4 Grams Of PUFA A Day Is Not A Threshold

[Amazoniac]

That's because essentially there is none: the more PUFA in the diet, the more predisposed an animal is to cancer up until a point where it isn't safe to venture.

Raj's opinion is below, skip to it if you want to.

I went through his articles on fats, trying to locate the review that he had in mind when he said:

https://raypeatforum.com/community/threads/kmud-phosphate-and-calcium-metablolism-2012.6392/
"They looked at various animal studies to see where starts the influence of polyunsaturated fats in increasing the cancer mortality; it's with 4 g per day for the average human bodyweight."​

Ray Peat

"In the 1940s, some of the toxic effects of fish oil (such as testicular degeneration, softening of the brain, muscle damage, and spontaneous cancer) were found to result from an induced vitamin E deficiency. Unfortunately, there isn't much reason to think that just supplementing vitamin E will provide general protection against the unsaturated fats. The half-life of fats in human adipose tissue is about 600 days, meaning that significant amounts of previously consumed oils will still be present up to four years after they have been removed from the diet. [4] According to Draper, et al., [5] enrichment of the tissues with highly unsaturated fatty acids results in an increase in lipid peroxidation in vivo even in the presence of normal concentrations of vitamin E. Fasting for more than 24 hours also results in an increase in MDA excretion, implying that lipolysis is associated with peroxidation of the fatty acids released."

"In a detailed study of the carcinogenicity of different quantities of unsaturated fat, Ip, et al., tested levels ranging from 0.5% to 10%, and found that the cancer incidence varied with the amount of "essential oils" in the diet. Some of their graphs make the point very clearly: [52] [Below]

This suggests that the optimal EFA intake might be 0.5% or less."

"Butter and coconut oil contain significant amounts of the short and medium-chain saturated fatty acids, which are very easily metabolized,[60] inhibit the release of histamine,[39] promote differentiation of cancer cells,[61] tend to counteract the stress-induced proteins,[62] decrease the expression of prolactin receptors, and promote the expression of the T3 (thyroid) receptor. [63] (A defect of the thyroid receptor molecule has been identified as an "oncogene," responsible for some cancers, as has a defect in the progesterone receptor.)"

"It has shown that it is probably impossible to experience a detectable deficiency of linoleic acid outside of the laboratory setting,[69]"

"Essential for Liver Damage: Both experimental and epidemiological studies have shown that dietary linoleic acid is required for the development of alcoholic liver damage.[75] Animals fed tallow and ethanol had no liver injury, but even 0.7% or 2.5% linoleic acid with ethanol caused fatty liver, necrosis, and inflammation. Dietary cholesterol at a level of 2% was found to cause no harm,[76] but omitting it entirely from the diet caused leakage of amino-transferase enzymes. This effect of the absence of cholesterol was very similar to the effects of the presence of linoleic acid with ethanol."

"If a certain small amount of dietary PUFA is essential for reproduction, but for no other life function, then it is analogous to the brief "estrogen surge," which must quickly be balanced by opposing hormones. The present approach to contraception through estrogen-induced miscarriage might give way to fertility regulation by diet. A self-actualizing pro-longevity diet, low in PUFA, might prolong our characteristically human condition of delayed reproductive maturity, and, if PUFA are really essential for reproduction, unsaturated vegetable oils could temporarily be added to the diet when reproduction is desired." [!]​

While not being able to find that source, there's the following recurrent reference [52] which one of the authors is another ultra-boss: Clement Ip.

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

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

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

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

.
"These observations suggest that there may be a requirement for polyunsaturated fat in mammary tumorigenesis, which is not satisfied by fats such as coconut oil or beef tallow, but can be provided by adding 3% sunflower seed oil to diets containing these fats."

If the proportion of linoleic acid in butter and coconut fat is about 2%, then, since the diets used in the experiment had 20% of their weight consisting of fat, that would be 0.4% of linoleic acid.​

.
"A recent paper by Cave and Jurkowski (6) also showed that when the polyunsaturated lipid content (corn oil) of the diet fell below 3% there was a decrease in tumor incidence in rats treated with N-methyl-N-nitrosourea. It is thought that linoleate may be the essential fatty acid primarily responsible for the tumor-promoting effect of unsaturated fat (14)."

"[..]the objective of the present study was not to determine whether dietary fat affects the initiation or promotion stage of carcinogenesis, but rather if the tumorigenic response depended on the EFA intake[.]"

