How Could We Better Get The Word Out About PUFA?

Gone Peating

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There are many knowledgable and kind-hearted people on this forum that I am very grateful for.

I think at this point it would make sense to use everything we have learned to put out some kind of material that would be more accessible to the public to learn about the dangers of vegetable oil.

There's no doubt it's behind most of the diseases, and general unwellness that people are experiencing - they just don't know it. We are all lucky to have stumbled upon Peat's work.

I was thinking maybe we could promote the forum some way some how? Or maybe use another avenue like social media?
 

lampofred

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Don't have any ideas as of now but following in case someone comes up with something
 

PhilParma

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We don't know for sure that PUFA is the driving force behind most modern disease, we just think we know. Most people know that sugar is the cause of all disease. They don't doubt it, they just blame themselves for lacking the self-control to resist the siren song of sugar's sweet kiss. Many highly intelligent people believe that sugar is evil. What make health, nutrition, biology, etc. so interesting is that their complexity is so high that it renders them effectively mysterious. That's why so many people are religiously ideological about their particular health/wellness paradigm. It's highly complex, and also highly important. We don't know, but we feel we need to know, so we pretend that we do, in order to prevent the discomfort of psychological chaos.

I believe PUFA is the primary cause of modern disease. But I don't know. And I won't proselytize about things that I don't know. I've been avoiding PUFA for years and I have no plan to stop. If its avoidance is health giving, then I will continue to become more energized and vibrant, and people will notice. They will ask if I have a secret. I will say, "no. I do try to avoid vegetable oil because I believe it's harmful, but who knows if that's actually true..."

But that's just me. I do enjoy listening to people with genius IQ's discuss these things, but I don't have the intelligence to shed blood in that arena. I can only experiment on myself and lead (or fall) by example.
 

tankasnowgod

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There are many knowledgable and kind-hearted people on this forum that I am very grateful for.

I think at this point it would make sense to use everything we have learned to put out some kind of material that would be more accessible to the public to learn about the dangers of vegetable oil.

There's no doubt it's behind most of the diseases, and general unwellness that people are experiencing - they just don't know it. We are all lucky to have stumbled upon Peat's work.

I was thinking maybe we could promote the forum some way some how? Or maybe use another avenue like social media?

I don't think there is much point to what you are suggesting. I didn't exactly "stumble" upon Peat's work, I found it as I was researching health subjects I was interested in. I think that's how most people will do it. Unless you have a good grasp of mass communications, or a following in that regard, or are willing to learn more about mass communication and build a following, I don't think you will accomplish much.

Also, people don't get most of their exposure to high PUFA oils from buying the oils themselves. It's either from restaurants or processed foods. A better use of time would be to try and get those entities to avoid using high PUFA oils and return to things like tallow and coconut oil. Price and availability would be two major obstacles to overcome. Or campaign for an end to soy subsidies. All those would take a lot of work and effort, but so would the first option, if it were to be done effectively.
 

olive

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More important than telling people to stop consuming PUFA is getting people to be more active and eat less calories. PUFA is burned preferentially for fuel. Meaning if not eating in a constant caloric surplus, no PUFA will accumulate. Look at the bigger picture, the issue is people are sedentary and over consume empty calories.

Before I get attacked, ask yourself this: why can usain bolt each hundreds of grams of PUFA from McDonald’s and break world records while being in tip top shape but memebers of this forum who pedantically track PUFA intake claim that they get fat as soon as PUFA intake increases from 2g to 4g per day? And before you answer generics, remember we are on the Ray Peat forum.
 
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Hans

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More important than telling people to stop consuming PUFA is getting people to be more active and eat less calories. PUFA is burned preferentially for fuel. Meaning if not eating in a constant caloric surplus, no PUFA will accumulate. Look at the bigger picture, the issue is people are sedentary and over consume empty calories.

