-
Nutrients Dec 2021Health authorities increasingly recommend a more plant-based diet, rich in fruits, vegetables, pulses, whole grains and nuts, low in red meat and moderate in dairy,...
Health authorities increasingly recommend a more plant-based diet, rich in fruits, vegetables, pulses, whole grains and nuts, low in red meat and moderate in dairy, eggs, poultry and fish which will be beneficial for both health and the environment. A systematic review of observational and intervention studies published between 2000 and January 2020 was conducted to assess nutrient intake and status in adult populations consuming plant-based diets (mainly vegetarian and vegan) with that of meat-eaters. Mean intake of nutrients were calculated and benchmarked to dietary reference values. For micronutrient status, mean concentrations of biomarkers were calculated and compared across diet groups. A total of 141 studies were included, mostly from Europe, South/East Asia, and North America. Protein intake was lower in people following plant-based diets compared to meat-eaters, but well within recommended intake levels. While fiber, polyunsaturated fatty acids (PUFA), folate, vitamin C, E and magnesium intake was higher, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) intake was lower in vegetarians and vegans as compared to meat-eaters. Intake and status of vitamin B12, vitamin D, iron, zinc, iodine, calcium and bone turnover markers were generally lower in plant-based dietary patterns compared to meat-eaters. Vegans had the lowest vitamin B12, calcium and iodine intake, and also lower iodine status and lower bone mineral density. Meat-eaters were at risk of inadequate intakes of fiber, PUFA, α-linolenic acid (ALA), folate, vitamin D, E, calcium and magnesium. There were nutrient inadequacies across all dietary patterns, including vegan, vegetarian and meat-based diets. As plant-based diets are generally better for health and the environment, public health strategies should facilitate the transition to a balanced diet with more diverse nutrient-dense plant foods through consumer education, food fortification and possibly supplementation.
Topics: Adult; Aged; Aged, 80 and over; Animals; Asia; Diet, Vegan; Diet, Vegetarian; Dietary Fiber; Dietary Proteins; Eating; Energy Intake; Europe; Feeding Behavior; Female; Humans; Male; Meat; Micronutrients; Middle Aged; North America; Nutrients; Nutritional Status; Vitamins
PubMed: 35010904
DOI: 10.3390/nu14010029 -
Cureus Oct 2022Omega is a polyunsaturated fatty acid (PUFA) that has an essential impact on cognitive performance at all stages of life. Eicosapentaenoic acid (EPA), docosahexaenoic... (Review)
Review
Omega is a polyunsaturated fatty acid (PUFA) that has an essential impact on cognitive performance at all stages of life. Eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and alpha-linolenic acid (ALA) are essential for brain functions. DHA, the dominant omega-3 in the brain, impacts neurotransmitters and functions of the brain. This systematic review aimed to assess the effects of omega-3 on brain functions. We searched for articles from 2010 to 2022 in PubMed, electronic databases: discover, academic search complete (EBSCO), and Cochrane. To increase search efficiency, search terms include database-specific indexed phrases and keywords. Search terms included "omega three," "DHA," "fish oil," "eicosapentaenoic acid," "EPA," "docosahexaenoic acid," "omega-3," "cognition," "brain," "mental health," and "PUFAs".We conducted a review of only randomized clinical trials (RCTs) that were published in English. We evaluated the quality of the studies using the Cochrane Collaboration bias assessment tool. Our search strategy yielded 174 articles, out of which 33 full-text articles were reviewed and nine articles were selected for data abstraction The overall number of individuals in all nine studies was 1319. Of the participants, 591 (44.81%) were men, and 728 (55.19%) were women. Participants who received omega-3 were 700 (65.06%) compared to 376 (34.94%) who received a placebo, and their mean age was 45. Ingestion of omega-3 fatty acids increases learning, memory, cognitive well-being, and blood flow in the brain. Omega-3 treatments are advantageous, well-tolerated, and risk-free. Lonelier people, the elderly, and those who eat fewer healthy foods containing omega-3 may benefit from an omega-3 supplement. We suggest that natural omega-3 consumption through the diet should be promoted.