"The diets contained 20% of fat by weight, with each varying in the composition of fats blended to achieve different levels of linoleate. All other ingredients, namely casein, dextrose, vitamin and salt mixes, and Alphacel, were held constant. The composition of the 20% fat synthetic diet has been described in detail in a previous publication (17)."

[17] Similarity between trans Fat and Saturated Fat in the Modification of Rat Mammary Carcinogenesis

Spoiler: Details

..collected not only from [17] but also from different experiments by them (such as (a)). Since they keep using the same method, every aspect is almost identical.

Initial weight: 180 g or so
Final weight: 320-360 g (more for those that consumed more P and U and F and A)
Food consumption a day: 15 g

g/100 g diet

Fat: 20
Caseid: 23.53
Dextrose: 44.71
AIN-76 mineral mix: 4.12
AIN-76 vitamin mix: 4.12
Alphacel (fiber): 5.88
DL-methionine: 0.35 (tut)
Choline bitartrate: 0.23

Calories/g diet: 4.53

% Calories:
20.8 Proteid
39.7 Fat
39.5 Carbohydrate

--
The carcinogen used was:
7,12-dimethylbenz(a)anthracene (DMBA)

.
"In Experiment 1, the fat blends consisted of a mixture of palm oil and corn oil in different proportions, such that when added at 20% by weight to the diet, it yielded increasing levels of linoleate (EFA): 2.0, 4.1, 6.5, or 12.1 %. In Experiment 2, the fat blends consisted of a mixture of coconut oil and corn oil to give a wide range of EFA in the diet: 0.5, 1.1, 1.7, 2.2, 3.5, 4.4, 8.5, or 11.5%."

"[..]the risk of a rat developing a tumor appears to increase with increasing intake of EFA."

Here are graphs showing the effects based on linoleic acid content of the diet:

Spoiler

It starts to count from week 15 because that's when they doubled the carcinogen dose because up until then the results were too clustered.

.
And these was at the end of the experiment, when they were able to include nonpalpable tumors that were only discovered after auto and psy:

Spoiler

.
"It can be seen that mammary tumorigenesis increased proportionately with the amount of dietary EFA from 0.5 to 4.4%, at which point there was a definite break in the pattern, suggesting that the requirement of EFA is quantifiable, with the critical inflection occurring around 4%."

This is the amount that maximizes the response to a certain carconigen.​

.
"[After doubling the carcinogen dose,] a pattern seemed to emerge in which rats fed the 0.5 and 1.1% EFA diets were gaining weight at a slightly slower rate than the rest."

"Surprisingly, we found that tissue PGE [Portland General Electric] levels were essentially insensitive to EFA intake, even at the lower range of the titration curve, in which susceptibility to cancer risk was most responsive."

"The lack of a correlation between mammary gland PGE levels and dietary EFA intake observed in this study does not necessarily mean that linoleate does not affect tumorigenesis via stimulation of prostaglandin synthesis. However, it does indicate that the interaction is probably far more complex than originally envisioned."

"Kidwell ef al. (12) and Wicha ef al. (23) have reported interesting data, showing that polyunsaturated fatty acids can influence the growth of normal rat mammary gland, as well as DMBA-induced mammary carcinoma in cell culture. These investigators found that supplementation of a hormone-enriched medium with linoleic acid increased thymidine incorporation and reduced cell-doubling time. Saturated fatty acids, such as stearic acid, had the opposite effect, thus inhibiting mitotic activity of these cells. A recent paper by Aylsworth et al. (1) suggests that polyunsaturated fatty acids could promote tumorigenesis by inhibition of intercellular communication. While the present study does not address the mechanism by which linoleate acts to enhance neoplastic development, it does reinforce the message that any working hypothesis should be consistent with the in vivo data that there is a linoleate (EFA) requirement for the maximal expression of mammary tumorigenesis."​

.
[52(3)] https://link.springer.com/article/10.1007/BF02533866

"[In previous experiments, polyunsaturated] fats such as cottonseed oil and sunflowerseed oil nearly doubled the number of tumors in rats treated with DMBA, when fed as 20% (w/w) of the diet, whereas fats such as coconut oil, butter or tallow, fed at the same level, produced little if any increase in tumor yield over that obtained with a low-fat diet. However, there did not seem to be a direct correspondence between degree of unsaturation and mammary tumor yield. For example, rats fed lard or olive oil developed about the same number of tumors as those fed corn oil or soybean oil, although the latter oils are much more highly unsaturated (13). A similar observation was made by Dayton et al. (14), who found that a high oleic safflower oil enhanced tumorigenesis in DMBA-treated rats to the same extent as a high-linoleic safflower oil."