Before I get attacked, ask yourself this: why can usain bolt each hundreds of grams of PUFA from McDonald’s and break world records while being in tip top shape but memebers of this forum who pedantically track PUFA intake claim that they get fat as soon as PUFA intake increases from 2g to 4g per day? And before you answer generics, remember we are on the Ray Peat forum.
This made me chuckle. I agree. People would do better from just stressing less, sleeping better, moving more and lead more productive/creative lives. Once people become more conscious of the above to improve their health, they'd also focus more on eating healthier and more natural and when people become more in tune with their bodies they'll automatically avoid foods that make them feel bad.
 

Dave Clark

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More important than telling people to stop consuming PUFA is getting people to be more active and eat less calories. PUFA is burned preferentially for fuel. Meaning if not eating in a constant caloric surplus, no PUFA will accumulate. Look at the bigger picture, the issue is people are sedentary and over consume empty calories.

Before I get attacked, ask yourself this: why can usain bolt each hundreds of grams of PUFA from McDonald’s and break world records while being in tip top shape but memebers of this forum who pedantically track PUFA intake claim that they get fat as soon as PUFA intake increases from 2g to 4g per day? And before you answer generics, remember we are on the Ray Peat forum.
This may not be a good analogy, but look at parrots, they eat tons of PUFA and live long lives. From what I read, the parrots have a high body temperature and burn up the PUFA before it can get stored in their body. Heck, my parrots eat all kinds of seeds and stuff we would not eat, they don't get fat, and they will probably outlive me, so there may be something to that.
 

redsun

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This may not be a good analogy, but look at parrots, they eat tons of PUFA and live long lives. From what I read, the parrots have a high body temperature and burn up the PUFA before it can get stored in their body. Heck, my parrots eat all kinds of seeds and stuff we would not eat, they don't get fat, and they will probably outlive me, so there may be something to that.

Probably because they were designed to eat seeds and humans are not.
 

tankasnowgod

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PUFA is burned preferentially for fuel.

Haidut just posted some studies that show exactly the opposite, that PUFA is preferentially stored, while SFA and MUFA are preferentially burned for fuel. SFA / MUFA are preferentially oxidized, while PUFA are stored/accumulated – To Extract Knowledge from Matter

That also jives with the population wide data that shows that people get fatter as high PUFA oils displace traditional fats that are more saturated. Why didn't people turn into lean "PUFA burning beasts" with higher basal temps if it is preferentially used for fuel?

Before I get attacked, ask yourself this: why can usain bolt each hundreds of grams of PUFA from McDonald’s and break world records while being in tip top shape but memebers of this forum who pedantically track PUFA intake claim that they get fat as soon as PUFA intake increases from 2g to 4g per day? And before you answer generics, remember we are on the Ray Peat forum.

Um, when did Usian Bolt eat "hundreds of grams" of PUFA from McDonalds? In a single meal? Was he on Man Vs. Food in a very special episode?

Did he eat 999 grams of PUFA (the upper limit of hundreds of grams) over, say, a 3 year period? Because, if so, that would be less than 1g a day.

Without a source for this claim, it doesn't mean much.
 

boris

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More important than telling people to stop consuming PUFA is getting people to be more active and eat less calories. PUFA is burned preferentially for fuel. Meaning if not eating in a constant caloric surplus, no PUFA will accumulate. Look at the bigger picture, the issue is people are sedentary and over consume empty calories.

Before I get attacked, ask yourself this: why can usain bolt each hundreds of grams of PUFA from McDonald’s and break world records while being in tip top shape but memebers of this forum who pedantically track PUFA intake claim that they get fat as soon as PUFA intake increases from 2g to 4g per day? And before you answer generics, remember we are on the Ray Peat forum.

Thyroid: Therapies, Confusion, and Fraud
"Until the second world war, hypothyroidism was diagnosed on the basis of BMR (basal metabolic rate) and a large group of signs and symptoms. In the late 1940s, promotion of the (biologically inappropriate) PBI (protein-bound iodine) blood test in the U.S. led to the concept that only 5% of the population were hypothyroid, and that the 40% identified by "obsolete" methods were either normal, or suffered from other problems such as sloth and gluttony"

He has a story about his friend that went to the doctor around the time the tests were changed. His hypothyroid overweight friend was then told he's not hypothyroid, but just gluttonous.