PubMed: 36381743
DOI: 10.7759/cureus.30091 -
BMJ (Clinical Research Ed.) Oct 2021To examine the associations between dietary intake and tissue biomarkers of alpha linolenic acid (ALA) and risk of mortality from all causes, cardiovascular disease... (Meta-Analysis)
Meta-Analysis
Dietary intake and biomarkers of alpha linolenic acid and risk of all cause, cardiovascular, and cancer mortality: systematic review and dose-response meta-analysis of cohort studies.
OBJECTIVE
To examine the associations between dietary intake and tissue biomarkers of alpha linolenic acid (ALA) and risk of mortality from all causes, cardiovascular disease (CVD), and cancer.
DESIGN
Systematic review and meta-analysis of prospective cohort studies.
DATA SOURCES
PubMed, Scopus, ISI Web of Science, and Google Scholar to 30 April 2021.
STUDY SELECTION
Prospective cohort studies that reported the risk estimates for death from all causes, CVD, and cancer.
DATA SYNTHESIS
Summary relative risks and 95% confidence intervals were calculated for the highest versus lowest categories of ALA intake using random effects and fixed effects models. Linear and non-linear dose-response analyses were conducted to assess the dose-response associations between ALA intake and mortality.
RESULTS
41 articles from prospective cohort studies were included in this systematic review and meta-analysis, totalling 1 197 564 participants. During follow-up ranging from two to 32 years, 198 113 deaths from all causes, 62 773 from CVD, and 65 954 from cancer were recorded. High intake of ALA compared with low intake was significantly associated with a lower risk of deaths from all causes (pooled relative risk 0.90, 95% confidence interval 0.83 to 0.97, I=77.8%, 15 studies), CVD (0.92, 0.86 to 0.99, I=48.2%, n=16), and coronary heart disease (CHD) (0.89, 0.81 to 0.97, I=5.6%, n=9), and a slightly higher risk of cancer mortality (1.06, 1.02 to 1.11, I=3.8%, n=10). In the dose-response analysis, a 1 g/day increase in ALA intake (equivalent to one tablespoon of canola oil or 0.5 ounces of walnut) was associated with a 5% lower risk of all cause (0.95, 0.91 to 0.99, I=76.2%, n=12) and CVD mortality (0.95, 0.91 to 0.98, I=30.7%, n=14). The pooled relative risks for the highest compared with lowest tissue levels of ALA indicated a significant inverse association with all cause mortality (0.95, 0.90 to 0.99, I=8.2%, n=26). Also, based on the dose-response analysis, each 1 standard deviation increment in blood concentrations of ALA was associated with a lower risk of CHD mortality (0.92, 0.86 to 0.98, I=37.1%, n=14).
CONCLUSIONS
The findings show that dietary ALA intake is associated with a reduced risk of mortality from all causes, CVD, and CHD, and a slightly higher risk of cancer mortality, whereas higher blood levels of ALA are associated with a reduced risk of all cause and CHD mortality only.
SYSTEMATIC REVIEW REGISTRATION
PROSPERO CRD42021229487.
Topics: Cardiovascular Diseases; Eating; Humans; Mortality; Neoplasms; Protective Factors; Risk Assessment; alpha-Linolenic Acid
PubMed: 34645650
DOI: 10.1136/bmj.n2213 -
The Cochrane Database of Systematic... Jul 2018Researchers have suggested that omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3), including eicosapentaenoic acid (EPA) and docosahexaenoic... (Meta-Analysis)
Meta-Analysis Review
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.
Topics: Adult; Cardiovascular Diseases; Cause of Death; Dietary Supplements; Docosahexaenoic Acids; Eicosapentaenoic Acid; Fatty Acids, Omega-3; Humans; Primary Prevention; Randomized Controlled Trials as Topic; Secondary Prevention; Treatment Outcome; alpha-Linolenic Acid
PubMed: 30019766
DOI: 10.1002/14651858.CD003177.pub3 -
Frontiers in Cardiovascular Medicine 2021The α-linolenic acid is a plant origin n-3 fatty acid that may reduce the risk of cardiovascular disease. However, the effect of α-linolenic acid (ALA) on the risk of...