Spoiler

.
"Rats treated with DMBA and fed a high fat diet containing 20% sunflowerseed oil developed about twice as many mammary tumors as those fed either a low fat diet containing 3% sunflowerseed oil or high fat diets containing 20% coconut oil or beef tallow. These results were predictable on the basis of our earlier observations (13). However, when 3% sunflowerseed oil was fed with 17% of either coconut oil or tallow, the yield of tumors increased to the level obtained by feeding 20% sunflowerseed oil (Fig. 1)."

"These findings indicate that there is a requirement for polyunsaturated fat in mammary tumorigenesis, which is not satisfied by fats such as coconut oil or beef tallow, but can be provided by adding 3% sunflowerseed oil to these fats. This may explain why fats such as lard and olive oil are nearly as effective as more unsaturated fats in promoting mammary tumorigenesis, since they would provide as much polyunsaturated fatty acid (linoleic acid) as 3% sunflowerseed oil, when fed as 20% (w/w) of the diet. The results of Dayton et al. (14) could also be explained on this basis, since the high oleic safflower oil used in their experiments would provide an even higher level of linoleic acid than either lard or olive oil. Our experiments also demonstrate that, in addition to the need for polyunsaturated fat, there must also be an overall requirement for a high fat diet, since neither 3% sunflowerseed oil in the present experiments nor 5% corn oil in earlier studies (13) were capable by themselves of enhancing the tumor yield."

"If these observations in the animal model are applicable to human populations, one might expect to see a relationship between human breast cancer mortality and the type, as well as the amount of fat consumed in different counties."

"[..]it seems probable that most human diets supply polyunsaturated fat at the level needed to demonstrate the promoting effect of dietary fat in the animal model. The observed positive correlation between dietary fat and breast cancer mortality in humans is therefore more likely to be related to total fat intake, which also influences mammary tumorigenesis in animals, as discussed above. The observation that human breast cancer mortality shows the best correlation with total fat intake and no correlation with vegetal fat intake (15,20) is thus in accord with our recent observations on the animal model. This has helped to restore our confidence that the model does provide information of relevance to the etiology of human breast cancer."​

.
While that's interesting, it isn't what our shaman had in the minds during the interview. There and fore I decided to put it on hold and contact him to know if he remembered the source:

Hi Ray,
In a KMUD interview, the theme was 'Calcium and Phosphate Metabolism' (2012), you mentioned the following:
"They looked at various animal studies to see where starts the influence of polyunsaturated fats in increasing the cancer mortality; it's with 4 g per day for the average human bodyweight."
What is the publication that you were referring to?

There were lots of experiments with different oils, all similar to Clarence Ip’s.

Cancer Res. 1985 May;45(5):1997-2001.
Requirement of essential fatty acid for mammary tumorigenesis in the rat.
Ip C, Carter CA, Ip MM.
In an attempt to determine the requirement of essential fatty acid for
dimethylbenz(a)anthracene-induced mammary tumorigenesis, rats were fed diets
containing different levels of linoleate: 0.5, 1.1, 1.7, 2.2, 3.5, 4.4, 8.5, or
11.5%. Each diet contained 20% of fat by weight, with varying amounts of coconut
oil and corn oil added to achieve the desired levels of linoleate. Mammary
tumorigenesis was very sensitive to linoleate intake and increased
proportionately in the range of 0.5 to 4.4% of dietary linoleate. Regression
analysis indicated that a breakpoint occurred at 4.4%, beyond which there was a
very poor linear relationship, suggesting the possibility of a plateau. From the
intersection of the regression lines in both the upper and lower ranges, the
level of linoleate required to elicit the maximal tumorigenic response was
estimated to be around 4%. The differences in tumor yield could not be correlated
with changes in prostaglandin E concentration in the mammary fat pads of normal
animals maintained on similar diets, suggesting that linoleate may act by some
other mechanism to stimulate mammary tumorigenesis.

Thanks.

Before sending you the message I went through most of your references in oily articles, so I happened to read that one (quite interesting).
But I'm curious if you can remember that specific publication. The reason for my insistence is because the '4 g' figure appears very often online and no one really knows for sure the source.

A variety of studies showed that the proportion that’s effective is consistent across species, and that’s based on body weight. I don’t think there is a threshold, but that’s where the statistics have shown a distinct linear increase beginning. I’m confident that two grams would also contribute to the development of cancer, but with a lower probability.

