Is Omega-3 Fish Oil Bad?

[Amazoniac]

This is interesting:
Certain Fatty Acids Require Additional Steps for Degradation - Biochemistry - NCBI Bookshelf

 

[Obi-wan]

I am starting to think that isolated oil consumption as a whole is bad, no matter the oil...so disappointed in olive oil

 

[MrSmart]

I am starting to think that isolated oil consumption as a whole is bad, no matter the oil...so disappointed in olive oil

Unsaturated fat are a bad idea, besides the trace amounts you find in animal products and plants. Only coconut oil is safe.

 

[Obi-wan]

Unsaturated fat are a bad idea, besides the trace amounts you find in animal products and plants. Only coconut oil is safe.

Agree

 

[Frankdee20]

If I get it through food like delicious shrimp, that’s one thing. Every time I supplement though, severe anxiety and agitation ensue. Must be increasing acetylcholine too much

 

[MrSmart]

If I get it through food like delicious shrimp, that’s one thing. Every time I supplement though, severe anxiety and agitation ensue. Must be increasing acetylcholine too much

No, it's because of the problem of all supplements. You are missing vital components in the food itself that is either a coactivator, a cosuppressor, or a stabilizer.

Like eating nuts, it's generally okay in moderate amounts, because the omega-6s are stabilized by Vitamin E. The calcium and iron in plant food is chelated by phytates, the omega-3 in salmon is stabilized by astaxanthin, and so forth. This is why whole foods are important to get the vitamins or minerals you want.

 

[Frankdee20]

No, it's because of the problem of all supplements. You are missing vital components in the food itself that is either a coactivator, a cosuppressor, or a stabilizer.

Like eating nuts, it's generally okay in moderate amounts, because the omega-6s are stabilized by Vitamin E. The calcium and iron in plant food is chelated by phytates, the omega-3 in salmon is stabilized by astaxanthin, and so forth. This is why whole foods are important to get the vitamins or minerals you want.

This is definitely a fact, but most isolated supplements don’t elicit strong anxiety like that. Leads me to believe EPA/DHA/AHA supplements are psycho active.

 

[MrSmart]

This is definitely a fact, but most isolated supplements don’t elicit strong anxiety like that. Leads me to believe EPA/DHA/AHA supplements are psycho active.

Because fish-oil taken alone, will peroxide almost completely within a couple of hours, and very little will actually be stored and metabolized properly into beneficial anti-inflammatory lipids, if it has not been rancid before ingestion already. This creates a cascade of stress and peroxide byproduct inflammation resulting in excitatory neural signaling and death, through arachnoid acid metabolism and cytokine storms.

But eating fish? It will be stored and metabolized appropriately when the need arises, exactly like how omega-3 is stored and metabolized properly in the living fish itself.

This can be somewhat mitigated by eating Algae oil instead, keeping it in the fridge, and taking vitamin E and lecithin with it.

 

[Frankdee20]

Because fish-oil taken alone, will peroxide almost completely within a couple of hours, and very little will actually be stored and metabolized properly into beneficial anti-inflammatory lipids, if it has not been rancid before ingestion already. This creates a cascade of stress and peroxide byproduct inflammation resulting in excitatory neural signaling and death, through arachnoid acid metabolism and cytokine storms.

But eating fish? It will be stored and metabolized appropriately when the need arises, exactly like how omega-3 is stored and metabolized properly in the living fish itself.

This can be somewhat mitigated by eating Algae oil instead, keeping it in the fridge, and taking vitamin E and lecithin with it.

Interesting

 

[boxers]

Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial

 

[boxers]

Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease. - PubMed - NCBI

 

[ecstatichamster]

I don’t really believe meta studies are helpful in most cases because of the ability to be very biased by throwing away good research and only paying attention to research confirming the PI’s opinion.

But this one says:

MAIN RESULTS:
We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias.

Trials were of 12 to 72 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet.

Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on

all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence),

cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs),

cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence),

coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs),

stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials)

or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs).

There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses - LCn3 probably makes little or no difference to CHD event risk.

All evidence was of moderate GRADE quality, except as noted.

Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and it may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence).

However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence), and probably reduces risk of CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs), and arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT).

Effects on stroke are unclear.

Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection.

LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes.

There were no dose or duration effects in subgrouping or meta-regression.

There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, although LCn3 slightly reduced triglycerides and increased HDL. ALA probably reduces HDL (high- or moderate-quality evidence).

AUTHORS' CONCLUSIONS:
This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia.

