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Author Topic: No effect of omega 3 supplements on risk of heart health or strokes  (Read 55 times)

Moses2

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30 Billion British Pounds each year. For nothing.

The study is a disaster for an industry built on belief and unscrupulous destruction of nature.

Do leave the Oceans!

They are not for you!



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Fool’s gold: what fish oil is doing to our health and the planet
Health & wellbeing

Omega-3 is one of our favourite supplements – but a huge new study has found it has little or no benefit for heart health or strokes. How did it become a $30bn business?

Paul Greenberg

Wed 25 Jul 2018 06.00 BST
Last modified on Thu 2 Aug 2018 16.00 BST

The omega-3 industry is in a twist. Again. Last week, Cochrane, an organisation that compiles and evaluates medical research for the general public, released a meta-analysis – a study of studies – to determine whether or not omega-3 pills, one of the world’s most popular dietary supplements, reduced the risk of coronary heart disease. After comparing 79 trials involving 112,059 people, the researchers could find “little or no difference to risk of cardiovascular events, coronary heart deaths, coronary heart disease events, stroke or heart irregularities”.
[...]

more:
https://www.theguardian.com/lifeandstyle/2018/jul/25/fish-oil-hype-health-planet-supplements-study-no-benefit


The press release and the study abstract:


https://newsroom.wiley.com/press-release/cochrane-library/new-evidence-published-today-shows-there-little-or-no-effect-omega-3-

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Wiley

New evidence published today shows there is little or no effect of omega 3 supplements on our risk of experiencing heart disease, stroke or death.

Omega 3 is a type of fat. Small amounts of omega 3 fats are essential for good health, and they can be found in the food that we eat. The main types of omega 3 fatty acids are; alpha­linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA).  ALA is normally found in fats from plant foods, such as nuts and seeds (walnuts and rapeseed are rich sources). EPA and DHA, collectively called long chain omega 3 fats, are naturally found in fatty fish, such as salmon and fish oils including cod liver oil.

Wednesday, July 18, 2018 12:01 am EDT

"We can be confident in the findings of this review which go against the popular belief that long-chain omega 3 supplements protect the heart. This large systematic review included information from many thousands of people over long periods.  Despite all this information, we don’t see protective effects."

Omega 3 is a type of fat. Small amounts of omega 3 fats are essential for good health, and they can be found in the food that we eat. The main types of omega 3 fatty acids are; alpha­linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA).  ALA is normally found in fats from plant foods, such as nuts and seeds (walnuts and rapeseed are rich sources). EPA and DHA, collectively called long chain omega 3 fats, are naturally found in fatty fish, such as salmon and fish oils including cod liver oil.

Increased consumption of omega 3 fats is widely promoted globally because of a common belief that that it will protect against heart disease. There is more than one possible mechanism for how they might help prevent heart disease, including reducing blood pressure or reducing cholesterol. Omega 3 fats are readily available as over-the-counter supplements and they are widely bought and used.

A new Cochrane systematic review, published today in the Cochrane Library, combines the results of seventy-nine randomised trials involving 112,059 people. These studies assessed effects of consuming additional omega 3 fat, compared to usual or lower omega 3, on diseases of the heart and circulation. Twenty-five studies were assessed as highly trustworthy because they were well designed and conducted.

The studies recruited men and women, some healthy and others with existing illnesses from North America, Europe, Australia and Asia. Participants were randomly assigned to increase their omega 3 fats or to maintain their usual intake of fat for at least a year. Most studies investigated the impact of giving a long-chain omega 3 supplement in a capsule form and compared it to a dummy pill.  Only a few assessed whole fish intake. Most ALA trials added omega 3 fats to foods such as margarine and gave these enriched foods, or naturally ALA-rich foods such as walnuts, to people in the intervention groups, and usual (non-enriched) foods to other participants.

The Cochrane researchers found that increasing long-chain omega 3 provides little if any benefit on most outcomes that they looked at. They found high certainty evidence that long-chain omega 3 fats had little or no meaningful effect on the risk of death from any cause. The risk of death from any cause was 8.8% in people who had increased their intake of omega 3 fats, compared with 9% in people in the control groups.

