Effect Of Omega-3 Dosage On Cardiovascular Outcomes

[b555]

https://www.mayoclinicproceedings.org/article/S0025-6196(20)30985-X/fulltext

“
Results
A total of 40 studies with a combined 135,267 participants were included. Supplementation was associated with reduced risk of MI (relative risk [RR], 0.87; 95% CI, 0.80 to 0.96), high certainty number needed to treat (NNT) of 272; CHD events (RR, 0.90; 95% CI, 0.84 to 0.97), high certainty NNT of 192; fatal MI (RR, 0.65; 95% CI, 0.46 to 0.91]), moderate certainty NNT = 128; and CHD mortality (RR, 0.91; 95% CI, 0.85 to 0.98), low certainty NNT = 431, but not CVD events (RR, 0.95; 95% CI, 0.90 to 1.00). The effect is dose dependent for CVD events and MI.
Conclusion
Cardiovascular disease remains the leading cause of death worldwide. Supplementation with EPA and DHA is an effective lifestyle strategy for CVD prevention, and the protective effect probably increases with dosage.”

 

[S-VV]

Uh oh, time to link to the fish oil great experiment article and the cherry picked studies.

 

[Tristan Loscha]

It is completely plausible, EPA is quite opposed to the actions of Arachidonic Acid activity. The thing about fish oil is just the ease of exploitation of the source material, properly fed animals contain a lot of "fish oil" in their adipose tissues. RP lumped the different pufa's together, for a lack of data during his formative years. SAT : MONO ratio 1 : 1, O6 : O3 1 : 1.

 

[mangoes]

I’m not really disputing it coz I don’t know but did yall read the footnotes?

 

[jb116]

This is why it's important to read all the way through...

"Potential Competing Interests: Dr Bernasconi is an employee of the Global Organization for EPA and DHA Omega-3s (GOED), a 501(c)6 not-for profit trade association. GOED’s goals are to increase consumption of omega-3s to adequate levels around the world and to ensure that the industry is producing quality omega-3 products that consumers can trust.

Dr Wiest has been a guest speaker with travel sponsored by DSM Nutritional Products and the Global Organization for EPA and DHA Omega-3s (GOED); and has received funding from GOED to conduct a meta-analysis on omega-3 fatty acids.

Dr Lavie has been a speaker for Amarin Corporation on Vascepa, has consulted for DSM Nutritional Products, and has made an omega-3 educational video at the American Heart Association meeting on November 14, 2016, for the Global Organization for EPA and DHA Omega-3s and also gave a presentation at a GOED-hosted omega-3 conference in Barcelona, Spain, in February 2020.

The remaining authors report no potential competing interests.

Grant Support: This study was supported by a grant from the Global Organization for EPA and DHA Omega-3s (GOED), Salt Lake City, UT."

 

[Tristan Loscha]

hahaha, that is very severe. Point still stands: Animals have the fats of fish oil if they are properly fed, and the ratios do matter.

 

[Atman]

If there is something left after correcting for conflict of interest, then it is probably the old "health conscious people have better health"-effect, which is also known from the various vegetarian/vegan studies.

Personally I just don't feel well after eating a big meal of fatty, PUFA-rich fish, so I tend to believe Peat's position is closer to the truth, especially if I consider the enormous interest in selling fish oil pills and farmed salmon.
Historically there was also no access to fatty sea food for the vast majority of humans. It doesn't make sense that we require large amounts of these fats for optimal development.

Aquaculture production of salmonids in tonnes
1950–2010

 

[schultz]

Omega-3 is very susceptible to lipid peroxidation, especially at body temperature. Does anybody dispute this? Personally I would feel more comfortable getting the same heart protective effect with something like aspirin, which also has other benefits as well.

 

[Tristan Loscha]

Omega-3 is very susceptible to lipid peroxidation, especially at body temperature. Does anybody dispute this? Personally I would feel more comfortable getting the same heart protective effect with something like aspirin, which also has other benefits as well.

When pufa gets incorporated, the phospholipid structure they get embedded in grants higher stability, half life of incorporated DHA in human brain is over 2.5 years. Do you think we do not have structural requirements for pufa?

 

[S-VV]

Do you think we do not have structural requirements for pufa?

Structure and function are interdependent at every level... except when we dont like them

 

[Tristan Loscha]

Structure and function are interdependent at every level... except when we dont like them

Do you think Peat makes a compelling case against the structural requirements of pufa? I only see listings of unfavorable attributes and the fragility of them, but no real proof of interchangeability of them with monounsaturates or saturates. Female Cats do not have live births without arachidonic acid, and male cats get the testicular atrophy if exposed to linoleic acid or arachidonic acid depletion, which was also observed in rodent models, and the other described defects. That they only lacked B6 is just conjecture at best.

 

[S-VV]

Do you think Peat makes a compelling case against the structural requirements of pufa?

Absolutely no. He says PUFA == bad, and that PUFA deficiency is really a b6 deficiency. Case closed. However, he wont even consider that PUFA peroxidation is probably due to low antioxidant status.

Its clear that the omega 6: omega 3 ratio matters a lot. The effect of structurally different prostaglandin series are evident. Estrogen differs from Testosterone by a single aromatisation reaction, but ray stresses that nuance is important and they have almost opposite effects due to the apparently small changes in structure. The same reasoning is applied to progesterone vs progestins. However, he doesn't even think of applying this structural reasoning to the multitude of prostanoids that have widely different structures, leading to oftentimes opposite effects, revealing that the prostanoid/leukotriene/thromboxane system is a complex and homeostatic mechanism.