——

I have not read the full study. I think that as Dr. Peat has said, and experience has shown in my own life, w-3 can help temporarily counter some of the immediately bad effects of w-6. The so-called “ratios” help reduce short term inflammatory effects of w-6.

But in the longer run, they are both very bad. It is hard to find studies that show w-3 is bad because of the huge bias in the political medical research industry.

 

[Kartoffel]

I don’t really believe meta studies are helpful in most cases because of the ability to be very biased by throwing away good research and only paying attention to research confirming the PI’s opinion.

But this one says:

MAIN RESULTS:
We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias.

Trials were of 12 to 72 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet.

Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on

all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence),

cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs),

cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence),

coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs),

stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials)

or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs).

There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses - LCn3 probably makes little or no difference to CHD event risk.

All evidence was of moderate GRADE quality, except as noted.

Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and it may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence).

However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence), and probably reduces risk of CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs), and arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT).

Effects on stroke are unclear.

Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection.

LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes.

There were no dose or duration effects in subgrouping or meta-regression.

There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, although LCn3 slightly reduced triglycerides and increased HDL. ALA probably reduces HDL (high- or moderate-quality evidence).

AUTHORS' CONCLUSIONS:
This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia.

——

I have not read the full study. I think that as Dr. Peat has said, and experience has shown in my own life, w-3 can help temporarily counter some of the immediately bad effects of w-6. The so-called “ratios” help reduce short term inflammatory effects of w-6.

But in the longer run, they are both very bad. It is hard to find studies that show w-3 is bad because of the huge bias in the political medical research industry.

If you look at Nanjii's work, for example, it seems as though the ω-3 are worse than the ω-6 fatty acids. Liver damage, or degree of cirrhosis, is more severe in rats fed fish oil than in those fed corn oil. ω-3 are a bit like morphine - they dull the pain but they make things even worse.

 

[FitnessMike]

That's true, but that doesn't make it essential. To my knowledge no experiment has demonstrated it's essentiality, and it's essential status is mostly based on it's theoretical role in theoretical membrane structures. The human studies supposedly showing it's beneficial role in some rare disorders, in which it (DHA) is thought to be lacking, are worse than most highschool science projects.

im dummie but isnt it true that we got plenty of DHA in the brain?

 

[not_James_Bond]

@FitnessMike have a read of this The Great Fish Oil Experiment

 

[frannybananny]

This is from Ray's website, I would start here to learn about fish oil and PUFAs, and read his other articles.
The Great Fish Oil Experiment

I know this is an old thread but thank you for the Fish Oil link ... I read the whole thing since I was just getting ready to ask about fish oil and this article is invaluable information. Thanks Dave, and thank you Ray Peat!

 

[Dave Clark]

I can't recall who posted these here on the forum, but credit to them for compiling these to peruse:
Functional Performance Systems has many studies using a search for the term "oil":

oil – Search Results – Functional Performance Systems (FPS)



How Vegetable Oils Replaced Animal Fats in the American Diet

How Vegetable Oils Replaced Animal Fats in the American Diet – Functional Performance Systems (FPS)

Fish Oils Increase Intestinal Permeability

Fish Oils Increase Intestinal Permeability – Functional Performance Systems (FPS)

Coconut Oil and Metabolism in Pigs

Coconut Oil and Metabolism in Pigs – Functional Performance Systems (FPS)

Ray Peat, PhD Quotes on Coconut Oil

Ray Peat, PhD Quotes on Coconut Oil – Functional Performance Systems (FPS)

Fish Oil and Lipid Peroxidation

https://www.functionalps.com/blog/2012/01/10/fish-oil-and-lipid-peroxidation/

Fish Oil Toxicity

https://www.functionalps.com/blog/2011/11/26/fish-oil-toxicity/

Fats and Oils: The significance of temperature

https://www.functionalps.com/blog/2011/11/02/fats-and-oils-the-significance-of-temperature/

PUFA, Fish Oil, and Alzheimers

https://www.functionalps.com/blog/2011/02/12/pufa-and-brain-degeneration/

Polyunsaturated oils (PUFA) and cancer

https://www.functionalps.com/blog/2011/01/28/polyunsaturated-oils-pufa-and-cancer/

Polyunsaturating America: Mazola’s Marketing

https://www.functionalps.com/blog/2016/02/21/polyunsaturating-america-mazolas-marketing/

Vitamin E Needs Increases with PUFA Consumption and Greater Unsaturation

https://www.functionalps.com/blog/2...th-pufa-consumption-and-greater-unsaturation/

Inflammatory C-Reactive Protein (CRP)

https://www.functionalps.com/blog/2014/06/08/inflammatory-c-reactive-protein-crp/

