Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

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Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

Postby JeffN » Tue Nov 18, 2014 8:15 am

The ongoing debate in the arena of essential fats centers around two issues...

1) Are marine sources (fish) better for you then plant sources

2) Are the short-chain Omega 3 fatty acids (ALA) as beneficial for you as the long-chain Omega 3 fatty acids (EPA &/or DHA) since the thought is that the body does not convert ALA to EPA & DHA very efficiently.

In my presentation and writings over the years, I have made the case many times that the 1) Plant sources are as good if not better then marine sources and 2) on a healthy minimally processed low fat, WFPB, low SOS diet, getting in adequate Omega 3 is more then enough and supplements of EPA/DHA are not necessary. as the body has the ability to make adequate conversions as needed.

These papers support both these positions.

In Health
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1) The Evidence for α-Linolenic Acid and Cardiovascular Disease Benefits: Comparisons with Eicosapentaenoic Acid and Docosahexaenoic Acid. Adv Nutr November 2014 Adv Nutr vol. 5: 863S-876S, 2014

http://advances.nutrition.org/content/5/6/863S

Abstract

"Our understanding of the cardiovascular disease (CVD) benefits of α-linolenic acid (ALA, 18:3n–3) has advanced markedly during the past decade. It is now evident that ALA benefits CVD risk. The expansion of the ALA evidence base has occurred in parallel with ongoing research on eicosapentaenoic acid (EPA, 20:5n–3) and docosahexaenoic acid (DHA, 22:6n–3) and CVD. The available evidence enables comparisons to be made for ALA vs. EPA + DHA for CVD risk reduction. The epidemiologic evidence suggests comparable benefits of plant-based and marine-derived n–3 (omega-3) PUFAs. The clinical trial evidence for ALA is not as extensive; however, there have been CVD event benefits reported. Those that have been reported for EPA + DHA are stronger because only EPA + DHA differed between the treatment and control groups, whereas in the ALA studies there were diet differences beyond ALA between the treatment and control groups. Despite this, the evidence suggests many comparable CVD benefits of ALA vs. EPA + DHA. Thus, we believe that it is time to revisit what the contemporary dietary recommendation should be for ALA to decrease the risk of CVD. Our perspective is that increasing dietary ALA will decrease CVD risk; however, randomized controlled clinical trials are necessary to confirm this and to determine what the recommendation should be. With a stronger evidence base, the nutrition community will be better positioned to revise the dietary recommendation for ALA for CVD risk reduction."


Science Daily Article

Nothing fishy about health benefits of plant-based omega-3 fatty acid
November 17, 2014

http://www.sciencedaily.com/releases/20 ... 174524.htm

Summary:
Increasing the amount of omega-3s in your diet, whether from fish or flax, will likely decrease your risk of getting heart disease, according to nutritionists. A substantial amount of evidence exists supporting the heart-health benefits of eicosapentaenoic acid and docosahexaenoic acid (EPA and DHA), marine-derived omega-3 fatty acids. However, much less evidence exists to demonstrate the positive effects of alpha-linolenic acid (ALA), a plant-based omega-3 fatty acid.

2) Plant compared with marine n-3 fatty acid effects on cardiovascular risk factors and outcomes: what is the verdict?
Am J Clin Nutr. 2014 Jul;100 Suppl 1:453S-8S. doi: 10.3945/ajcn.113.071555. Epub 2014 Jun 4.

http://www.ncbi.nlm.nih.gov/pubmed/24898234

Abstract
Plants provide α-linolenic acid [ALA; 18:3n-3 (18:3ω-3)], which can be converted via eicosapentaenoic acid (EPA; 20:5n-3) to docosahexaenoic acid (DHA; 22:6n-3), which is required for normal visual and cognitive function. Dietary ALA is provided mainly by vegetable oils, especially soybean and rapeseed oils, but is destroyed by partial hydrogenation; it is also present in high amounts in walnuts and flaxseed. Dietary EPA and DHA are provided mainly by fish and so are absent from vegan diets and only present in trace amounts in vegetarian diets. Vegetarians and vegans have lower proportions of DHA in blood and tissue lipids compared with omnivores. High intakes of EPA and DHA (typically in the range of 3-5 g/d) but not ALA have favorable effects on several cardiovascular disease (CVD) risk factors and have been postulated to delay arterial aging and cardiovascular mortality, but these intakes are beyond the range of normal dietary intake. Arterial stiffness, which is a measure of arterial aging, appears to be lower in vegans than in omnivores; and risk of CVD in vegetarians and vegans is approximately one-third that in omnivores. Prospective cohort studies showed higher intakes of EPA+DHA, and less consistently ALA, to be associated with a lower risk of CVD, especially fatal coronary heart disease, but meta-analyses of randomized controlled trials of supplementation of EPA+DHA or ALA in secondary prevention of CVD showed no clear benefit. Current evidence is insufficient to warrant advising vegans and vegetarians to supplement their diets with EPA or DHA for CVD prevention.


