Omega-3 Deficiency In Psychiatric Disease, Fish Oil Opinions?

Sobieski

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Stay away from fish oil. If you feel you must consume some form of long chain omega 3, I recommend eating lean white fish (cod, haddock etc) as this will contain very small amounts that is enough to supply the supposed amounts our body 'needs'. I can tell you first hand that fish oil stopped my joint aches and pains... temporarily; then they came back worse. Repeated the cycle over and over because this was before I found Peat. Moral of the story; fish oil is toxic.
 

GutFeeling

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My infant formula was powdered cow milk with dha and fish oil. I had such a bad reaction that my family thought I was dying. After change to pure cow milk everything is alright.
 

ATP

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I do remember reading a study a while ago which was arguing that there was a correlation between a lack of arachidonic acid and mental illness, I can’t recall the specifics.

Which is ironic to think that a lack of pro inflammatory substances could be cause a of mental illness.
 
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TreasureVibe

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I hope anyone knows, what can be a substitute for the cheap coconut oil that @Anabolic suggested, as it does work!! But it gives my relative acne. He hasn't been online for 2 months so I hope someone else can tell!

His suggestions do work!!
 

LegendeLic

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as far as I know ray argues that omega 3 and such are not essential because the body can produce mead acid... but what if in some persons for whatever reason the mechanism of mead acid production is hindered? on those people might benefit from low amounts of omega3 for example? i mean it would be better to why the mead acid production isn't working and how to fix that... ... genes can be activated/deactivated Identification of genes and pathways involved in the synthesis of Mead acid (20:3n-9), an indicator of essential fatty acid deficiency. - PubMed - NCBI
so might be when the autoimmune disease is triggered or on those genes for mead acid aren't on.
 

Motif

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Fish oil is recommended by people on the basis of its DHA content, a large lipid with six double‐bonds found in the brain. This is absolutely essential as is demonstrated by those having Zellweger's syndrome. However, we don't need to consume DHA to have it in our brains; most animals and over 99% of people can simply make it themselves from the precursor α-linolenic acid, which is found in leaves and grass‐fed cheese.

Beta‐carotene is also found in leaves and vitamin A in cheese, should that be the argument for fish oil.

I personally don't think its worth taking. It is smelly, oxidized, and the high vitamin A + PUFA content of CLO can give a person liver damage. If someone is depressed, I think things like lotus stamens and vitamin D would be better—and safer. A person could perhaps even grow poppies.. .


High vitamin A is bad for the liver?
Damn
 

benaoao

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Just don’t go over an average of 1000iu of retinol per day. If you have a tin of cod liver every week it’ll be alright.

Fish oil / algae DHA are indeed an oxidized scam.
 

Travis

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as far as I know ray argues that omega 3 and such are not essential because the body can produce mead acid... but what if in some persons for whatever reason the mechanism of mead acid production is hindered? on those people might benefit from low amounts of omega3 for example? i mean it would be better to why the mead acid production isn't working and how to fix that... ... genes can be activated/deactivated Identification of genes and pathways involved in the synthesis of Mead acid (20:3n-9), an indicator of essential fatty acid deficiency. - PubMed - NCBI
so might be when the autoimmune disease is triggered or on those genes for mead acid aren't on.

Mead acid is synthesized upon ω−6 'deficiency,' yet it is impossible to avoid all ω−3 fatty acids. Without small amounts of DHA (22∶6ω−3), or its ubiquitous precursor α-linolenic acid (18∶3ω−3), we would surely die. That is not to say that we should be eating large amounts of these, only that they are the truly the only 'essentially fatty acids.' All ω−9 fatty acids—such as oleic (18∶1ω−9) and Mead acids (20∶3ω−9)—can be synthesized via stearate, and there is no good reason to ever consume ω−6 fatty acids.

Omega−6 fatty acids are in no way essential, a mythology that had arisen mostly because the original 1940s studies did not discern between α-linolenic acid (18∶3ω−3) and γ-linolenic acid (18∶3ω−6). I will make the case that the skin problems observed were not an omega−6 deficiency nor a B vitamin deficiency, but simply due to increased evapotranspiration consequent of decreased skin lipid desaturation. Some experimenters had even eliminated the possibility of B vitamin deficiency via supplementation, and greatly increased water consumption had been noted in experimental mice.
 

