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Funk has been telling us this all along...

 

 

Meta-analysis finds no CV benefit of omega-3 fatty acids

September 13, 2012 Michael O'Riordan

 

Ioannina, Greece - A new meta-analysis looking at the effects of omega-3 fatty acids in patients at high risk for cardiovascular events has shown that the supplements have no effect on hard clinical outcomes, including all-cause mortality, cardiac death, sudden death, MI, or stroke [1]. There was a trend toward benefit in the prevention of sudden death, but the reduction failed to reach statistical significance, a finding the researchers believe refutes any supposed antiarrhythmic-mediated effect of omega-3 fatty acids.

 

"The meta-analysis, taking into account the recent and previously published trials, showed that omega-3 fatty acids did not significantly reduce the incidence of cardiovascular events," senior investigator Dr Moses Elisaf (University Hospital of Ioannina, Greece) told heartwire. "However, there was a trend toward benefit in terms of sudden death, about a 13% reduction, and myocardial infarction, about a 10% reduction, but the decrease was not statistically significant. So, we can conclude from this meta-analysis and other recently published trials that the effect of omega-3 fatty-acid supplementation in high-risk patients is rather low. They are without side effects, but without significant efficacy."

 

The study is published in the September 12, 2012 issue of the Journal of the American Medical Association.

 

Some clinical guidelines, including those of the European Society of Cardiology (ESC), recommend omega-3 polyunsaturated fats, either through supplements or dietary changes, after MI. Despite the recommendations, there is a large degree of controversy and uncertainty regarding the benefits of omega-3 polyunsaturated fats on the risk of major cardiovascular events. Currently, the US Food and Drug Administration (FDA) has approved high-dose omega-3 fatty acids for the treatment of high triglyceride levels in patients with overt hypertriglyceridemia.

 

Speaking with heartwire, Elisaf said few trials included in the meta-analysis used the high-dose omega-3 fatty-acid supplements, that being 2 to 4 g per day as approved by the FDA, so more studies are needed to study the benefit of using the high-dose supplements to lower triglyceride levels and prevent cardiovascular events. "We need more data to clearly define the role of omega-3 fatty acids in clinical practice," said Elisaf.

Efficacy of omega-3 fatty acids across clinical outcomes

 

Outcome

Relative risk (95% CI)

All-cause mortality

0.96 (0.91-1.02)

Cardiac death

0.91 (0.85-0.98)*

Sudden death

0.87 (0.75-1.01)

MI

0.89 (0.76-1.04)

Stroke

1.05 (0.93-1.18)

 

*Reduction in cardiac death events not significant after corrected for multiple comparisons

 

The meta-analysis included 20 clinical trials of 68 680 patients. Some of the studies were published as early as 1989, but more than half of the clinical trials were published when statins were routinely recommended for the reducing the risk of cardiovascular disease. The mean omega-3 dose used in the trial was 1.5 g/day, or 0.77 g/day eicosapentaenoic acid (EPA) and 0.60 g/day docosahexaenoic acid (DHA). The median treatment duration was two years, and the maximum was 6.2 years.

 

Given the negative results, Elisaf said that one of the reasons can be explained by contemporary treatment of patients at high risk for cardiovascular disease. One of the pivotal trials that first suggested omega-3 fatty acids could reduce the risk of cardiovascular disease, GISSI, was undertaken before patients were regularly treated with other cardiovascular medications, including cholesterol-lowering agents. "Today, our high-risk patients take aspirin and statins," he said. "So, we have patients with much lower levels of LDL cholesterol, and the potential benefits of reducing mortality further with other agents, including omega-3 fatty acids, might be marginal."

 

While many patients might take omega-3 fatty acids over the counter, Elisaf said the present trial included only doses and formulations recommended by FDA and other medical authorities around the world. Low-dose formulations purchased over the counter were not included in the analysis. Elisaf noted that the meta-analysis included clinical trials with varying methodologies and clinical hypotheses, as well as different prevention settings, in order to provide a big-picture assessment of the evidence.