The α-linolenic acid is a plant origin n-3 fatty acid that may reduce the risk of cardiovascular disease. However, the effect of α-linolenic acid (ALA) on the risk of heart failure (HF) remains unclear. In this meta-analysis, we aimed to determine the role of ALA in the risk of incident HF. Electronic databases were searched for studies up to August 10, 2021. Studies were included for meta-analysis if the adjusted risk of HF in different dietary intake or circulating levels of ALA was reported. We used the random-effects model to calculate the estimated hazard ratios (HRs) and 95% CI for higher ALA. A total of 6 studies (7 cohorts) comprising 135,270 participants were included for meta-analysis. After a median follow-up duration of 10 years, 5,905 cases of HF were recorded. No significant heterogeneity was observed among all the included studies. Random-effects model analyses showed that there was no significant association between ALA and the risk of incident HF, either assessed as quintiles (highest quintile vs. lowest quintile: HR = 0.95, 95% CI = 0.86-1.06) or per 1 increment (HR = 0.99, 95% CI = 0.95-1.01). Furthermore, we did not observe any association between ALA and the risk of HF in subgroup analyses performed according to age, sex, follow-up duration, and measuring method of ALA. We found no association between ALA and the risk of incident HF, suggesting that ALA might not be effective in the prevention of HF.
PubMed: 35059448
DOI: 10.3389/fcvm.2021.788452 -
BMJ (Clinical Research Ed.) Aug 2019To assess effects of increasing omega-3, omega-6, and total polyunsaturated fatty acids (PUFA) on diabetes diagnosis and glucose metabolism. (Meta-Analysis)
Meta-Analysis
Omega-3, omega-6, and total dietary polyunsaturated fat for prevention and treatment of type 2 diabetes mellitus: systematic review and meta-analysis of randomised controlled trials.
OBJECTIVE
To assess effects of increasing omega-3, omega-6, and total polyunsaturated fatty acids (PUFA) on diabetes diagnosis and glucose metabolism.
DESIGN
Systematic review and meta-analyses.
DATA SOURCES
Medline, Embase, Cochrane CENTRAL, WHO International Clinical Trials Registry Platform, Clinicaltrials.gov, and trials in relevant systematic reviews.
ELIGIBILITY CRITERIA
Randomised controlled trials of at least 24 weeks' duration assessing effects of increasing α-linolenic acid, long chain omega-3, omega-6, or total PUFA, which collected data on diabetes diagnoses, fasting glucose or insulin, glycated haemoglobin (HbA), and/or homoeostatic model assessment for insulin resistance (HOMA-IR).
DATA SYNTHESIS
Statistical analysis included random effects meta-analyses using relative risk and mean difference, and sensitivity analyses. Funnel plots were examined and subgrouping assessed effects of intervention type, replacement, baseline risk of diabetes and use of antidiabetes drugs, trial duration, and dose. Risk of bias was assessed with the Cochrane tool and quality of evidence with GRADE.
RESULTS
83 randomised controlled trials (mainly assessing effects of supplementary long chain omega-3) were included; 10 were at low summary risk of bias. Long chain omega-3 had little or no effect on likelihood of diagnosis of diabetes (relative risk 1.00, 95% confidence interval 0.85 to 1.17; 58 643 participants, 3.7% developed diabetes) or measures of glucose metabolism (HbA mean difference -0.02%, 95% confidence interval -0.07% to 0.04%; plasma glucose 0.04, 0.02 to 0.07, mmol/L; fasting insulin 1.02, -4.34 to 6.37, pmol/L; HOMA-IR 0.06, -0.21 to 0.33). A suggestion of negative outcomes was observed when dose of supplemental long chain omega-3 was above 4.4 g/d. Effects of α-linolenic acid, omega-6, and total PUFA on diagnosis of diabetes were unclear (as the evidence was of very low quality), but little or no effect on measures of glucose metabolism was seen, except that increasing α-linolenic acid may increase fasting insulin (by about 7%). No evidence was found that the omega-3/omega-6 ratio is important for diabetes or glucose metabolism.