Another thread on the topic that also covers the issue of our ability to convert ALA > EPA >DHA

viewtopic.php?f=22&t=19443&p=181741
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Re: Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

Postby JeffN » Tue Jun 28, 2016 10:02 am

JAMA Article

ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease
Pooling Project of 19 Cohort Studies
Original Investigation
June 27, 2016

http://archinte.jamanetwork.com/article.aspx?articleid=2530286

ABSTRACT

Importance
The role of ω-3 polyunsaturated fatty acids for primary prevention of coronary heart disease (CHD) remains controversial. Most prior longitudinal studies evaluated self-reported consumption rather than biomarkers.

Objective
To evaluate biomarkers of seafood-derived eicosapentaenoic acid (EPA; 20:5ω-3), docosapentaenoic acid (DPA; 22:5ω-3), and docosahexaenoic acid (DHA; 22:6ω-3) and plant-derived α-linolenic acid (ALA; 18:3ω-3) for incident CHD.

Data Sources
A global consortium of 19 studies identified by November 2014.

Study Selection
Available prospective (cohort, nested case-control) or retrospective studies with circulating or tissue ω-3 biomarkers and ascertained CHD.

Data Extraction and Synthesis
Each study conducted standardized, individual-level analysis using harmonized models, exposures, outcomes, and covariates. Findings were centrally pooled using random-effects meta-analysis. Heterogeneity was examined by age, sex, race, diabetes, statins, aspirin, ω-6 levels, and FADS desaturase genes.

Main Outcomes and Measures
Incident total CHD, fatal CHD, and nonfatal myocardial infarction (MI).

Results
The 19 studies comprised 16 countries, 45 637 unique individuals, and 7973 total CHD, 2781 fatal CHD, and 7157 nonfatal MI events, with ω-3 measures in total plasma, phospholipids, cholesterol esters, and adipose tissue. Median age at baseline was 59 years (range, 18-97 years), and 28 660 (62.8%) were male. In continuous (per 1-SD increase) multivariable-adjusted analyses, the ω-3 biomarkers ALA, DPA, and DHA were associated with a lower risk of fatal CHD, with relative risks (RRs) of 0.91 (95% CI, 0.84-0.98) for ALA, 0.90 (95% CI, 0.85-0.96) for DPA, and 0.90 (95% CI, 0.84-0.96) for DHA. Although DPA was associated with a lower risk of total CHD (RR, 0.94; 95% CI, 0.90-0.99), ALA (RR, 1.00; 95% CI, 0.95-1.05), EPA (RR, 0.94; 95% CI, 0.87-1.02), and DHA (RR, 0.95; 95% CI, 0.91-1.00) were not. Significant associations with nonfatal MI were not evident. Associations appeared generally stronger in phospholipids and total plasma. Restricted cubic splines did not identify evidence of nonlinearity in dose responses.

Conclusions and Relevance
On the basis of available studies of free-living populations globally, biomarker concentrations of seafood and plant-derived ω-3 fatty acids are associated with a modestly lower incidence of fatal CHD.



Mass Media Article

Science News
Consumption of omega-3s linked to lower risk of fatal heart disease
Date: June 27, 2016
Source: Tufts University, Health Sciences Campus
Summary:

A global consortium of researchers banded together to conduct an epidemiological study analyzing specific omega-3 fatty acid biomarkers and heart disease. They found that blood levels of omega-3 fatty acids from seafood and plant-based foods are associated with a lower risk of fatal heart attack.

https://www.sciencedaily.com/releases/2016/06/160627124433.htm

"Overall, both plant-based and seafood-based omega-3s were associated with about a 10 percent lower risk of fatal heart attacks."
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Re: Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

Postby JeffN » Wed Jul 18, 2018 6:12 pm

Not Fish, Not Supplements. Plants!

