Summary: Studies reveal there is no demonstrable value in people taking omega 3 oil supplements for the prevention or treatment of cancer. Findings reveal there may be a slightly increased risk of men developing prostate cancer following long-term omega 3 consumption.
Source: University of East Anglia
Increased consumption of omega 3 fats is widely promoted globally because of a common belief that it will protect against, or even reverse, diseases such as cancer, heart attacks and stroke.
But two systematic reviews published today find that omega 3 supplements may slightly reduce coronary heart disease mortality and events, but slightly increase risk of prostate cancer. Both beneficial and harmful effects are small.
If 1,000 people took omega 3 supplements for around four years, three people would avoid dying from heart disease, six people would avoid a coronary event (such as a heart attack) and three extra people would develop prostate cancer.
The sister systematic reviews are published today in the British Journal of Cancer and the Cochrane Database of Systematic Reviews.
Omega 3 is a type of fat. Small amounts are essential for good health and can be found in the food that we eat including nuts and seeds and fatty fish, such as salmon.
Omega 3 fats are also readily available as over-the-counter supplements and they are widely bought and used.
The research team looked at 47 trials involving adults who didn’t have cancer, who were at increased risk of cancer, or had a previous cancer diagnosis, and 86 trials with evidence on cardiovascular events or deaths.
More than 100,000 participants were randomised to consume more long-chain omega-3 fats (fish oils), or maintain their usual intake, for at least a year for each of the reviews.
They studied the number of people who died, received a new diagnosis of cancer, heart attack or stroke and/or died of any of the diseases.
Lead author Dr Lee Hooper, from UEA’s Norwich Medical School, said: “Our previous research has shown that long-chain omega 3 supplements, including fish oils, do not protect against conditions such as anxiety, depression, stroke, diabetes or death.
“These large systematic reviews included information from many thousands of people over long periods. This large amount of information has clarified that if we take omega 3 supplements for several years we may very slightly reduce our risk of heart disease, but balance this with very slightly increasing our risk of some cancers. The overall effects on our health are minimal.
“The evidence on omega 3 mostly comes from trials of fish oil supplements, so health effects of oily fish, a rich source of long-chain omega 3, are unclear. Oily fish is a very nutritious food as part of a balanced diet, rich in protein and energy as well as important micronutrients such as selenium, iodine, vitamin D and calcium – it is much more than an omega 3 source.
“But we found that there is no demonstrable value in people taking omega 3 oil supplements for the prevention or treatment of cancer. In fact, we found that they may very slightly increase cancer risk, particularly for prostate cancer.
“However this risk is offset by a small protective effect on cardiovascular disease.
“Considering the environmental concerns about industrial fishing and the impact it is having on fish stocks and plastic pollution in the oceans, it seems unhelpful to continue to take fish oil tablets that give little or no benefit.”
Funding: The research was funded by the World Health Organisation (WHO).
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Source: University of East Anglia Media Contacts: Lisa Horton – University of East Anglia Image Source: The image is in the public domain.
Omega-3, omega-6 and total dietary polyunsaturated fat on cancer incidence: systematic review and meta-analysis of randomised trials
Background The relationship between long-chain omega-3 (LCn3), alpha-linolenic acid (ALA), omega-6 and total polyunsaturated fatty acid (PUFA) intakes and cancer risk is unclear.
Methods We searched Medline, Embase, CENTRAL and trials registries for RCTs comparing higher with lower LCn3, ALA, omega-6 and/or total PUFA, that assessed cancers over ≥12 months. Random-effects meta-analyses, sensitivity analyses, subgrouping, risk of bias and GRADE were used.
Results We included 47 RCTs (108,194 participants). Increasing LCn3 has little or no effect on cancer diagnosis (RR1.02, 95% CI 0.98–1.07), cancer death (RR0.97, 95% CI 0.90–1.06) or breast cancer diagnosis (RR1.03, 95% CI 0.89–1.20); increasing ALA has little or no effect on cancer death (all high/moderate-quality evidence). Increasing LCn3 (NNTH 334, RR1.10, 95% CI 0.97–1.24) and ALA (NNTH 334, RR1.30, 95% CI 0.72–2.32) may slightly increase prostate cancer risk; increasing total PUFA may slightly increase risk of cancer diagnosis (NNTH 125, RR1.19, 95% CI 0.99–1.42) and cancer death (NNTH 500, RR1.10, 95% CI 0.48–2.49) but total PUFA doses were very high in some trials.
Conclusions The most extensive systematic review to assess the effects of increasing PUFAs on cancer risk found increasing total PUFA may very slightly increase cancer risk, offset by small protective effects on cardiovascular diseases.