 

From HeartWire at www.theheart.org

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A new study published in Mayo Clinic Proceedings provides the most comprehensive analysis of the role of omega-3 dosage on cardiovascular prevention to date. The meta-analysis, which is an in-depth re

"According to the study, which was funded by the National Institutes of Health (NIH), a higher Omega-3 Index was associated with a lower risk for total CVD events, total coronary heart disease events,

Did he forget that he wrote this?   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330561/   Dude is also a huge statin fan.        

I have no opinion yet on the study design or the reported results, though I do like to infer a researcher's potential cognitive biases by examining his/her background and industry collaborations; in this case there is a correlation with statin manufacturers Pfizer and Merck (causation should not be assumed).

 

"Moses S. Elisaf, MD, FRSH, FASA

Professor of Medicine, School of Medicine

University of Ioannina

Ioannina, Greece

 

Prof. Elisaf has disclosed that he is a recipient of research/grant funding from MSD, Solvay and Fournier; is a consultant/advisor for MSD, Solvay and Schering Plough; and is a member of the speakers bureaus for Merck, Sharpe & Dohme, Schering Plough, Pfizer and AstraZeneca."

http://www.cmrojournal.com/ipi/ih/editorial-advisory-board.jsp

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Most problems with fish oil derive from the fact that it's the most fragile, easily oxidized substance that's edible. If all it did were transiently increase oxidative stress that would be bad enough but your body incorporates this stuff into cell and mitochondrial membranes, and now YOU become fragile and easily oxidized. There's a direct relationship between the mitochondrial membrane content of PUFA and the rate of aging across species.

 

Most benefits of fish oil derive from its competition with Omega-6 fatty acids. I advocate eating as little of both O3 and O6 as is practical. These fatty acids are claimed to be essential but no minimum requirement has ever been identified to my knowledge. The USDA used the average american's intake as the adequate intake level, with the rationale that no deficiency symptoms are observed in the average american (possibly the laziest science ever). In practice it's impossible to avoid consuming a significant quantity of these fatty acids as they are ubiquitous in foods, which probably renders any deficiency concerns moot, but you can still reduce your intake dramatically.

 

The benefits of O6 restriction can be striking -- I cleared up a lifelong (post-puberty anyway) case of acne within a month of reducing my O6 intake to

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you got to love the bolded part here

 

Effect of Fish Oil Supplementation on Fasting Vascular Endothelial Function in Humans: A Meta-Analysis of Randomized Controlled Trials

 

free full-text @ http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0046028

 

Background

 

Effect of fish oil supplementation on flow-mediated dilation, an index of endothelial function in humans, remains controversial. We performed a meta-analysis to determine whether fish oil supplementation could improve endothelial function.

Methods

 

Human intervention studies were identified by systematic searches of Medline, Embase, Cochrane's library and references of related reviews and studies. A random-effect model was applied to estimate the pooled results. Meta-regression and subgroup analyses were performed to evaluate the impact of study characteristics on the effect of fish oil supplementation on flow-mediated dilation.

Results

 

A total of sixteen records with 1,385 subjects were reviewed. The results of the pooled analysis showed that fish oil supplementation significantly improved flow-mediated dilation (weighed mean difference: 1.49%, 95% confidence interval 0.48% to 2.50%, p = 0.004). Meta-regression and subgroup analysis suggested that the quality of included studies were inversely related to the overall effect (regression coefficient = −1.60, p = 0.04), and the significance of the effect was mainly driven by the studies with relatively poor quality. Sensitivity analysis including only double-blind, placebo-controlled studies indicated fish oil supplementation has no significant effect on endothelial function (weighed mean difference: 0.54%, 95% confidence interval −0.25% to 1.33%, p = 0.18). Besides, normoglycemic subjects or participants with lower diastolic blood pressure seemed to be associated with remarkable improvement of endothelial function after fish oil supplementation.

Conclusions

 

Although current evidence suggested a possible role of fish oil in improving endothelial function, large-scale and high-quality clinical trials are needed to evaluate these effects before we can come to a definite conclusion.