CONCLUSIONS
This is the most extensive systematic review of trials to date to assess effects of polyunsaturated fats on newly diagnosed diabetes and glucose metabolism, including previously unpublished data following contact with authors. Evidence suggests that increasing omega-3, omega-6, or total PUFA has little or no effect on prevention and treatment of type 2 diabetes mellitus.
SYSTEMATIC REVIEW REGISTRATION
PROSPERO CRD42017064110.
Topics: Adult; Blood Glucose; Diabetes Mellitus, Type 2; Dietary Fats, Unsaturated; Dietary Supplements; Fasting; Fatty Acids, Omega-3; Fatty Acids, Omega-6; Fatty Acids, Unsaturated; Female; Glycated Hemoglobin; Humans; Insulin; Insulin Resistance; Male; Primary Prevention; Randomized Controlled Trials as Topic; Secondary Prevention
PubMed: 31434641
DOI: 10.1136/bmj.l4697 -
The Cochrane Database of Systematic... Feb 2020Omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3)), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from... (Meta-Analysis)
Meta-Analysis
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.
Topics: Adiposity; Adult; Arrhythmias, Cardiac; Cardiovascular Diseases; Cause of Death; Coronary Disease; Dietary Supplements; Docosahexaenoic Acids; Eicosapentaenoic Acid; Fatty Acids, Omega-3; Hemorrhage; Humans; Primary Prevention; Pulmonary Embolism; Randomized Controlled Trials as Topic; Regression Analysis; Secondary Prevention; Stroke; Treatment Outcome; alpha-Linolenic Acid
PubMed: 32114706
DOI: 10.1002/14651858.CD003177.pub5 -
The Cochrane Database of Systematic... Dec 2019Polyunsaturated fatty acid (PUFA) supplements, involving omega-3 and/or omega-6 components, have been proposed as a therapy for dry eye. Omega-3 PUFAs exist in both... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Polyunsaturated fatty acid (PUFA) supplements, involving omega-3 and/or omega-6 components, have been proposed as a therapy for dry eye. Omega-3 PUFAs exist in both short- (alpha-linolenic acid [ALA]) and long-chain (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) forms, which largely derive from certain plant- and marine-based foods respectively. Omega-6 PUFAs are present in some vegetable oils, meats, and other animal products.
OBJECTIVES
To assess the effects of omega-3 and omega-6 polyunsaturated fatty acid (PUFA) supplements on dry eye signs and symptoms.
SEARCH METHODS
CENTRAL, Medline, Embase, two other databases and three trial registries were searched in February 2018, together with reference checking. A top-up search was conducted in October 2019, but the results have not yet been incorporated.
SELECTION CRITERIA
We included randomized controlled trials (RCTs) involving dry eye participants, in which omega-3 and/or omega-6 supplements were compared with a placebo/control supplement, artificial tears, or no treatment. We included head-to-head trials comparing different forms or doses of PUFAs.
DATA COLLECTION AND ANALYSIS
We followed standard Cochrane methods and assessed the certainty of the evidence using GRADE.