(a) Fat and essential fatty acid in mammary carcinogenesis (Clement Ip)

"It is thought that linoleate may be the essential fatty acid (EFA) primarily responsible for the tumor-promoting effect of unsaturated fatty acids."

"In the text, the terms linoleate and EFA are used interchangeably, because from a nutritional standpoint as well as from the basis of the experimental design, linoleate is the major source of EFA in the diet."​

"Carroll (16) was the first to document that rats treated with DMBA developed fewer mammary tumors when fed a closed-formula commercial chow diet compared with those fed a purified diet containing a comparable level of fat."

"Although the enhancing effect of fat was expressed in rats fed either the natural-ingredient or purified diets, the tumorigenic response at each fat level was much attenuated in rats maintained on the natural-ingredient diet compared with those given the purified diet. Animals on the basal NIH-07 diet developed half as many tumors as those on the 5%-fat purified diet. This differential was sustained for the 10% and 20% fat levels. In summary, rats fed a natural-ingredient diet were found to be less sensitive to carcinogenesis even in the presence of a high-fat intake."

Spoiler

.
"Results of the present study confirm the conclusion of Carroll and Hopkins (12) that EFA is required for the maximal expression of mammary neoplasia."

"Once the EFA requirement for optimal tumor expression is met, further enhancement of development would depend on the amount and not on the type of dietary fat."

"Kritchevsky et al (19) suggested that caloric intake may be a greater determinant than dietary fat in influencing the development of tumors. Caloric restriction during the postinitiation phase of DMBA-induced mammary carcinogenesis markedly suppresses the formation of tumors despite the high-fat content of the diet and increased fat consumption of the food restricted animals. Similarly, Clinton et al (20) showed that in addition to the response to dietary fat, mammary tumorigenesis is increased in rats with greater ad libitum food consumption. In conclusion, the enhancing effect of fat on mammary tumorigenesis should be viewed in the context of a requirement for EFA and caloric intake as well as composition of the other dietary ingredients."​

.
So the practical considerations are: to restrict PUFA intake the most in a way that doesn't compromise nutrition and to treat your body like a temple giving it the pure building blocks it needs.

 

[HDD]

+1
Thank you for pulling this all together like this!

 

[Tenacity]

Excellent thread, thank you very much. Puts a spanner in the works for egg consumption, at least. So, it doesn't depend on the ratio of saturated to unsaturated fat?

 

[Hugh Johnson]

At least in humans the liver is capable of getting rid of PUFA. This might not happen in mice, they have a different metabolism. So it might not be necessary to have zero intake of PUFA to induce a deficiency.

 

[Amazoniac]

+1
Thank you for pulling this all together like this!

Unfortunately Ramón couldn't make the recallings on the specific review that he had in mind.

Excellent thread, thank you very much. Puts a spanner in the works for egg consumption, at least. So, it doesn't depend on the ratio of saturated to unsaturated fat?

These were acute inductions. Since our tissues reflect the composition of our diets, I guess it does matter. If someone's diet is already low in them, the amounts stored might still provide enough to put the person in the range of increased probability.

Some authors comment that a higher fat diet is more concerned with promotion rather than initiation.

In one of the experiments, coconut oil + linoleic acid gave the worst outcome. Perhaps this is because if the animal is being injured by a carcinogen, the diet is providing enough PUFA, then, as a consequence the liver might become burdened. The fats in coconut that were supposed to be used for energy and now accumulating in it and impairing its function and affecting everything else. Another possibility is that once they're consumed in the body, what you're left with is only a fraction of the total saturated fat content; so you might end up with a ratio much greater than those 1.5-2% of linoleic acid and no longer the same amount of fat protect it.

--
A part that suggests that there is a minimum requirement was this:

"These observations suggest that there may be a requirement for polyunsaturated fat in mammary tumorigenesis, which is not satisfied by fats such as coconut oil or beef tallow, but can be provided by adding 3% sunflower seed oil to diets containing these fats."

But it isn't supported by this:

(1)

"[In previous experiments, polyunsaturated] fats such as cottonseed oil and sunflowerseed oil nearly doubled the number of tumors in rats treated with DMBA, when fed as 20% (w/w) of the diet, whereas fats such as coconut oil, butter or tallow, fed at the same level, produced little if any increase in tumor yield over that obtained with a low-fat diet.

But also the following graphs (from the original post):

(2)

Spoiler

(3)

Spoiler

How likely it is that it just drops to nothing as you experiment with the lowest range that wasn't tested?

