Why Fish Oil Fails

haidut

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Not sure if this has been posted before, but a few emails from advocates of fish oil promoted my search. I found this study, which was promptly retracted upon publishing due to the author apparently not declaring conflict of interest and misstating his educational credentials. Note that the study was not retracted due to the findings of it being disputed, it's the author they attacked. Given that it is retracted, feel free to take the findings with a grain of salt. However, what is indisputable is that the study cites quite a few other sources which significantly back up its claims.
Overall, a must read for anyone having doubts about PUFA and especially fish oil. The study has references that I had not see so far and they implicate fish oil, and oxidized omega-6 in virtually all degenerative conditions seen today.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3914521/

"...With dietary marine/fish oil supplementation and its EPA/DHA modification of membrane fatty acid composition, which accelerates unnatural lipid peroxidation, significant effects of oxidative damage to many and varied cellular macromolecules occur. For example, peroxidized cardiolipin in the mitochondrial membrane can inactivate cytochrome oxidase by mechanisms similar to those of hydrogen peroxide as well as mechanisms unique to organic hydroperoxides. Dr. Hulbert warns, “Lipid peroxidation should not be perceived solely as ‘damage to lipids,' but should also be considered as a significant endogenous source of damage to other cellular macromolecules, such as proteins and DNA (including mutations)” [18].
Furthermore, the noncharged structure of aldehydes allows their migration with relative ease through hydrophobic membranes and hydrophilic cytosolic media, thereby extending the migration distance far from the production site. On the basis of these features alone, these carbonyl compounds can be more destructive than free radicals and may have far-reaching damaging effects on target sites both within and outside membranes.
Dr. Hulbert makes the importance of mitochondrial functionality clear with his statement, “The insight that the exceptionally long-living species, Homo sapiens, potentially provides for understanding the mechanisms determining animal longevity, is that the fatty acid composition of mitochondrial membranes may be much more important than the composition of other cellular membranes” [17]. A pharmacologic overdose of ALA metabolites exacerbates a shorter lifespan by altering the lipid (mitochondrial) membranes [23].
Mitochondrial cardiolipin molecules are targets of oxygen free radical attack, due to their high content of fatty acids—normally containing negligible long-chain omega-3 metabolites like DHA—unless pharmacologically overdosed as with marine/fish oil. Mitochondrial mediated ROS generation affects the activity of complex I, as well as complexes III and IV, via peroxidation of cardiolipin following oxyradical attack to its fatty acid constituents [18]."

"...Alteration of mitochondrial structure by fish oil was known in 1990 and published at that time in an article in the Proceedings of the National Academy of Science, as follows: “Phospholipase A2 activity and mitochondrial damage are enhanced when mitochondrial membranes are enriched with n-3 fatty acids [from marine/fish oil].

"...Fish oil cannot work, based on human physiology and biochemistry. Humans do not live in frigid waters where an “anti-freeze” is required, that is, EPA/DHA. These so-called active components spontaneously oxidize (radical induced oxidation) at room temperature and are even more problematic at physiologic body temperatures, causing numerous deleterious aldehyde secondary/end products regardless of antioxidant levels. It has been clearly shown that the general population does not suffer impairment of delta-6/-5 desaturation enzyme impairments, as previously thought in the 20th century. Prostate and other cancers along with CVD are predicted to increase in patients consuming fish oil on purely theoretical grounds, utilizing known physiology and biochemistry—and they do—in particular, epithelial cancers and impaired arterial intima."

"...Marine/fish oil, in the supraphysiologic, prophylactic amounts often consumed, is harmful, possibly even more harmful than trans fats [3]. If proper physiologic amounts were utilized (<20 mg EPA/DHA), perhaps their furan acid content would be a significant positive factor; the concern of rampant oxidation is alleviated. Otherwise, given today's high quantities of fish oil recommendation, we see that their furan acid component is rendered ineffective. The medical profession needs to thoroughly review highly quantitative 21st century lipid physiology and biochemistry and offer the appropriate patient warnings. It is sincerely hoped that future researchers will approach the fish oil controversy with a more comprehensive grasp of the lipid biochemistry and physiology involved. Science must take precedence over “studies” which are often open to (mis)interpretation, leading to continual reversals and inconsistent results in clinical trials.
Using the most direct and effective physiologic measure, fish oil in the doses suggested is unequivocally shown to be an anti-antiaging substance, increasing vascular “biologic aging” by over a decade—causing “hardening of the arteries”—compared to PEO consumption. Compared to taking nothing, fish oil decreased subjects' arterial compliance (a bad outcome), by nearly four years [60]. Prophylactic marine oil consumption given its supraphysiologic EPA/DHA amounts—both theoretically and in clinical use—leads to increased inflammation, increased CVD, and increased cancer risk."
 