They also found that taking more long-chain omega 3 fats (including EPA and DHA), primarily through supplements probably makes little or no difference to risk of cardiovascular events, coronary heart deaths, coronary heart disease events, stroke or heart irregularities. Long-chain omega 3 fats probably did reduce some blood fats, triglycerides and HDL cholesterol. Reducing triglycerides is likely to be protective of heart diseases, but reducing HDL has the opposite effect. The researchers collected information on harms from the studies, but information on bleeding and blood clots was very limited.

The systematic review suggests that eating more ALA through food or supplements probably has little or no effect on cardiovascular deaths or deaths from any cause. However, eating more ALA probably reduces the risk of heart irregularities from 3.3 to 2.6%. The review team found that reductions in cardiovascular events with ALA were so small that about 1000 people would need to increase consumption of ALA for one of them to benefit. Similar results were found for cardiovascular death. They did not find enough data from the studies to be able to measure the risk of bleeding or blood clots from using ALA.

Increasing long-chain omega 3 or ALA probably does not affect body weight or fatness.

Cochrane lead author, Dr. Lee Hooper from the University of East Anglia, UK said: “We can be confident in the findings of this review which go against the popular belief that long-chain omega 3 supplements protect the heart. This large systematic review included information from many thousands of people over long periods.  Despite all this information, we don’t see protective effects.

“The review provides good evidence that taking long-chain omega 3 (fish oil, EPA or DHA) supplements does not benefit heart health or reduce our risk of stroke or death from any cause.  The most trustworthy studies consistently showed little or no effect of long-chain omega 3 fats on cardiovascular health. On the other hand, while oily fish is a healthy food, it is unclear from the small number of trials whether eating more oily fish is protective of our hearts.

“This systematic review did find moderate evidence that ALA, found in plant oils (such as rapeseed or canola oil) and nuts (particularly walnuts) may be slightly protective of some diseases of the heart and circulation. However, the effect is very small, 143 people would need to increase their ALA intake to prevent one person developing arrhythmia. One thousand people would need to increase their ALA intake to prevent one person dying of coronary heart disease or experiencing a cardiovascular event.  ALA is an essential fatty acid, an important part of a balanced diet, and increasing intakes may be slightly beneficial for prevention or treatment of cardiovascular disease.”

--END--

Editor’s notes:

Full citation: Abdelhamid AS, Brown TJ, Brainard JS, Biswas P, Thorpe GC, Moore HJ, Deane KHO, AlAbdulghafoor FK, Summerbell CD, Worthington HV, Song F, Hooper L. Omega 3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews 2018, Issue 7. Art. No.: CD003177. DOI: 10.1002/14651858.CD003177.pub3.

For further information and media enquiries, please contact,

Katie Abbotts

Media Officer, Cochrane

M +44(0) 7810 504380 E kabbotts[etta]cochrane.org or pressoffice[etta]cochrane.org

 

Dawn Peters Wiley (US)

+1 781-388-8408
sciencenewsroom[etta]wiley.com

Dr. Lee Hooper
Norwich Medical School
University of East Anglia
Norwich Research Park
Norwich
Norfolk, UK
l.hooper[etta]uea.ac.uk.


About Cochrane
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Contact:

Katie Abbotts
Media Officer, Cochrane
M +44(0) 7810 504380 E kabbotts[etta]cochrane.org or pressoffice[etta]cochrane.org
Dawn Peters Wiley (US)
+1 781-388-8408
sciencenewsroom[etta]wiley.com
Tags:
Cardiovascular Disease, The Cochrane Library

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Title Abstract Keyword
Cochrane Database of Systematic Reviews

Omega‐3 fatty acids for the primary and secondary prevention of cardiovascular disease

Cochrane Systematic Review - Intervention Version published: 18 July 2018 see what's new

    New search
    Conclusions changed

Article has an altmetric score of 1165
View article information

    Asmaa S Abdelhamid
    Tracey J Brown
    Julii S Brainard
    Priti Biswas
    Gabrielle C Thorpe
    Helen J Moore
    Katherine HO Deane
    Fai K AlAbdulghafoor
    Carolyn D Summerbell
    Helen V Worthington
    Fujian Song
    Lee Hooper

View authors' declarations of interest

Abstract available in English Español

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 available in English Deutsch Español 日本語 Bahasa Malaysia Polski

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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