 

in other words: THE BETTER THE STUDY THE LESS PRONOUNCED THE EFFECT - got to make you think about the damn hype around fish oil

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Most problems with fish oil derive from the fact that it's the most fragile, easily oxidized substance that's edible. If all it did were transiently increase oxidative stress that would be bad enough but your body incorporates this stuff into cell and mitochondrial membranes, and now YOU become fragile and easily oxidized. There's a direct relationship between the mitochondrial membrane content of PUFA and the rate of aging across species.

 

Most benefits of fish oil derive from its competition with Omega-6 fatty acids. I advocate eating as little of both O3 and O6 as is practical. These fatty acids are claimed to be essential but no minimum requirement has ever been identified to my knowledge. The USDA used the average american's intake as the adequate intake level, with the rationale that no deficiency symptoms are observed in the average american (possibly the laziest science ever). In practice it's impossible to avoid consuming a significant quantity of these fatty acids as they are ubiquitous in foods, which probably renders any deficiency concerns moot, but you can still reduce your intake dramatically.

 

The benefits of O6 restriction can be striking -- I cleared up a lifelong (post-puberty anyway) case of acne within a month of reducing my O6 intake to <3g daily. Plug your diet into something like cronometer to determine your current intake and identify the worst offenders.

 

I thought you people used to ask for references

 

W-6 is irrelevant here

 

excellent example (maybe not intended) of rhetoric instead of logic

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And before you ask for it...

 

Food Nutr Res. 2011;55. doi: 10.3402/fnr.v55i0.5792. Epub 2011 Jun 10.

Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements.

Halvorsen BL, Blomhoff R.

Source

 

Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.

Abstract

BACKGROUND:

 

There is convincing evidence that replacing dietary saturated fats with polyunsaturated fats (PUFA) decreases risk of cardiovascular diseases. Therefore, PUFA rich foods such as vegetable oils, fatty fish, and marine omega-3 supplements are recommended. However, PUFA are easily oxidizable and there is concern about possible negative health effects from intake of oxidized lipids. Little is known about the degree of lipid oxidation in such products.

OBJECTIVE:

 

To assess the content of lipid oxidation products in a large selection of vegetable oils and marine omega-3 supplements available in Norway. Both fresh and heated vegetable oils were studied.

DESIGN:

 

A large selection of commercially available vegetable oils and marine omega-3 supplements was purchased from grocery stores, pharmacies, and health food stores in Norway. The content of lipid oxidation products were measured as peroxide value and alkenal concentration. Twelve different vegetable oils were heated for a temperature (225°C) and time (25 minutes) resembling conditions typically used during cooking.

RESULTS:

 

The peroxide values were in the range 1.04-10.38 meq/kg for omega-3 supplements and in the range 0.60-5.33 meq/kg for fresh vegetable oils. The concentration range of alkenals was 158.23-932.19 nmol/mL for omega-3 supplements and 33.24-119.04 nmol/mL for vegetable oils. After heating, a 2.9-11.2 fold increase in alkenal concentration was observed for vegetable oils.

CONCLUSIONS:

 

The contents of hydroperoxides and alkenals in omega-3 supplements are higher than in vegetable oils. After heating vegetable oils, a large increase in alkenal concentration was observed.

 

PMID: 21691461

 

FT

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What is it you are questioning here?

I can't speak for Elle, but I'm having trouble accepting FunkO's statement "Most benefits of fish oil derive from its competition with Omega-6 fatty acids". I want a hefty dose of experimental data and citations to back up a claim like that.

 

Previously Funk attributed improvements in his skin to reduced intake of milk. So what's the causative agent -- milk, omega 6, or some other change that Funk made around the same time?

 

If FunkO's statement about Fish Oil is true, does it apply equally to O3 from fresh fish? Surely the level of oxidation from capsules vs fresh is a confounding factor in any hypothesis. So, in general I see a lot of confounds abounding.

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If FunkO's statement about Fish Oil is true, does it apply equally to O3 from fresh fish? Surely the level of oxidation from capsules vs fresh is a confounding factor in any hypothesis. So, in general I see a lot of confounds abounding.

 

I believe he was speaking of fish oil supplements as are generally available to consumers.