Agent207

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What about a minimal amount of wild caught fish like fresh anchovys with moderated amounts of DHA and low overall PUFA content?

Fish oil supplements are crap.
 

haidut

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Agent207 said:
post 105617 What about a minimal amount of wild caught fish like fresh anchovys with moderated amounts of DHA and low overall PUFA content?

Fish oil supplements are crap.

I think eating fish occasionally is probably OK. Peat said he likes cod and trout but he eats them sparingly. Lean fish would be better than fatty fish, that's all.
 
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J

jb116

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Cod is a very good low fat fish with an exceptional protein profile, including AAs like taurine and glycine.
 

Ideonaut

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"A pharmacologic overdose of ALA metabolites exacerbates a shorter lifespan by altering the lipid (mitochondrial) membranes [23]."

Is the ALA reference to alpha-lipoic acid? hope not; I've been taking a lot of that "master antioxidant" for years. aarrgghh!
 
J

jb116

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brumpfschmlog said:
post 105963 "A pharmacologic overdose of ALA metabolites exacerbates a shorter lifespan by altering the lipid (mitochondrial) membranes [23]."

Is the ALA reference to alpha-lipoic acid? hope not; I've been taking a lot of that "master antioxidant" for years. aarrgghh!
That's alpha-linolenic, n-3 type.
Although what you take is a sythetic form
 
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rei

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I don't see anything wrong with the paper at first glance, i guess the retraction is another seal of approval that the higher ups did not want this citable.
 

Amazoniac

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..

"There are only two true 18-chain carbon essential fatty acids (EFAs): linoleic acid (LA) with two double bonds and alphalinolenic acid (ALA) with three double bonds. Neither can be manufactured in the body; both must come from food. Longer-chain metabolites are synthesized from LA and ALA. These long-chain metabolites—not essential and often incorrectly termed “EFAs”—are correctly termed “derivatives.” For example, common derivatives of the omega-3 series are EPA (eicosapentaenoic acid) with five double bonds and DHA (docosahexaenoic acid) with six double bonds. To clarify the issue, I term LA and ALA “Parent Essential Oils” (PEOs) or “Parents.” I properly term all of their long-chain metabolites “derivatives.” The body makes these important derivatives from Parents “as needed” in naturally minute amounts.The literature often fails to clearly distinguish these two vastly different substances."

"Most Parents Stay as Parents. A major mistake was made in the 20th century, which misdirected researchers. It was wrongly assumed that the vast majority of “Parents” would be converted into “derivatives.” This did not occur, causing the medical research community to proclaim that there were ubiquitous metabolic deficiencies impacting the delta-6 and delta-5 desaturase enzymes in the general population. This has been shown to be categorically false by advanced 21st century quantitative methods (described later). In humans, no more than one percent (1%) of Parents are naturally converted into derivatives. Fish oil mania wrongly (and hazardously) assumes the converse."

"[..]nonfunctional LA-based trans fats, oxidized LA entities, and inappropriate omega-6/omega-3 ratios (caused in part from normally recommended, yet supraphysiologic, marine oil supplementation) are all potential sources of unsaturated fatty acids—in particular, LA (Parent omega-6)—that can disrupt the normal membrane structure, significantly increasing the potential for cancer [11]. All of the supraphysiologic, excess EPA/DHA cannot be betaoxidized away. Thus a significant amount of the excess will be physiologically incorporated into all cell membranes, detrimentally."