We know that PUFA inhibits the thyroid. Peat is sedentary for the last decade and he's not overweight.

Also "calories are not calories". 500 calories from orange juice is not the same as 500 calories from fat.

Selye demonstrated that PUFA does no immediate damage in cells when a higher ratio of saturated fats is present. That means we preferentially use saturated fat that's why a ratio of more SAT to PUFA protects from the immediate effects of PUFA and stores them. The problem is then in stress situations when the stored PUFA gets released.
 

Dave Clark

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Probably because they were designed to eat seeds and humans are not.
Yes, the article I read said that they were designed to have normal body temperatures over 100 degrees which metabolize the seed oils before they get a chance to get stored. I made that point to sort of agree with Olive's assertion that if we burn it up and not store the PUFAs they would be less harm, by that theory.
 

Hans

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Haidut just posted some studies that show exactly the opposite, that PUFA is preferentially stored, while SFA and MUFA are preferentially burned for fuel. SFA / MUFA are preferentially oxidized, while PUFA are stored/accumulated – To Extract Knowledge from Matter
That study was in trout and I doubt it's the same in humans.

Selective release of human adipocyte fatty acids according to molecular structure.
"Conversely, the percentage of very-long-chain (20-22 carbon atoms) saturated and monounsaturated fatty acids was approx. 2 times lower in NEFA than in TAG. The relative mobilization (% in NEFA/% in TAG) of the most readily mobilized fatty acid (C20:5, n-3; 2.25) was more than 6-fold higher than that of the least readily mobilized (C22:1,n-11; 0.37). Relationships were found between the molecular structure of fatty acids and their mobilization rate. For a given chain length, the relative mobilization rate increased with increasing unsaturation, whereas for a given unsaturation, it decreased with increasing chain length. The relative mobilization rate for essential fatty acids decreased in the following order: C20:5,n-3>C20:4,n-6>C18:3,n-3>C18:2, n-6>C22:6,n-3. Interestingly, C20:5,n-3 and C20:4,n-6, which are respectively precursors of the 3- and 2-series of prostaglandins, were preferentially mobilized. It is concluded that fatty acids are selectively mobilized from human fat cells according to molecular structure, in full agreement with animal studies."

Net release of individual fatty acids from white adipose tissue during lipolysis in vitro: evidence for selective fatty acid re-uptake. - PubMed - NCBI
"Thus the greater the fatty acid re-uptake, the higher the proportion of polyunsaturated fatty acids and the lower the proportion of long-chain saturated and monounsaturated fatty acids in NEFA. Moreover, the relative mobilization (%NEFA/%TAG) of the least readily mobilized fatty acid (C(22:1,n-11)) was 6.2-fold lower than that of the most readily mobilized fatty acid (C(20:5,n-3)) under conditions of very low fatty acid re-uptake, and 14.8-fold lower under conditions of high fatty acid re-uptake, indicating a widening of the range of relative mobilizations."

Association between Plasma Nonesterified Fatty Acids Species and Adipose Tissue Fatty Acid Composition
"Mobilization studies were mostly performed in-vitro [12], in animals with induced lipolysis [13] or using venous-arterial differences of human AT, which indicated a preferential mobilization of PUFA [14], [15]."
"PUFA are preferentially mobilized from AT in in-vitro studies with adipocytes [12], in in-vivo studies in animals [13] and in humans [15]."

It's difficult to accurately determine which fats in most released and which is preferably oxidized because:
Association between Plasma Nonesterified Fatty Acids Species and Adipose Tissue Fatty Acid Composition
"These approaches do not reflect the relation of AT and pNEFA FA percentages, because the pNEFA pool is affected by a complex interaction of AT lipolysis [10], reincorporation of NEFA into AT triacylglycerols (TAG) [16], uptake of pNEFA by peripheral tissues, oxidation rates of individual FA [17], intracellular metabolism [18] and contribution of pNEFA derived from plasma TAG or phospholipid hydrolysis [19]."