Ps.: the percentages of fat compositions of diets discussed here were not in relation to total calories, but to food weight. This was more precise for them since they were working with purified diets but might be confusing when trying to find relatable doses.

 

[Amazoniac]

Oh craρ, forgot to comment that the reason for creating this thread was not to encourage unhealthy habits, but to start a discussion on the arbitrary figure that circulates quite often on the forum. I'm calling it arbitrary because I never found an objective discussion on it.

--
I'm not completely sure if the following approach is correct, let me know if it's not.

The values were given based on weight of the diet, we have more relevant information in the 'Details' box.

- Rats weighted 180 g.
- Ate 15 g of food daily.
- 0.5% (min linoleic acid) and 4% (maximized linoleic acid) of that is: 75 mg and 600 mg.
- 75 mg/180 g = 420 mg/kg | 600 mg/180 g = 3300 mg/kg
- Humanoid equivalent amount: (420/6.2) 70 mg/kg | (3300/6.2) 530 mg/kg
- 70 kg adult: 5 g/d | 37 g/d

Coconut and dairy fat are about 2% linoleic acid.
- 20% (fat composition) * 2% (linoleic acid content of that): 0.4%
We don't have to repeat everything over again. Since the amount that maximizes is 4% and now we have 0.4%, we can just divide our final value of 37 by 10, which leaves us with what Rajesh refers to as a reasonable amount of 3.7 g/d.

 

[Amazoniac]

And this is what I mean by the title:

Spoiler

It's not like on one side of the border you're safe and, as soon as you cross it, you're all of the sudden on the dangerous territory.
My bad for the snobbish commas.

 

[Tenacity]

It's like what Ray has said about radiation: PUFA are toxic at any dose. Is that right?

 

[Waynish]

I wonder how much PUFA is actually in pork bone broth. There's often plenty of fat on the meat that's left on the bone. And even after siphoning off the floating fat, I wonder how much is dispersed through the broth. Ideas?

 

[vulture]

What I get here is that we shall minimize fat intake because, in whole milk for example, there's always some PUFA and no matter how much it's like just taking poison in small vs tiny amounts?
And another interest thing is that a lot of the benefit from PUFA reduction might be more evident about 2 years after reduction of PUFA in diet?
Of course there are other more immediate benefits Peating, but PUFA related benefits might take a lot more. What about non-fat diet for a month which was proposed here?

 

[Waynish]

What I get here is that we shall minimize fat intake because, in whole milk for example, there's always some PUFA and no matter how much it's like just taking poison in small vs tiny amounts?
And another interest thing is that a lot of the benefit from PUFA reduction might be more evident about 2 years after reduction of PUFA in diet?
Of course there are other more immediate benefits Peating, but PUFA related benefits might take a lot more. What about non-fat diet for a month which was proposed here?

I don't think so. Where is the study saying fats always cause problems. For example, well timed coconut oil, butter, or beef? From experience we can say cutting out all fat is orthorexia.

 

[Amazoniac]

It's like what Ray has said about radiation: PUFA are toxic at any dose. Is that right?

From what I understand, anything beyond the requirement is unnecessary stress. But once the diet is consistently low in PUFA, other factors are more important than varying a few grams or so.

What I get here is that we shall minimize fat intake because, in whole milk for example, there's always some PUFA and no matter how much it's like just taking poison in small vs tiny amounts?
And another interest thing is that a lot of the benefit from PUFA reduction might be more evident about 2 years after reduction of PUFA in diet?
Of course there are other more immediate benefits Peating, but PUFA related benefits might take a lot more. What about non-fat diet for a month which was proposed here?

The main concern is polyunsaturated oils, the safe fats are just that. If the person has been eating a great deal of PUFA for a while, it's worth considering that what's being released from storage might be enough to make the person more vulnerable for some years (those 600 days is the average time that it's reduced in half).

If you read this thread, you can find many habits that can challenge our views. They commented above about calorie intake having an effect and I never heard of a person that lived long who seemed to eat copious amounts of foods.
But the point is that it isn't as simple as PUFA restriction, although it clearly makes animals more resistant; however this can be undermined by a poor diet that often goes along with restrictive habits.

What's really important is to not try to scroll down the text with keyboard arrow when you left the text cursor on other pages.

 

[Kartoffel]

From what I understand, anything beyond the requirement is unnecessary stress. But once the diet is consistently low in PUFA, other factors are more important than varying a few grams or so.