"Polyunsaturated fatty acids including LA contain the system HC=CH–CH2–CH=CH. Long-chain fatty acids contain bis-allylic hydrogens whereby the –C=C– units are separated by a single-bonded –C– (carbon) atom. The hydrogen atoms attached to each of these intermediate –C– atoms are called bis-allylic hydrogens and have the lowest C–H (weakest) bond-energies of the fatty acid chain. The weak bond makes them enormously susceptible to attack by reactive oxygen species (ROS) generated elsewhere in the body [17]. Because of the five double bonds in EPA and six double bonds in DHA, these metabolites are highly sensitive to temperature. In particular, DHA, with its 6 double bonds, contains 5 bis-allylic bonds and is therefore 320 times more susceptible to oxidative attack, that is, becoming rancid, than monounsaturated oleic acid (18:1), which has no bis-allylic hydrogens in its chain. A saturated fat membrane containing just 5% DHA (fish oil) is 16 times more susceptible to peroxidative damage [18]. Fish oil’s DHA is 7 times more susceptible to peroxidative damage than LA (Parent omega-6), the most significant fatty acid by both weight and functionality in the cell’s bilipid membrane. The shifting of the body’s antioxidants required to combat this physiologic insult causes a shortage elsewhere. This fact should cause the medical community great concern. Keeping tissue fluid in frigid waters is not a physiologic concern of humans."

"Regardless of antioxidant level added to the fish oil supplement, rancidity/peroxidation upon ingestion (in vivo) becomes a very significant and problematic issue. Oxidation of EPA leads to generation of a mixture of aldehydes, peroxides, and other oxidation products. Highly polyunsaturated, long-chained EPA and more so with DHA, due to its additional double bond, is readily oxidized at room temperature even in the absence of exogenous oxidizing reagents. Importantly, in vivo, a large increase in tissue and plasma accumulation of fatty acid oxidation products is noted in subjects consuming fish oil even after addition of antioxidant supplements to the diet—this effect strongly suggests extensive oxidation of omega-3 fatty acids such as EPA in vivo. This deleterious effect is true as evidenced by the trial in which a 14% decrease in life expectancy occurred in those animals fed fish oil [23]."

"In humans and primates such as the monkey, no quantity of in vivo antioxidants will stop EPA/DHA damage as measured by lipofuscin, the peroxidized “age spots.” Lipofuscin was three-fold (3Xs) greater in the livers of monkeys fed fish oil. Furthermore, another measure of oxidative damage, the levels of basal thiobarbituric acid reactive substances (TBARS), was four-fold (4Xs) greater than that of the monkeys fed corn oil with no EPA/DHA. The researchers found that even a ten-fold (10Xs) increase in alpha-tocopherol, a potent antioxidant, was not fully able to prevent the peroxidative damage from fish oil [24]."

"What percentage of PEOs [Parent Essential Oils] does become converted (naturally) to long-chain metabolites such as EPA and DHA? This important question must be addressed and answered before their correct supplemental dosage (if any) can be determined. This fundamental research was neglected concerning marine oils, which tragically led to recommendations of haphazard supraphysiologic overdoses of marine oil’s EPA/DHA. New, twenty-first century quantitative research from both NIH and USDA shows considerably lesser amounts of natural DHA conversion/usage from ALA than the medical community has been led to believe. These findings will be upsetting to those health professionals recommending fish oil prophylactically. The conversion amount is much less than the medical field assumes: it is less than 5%—often less than 1%—with at least 95% of PEOs staying in Parent form. This singular mistake of assuming very high conversion amounts, whereas in actuality their conversion amounts are extremely low, led to the irrational fish oil mania."

"Contrary to wrong dogma, the enzymes that produce PEO derivatives (the delta-6 and delta-5 desaturase enzymes) are not impaired in the vast majority of patients [32]. Conversion of ALA (Parent omega-3) to DHA is unlikely to ever normally exceed 1% in humans [33]."

"Research at the United States Department of Agriculture’s USDA Food Composition Laboratory (2001) reported a natural net conversion rate of a mere 0.046% of ALA to DHA and 0.2% to EPA—not the highly misleading 15% conversion rate that is often quoted [34]. This is a mistake of nearly 2 orders of magnitude (100-fold). In 2009 NIH researchers determined the amount of DHA utilized in human brain tissue to be a mere 3.8 mg ± 1.7 mg/day. Therefore, based on the variance, brain tissue in 95% of all subjects, allowing for variation in brain size, would consume no more than 0.4 mg–7.2 mg of DHA per day [32]."