There is evidence that taking omega-3 capsules does not reduce heart disease, stroke or death. There is little evidence of effects of eating fish. Although EPA and DHA reduce triglycerides, supplementary omega-3 fats are probably not useful for preventing or treating heart and circulatory diseases. However, increasing plant-based ALA may be slightly protective for some heart and circulatory diseases.

Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease
First published: 18 July 2018
Editorial Group: Cochrane Heart Group
DOI: 10.1002/14651858.CD003177.pub3

http://cochranelibrary-wiley.com/doi/10 ... .pub3/full

Press Release
https://www.cochrane.org/news/new-cochr ... rt-disease

Abstract

Background

Researchers have suggested that omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from plants (alpha-linolenic acid (ALA)) benefit cardiovascular health. Guidelines recommend increasing omega-3-rich foods, and sometimes supplementation, but recent trials have not confirmed this.

Objectives
To assess effects of increased intake of fish- and plant-based omega-3 for all-cause mortality, cardiovascular (CVD) events, adiposity and lipids.

Search methods
We searched CENTRAL, MEDLINE and Embase to April 2017, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to September 2016, with no language restrictions. We handsearched systematic review references and bibliographies and contacted authors.

Selection criteria
We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation and/or advice to increase LCn3 or ALA intake versus usual or lower intake.

Data collection and analysis\
Two review authors independently assessed studies for inclusion, extracted data and assessed validity. We performed separate random-effects meta-analysis for ALA and LCn3 interventions, and assessed dose-response relationships through meta-regression.

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.
Plain language summary

Omega-3 intake for cardiovascular disease

Review question

We reviewed randomised trials (where participants have an equal chance of being assigned to either treatment) examining effects of increasing fish- and plant-based omega-3 fats on heart and circulatory disease (called cardiovascular diseases, CVD, which include heart attacks and stroke), fatness and blood fats (lipids, including cholesterol, triglycerides, high-density lipoprotein (HDL – 'good' cholesterol) and low-density lipoprotein (LDL – 'bad' cholesterol)).

Background

Omega-3 fats are essential – to stay healthy we must obtain some from food. The main types of omega-3 fats are alpha-linolenic acid (ALA), a fat found in plant foods, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), both found in fish. There is a common belief that eating more fish or taking omega-3 supplements reduces our risk of heart disease, stroke and death.

Study characteristics

The evidence is current to April 2017. The review included 79 trials involving over 112,000 people. These studies assessed effects of greater omega-3 intake versus lower or no omega-3 intake for heart and circulatory disease. Twenty-five studies were very trustworthy (well-designed so as not to give biased results). Participants were adults, some with existing illness and some healthy, living in North America, Europe, Australia and Asia. Participants increased omega-3 fats, or maintained their usual fats for at least a year. Most EPA and DHA trials provided capsules, few gave oily fish.

Key results

Increasing EPA and DHA has little or no effect on all-cause deaths and cardiovascular events (high-quality evidence) and probably makes little or no difference to cardiovascular death, coronary deaths or events, stroke, or heart irregularities (moderate-quality evidence, coronary events are illnesses of the arteries which supply the heart). EPA and DHA slightly reduce serum triglycerides and raise HDL (high-quality evidence).

Eating more ALA (for example, by increasing walnuts or enriched margarine) probably makes little or no difference to all-cause or cardiovascular deaths or coronary events but probably slightly reduce cardiovascular events, coronary mortality and heart irregularities (moderate/low-quality evidence). Effects of ALA on stroke are unclear as the evidence was of very low quality.

There is evidence that taking omega-3 capsules does not reduce heart disease, stroke or death. There is little evidence of effects of eating fish. Although EPA and DHA reduce triglycerides, supplementary omega-3 fats are probably not useful for preventing or treating heart and circulatory diseases. However, increasing plant-based ALA may be slightly protective for some heart and circulatory diseases.
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Re: Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

Postby JeffN » Thu Jul 19, 2018 7:52 am

Well, what about the brain?

Cochrane 2012 on Fish oils for the prevention of dementia in older people
Authors' conclusions:
Direct evidence on the effect of omega-3 PUFA on incident dementia is lacking. The available trials showed no benefit of omega-3 PUFA supplementation on cognitive function in cognitively healthy older people.