Kartoffel

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Fish oil is recommended by people on the basis of its DHA content, a large lipid with six double‐bonds found in the brain. This is absolutely essential as is demonstrated by those having Zellweger's syndrome.

Can you please elaborate on why or how people with Zellweger's prove that DHA is essential?
 

Travis

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Can you please elaborate on why or how people with Zellweger's prove that DHA is essential?

Because they have profound cholesterol ingression in the brain—visualized via MRI as 'white matter' in the 'grey matter'—and have IQ's under 70. While you may be able to actually survive for some having cell membranes composed of only ω−9 fatty acids, this represents such a pathology that ω−3 fatty acids should be considered essential. Only small amounts are needed for DHA synthesis however, amounts so small as to be unavoidable. The real danger is consuming so much ω−6 fatty acids that DHA elongation enzymes are inhibited, raising the requirement and causing a mild form of Zellweger's. Arachidonic acid (20∶4ω−6) is not as effective as DHA in excluding sterols from the cell membrane, and the enhanced potency of its eicosanoid derivatives represent a pathology of an entirely different nature. I think the best science indicates that trace amounts of ω−3 fatty acids are needed, but also that we can rest assured that ω−6 fatty acids are still 100% unnecessary and entirely inimical.
 

Kartoffel

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Because they have profound cholesterol ingression in the brain—visualized via MRI as 'white matter' in the 'grey matter'—and have IQ's under 70. While you may be able to actually survive for some having cell membranes composed of only ω−9 fatty acids, this represents such a pathology that ω−3 fatty acids should be considered essential. Only small amounts are needed for DHA synthesis however, amounts so small as to be unavoidable. The real danger is consuming so much ω−6 fatty acids that DHA elongation enzymes are inhibited, raising the requirement and causing a mild form of Zellweger's. Arachidonic acid (20∶4ω−6) is not as effective as DHA in excluding sterols from the cell membrane, and the enhanced potency of its eicosanoid derivatives represent a pathology of an entirely different nature. I think the best science indicates that trace amounts of ω−3 fatty acids are needed, but also that we can rest assured that ω−6 fatty acids are still 100% unnecessary and entirely inimical.

Ok, but I don't see how Zellwegers disease proves that DHA is essential, because to my knowledge nobody has demonstrated that DHA deficiency causes Zellweger's nor that supplementation of it significantly, or consistently, improves the symptoms of the disease. Just because Zellwegers people can not synthesize C22:6n-3 because of their defective peroxisomes doesn't necessarily mean that the disease or it's symptoms can be attributed to the "deficiency".
 

Travis

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Ok, but I don't see how Zellwegers disease proves that DHA is essential, because to my knowledge nobody has demonstrated that DHA deficiency causes Zellweger's...

There are review articles on Zellweger's disease.
 

Kartoffel

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There are review articles on Zellweger's disease.

You have a particular one in mind? Most rat experiments and human trials I have seen show DHA to be ineffective. The papers by Martinez et al. that people cite most often, and which supposedly show that DHA improves myelination and other things in Zellwegers, (1996) use no control groups and often change many other variables.

"Treatment has been always accompanied by a nutritious diet, normal for the age, in order to provide all the necessary nutrients and avoid a polyunsaturated fatty acid (PUFA) imbalance." (Martinez 2001)
Docosahexaenoic acid therapy in peroxisomal diseases: results of a double-blind, randomized trial.
Neurology. 2010 Aug 31;75(9):826-30
Paker AM1, Sunness JS, Brereton NH, Speedie LJ, Albanna L, Dharmaraj S, Moser AB, Jones RO, Raymond GV.

OBJECTIVES:
Peroxisome assembly disorders are genetic disorders characterized by biochemical abnormalities, including low docosahexaenoic acid (DHA). The objective was to assess whether treatment with DHA supplementation would improve biochemical abnormalities, visual function, and growth in affected individuals.

METHODS:
This was a randomized, double-blind, placebo-controlled trial conducted at a single center. Treatment groups received supplements of DHA (100 mg/kg per day). The primary outcome measures were the change from baseline in the visual function and physical growth during the 1 year follow-up period.