I recently experienced that just a little more PUFA can make a tremendous difference. I usually eat one whole egg per day, and for about two weeks I started eating 3. One morning I was suddenly horrified because I noticed a black spot on one of my finger where there had only been clear skin before. It looked like a cancerous mole. When I checked the rest of my body, I saw that there was another black spot on one of my moles on my chest. After I while I remembered what Peat mentioned about lipofuscin and people getting age spots when they eat a lot of PUFA. Long story short: I stopped eating any eggs and cut out every source of PUFA, and after 3 days both black spots simply fell of, leaving a tiny dent. I'm pretty sure that the relatively small quantitiy of extra PUFA from the egg yolks caused some lipofuscin to accumulate and migrate to those two places on my skin.

 

[Amazoniac]

I recently experienced that just a little more PUFA can make a tremendous difference. I usually eat one whole egg per day, and for about two weeks I started eating 3. One morning I was suddenly horrified because I noticed a black spot on one of my finger where there had only been clear skin before. It looked like a cancerous mole. When I checked the rest of my body, I saw that there was another black spot on one of my moles on my chest. After I while I remembered what Peat mentioned about lipofuscin and people getting age spots when they eat a lot of PUFA. Long story short: I stopped eating any eggs and cut out every source of PUFA, and after 3 days both black spots simply fell of, leaving a tiny dent. I'm pretty sure that the relatively small quantitiy of extra PUFA from the egg yolks caused some lipofuscin to accumulate and migrate to those two places on my skin.

That's interesting. I could notice effects from subtle changes when my skin was more susceptible to a and c and n and e.

 

[ecstatichamster]

I recently experienced that just a little more PUFA can make a tremendous difference. I usually eat one whole egg per day, and for about two weeks I started eating 3. One morning I was suddenly horrified because I noticed a black spot on one of my finger where there had only been clear skin before. It looked like a cancerous mole. When I checked the rest of my body, I saw that there was another black spot on one of my moles on my chest. After I while I remembered what Peat mentioned about lipofuscin and people getting age spots when they eat a lot of PUFA. Long story short: I stopped eating any eggs and cut out every source of PUFA, and after 3 days both black spots simply fell of, leaving a tiny dent. I'm pretty sure that the relatively small quantitiy of extra PUFA from the egg yolks caused some lipofuscin to accumulate and migrate to those two places on my skin.

Wow. Quite interesting. You could be right. Dr. Peat is probably right as usual.

 

[Mito]

I recently experienced that just a little more PUFA can make a tremendous difference. I usually eat one whole egg per day, and for about two weeks I started eating 3. One morning I was suddenly horrified because I noticed a black spot on one of my finger where there had only been clear skin before. It looked like a cancerous mole. When I checked the rest of my body, I saw that there was another black spot on one of my moles on my chest. After I while I remembered what Peat mentioned about lipofuscin and people getting age spots when they eat a lot of PUFA. Long story short: I stopped eating any eggs and cut out every source of PUFA, and after 3 days both black spots simply fell of, leaving a tiny dent. I'm pretty sure that the relatively small quantitiy of extra PUFA from the egg yolks caused some lipofuscin to accumulate and migrate to those two places on my skin.

I thought lipofuscin was brown not black?

 

[Dobbler]

Eat SAFA dominant diet, low PUFA foods, exception is eggs. You already doing better than 99,9% of population. Take things that increase lifespan = gelatin, anti-cortisol stuff etc. Be lean and build some muscle. Sunbath and do grounding.
If you do all those daily then there is nothing to worry. If you wanna go to extreme then do a long fast or eat 0 fat diet.

 

[Peatful]

I thought lipofuscin was brown not black?

Yes, and that it is underneath the skin not growing out from the skin? @Kartoffel

 

[Kartoffel]

Yes, and that it is underneath the skin not growing out from the skin? @Kartoffel

Well, maybe it wasn't lipofuscin, that was just a guess. I couldn't think of anything else that might appear and disappear so quickly. Maybe I'll ask Ray about it. He talked about how he had moles developing dark growths the size of a small cherry that disappeared when he used DHEA/vitamin A applications. I regret that I didn't make any pictures, I didn't think of it then because it was a little scarry.

 

[Peatful]

Well, maybe it wasn't lipofuscin, that was just a guess. I couldn't think of anything else that might appear and disappear so quickly. Maybe I'll ask Ray about it. He talked about how he had moles developing dark growths the size of a small cherry that disappeared when he used DHEA/vitamin A applications. I regret that I didn't make any pictures, I didn't think of it then because it was a little scarry.

Yes, if you do indeed find out from Peat repost and let us know. Thx @Kartoffel