 

If you read the FT, you find that they took a number of steps to control for "freshness"...they tested four brands of encapsulated fish oil purchased online in addition to locally purchased samples where they bought some from three different retailers...everything was stored in original packaging according the manufacturer's recommendations so unless you are catching your fish oil on the fin, their findings probably apply to the stuff in your cupboard.

 

I can't speak to Funk's skin improvements but it is pretty clear that marine oils are particularly unstable, even among PUFAs, and the level of oxidization found in commercially available fish oil is much higher than that found in commercially available vegetable oils. And your body does readily incorporate these dietary oils into cellular membranes so his observation that this would tend to make your cells more susceptible to oxidation damage is reasonable.

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now things are finally getting interesting, as we are moving beyond hear-say bro-science - omega3:omega6 ratio stuff and looking at the mechanisms

 

J Nutr Biochem. 2012 Feb;23(2):101-5. Epub 2011 Dec 1.

Biophysical and biochemical mechanisms by which dietary N-3 polyunsaturated fatty acids from fish oil disrupt membrane lipid rafts.

Shaikh SR.

Source

 

Department of Biochemistry and Molecular Biology, Brody School of Medicine, East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC 27834, USA. shaikhsa@ecu.edu

Abstract

 

N-3 polyunsaturated fatty acids (PUFAs) from fish oil exert their functional effects by targeting multiple mechanisms. One mechanism to emerge in the past decade is the ability of n-3 PUFA acyl chains to perturb the molecular organization of plasma membrane sphingolipid/cholesterol-enriched lipid raft domains. These domains are nanometer-scale assemblies that coalesce to compartmentalize select proteins for optimal function. Here we review recent evidence on how n-3 PUFAs modify lipid rafts from biophysical and biochemical experiments from several different model systems. A central theme emerges from these studies. N-3 PUFA acyl chains display tremendous conformational flexibility and a low affinity for cholesterol and saturated acyl chains. This unique flexibility of n-3 PUFA acyl chains impacts the organization of inner and outer leaflet lipid rafts by disrupting acyl chain packing and molecular order within rafts. Ultimately, the disruption in raft organization has consequences for protein clustering and thereby signaling. Overall, elucidating the complex mechanisms by which n-3 PUFA acyl chains reorganize membrane architecture will enhance the translation of these fatty acids into the clinic for treating several diseases.

 

Copyright © 2012 Elsevier Inc. All rights reserved.

I guess whether these effects on the cell membrane are good or bad depends on the type of cell e.g.

 

* Breast cancer => http://www.ncbi.nlm.nih.gov/pubmed/22622660 = positive or

* susceptibility to ethanol induced oxidation => http://www.ncbi.nlm.nih.gov/pubmed/21945097 "the ability of EPA to modify lipid raft physical and chemical properties plays a key role in the enhancement, by this dietary n-3 PUFA, of ethanol-induced oxidative stress." = negative

 

... as well as the circumstances in which they take place.

 

Also, it is false to assume that the main benefits of O3 come from replacing O6, when there is more than enough evidence that they directly interact with G-protein-coupled receptors (GPRs)

 

e.g.

GPR84 increases IL-12 production in macrophages,

GPR119 increases GLP-1 and PYY, insulin secretion, reduces food intake and

GPR120 directly decreases inflammatory cytokine production by macrophages, increases GLP-1 & CCK, increases GLUT-4 expression

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Everything I think I know always turns out to be wrong.

Probably even this.

 

 

To clarify, are we then suggesting that diets high in fish intake are potentially harmful, or consumption of fish oil supplements?

 

 

 

Can we patent and market egg yolk fat supplements?

No seriously @funk, if you are trying to abstain from dairy fat and fish fats, what are you mostly consuming? Or are you just trying to avoid fats in general?

Just tell me I can load up on pig butter.

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To clarify, are we then suggesting that diets high in fish intake are potentially harmful, or consumption of fish oil supplements?

 

The data we have seen regarding the instablity of marine oils deals with fish oil supplements and not fresh fish.

 

That said, coldwater fish tend to accumulate the crap we put in the oceans like mercury and pcbs so I am less than convinced that eating fresh fish is all that good for you.