RESULTS:
Fifty individuals were enrolled and randomized. Two were subsequently excluded from study analysis when it was determined that they had a single enzyme disorder of peroxisomal beta oxidation. Thirty-four returned for follow-up. Nine patients died during the trial of their disorder, and 5 others were lost to follow-up. DHA supplementation was well tolerated. There was no difference in the outcomes between the treated and untreated groups in biochemical function, electroretinogram, or growth. Improvements were seen in both groups in certain individuals.

CONCLUSIONS:
DHA supplementation did not improve the visual function or growth of treated individuals with peroxisome assembly disorders.

CLASSIFICATION OF EVIDENCE:
This interventional study provides Class II evidence that DHA supplementation did not improve the visual function or growth of treated individuals with peroxisome assembly disorders during an average of 1 year of follow-up in patients aged 1 to 144 months.


 

Travis

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Most rat experiments and human trials I have seen show DHA to be ineffective.

Most? I suppose you hadn't actually bothered to read the study you'd linked.

'In previous open studies [7,8], it had been stated that DHA supplementation was associated with improvements in vision and growth of these children.' ―Parker

[7.] Martinez M. "Docosahexaenoic acid: a new therapeutic approach to peroxisomal-disorder patients—experience with two cases." Neurology (1993)
[8.] Martinez M. "Restoring the DHA levels in the brains of Zellweger patients." J Mol Neurosci (2001)

Now which rat experiments exactly had you been referring to?
 

Kartoffel

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Most? I suppose you hadn't actually bothered to read the study you'd linked.

'In previous open studies [7,8], it had been stated that DHA supplementation was associated with improvements in vision and growth of these children.' ―Parker

[7.] Martinez M. "Docosahexaenoic acid: a new therapeutic approach to peroxisomal-disorder patients—experience with two cases." Neurology (1993)
[8.] Martinez M. "Restoring the DHA levels in the brains of Zellweger patients." J Mol Neurosci (2001)

Now which rat experiments exactly had you been referring to?

I just mentioned source number [8] above. They supplemented the children with lots of nutrients and DHA, and had no control group. That's no evidence that DHA does anything for Zellwegers. It could have been, and probably was, one of the many other nutrients, or maybe the children would have seen the same improvement without any intervention over time. You can't tell without a control group. Source number [7] is a case study with two (!) subjects, of course no controls. That's also no evidence. That's why the paper I cited talks about an association.
This one that was published in nature is one of the studies I had in mind.

Lab Invest. 2000 Jan;80(1):31-5.
Docosahexaenoic acid deficit is not a major pathogenic factor in peroxisome-deficient mice.
Janssen A1, Baes M, Gressens P, Mannaerts GP, Declercq P, Van Veldhoven PP.


Docosahexaenoic acid (DHA), a major component of membrane phospholipids in brain and retina, is profoundly reduced in patients with peroxisome biogenesis disorders (Zellweger syndrome). Supplementing newborn patients with DHA resulted in improved muscular tone and visual functions. The purpose of this study was to investigate (a) whether DHA levels were also reduced in newborn PEX5 knockout mice, the mouse model of Zellweger syndrome that we recently generated; (b) whether these levels could be normalized by supplying DHA; and (c) whether this results in longer survival. The DHA concentration in brain of newborn PEX5-/- mice was reduced by 40% as compared with levels in normal littermates; in liver, no differences were noticed. The daily administration of 10 mg of DHA-ethyl ester (EE) to pregnant heterozygous mothers during the last 8 days of gestation resulted in a normalization of brain DHA levels in Zellweger pups. However, no clinical improvement was observed in these pups, and the neuronal migration defect was unaltered. These data suggest that the accretion of DHA in the brain at the end of embryonic development is not only supported by the maternal supply but also depends on synthesis in the fetal brain. Furthermore, the DHA deficit does not seem to be a major pathogenic factor in the newborn Zellweger mice.
 

Travis

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That's no evidence that DHA does anything for Zellwegers.
Yes there is, here are some quotes from the study you'd posted:

'A profound deficiency of docosahexaenoic acid (DHA) (30% of normal levels), a n-3 polyunsaturated fatty acid (PUFA), has been documented in Zellweger patients (Martinez, 1992a).' ―Janssen

'Dietary deficiency of n-3 fatty acids is associated with disturbances in vision and other neurological abnormalities (Green and Yavin, 1998).' ―Janssen

'Because Zellweger patients have a manifest deficit of DHA, Martinez supplemented several patients (3–7 months old) with DHA-EE (Martinez, 1996; Martinez and Vazquez, 1998). Beneficial effects were noticed including increased muscular tone, better visual function, and improvement of myelination.' ―Janssen

'Although the lack of DHA in Zellweger patients is well established during the first months of life (Martinez, 1992a)...' ―Janssen

The mice you cite as proof had been treated for only ten days.