The Observations of George Catlin

https://www.functionalps.com/blog/2013/09/11/the-observations-of-george-catlin/

PUFA, Ketones, and Sugar Restriction Promote Tumor Growth

https://www.functionalps.com/blog/2...s-and-sugar-restriction-promote-tumor-growth/

PUFA Promote Stress Response; Saturated Fats Suppress Stress Response

https://www.functionalps.com/blog/2...esponse-saturated-fats-blunt-stress-response/

Unsaturated Fats, Oxidative Stress, and Atherosclerosis

https://www.functionalps.com/blog/2012/10/26/unsaturated-fats-oxidative-stress-and-atherosclerosis/

Phospholipases, PUFA, and Inflammation

https://www.functionalps.com/blog/2012/10/03/phospholipase-a2-pla2-prostaglandins-and-inflammation/

Dietary PUFA Reflected in Human Subcutaneous Fat Tissue

https://www.functionalps.com/blog/2...a-reflected-in-human-subcutaneous-fat-tissue/

PUFA Kill Thymocytes

https://www.functionalps.com/blog/2012/07/04/pufa-kill-thymocytes/

PUFA, Inflammation, and Rheumatoid Arthritis

https://www.functionalps.com/blog/2012/06/28/pufa-inflammation-and-rheumatoid-arthritis/

Israeli Paradox: High Omega -6 Diet Promotes Disease

https://www.functionalps.com/blog/2012/06/28/israeli-paradox-high-omega-6-diet-promotes-disease/

PUFA, Estrogen, Obesity and Early Onset of Puberty

https://www.functionalps.com/blog/2012/06/23/pufa-estrogen-and-early-onset-of-puberty/

PUFA Decrease Cellular Energy Production

https://www.functionalps.com/blog/2012/06/15/pufa-decrease-cellular-energy-production/

Unsaturated Fats and Age Pigment

https://www.functionalps.com/blog/2012/04/23/unsaturated-fats-and-age-pigment/

Toxicity of Stored PUFA

https://www.functionalps.com/blog/2012/04/22/fatty-acid-composition-of-diet-reflected-in-fat-tissue/

Fats and AGEs: PUFAs Are Even Worse than Fructose

https://www.functionalps.com/blog/2012/04/03/fats-and-ages-pufas-are-even-worse-than-fructose/

Unsaturated Fats and Heart Damage

https://www.functionalps.com/blog/2012/01/31/unsaturated-fats-and-heart-damage/

Brain Swelling Induced by Polyunsaturated Fats (PUFA)

https://www.functionalps.com/blog/2011/12/22/brain-swelling-induced-by-polyunsaturated-fats-pufa/

 

[Dr. B]

I don’t really believe meta studies are helpful in most cases because of the ability to be very biased by throwing away good research and only paying attention to research confirming the PI’s opinion.

But this one says:

MAIN RESULTS:
We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias.

Trials were of 12 to 72 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet.

Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on

all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence),

cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs),

cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence),

coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs),

stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials)

or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs).

There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses - LCn3 probably makes little or no difference to CHD event risk.

All evidence was of moderate GRADE quality, except as noted.

Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and it may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence).

However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence), and probably reduces risk of CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs), and arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT).

Effects on stroke are unclear.

Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection.

LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes.

There were no dose or duration effects in subgrouping or meta-regression.

There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, although LCn3 slightly reduced triglycerides and increased HDL. ALA probably reduces HDL (high- or moderate-quality evidence).

AUTHORS' CONCLUSIONS:
This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia.

——

I have not read the full study. I think that as Dr. Peat has said, and experience has shown in my own life, w-3 can help temporarily counter some of the immediately bad effects of w-6. The so-called “ratios” help reduce short term inflammatory effects of w-6.

But in the longer run, they are both very bad. It is hard to find studies that show w-3 is bad because of the huge bias in the political medical research industry.

Vitamin d somehow has those similar effects to fish oil... both are known to raise serotonin and I think both mimic and increase cortisol too...

 

[yerrag]

Vitamin d somehow has those similar effects to fish oil... both are known to raise serotonin and I think both mimic and increase cortisol too...

Do you know how vitamin D raises serotonin and cortisol? Does your take on vitamin D apply to the vitamin D endogenously produced by exposure to sunlight from cholesterol as well as to the supplementary vitamin D3?

 

[Dr. B]

Do you know how vitamin D raises serotonin and cortisol? Does your take on vitamin D apply to the vitamin D endogenously produced by exposure to sunlight from cholesterol as well as to the supplementary vitamin D3?

Only the oral supplements not the sunlight... sunlight does lots of things...