Cochrane 2016 on Omega-3 fatty acids for the treatment of dementia
Authors' conclusions:
We found no convincing evidence for the efficacy of omega-3 PUFA supplements in the treatment of mild to moderate AD. This result was consistent for all outcomes relevant for people with dementia.
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Re: Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

Postby JeffN » Wed Jun 26, 2019 8:44 am

As we know, nuts, olive oil and a few other foods have been awarded low level qualified health claims. Basically these claims are meaningless and the equivalent of advertising and are only allowed as a result of the food & supplement industries pressure on Congress.

Now we can add EPA & DHA to the insanity.

Here is a great article on it by Marion Nestle


FDA approves qualified health claim for omega-3s
Marion Nestle, PhD

https://www.foodpolitics.com/2019/06/fd ... -omega-3s/

I love the FDA’s qualified health claims for food products because they are so patently ridiculous.

These are health claims so poorly supported by science that the FDA insists on a disclaimer.

What’s their point? Companies can use them for marketing and put the disclaimer in tiny print.

The latest is the FDA’s response to a petition from the Global Organization for EPA and DHA Omega-3s, which asked the FDA to approve these health claims:

* EPA and DHA help lower blood pressure in the general population.
* EPA and DHA reduce BP, a risk factor for CHD (coronary heart disease).
* EPA and DHA reduce the risk of CHD.
* Research shows that EPA and DHA may be beneficial for moderating BP, a risk factor for CHD.
* Convincing scientific evidence indicates that EPA and DHA help lower blood pressure in the general population, with comparable reductions to those achieved with other diet and lifestyle interventions.

Not a chance.

The FDA did its own review of the literature and quite sensibly concluded that evidence supporting such claims is too weak to take seriously.

Instead, the FDA said that

* In light of the above considerations, FDA intends to consider the exercise of its enforcement discretion for the following qualified health claims [with my emphasis in red]:

* Consuming EPA and DHA combined may help lower blood pressure in the general population and reduce the risk of hypertension. However, FDA has concluded that the evidence is inconsistent and inconclusive. One serving of [name of the food or dietary supplement] provides [ ] gram(s) of EPA and DHA.

* Consuming EPA and DHA combined may reduce blood pressure and reduce the risk of hypertension, a risk factor for CHD (coronary heart disease). However, FDA has concluded that the evidence is inconsistent and inconclusive. One serving of [name of the food or dietary supplement] provides [ ] gram(s) of EPA and DHA.

* Consuming EPA and DHA combined may reduce the risk of CHD (coronary heart disease) by lowering blood pressure. However, FDA has concluded that the evidence is inconsistent and inconclusive. One serving of [name of the food or dietary supplement] provides [ ] gram(s) of EPA and DHA.

* Consuming EPA and DHA combined may reduce the risk of CHD (coronary heart disease) by reducing the risk of hypertension. However, FDA has concluded that the evidence is inconsistent and inconclusive. One serving of [name of the food or dietary supplement] provides [ ] gram(s) of EPA and DHA.

* Research shows that consuming EPA and DHA combined may be beneficial for moderating blood pressure, a risk factor for CHD (coronary heart disease). However, FDA has concluded that the evidence is inconsistent and inconclusive. One serving of [name of the food or dietary supplement] provides [ ] gram(s) of EPA and DHA.

In order to use these claims, the products would have to contain at least 0.8 g EPA and DHA (combined total).
(Note: this is 2-4x whatis in most vegan varieties.)

Absurd as all this may seem, the approval of qualified claims is considered a win for the omega 3 industry.

Why does the FDA allow such claims? Because Congress said it had to permit claims even if evidence was insufficient to back them up.

Sigh.
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Re: Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

Postby JeffN » Mon Nov 04, 2019 2:21 pm

Here is a great video presentation on the issue by a colleague

https://www.youtube.com/watch?v=NI7_QekdVoI&t=237s

And his update website discussion on it.

https://radaktim.wixsite.com/website/po ... ain-health

Full reference list
https://radaktim.wixsite.com/website/po ... tober-2019

In Health
Jeff
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Re: Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

Postby JeffN » Mon Nov 04, 2019 4:27 pm

Doesn't look like they help with depression and anxiety either


https://www.cambridge.org/core/journals ... 961E9EADF8

Omega-3 and polyunsaturated fat for prevention of depression and anxiety symptoms: systematic review and meta-analysis of randomised trials
Katherine H. O. Deane (a1), Oluseyi F. Jimoh (a2), Priti Biswas (a3), Alex O'Brien (a4) ...
DOI: https://doi.org/10.1192/bjp.2019.234Published online by Cambridge University Press: 24 October 2019
Abstract

Background
There is strong public belief that polyunsaturated fats protect against and ameliorate depression and anxiety.
Aims

To assess effects of increasing omega-3, omega-6 or total polyunsaturated fat on prevention and treatment of depression and anxiety symptoms.