'A possible explanation for this discrepancy might be that the mice were treated for a much shorter time period (10 days), not allowing visible clinical improvements.' ―Janssen

These particular mice were genetically engineered to be deficient in PEX5, not exclusively-characteristic of actual human Zellweger's disease. Although these mice had a 40% reduction in brain DHA (22∶6ω−3), they actually had an equivalent lipid present. Because these mice could freely elongate ω−3 fatty acids yet could not β-oxidize tetracosahexaenoic acid (24∶6ω−3) down to docosahexaenoic acid (22∶6ω−3), they had accumulated a lipid species even more effective at excluding membrane cholesterol:

'By spiking the extracts with synthetic C24:6n-3, the peak was tentatively identified as C24:6n-3.' ―Janssen

Now why would you expect to see any changes from a study of such short duration?
 

SOMO

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After I ruined my health with Veganism, fish oil brought my mental state back to normal. After several years of being on the vegan diet, I started getting depressed and it wasn't anything to do with my environment or home life. Also Fish oil cured my back acne.

There are definite neurological effects of Fish Oil, likely due to the DHA.

Regardless of how you feel about PUFA, there are people who find benefit from Omega 6 supplements like Borage/Evening Primrose Oil or Omega 3s like Fish Oil/Cod Liver Oil.
 

Travis

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After I ruined my health with Veganism, fish oil brought my mental state back to normal. After several years of being on the vegan diet, I started getting depressed and it wasn't anything to do with my environment or home life. Also Fish oil cured my back acne.

There are definite neurological effects of Fish Oil, likely due to the DHA.

Regardless of how you feel about PUFA, there are people who find benefit from Omega 6 supplements like Borage/Evening Primrose Oil or Omega 3s like Fish Oil/Cod Liver Oil.

But aren't you the same guy who'd said he'd been hospitalized for sodium deficiency?
 

SOMO

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But aren't you the same guy who'd said he'd been hospitalized for sodium deficiency?

Yes.
Are you implying Fish Oil messes with electrolytes? Or does being hospitalized for dehydration affect my earlier experience with using fish oil? I'm not sure what the connection you're trying to make there is. :fearful:

Even if those 2 things affected each other, I had severe, persistent depression and allergic reactions to many foods, including completely vegan foods like fruits, vegetables and starches. My reactions to food and my mood resolved rapidly after reintroducing fish oil and also seafood (the first "animal" food I tried.) Whatever is in seafood fixed my transient depression.

Interestingly, two common pathways, neuroprotection and anti-inflammation, have been found to be associated with all the antidepressant drugs.21,24) More importantly, these two common mechanisms link to antidepressant effects not only for drugs but also for non-pharmacological treatment omega-3 PUFAs.6,11,20) Indeed, the effects on neuroprotection and anti-inflammation support the promising hypothesis of psychoneuroimmunology of mood and anxiety disorders and provide an excellent interface between “mind” and “body”.

The deficits in omega-3 PUFA levels have been reported in other populations with mood disorders, including lower DHA and total n-3 PUFAs in postpartum depression 31) and lower DHA and EPA in social anxiety disorder.32) In the elderly patients, lower DHA and higher AA, n-6/n-3, AA/EPA, and AA/DHA ratios were associated with depressive disorders compared to healthy volunteers.33) In samples of patients with acute coronary syndromes, the depressed patients had lower DHA, total DHA and EPA; and higher AA, n-6/n-3, AA/EPA and AA/DHA than those without depression.34) Interestingly, lower DHA levels before starting interferon (IFN)-α therapy predicted IFN-α-induced depression in patients with chronic hepatitis C viral (HCV) infection.13)

So, a ratio between O6 AA and O3 exist and different prostaglandins are formed by AA and EPA/DHA. RP would say it was the "immune-suppressive" effects of Omega-3s that I was noticing, but RP has also spoken about the SFA:PUFA ratio, so it's possible there is a healthy level of Omega-3s, greater than 0.
 

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