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Can someone explain to me why, if at all, taking say, 2g only of fish oil per day to bring up the O3 balance would be bad? I just dont see why moderation would be deleterious. I see here that high consumption increases oxidation potential but in low doses, would it even matter? Enough to negate benefits on PPARa and inflammation?

 

I'm open minded but perhaps lacking in understanding.

 

Sent from my SPH-M820-BST using Tapatalk 2

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Can someone explain to me why, if at all, taking say, 2g only of fish oil per day to bring up the O3 balance would be bad? I just dont see why moderation would be deleterious. I see here that high consumption increases oxidation potential but in low doses, would it even matter? Enough to negate benefits on PPARa and inflammation?

 

I'm open minded but perhaps lacking in understanding.

 

Sent from my SPH-M820-BST using Tapatalk 2

 

if you mean 2g = 2x 1g caps - not a problem. If we are talking 2g = only EPA + DHA you can check out studies like

 

Eur J Appl Physiol. 2011 Aug;111(8):1829-39. Epub 2011 Jan 11.

Effects of 6 weeks of n-3 fatty acids and antioxidant mixture on lipid peroxidation at rest and postexercise.

Filaire E, Massart A, Rouveix M, Portier H, Rosado F, Durand D.

Source

 

Laboratoire CTI Inserm 658, UFRSTAPS, 2 allée du Château, BP 6237, 45062, Orléans Cedex, France. edith.filaire@univ-orleans.fr

Abstract

 

The purpose of this randomized study was to measure the influence of 6 weeks of LCPUFA (600 mg EPA and 400 mg DHA per day) supplementation alone or in association with 30 mg vitamin E, 60 mg vitamin C and 6 mg β-carotene on resting and exercise-induced lipid peroxidation in judoists (n = 36). Blood samples were collected at rest before (T (1)) and after the supplementation period, in preexercise (T (2)) and postexercise (T (3)) conditions, for analysis of α-tocopherol, retinol, lag phase (Lp) before free radical-induced oxidation, maximum rate of oxidation (R (max)) during the propagating chain reaction, maximum amount of conjugated dienes (CD(max)) accumulated after the propagation phase, and nitric oxide, malondialdehyde and lipoperoxide (POOL) concentrations. Dietary data were collected using a 7-day diet record. There were no significant differences among treatment groups with respect to habitual intakes of energy from fat, carbohydrate, or protein. At T (1), there were no significant differences among treatment groups with respect to lipid peroxidation, lag phase, and levels of α-tocopherol or retinol. The consumption of an n-3 LC PUFA supplement increased oxidative stress at rest and did not attenuate the exercise-induced oxidative stress. The addition of antioxidants did not prevent the formation of oxidation products at rest. On the contrary, it seems that the combination of antioxidants added to the n-3 LCPUFA supplement led to a decrease in, CD(max), R (max), and POOL and MDA concentrations after a judo training session.

 

PMID:

21222131

[PubMed - indexed for MEDLINE]

 

As far as fish goes, I wonder if it's not rather the consumption of ALREADY OXIDIZED fish oil (in cooked / grilled fish) that could be an advantage, I know that sounds counter-intuitive, but check out a previous post of mine on the benign nature of oxidized fish oil > http://suppversity.blogspot.de/2011/12/some-things-fishy-oxidized-fish-oil.html

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if you mean 2g = 2x 1g caps - not a problem. If we are talking 2g = only EPA + DHA you can check out studies like

 

This is the problem I see with so many fish oil recs - a total amount of fish oil is recommended, but they all vary in EPA + DHA content. Thanks for bringing this up.

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The first post is on fish oil pills then we get into whether O3's are bad or unnecessary (because of stability and oxidation potential either of themselves or cells they are in). I'm out of my element but I will try.

 

Are we throwing the DHA out with the Fish Oil pills?