"Increasing chain-length and increasing saturation negatively impact correlation coefficients. In previous studies, this has been ascribed to lower mobilization as well as lower clearance of SFA and MUFA, especially of 18∶0"

'The influence of flux to the different tissues may be confirmed by the significantly lower percentages of medium-chain FA 12∶0, 12∶1, 14∶0 and 14∶1, as these FA have a higher flux to tissue due to direct transport through cell membrane and rapid mitochondrial oxidation independently of the carnitine transport system "
Short chain fats are rapidly oxidized, but as the chain gets longer, it slows down, but increases with unsaturation.

"Additionally, the lower flux to tissue and elevated pNEFA levels may result in an increased (re-)uptake of pNEFA to AT which strengthen the correlation of SFA between pNEFA and AT in obese subjects"

It's not just lipolysis and fat oxidation that promote fat loss, but a decrease in fat uptake in adipose tissue. PUFAs increase lipogenesis, fat uptake and deposition in fat tissue.
Polyunsaturated fatty acid-rich diets: effect on adipose tissue metabolism in rats. - PubMed - NCBI
"These results indicate that enrichment of the diet with polyunsaturated fatty acids causes changes in adipose tissue metabolism that favour fat deposition. Different metabolic pathways were preferentially affected by each type of fatty acid used."

Lastly, on oxidation rates, in vivo (in rats though)
Differential oxidation of saturated and unsaturated fatty acids in vivo in the rat. - PubMed - NCBI
"The oxidation rates of lauric, myristic, palmitic, stearic, oleic, alpha-linolenic, linoleic, kappa-linolenic, dihomo-gamma-linolenic and arachidonic acids were studied by use of a radioisotope tracer technique in weanling rats at rest in a metabolism chamber over 24 h. Of the saturated fatty acids, lauric acid (12:0) was the most efficient energy substrate: the longer the chain length of the saturated fatty acids, the slower the rate of oxidation. Oleic acid (18:1) was oxidized at a remarkably fast rate, similar to that of lauric acid. Of the omega 6 essential fatty acids studied, linoleic acid (18:2 omega 6) was oxidized at a faster rate than any of its metabolites, with arachidonic acid (20:4 omega 6) being oxidized at the slowest rate. The rate of oxidation of gamma-linolenic acid (18:3 omega 3) was almost as fast as that of lauric and oleic acids."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6140086/
"Medium-chain saturated fatty acids (C6–C12), alpha-linolenic acid (ALA), oleic acid, and linoleic acid have particularly high oxidation rates compared to certain long-chain saturated fats such as palmitate (16:0) and stearate (18:0).1 In one study, the cumulative oxidation of different fats in humans over a nine-hour period from highest to lowest was laurate (41%), oleate (18%), palmitate (16%) and stearate (13%).2 In other words, long-chain saturated fats were less likely to be burned (lower oxidation rate) compared to laurate (found in coconut oil) and oleate (found in olive oil)."

Interestingly:
https://www.ncbi.nlm.nih.gov/pubmed/2615563
"Total and peroxisomal oxidation rates of palmitic, oleic and linoleic acid were 3-4 times higher than those of arachidonic and adrenic acid which had higher oxidation rates than those of lignoceric and erucic acid."
 

Aries

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Hans

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That study was in trout and I doubt it's the same in humans.