Omega‐3 fatty acids for the primary and secondary prevention of cardiovascular diseases
Background 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)) may benefit cardiovascular health. Guidelines recommend increasing omega‐3‐rich foods, and sometimes supplementation, but recent trials have not confirmed this.
Objectives To assess the effects of increased intake of fish‐ and plant‐based omega‐3 fats for all‐cause mortality, cardiovascular events, adiposity and lipids.
Search methods We searched CENTRAL, MEDLINE and Embase to February 2019, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to August 2019, with no language restrictions. We handsearched systematic review references and bibliographies and contacted trial authors.
Selection criteria We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation or advice to increase LCn3 or ALA intake, or both, versus usual or lower intake.
Data collection and analysis Two review authors independently assessed trials 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 86 RCTs (162,796 participants) in this review update and found that 28 were at low summary risk of bias. Trials were of 12 to 88 months’ duration and included adults at varying cardiovascular risk, mainly in high‐income countries. Most trials assessed LCn3 supplementation with capsules, but some used LCn3‐ or ALA‐rich or enriched foods or dietary advice compared to placebo or usual diet. LCn3 doses ranged from 0.5 g a day to more than 5 g a day (19 RCTs gave at least 3 g LCn3 daily).
Meta‐analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on all‐cause mortality (risk ratio (RR) 0.97, 95% confidence interval (CI) 0.93 to 1.01; 143,693 participants; 11,297 deaths in 45 RCTs; high‐certainty evidence), cardiovascular mortality (RR 0.92, 95% CI 0.86 to 0.99; 117,837 participants; 5658 deaths in 29 RCTs; moderate‐certainty evidence), cardiovascular events (RR 0.96, 95% CI 0.92 to 1.01; 140,482 participants; 17,619 people experienced events in 43 RCTs; high‐certainty evidence), stroke (RR 1.02, 95% CI 0.94 to 1.12; 138,888 participants; 2850 strokes in 31 RCTs; moderate‐certainty evidence) or arrhythmia (RR 0.99, 95% CI 0.92 to 1.06; 77,990 participants; 4586 people experienced arrhythmia in 30 RCTs; low‐certainty evidence). Increasing LCn3 may slightly reduce coronary heart disease mortality (number needed to treat for an additional beneficial outcome (NNTB) 334, RR 0.90, 95% CI 0.81 to 1.00; 127,378 participants; 3598 coronary heart disease deaths in 24 RCTs, low‐certainty evidence) and coronary heart disease events (NNTB 167, RR 0.91, 95% CI 0.85 to 0.97; 134,116 participants; 8791 people experienced coronary heart disease events in 32 RCTs, low‐certainty evidence). Overall, effects did not differ by trial duration or LCn3 dose in pre‐planned subgrouping or meta‐regression. There is little evidence of effects of eating fish.
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 in 5 RCTs, moderate‐certainty evidence),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25; 18,619 participants; 219 cardiovascular deaths in 4 RCTs; moderate‐certainty evidence), coronary heart disease mortality (RR 0.95, 95% CI 0.72 to 1.26; 18,353 participants; 193 coronary heart disease deaths in 3 RCTs; moderate‐certainty evidence) and coronary heart disease events (RR 1.00, 95% CI 0.82 to 1.22; 19,061 participants; 397 coronary heart disease events in 4 RCTs; low‐certainty evidence). However, increased ALA may slightly reduce risk of cardiovascular disease events (NNTB 500, RR 0.95, 95% CI 0.83 to 1.07; but RR 0.91, 95% CI 0.79 to 1.04 in RCTs at low summary risk of bias; 19,327 participants; 884 cardiovascular disease events in 5 RCTs; low‐certainty evidence), and probably slightly reduces risk of arrhythmia (NNTB 91, RR 0.73, 95% CI 0.55 to 0.97; 4912 participants; 173 events in 2 RCTs; moderate‐certainty evidence). Effects on stroke are unclear.
Increasing LCn3 and ALA had little or no effect on serious adverse events, adiposity, lipids and blood pressure, except increasing LCn3 reduced triglycerides by ˜15% in a dose‐dependent way (high‐certainty evidence).
Authors’ conclusions This is the most extensive systematic assessment of effects of omega‐3 fats on cardiovascular health to date. Moderate‐ and low‐certainty evidence suggests that increasing LCn3 slightly reduces risk of coronary heart disease mortality and events, and reduces serum triglycerides (evidence mainly from supplement trials). Increasing ALA slightly reduces risk of cardiovascular events and arrhythmia.
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