"Because the body cannot oxidize away these tremendous overdoses of EPA/DHA, they become incorporated into tissue and organs with deleterious effects as confirmed by the skyrocketing increase in all epithelial-based cancers (described later). Supraphysiologic amounts are forced into tissue, causing gross physiologic imbalance and great potential for harm."

"Vegans—Consuming No Fish—Produce Sufficient DHA. Even vegetarians consuming little or no fish had acceptable EPA/DHA levels [36]. This is a group that absolutely would be expected to manifest gross neurological abnormalities, including both visual impairment and cognitive impairment, yet there is no clinical evidence of such neurologic and cognitive abnormalities in vegetarians [36, 37]. Confirmation in 2010 showed that vegetarians with an intake of 0.3% DHA compared to fish eaters produced 85% of the EPA levels and 83% of the DHA levels that consumers of fish did. These amounts are within the “normal” ranges [37]."

"Given the above analyses, how much EPA/DHA does the typical marine oil/fish oil supplement provide? An average 1,000mg health-food-grade fish oil capsule contains approximately 180mg EPA and 120mg DHA. Pharmaceutical-grade versions contain higher doses. Furthermore EPA ⇔ DHA. This is not the case with PEOs. They are unidirectional. The American Heart Association states that those with documented CHD are advised to consume about 1 gm (1,000mg) of EPA + DHA per day. Is this advice rational? No. As an example, using the USDA food composition research formulas covered earlier, if patients consumed a supplement of 600mg of Parent ALA, they would naturally convert it to EPA by no more than the (generous) factor of 0.25% = 1.5 mg EPA and 1.5 mg × 0.63 × 0.37 = 0.35 mg to DHA in patient plasma. Therefore, just one capsule provides the amounts shown in the analysis below, and many people are overdosing even more by taking 2 to 4 fish oil capsules each day, likely in part because the cardiology and heart recommendations are often “EPA + DHA ranging from 0.5 to 1.8 grams per day.”What overdose does this translate to?"

"Potential EPA/DHA Overdoses Are Frequent. Potential Overdose equates to the following plasma overdoses: EPA = 180 mg/1.5 mg = 120 times overdose and DHA = 120 mg/0.35 mg = 340 times overdose. These facts should cause great pause and concern. (Technically, a bit more is required for additional metabolic pathways aside from direct tissue incorporation like prostaglandin production, but it is not a significant amount by weight on a daily basis.) The medical community and most physicians and other health professionals may unknowingly be overdosing patients prophylactically with supraphysiologic supplemental amounts of omega-3 derivatives."

"The concentration in adipose tissue triacylglycerols is roughly proportional to dietary concentration and is now frequently used as a measure of relative dietary intake. It has been long known that the fatty acid composition of the diet can influence membrane fatty acid composition [43, 44]. Fortunately, tissue alteration caused by supraphysiologic amounts of marine oil consumption can be remedied. Once removed, it takes 18 weeks to fully rid patients of the negative effects of fish oil [45]."

"Cardiolipin is a fat-based complex phospholipid found in all mitochondrial membranes, almost exclusively in the inner membrane, and is intimately involved in maintaining mitochondrial functionality and membrane integrity. It is used for ATP (energy) synthesis and consists roughly of 20% lipids [82]."
"With dietary marine/fish oil supplementation and its EPA/DHA modification of membrane fatty acid composition, which accelerates unnatural lipid peroxidation, significant effects of oxidative damage to many and varied cellular macromolecules occur. For example, peroxidized cardiolipin in the mitochondrial membrane can inactivate cytochrome oxidase by mechanisms similar to those of hydrogen peroxide as well as mechanisms unique to organic hydroperoxides. Dr. Hulbert warns, “Lipid peroxidation should not be perceived solely as ‘damage to lipids,’ but should also be considered as a significant endogenous source of damage to other cellular macromolecules, such as proteins and DNA (including mutations)” [18]."

"Furthermore, the noncharged structure of aldehydes allows their migration with relative ease through hydrophobic membranes and hydrophilic cytosolic media, thereby extending the migration distance far from the production site. On the basis of these features alone, these carbonyl compounds can be more destructive than free radicals and may have far-reaching damaging effects on target sites both within and outside membranes."
 

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