Finally, DHA really is needed for membrane fluidity. Of course, mentioning the membrane as even minimally relevant is heresy, contradicting 60+ years of established research and going down rabbit holes that lead nowhere, for example, denying the importance of receptors. Never mind the studies showing that a single amino-acid substitution in most selective ion channels or pumps renders them non-funtional or leads to a loss of selectivity. And dont ever mention the established channelopathies like cystic fibrosis that been conclusively traced to several SNPs or deletions.

The PUFA affair reminds me of ray saying estrogen is almost always bad, peaters take an ai (as i did) and then joints go to hell. What a surprise, who would have thought that a metabolite that the body spends resources producing has an important physiologic role!

I dont want to seem like a mindless hater, I really appreciate peat for his different perspectives, and especially the ray peat forum for allowing productive debate.

On a personal note, I have tried most of peats suggestions, after carefully reading almost every article, and results have been lackluster to negative, except for pregnenolone.

 

[Tristan Loscha]

Absolutely no. He says PUFA == bad, and that PUFA deficiency is really a b6 deficiency. Case closed. However, he wont even consider that PUFA peroxidation is probably due to low antioxidant status.

Its clear that the omega 6: omega 3 ratio matters a lot. The effect of structurally different prostaglandin series are evident. Estrogen differs from Testosterone by a single aromatisation reaction, but ray stresses that nuance is important and they have almost opposite effects due to the apparently small changes in structure. The same reasoning is applied to progesterone vs progestins. However, he doesn't even think of applying this structural reasoning to the multitude of prostanoids that have widely different structures, leading to oftentimes opposite effects, revealing that the prostanoid/leukotriene/thromboxane system is a complex and homeostatic mechanism.

Finally, DHA really is needed for membrane fluidity. Of course, mentioning the membrane as even minimally relevant is heresy, contradicting 60+ years of established research and going down rabbit holes that lead nowhere, for example, denying the importance of receptors. Never mind the studies showing that a single amino-acid substitution in most selective ion channels or pumps renders them non-funtional or leads to a loss of selectivity. And dont ever mention the established channelopathies like cystic fibrosis that been conclusively traced to several SNPs or deletions.

The PUFA affair reminds me of ray saying estrogen is almost always bad, peaters take an ai (as i did) and then joints go to hell. What a surprise, who would have thought that a metabolite that the body spends resources producing has an important physiologic role!

I dont want to seem like a mindless hater, I really appreciate peat for his different perspectives, and especially the ray peat forum for allowing productive debate.

On a personal note, I have tried most of peats suggestions, after carefully reading almost every article, and results have been lackluster to negative, except for pregnenolone.

A good and fair critique. Very well.

 

[schultz]

When pufa gets incorporated, the phospholipid structure they get embedded in grants higher stability, half life of incorporated DHA in human brain is over 2.5 years. Do you think we do not have structural requirements for pufa?

I think we can handle them to a certain extent, as evidenced by people consuming such things consistently. But these things don't remain in storage for one thing. They can be released as FFA into the oxygen and iron rich blood. The mere fact that we can find highly damaging breakdown products of these fats, linked to dozens of degenerative diseases, tells me that they are not stable inside the body. Even if it's just 1% of the consumed fats.

I should note that omega-3 is a bit more tricky to study regarding its breakdown products as it is reduced to smaller aldehydes, many of which we may not have discovered yet.

Omega-6 is not stable in the body and it's more stable than omega-3.

Lipofuscin is the hallmark of aging. Just take a look at what it is composed of.

 

[PxD]

https://www.mayoclinicproceedings.org/article/S0025-6196(20)30985-X/fulltext

“
Results
A total of 40 studies with a combined 135,267 participants were included. Supplementation was associated with reduced risk of MI (relative risk [RR], 0.87; 95% CI, 0.80 to 0.96), high certainty number needed to treat (NNT) of 272; CHD events (RR, 0.90; 95% CI, 0.84 to 0.97), high certainty NNT of 192; fatal MI (RR, 0.65; 95% CI, 0.46 to 0.91]), moderate certainty NNT = 128; and CHD mortality (RR, 0.91; 95% CI, 0.85 to 0.98), low certainty NNT = 431, but not CVD events (RR, 0.95; 95% CI, 0.90 to 1.00). The effect is dose dependent for CVD events and MI.
Conclusion
Cardiovascular disease remains the leading cause of death worldwide. Supplementation with EPA and DHA is an effective lifestyle strategy for CVD prevention, and the protective effect probably increases with dosage.”

If you have a, say, 10% chance of MI a RR of 0.87 means omega-3 supplementation drops the risk to 8.7%. This might be meaningful across a very large population but from an individual perspective I find the power of this effect to be fairly modest IMO, even if it is statistically significant.

 

[lampofred]

EPA is like statins. Lowers heart disease risk but proportionately raises cancer risk.

DHA is poison.

 

[Daft]

O3 may do good, but it looks like vitamin e still needed to prevent oxidation of tissue omega 3:

Relationship between vitamin E requirement and polyunsaturated fatty acid intake in man: a review - PubMed

Vitamin E is the general term for all tocopherols and tocotrienols, of which alpha-tocopherol is the natural and biologically most active form. Although gamma-tocopherol makes a significant contribution to the vitamin E CONTENT in foods, it is less effective in animal and human tissues, where...

pubmed.ncbi.nlm.nih.gov

"a calculation of the vitamin E requirement, using recent nutritional intake data, shows that a reduction in total fat intake with a concomitant increase in PUFA consumption, including EPA and DHA, will result in an increased amount of vitamin E required."

and

Vitamin E function and requirements in relation to PUFA - PubMed

Vitamin E (α-tocopherol) is recognised as a key essential lipophilic antioxidant in humans protecting lipoproteins, PUFA, cellular and intra-cellular membranes from damage. The aim of this review was to evaluate the relevant published data about vitamin E requirements in relation to dietary PUFA...

pubmed.ncbi.nlm.nih.gov