrogenated coconut oil. Ray has mentioned he averages about 60 grams per day. Im done here sharing my opinions, I just get upset when people come to a forum which the subject matter is not in agreement with their own opinions, and post anyways. Almost comparable to an athiest posting his or her ideas on a Christian forum... You see where Im getting at? Your opinions are important, and make you the person who you are, which is good, and you could be correct, but why come to a forum that is based off the work of a man in which you dont agree with? seems quite bizarre to me. I have seen this slowly happen to this forum over the years, where more and more come and state that they think Ray is wrong.. Then why come and post here?? I think my time on this forum is closely coming to an end.
 

Drareg

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@Drareg The title of that video is misleading, and only pertains to people consuming a " moderate amount " of fat from butter and or regular coconut oil, as Ray said in the video. People keeping pufa very low by eating a truly low fat diet, or eating a normal amount of fat that is from hydrogenated coconut oil can become "deficient" in the Polyunsaturated fatty acids.

Thanks, Its just the point on how he comprehends how hard it is to eliminate them because of our environment.
Thanks for the other quotes,there is more I'm going to post when I have more time,he has issue with pufa crossing the cell membrane and the interpretation of whether the speeding up is from the damage it causes at the surface.
 

Drareg

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Thanks for this. I think it is pretty clear from Ray's writings on where stands on PUFA levels. I get accused of somehow ascribing to him extreme views when the man is pretty willing to say so directly in email or in his articles. I understand that we all have different views. But Peat's position on PUFA is pretty clear, especially on the depletion of body stores.

When will your research on pufa depletion be starting? Will you check DHA in the eye?
 

haidut

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haidut

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nice, @haidut so you tested your mead acid level. can you please share the numbers?

Yes, I think my doctor used this test:
http://www.questdiagnostics.com/testcenter/BUOrderInfo.action?tc=11254X&labCode=SJC

My Mead reading was 37 nMol/L and the upper "normal" limit is 30 nMol/L.

Btw, here is an interesting study that shows feeding mice omega-3 or omega-6 directly increases the "caloric efficiency" of food. By caloric effiency they simply mean how much weight animals gained for every kcal of ingested food. So, you could say it was a measure of how fattening the diet was. As you can see, the 1% fish oil diet got the mice to be EFA deficient and had negative caloric efficiency - they were losing weight.
FISH OIL PREVENTS ESSENTIAL FATTY ACID DEFICIENCY AND ENHANCES GROWTH: CLINICAL AND BIOCHEMICAL IMPLICATIONS
 

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tyw

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@tca300 It's fine to disagree. I've substantiated my points fairly well, and listed the uncertainties in place.

If I disagree with Ray, why post here?

(a) I will disagree with some of what Peat says, and will agree with more than I disagree. Some of the disagreements are on principles, and most are just on relatively minor practical tweaks.

Discussing those points of disagreement may help other people understand the topics discussed better, and make better decisions for themselves.

For example, my position on fructose has been that some is beneficial, and too much is bad, and the middle ground is probably to consume no more than what is needed to fill liver glycogen stores on a daily basis (generally about 50-75g of total fructose as a maximum). The reasoning is simply "try not exceed what your body needs", and I have gone into some details.

Then, it is up to the individual to experiment with what their ideal dose should be, hopefully now free from the dogma of either "fructose is the devil", or "more fructose means better metabolism", and eventually settle upon, "fructose in balance".

Similarly, the discussion regarding definitions of "starch", and being more discriminatory about "starch sources", has helped clarify what sources some people can and cannot tolerate. I view that as useful discussion that is beneficial as a whole.​


(b) I come here with a clinical bias. A statement like, "nothing in life is ever easy", is not very effective when trying to get people to adopt lifestyle changes.

"Try to reduce PUFA" is good and friendly advice. Having to be militant about it breeds a dogmatic stance that can lead to negative outcomes (be it an overly-restrictive diet, or just plain obsession over trying to do the diet "correctly").

I simply highlight the inconsistencies and uncertainties as factually as possible, state some practical considerations (which do not really differ much from the general consensus here), and let people make up their mind.

Accordingly, some people here who have found issues when trying to restrict PUFA too much, found that adding small amounts was helpful (eg: regular consumption of eggs). This is additional information used for better individualisation, not a gross disagreement with Peat.​


That is perfectly within the bounds of rational discourse, and perfectly relevant material for raypeatforum.com. Based on the feedback that I've gotten, I think most would agree with that sentiment.

.....
 

Drareg

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@tca300 It's fine to disagree. I've substantiated my points fairly well, and listed the uncertainties in place.

If I disagree with Ray, why post here?

(a) I will disagree with some of what Peat says, and will agree with more than I disagree. Some of the disagreements are on principles, and most are just on relatively minor practical tweaks.

Discussing those points of disagreement may help other people understand the topics discussed better, and make better decisions for themselves.