 

DHA seems to have quite a history of importance it in terms of how it's taken part in brain growth evolution. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257695/

 

3M years of evolution did not have a huge impact on brain capacity of Australopithecus. But brain size doubled in 1M years from Homo erectus --> Sapiens. Exponetial growth rate in the last 200K years. “The nutrition at the water's front would have given evolving humans the edge over other hominid species. They would have had access to a rich, plentiful and easily harvested food resource, rich in DHA, trace elements and anti-oxidants, for little energy expenditure.†"We suggest that the evolution of the large human brain could not have occurred on the savannahs of Africa."

http://www.ncbi.nlm.nih.gov/pubmed/12083408 http://www.ncbi.nlm.nih.gov/pubmed/11923081 http://www.ncbi.nlm.nih.gov/pubmed/10419087

 

And the idea that it gets in cells and is prone to oxidation seems a paradox in that it is found and hoarded in highest levels in the very places that are metabolically most active. Maybe the antioxidant system counterbalances it somewhat?

"Further, DHA prevented the activation of NF-κB by up-regulating intracellular glutathione to a level high enough to effectively balance the oxidative stress. It is interesting to note that these anti-inflammatory effects of DHA are mediated via increasing the availability of intracellular antioxidants."

 

EPA doesn't convert very well so it it probably not enough to ensure DHA levels remain good.

"Human plasma and tissues are responsive to dietary intake of the long-chain n−3 fatty acids, and levels increase in plasma and tissues in a dose-dependent manner. The most effective way to increase a particular n−3 fatty acid is to provide that specific dietary fatty acid, because interconversion of the n−3 fatty acids is limited in humans. ALA accumulates only to a minor extent, most likely as the result of increased oxidation at higher doses, and modestly raises EPA but not DHA." http://ajcn.nutrition.org/content/83/6/S1467.full

 

If you are not eating DHA in an intact form are you concerned about Macular Degeneration? DHA isn't much stored in the adipose tissue but will the brain/heart not try to find it from elsewhere in the body, such as the nearby and DHA rich retina? http://ajcn.nutrition.org/content/83/6/S1467/F1.large.jpg

 

To Benson's point if it's the pills that are bad and cold water fish are contaminated are maybe we are just screwed.

 

Or someone like me who was deemed allergic to fish proteins @ age 5 (at least the varieties I tried to that point) is double screwed so I take a little Jarrow DHA Max in hopes that it may help keep DHA levels adequate.

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I can't speak for Elle' date=' but I'm having trouble accepting FunkO's statement "[i']Most benefits of fish oil derive from its competition with Omega-6 fatty acids[/i]". I want a hefty dose of experimental data and citations to back up a claim like that.

 

That's fair and I'll see what I can dig up.

 

Previously Funk attributed improvements in his skin to reduced intake of milk. So what's the causative agent -- milk' date=' omega 6, or some other change that Funk made around the same time?[/quote']

 

Eliminating dairy definitely helps and I've gone on and off dairy a number of times in the past to prove it. However, the reduction in O6 intake combined with dairy avoidance improved my skin to a level beyond what I ever achieved previously.

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It may be worth noting that the first actual evidence for significant fishing/fish consumption among humans only dates back <50k years...not a lot of time to influence human evolution.

 

 

Science News Article

 

They probably ate whatever was easy to catch, just like we do today (twinkies). Anyway, this seems to point to the possibility fish were a part of the diet a little longer ago, granted it's not as "direct" as human bone evidence.

 

http://blogs.discovermagazine.com/80beats/2010/06/02/did-dining-on-seafood-help-early-humans-grow-these-big-brains/

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No seriously @funk, if you are trying to abstain from dairy fat and fish fats, what are you mostly consuming? Or are you just trying to avoid fats in general?

Just tell me I can load up on pig butter.

 

Fats from ruminant animals have excellent fatty acid profiles, both the meat and the milk. Beef, lamb, butter, tallow, cow milk, goat milk, etc. There's also coconuts and coconut oil, macadamia nuts and macadamia nut oil. None of the above fat sources contain more than ~5% PUFA. Cocoa butter (as in dark chocolate) is also very good. Since I usually avoid dairy for the benefit of my skin most of my fat comes from grass-fed beef, coconut and macadamia.

 

These include a bit more PUFA so I don't eat more than one serving out of this group per day: eggs, olive oil, chicken, pork, avocado.

 

I avoid vegetable oils, grains (except white rice), nuts (except coconut & macadamia), and legumes completely. Carbs come from fruits, tubers and white rice.

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