Selective release of human adipocyte fatty acids according to molecular structure.
"Conversely, the percentage of very-long-chain (20-22 carbon atoms) saturated and monounsaturated fatty acids was approx. 2 times lower in NEFA than in TAG. The relative mobilization (% in NEFA/% in TAG) of the most readily mobilized fatty acid (C20:5, n-3; 2.25) was more than 6-fold higher than that of the least readily mobilized (C22:1,n-11; 0.37). Relationships were found between the molecular structure of fatty acids and their mobilization rate. For a given chain length, the relative mobilization rate increased with increasing unsaturation, whereas for a given unsaturation, it decreased with increasing chain length. The relative mobilization rate for essential fatty acids decreased in the following order: C20:5,n-3>C20:4,n-6>C18:3,n-3>C18:2, n-6>C22:6,n-3. Interestingly, C20:5,n-3 and C20:4,n-6, which are respectively precursors of the 3- and 2-series of prostaglandins, were preferentially mobilized. It is concluded that fatty acids are selectively mobilized from human fat cells according to molecular structure, in full agreement with animal studies."

Net release of individual fatty acids from white adipose tissue during lipolysis in vitro: evidence for selective fatty acid re-uptake. - PubMed - NCBI
"Thus the greater the fatty acid re-uptake, the higher the proportion of polyunsaturated fatty acids and the lower the proportion of long-chain saturated and monounsaturated fatty acids in NEFA. Moreover, the relative mobilization (%NEFA/%TAG) of the least readily mobilized fatty acid (C(22:1,n-11)) was 6.2-fold lower than that of the most readily mobilized fatty acid (C(20:5,n-3)) under conditions of very low fatty acid re-uptake, and 14.8-fold lower under conditions of high fatty acid re-uptake, indicating a widening of the range of relative mobilizations."

Association between Plasma Nonesterified Fatty Acids Species and Adipose Tissue Fatty Acid Composition
"Mobilization studies were mostly performed in-vitro [12], in animals with induced lipolysis [13] or using venous-arterial differences of human AT, which indicated a preferential mobilization of PUFA [14], [15]."
"PUFA are preferentially mobilized from AT in in-vitro studies with adipocytes [12], in in-vivo studies in animals [13] and in humans [15]."

It's difficult to accurately determine which fats in most released and which is preferably oxidized because:
Association between Plasma Nonesterified Fatty Acids Species and Adipose Tissue Fatty Acid Composition
"These approaches do not reflect the relation of AT and pNEFA FA percentages, because the pNEFA pool is affected by a complex interaction of AT lipolysis [10], reincorporation of NEFA into AT triacylglycerols (TAG) [16], uptake of pNEFA by peripheral tissues, oxidation rates of individual FA [17], intracellular metabolism [18] and contribution of pNEFA derived from plasma TAG or phospholipid hydrolysis [19]."

"Increasing chain-length and increasing saturation negatively impact correlation coefficients. In previous studies, this has been ascribed to lower mobilization as well as lower clearance of SFA and MUFA, especially of 18∶0"

'The influence of flux to the different tissues may be confirmed by the significantly lower percentages of medium-chain FA 12∶0, 12∶1, 14∶0 and 14∶1, as these FA have a higher flux to tissue due to direct transport through cell membrane and rapid mitochondrial oxidation independently of the carnitine transport system "
Short chain fats are rapidly oxidized, but as the chain gets longer, it slows down, but increases with unsaturation.

"Additionally, the lower flux to tissue and elevated pNEFA levels may result in an increased (re-)uptake of pNEFA to AT which strengthen the correlation of SFA between pNEFA and AT in obese subjects"

It's not just lipolysis and fat oxidation that promote fat loss, but a decrease in fat uptake in adipose tissue. PUFAs increase lipogenesis, fat uptake and deposition in fat tissue.
Polyunsaturated fatty acid-rich diets: effect on adipose tissue metabolism in rats. - PubMed - NCBI
"These results indicate that enrichment of the diet with polyunsaturated fatty acids causes changes in adipose tissue metabolism that favour fat deposition. Different metabolic pathways were preferentially affected by each type of fatty acid used."