For example, my position on fructose has been that some is beneficial, and too much is bad, and the middle ground is probably to consume no more than what is needed to fill liver glycogen stores on a daily basis (generally about 50-75g of total fructose as a maximum). The reasoning is simply "try not exceed what your body needs", and I have gone into some details.

Then, it is up to the individual to experiment with what their ideal dose should be, hopefully now free from the dogma of either "fructose is the devil", or "more fructose means better metabolism", and eventually settle upon, "fructose in balance".

Similarly, the discussion regarding definitions of "starch", and being more discriminatory about "starch sources", has helped clarify what sources some people can and cannot tolerate. I view that as useful discussion that is beneficial as a whole.​


(b) I come here with a clinical bias. A statement like, "nothing in life is ever easy", is not very effective when trying to get people to adopt lifestyle changes.

"Try to reduce PUFA" is good and friendly advice. Having to be militant about it breeds a dogmatic stance that can lead to negative outcomes (be it an overly-restrictive diet, or just plain obsession over trying to do the diet "correctly").

I simply highlight the inconsistencies and uncertainties as factually as possible, state some practical considerations (which do not really differ much from the general consensus here), and let people make up their mind.

Accordingly, some people here who have found issues when trying to restrict PUFA too much, found that adding small amounts was helpful (eg: regular consumption of eggs). This is additional information used for better individualisation, not a gross disagreement with Peat.​


That is perfectly within the bounds of rational discourse, and perfectly relevant material for raypeatforum.com. Based on the feedback that I've gotten, I think most would agree with that sentiment.

.....

Everyone appreciates the discussion,we can all learn.

I think the points made to you was that Ray Peat is encouraging the things you speak of,I'm not sure how you are seeing it any other way ,he speaks in terms of ideals intertwined with how to apply this in the real world,he is getting PUFA in his diet albeit extremely low,he also encourages shellfish as you noted but to claim this is Ray sending out mixed signals is taking him out of context,essentially doing what many do with dietary advice,he fully comprehends the context people are in,pufa is extremely difficult to avoid,his only 2 supplements he recommended regularly were vitamin E and thyroid,this is a clear message imo. He recommends liver but warns it should be in moderation as it can suppress thyroid,if you view this statement without reading the guys other articles you will be confused,why recommend liver if your entire body of work is about supporting thyroid?

I understand you are encouraging balance but your criticisms are not clear without the quotes form Peat,I think you are reading members anecdotes but this isn't Peat,it's the interpretion of his work,most are not reading his articles and trying to understand what he is saying.

In relation to starch he spoke about certain potatoes in a KMUd interview,the baby/new potatoes being better because of their starch content,it wasn't just you who spotted this,he may have discussed rice also.
Peat recommends eggs.
 

tyw

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Everyone appreciates the discussion,we can all learn.

I think the points made to you was that Ray Peat is encouraging the things you speak of,I'm not sure how you are seeing it any other way ,he speaks in terms of ideals intertwined with how to apply this in the real world,he is getting PUFA in his diet albeit extremely low,he also encourages shellfish as you noted but to claim this is Ray sending out mixed signals is taking him out of context,essentially doing what many do with dietary advice,he fully comprehends the context people are in,pufa is extremely difficult to avoid,his only 2 supplements he recommended regularly were vitamin E and thyroid,this is a clear message imo. He recommends liver but warns it should be in moderation as it can suppress thyroid,if you view this statement without reading the guys other articles you will be confused,why recommend liver if your entire body of work is about supporting thyroid?

I understand you are encouraging balance but your criticisms are not clear without the quotes form Peat,I think you are reading members anecdotes but this isn't Peat,it's the interpretion of his work,most are not reading his articles and trying to understand what he is saying.

In relation to starch he spoke about certain potatoes in a KMUd interview,the baby/new potatoes being better because of their starch content,it wasn't just you who spotted this,he may have discussed rice also.
Peat recommends eggs.

And thus the response was specifically to tca300 ;)

.....
 

amethyst

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Well I think tyw has a lot of salient points that he has very succinctly brought out, in a diplomatic and thought provoking way, so thank you tyw. I appreciate what you have written :) And, I tend to agree with you that avoiding some form of PUFA is near next to impossible, (if I understand you correctly) as it is in virtually everything we eat but, we should make it a point to avoid the obvious sources of PUFA (something I am personally trying to do).

Also, I am not 100% convinced that some cultures do so badly with a larg(er) amount of PUFA better than other cultures. This is just my own opinion. For example, the Japanese. They eat a LOT of fish and seafood and soy products. Whereas, other cultures such as European ones, may do better with less Pufa. Something to think about no?

This might even fall into the category of certain blood types doing better with more or less PUFA. Something I've thought about. But that's another topic. Regardless, after reading some of Peat's dedicated research in this area, actively trying to avoid unnecessary PUFA in our food sources is a positive and healthy thing to do and something I will continue to try and pursue, as I am convinced it is a great detriment to me to be over PUFAsized.
 

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