Method
We searched widely (Central, Medline and EMBASE to April 2017, trial registers to September 2016, ongoing trials updated to August 2019), including trials of adults with or without depression or anxiety, randomised to increased omega-3, omega-6 or total polyunsaturated fat for ≥24 weeks, excluding multifactorial interventions. Inclusion, data extraction and risk of bias were assessed independently in duplicate, and authors contacted for further data. We used random-effects meta-analysis, sensitivity analyses, subgrouping and Grading of Recommendations, Assessment, Development and Evaluations (GRADE) assessment.

Results
We included 31 trials assessing effects of long-chain omega-3 (n = 41 470), one of alpha-linolenic acid (n = 4837), one of total polyunsaturated fat (n = 4997) and none of omega-6. Meta-analysis suggested that increasing long-chain omega-3 probably has little or no effect on risk of depression symptoms (risk ratio 1.01, 95% CI 0.92–1.10, I2 = 0%, median dose 0.95 g/d, duration 12 months) or anxiety symptoms (standardised mean difference 0.15, 95% CI 0.05–0.26, I2 = 0%, median dose 1.1 g/d, duration 6 months; both moderate-quality evidence). Evidence of effects on depression severity and remission in existing depression were unclear (very-low-quality evidence). Results did not differ by risk of bias, omega-3 dose, duration or nutrients replaced. Increasing alpha-linolenic acid by 2 g/d may increase risk of depression symptoms very slightly over 40 months (number needed to harm, 1000).

Conclusions
Long-chain omega-3 supplementation probably has little or no effect in preventing depression or anxiety symptoms.
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Re: Essential Fats: Plant vs Marine & ALA vs EPA &/or DHA

Postby JeffN » Sun Aug 07, 2022 7:25 am

If you read my long thread on Omega 3's and conversion, this is basically the same conclusion it comes to.

Dietary and Plasma Phospholipid Profiles in Vegans and Omnivores-Results from the RBVD Study
Nutrients. 2022 Jul 14;14(14):2900.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9320578/

“Accordingly, our study shows that vegans had a very low intake of EPA and DHA but a respectable plasma proportion of EPA and DHA.”

α-linolenic acid interconversion is sufficient as a source of longer chain ω-3 polyunsaturated fatty acids in humans: An opinion
Lipids. 2022 Jul 31.


α-linolenic acid (αLNA) conversion into the functionally important ω-3 polyunsaturated fatty acids (PUFA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), has been regarded as inadequate for meeting nutritional requirements for these PUFA. This view is based on findings of small αLNA supplementation trials and stable isotope tracer studies that have been interpreted as indicating human capacity for EPA and, in particular, DHA synthesis is limited. The purpose of this review is to re-evaluate this interpretation. Markedly differing study designs, inconsistent findings and lack of trial replication preclude robust consensus regarding the nutritional adequacy of αLNA as a source of EPC and DHA. The conclusion that αLNA conversion in humans is constrained is inaccurate because it presupposes the existence of an unspecified, higher level of metabolic activity. Since capacity for EPA and DHA synthesis is the product of evolution it may be argued that the levels of EPA and DHA it maintains are nutritionally appropriate. Dietary and supra-dietary EPA plus DHA intakes confer health benefits. Paradoxically, such health benefits are also found amongst vegetarians who do not consume EPA and DHA, and for whom αLNA conversion is the primary source of ω-3 PUFA. Since there are no reported adverse effects on health or cognitive development of diets that exclude EPA and DHA, their synthesis from αLNA appears to be nutritionally adequate. This is consistent with the dietary essentiality of αLNA and has implications for developing sustainable nutritional recommendations for ω-3 PUFA.

https://pubmed.ncbi.nlm.nih.gov/35908848/
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