Lastly, on oxidation rates, in vivo (in rats though)
Differential oxidation of saturated and unsaturated fatty acids in vivo in the rat. - PubMed - NCBI
"The oxidation rates of lauric, myristic, palmitic, stearic, oleic, alpha-linolenic, linoleic, kappa-linolenic, dihomo-gamma-linolenic and arachidonic acids were studied by use of a radioisotope tracer technique in weanling rats at rest in a metabolism chamber over 24 h. Of the saturated fatty acids, lauric acid (12:0) was the most efficient energy substrate: the longer the chain length of the saturated fatty acids, the slower the rate of oxidation. Oleic acid (18:1) was oxidized at a remarkably fast rate, similar to that of lauric acid. Of the omega 6 essential fatty acids studied, linoleic acid (18:2 omega 6) was oxidized at a faster rate than any of its metabolites, with arachidonic acid (20:4 omega 6) being oxidized at the slowest rate. The rate of oxidation of gamma-linolenic acid (18:3 omega 3) was almost as fast as that of lauric and oleic acids."

Good Fats versus Bad Fats: A Comparison of Fatty Acids in the Promotion of Insulin Resistance, Inflammation, and Obesity
"Medium-chain saturated fatty acids (C6–C12), alpha-linolenic acid (ALA), oleic acid, and linoleic acid have particularly high oxidation rates compared to certain long-chain saturated fats such as palmitate (16:0) and stearate (18:0).1 In one study, the cumulative oxidation of different fats in humans over a nine-hour period from highest to lowest was laurate (41%), oleate (18%), palmitate (16%) and stearate (13%).2 In other words, long-chain saturated fats were less likely to be burned (lower oxidation rate) compared to laurate (found in coconut oil) and oleate (found in olive oil)."

Interestingly:
Total and peroxisomal oxidation of various saturated and unsaturated fatty acids in rat liver, heart and m. quadriceps. - PubMed - NCBI
"Total and peroxisomal oxidation rates of palmitic, oleic and linoleic acid were 3-4 times higher than those of arachidonic and adrenic acid which had higher oxidation rates than those of lignoceric and erucic acid."
I should add that during exercise, saturated fat, especially the medium chain ones, are being mobilized and oxidized.
Priority use of medium-chain fatty acids during high-intensity exercise in cross-country skiers
"We observed that the level of capric acid (С10:0) (p = 0.013) rose considerably (60%) at cycle load (Fig. 2) and after various skiing competition distances (p = 0.001) (Figs. 3, and 4). We also noted a significant, twofold increase in lauric acid (С12:0) concentrations at the peak of cycle load (p = 0.008) and upon completion of 1.3-km (p = 0.004) and 15-km (p = 0.011) races. Furthermore, we observed a trend for increasing myristic (C14:0) acid concentrations from 30 to 70% relative to baseline values after competition (p > 0.05)."

"Octanoate (C10:0) contributes 50% of the acetyl-CoA pool in the heart and soleus muscle under normal physiological conditions."

"No significant differences in long-chain saturated FA (palmitic and stearic acid) content relative to baselines during exercise tests or competitions were revealed."
 

MatheusPN

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More important than telling people to stop consuming PUFA is getting people to be more active and eat less calories. PUFA is burned preferentially for fuel. Meaning if not eating in a constant caloric surplus, no PUFA will accumulate. Look at the bigger picture, the issue is people are sedentary and over consume empty calories.

Before I get attacked, ask yourself this: why can usain bolt each hundreds of grams of PUFA from McDonald’s and break world records while being in tip top shape but memebers of this forum who pedantically track PUFA intake claim that they get fat as soon as PUFA intake increases from 2g to 4g per day? And before you answer generics, remember we are on the Ray Peat forum.
At 5'3, 161,5 cm and 47,5 to 52 kg if I ate less than 7000 or 65000 kcal I would lose weight quite quickly, why? Diet! Being sedentary or not, created very little difference. Now at 55,5 kg, I changed my diet, eating only 2750 to 3500 kcal because now is tough to eat more, I gained the max and most rapidly in my life

One reason why is because Usain uses steroids. Nate Diaz: "Everyone's on steroids". Or search for: Devon Larratt about Steroids in Armwresling
 
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