MAIN RESULTS
We included 34 RCTs, involving 4314 adult participants from 13 countries with dry eye of variable severity and etiology. Follow-up ranged from one to 12 months. Nine (26.5%) studies had published protocols and/or were registered. Over half of studies had high risk of bias in one or more domains. Long-chain omega-3 (EPA and DHA) versus placebo or no treatment (10 RCTs) We found low certainty evidence that there may be little to no reduction in dry eye symptoms with long-chain omega-3 versus placebo (four studies, 677 participants; mean difference [MD] -2.47, 95% confidence interval [CI] -5.14 to 0.19 units). We found moderate certainty evidence for a probable benefit of long-chain omega-3 supplements in increasing aqueous tear production relative to placebo (six studies, 1704 participants; MD 0.68, 95% CI 0.26 to 1.09 mm/5 min using the Schirmer test), although we did not judge this difference to be clinically meaningful. We found low certainty evidence for a possible reduction in tear osmolarity (one study, 54 participants; MD -17.71, 95% CI -28.07 to -7.35 mOsmol/L). Heterogeneity was too substantial to pool data on tear break-up time (TBUT) and adverse effects. Combined omega-3 and omega-6 versus placebo (four RCTs) For symptoms (low certainty) and ocular surface staining (moderate certainty), data from the four included trials could not be meta-analyzed, and thus effects on these outcomes were unclear. For the Schirmer test, we found moderate certainty evidence that there was no intergroup difference (four studies, 455 participants; MD: 0.66, 95% CI -0.45 to 1.77 mm/5 min). There was moderate certainty for a probable improvement in TBUT with the PUFA intervention relative to placebo (four studies, 455 participants; MD 0.55, 95% CI 0.04 to 1.07 seconds). Effects on tear osmolarity and adverse events were unclear, with data only available from a single small study for each outcome. Omega-3 plus conventional therapy versus conventional therapy alone (two RCTs) For omega-3 plus conventional therapy versus conventional therapy alone, we found low certainty evidence suggesting an intergroup difference in symptoms favoring the omega-3 group (two studies, 70 participants; MD -7.16, 95% CI -13.97 to -0.34 OSDI units). Data could not be combined for all other outcomes. Long-chain omega-3 (EPA and DHA) versus omega-6 (five RCTs) For long-chain omega-3 versus omega-6 supplementation, we found moderate certainty evidence for a probable improvement in dry eye symptoms (two studies, 130 participants; MD -11.88, 95% CI -18.85 to -4.92 OSDI units). Meta-analysis was not possible for outcomes relating to ocular surface staining, Schirmer test or TBUT. We found low certainty evidence for a potential improvement in tear osmolarity (one study, 105 participants; MD -11.10, 95% CI -12.15 to -10.05 mOsmol/L). There was low level certainty regarding any potential effect on gastrointestinal side effects (two studies, 91 participants; RR 2.34, 95% CI 0.35 to 15.54).
AUTHORS' CONCLUSIONS
Overall, the findings in this review suggest a possible role for long-chain omega-3 supplementation in managing dry eye disease, although the evidence is uncertain and inconsistent. A core outcome set would work toward improving the consistency of reporting and the capacity to synthesize evidence.
Topics: Dry Eye Syndromes; Fatty Acids, Omega-3; Fatty Acids, Omega-6; Humans; Lubricant Eye Drops; Ophthalmic Solutions; Randomized Controlled Trials as Topic
PubMed: 31847055
DOI: 10.1002/14651858.CD011016.pub2 -
The American Journal of Clinical... Dec 2012Prior studies of α-linolenic acid (ALA), a plant-derived omega-3 (n-3) fatty acid, and cardiovascular disease (CVD) risk have generated inconsistent results. (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Prior studies of α-linolenic acid (ALA), a plant-derived omega-3 (n-3) fatty acid, and cardiovascular disease (CVD) risk have generated inconsistent results.
OBJECTIVE
We conducted a meta-analysis to summarize the evidence regarding the relation of ALA and CVD risk.
DESIGN
We searched multiple electronic databases through January 2012 for studies that reported the association between ALA (assessed as dietary intake or as a biomarker in blood or adipose tissue) and CVD risk in prospective and retrospective studies. We pooled the multivariate-adjusted RRs comparing the top with the bottom tertile of ALA using random-effects meta-analysis, which allowed for between-study heterogeneity.
RESULTS
Twenty-seven original studies were identified, including 251,049 individuals and 15,327 CVD events. The overall pooled RR was 0.86 (95% CI: 0.77, 0.97; I² = 71.3%). The association was significant in 13 comparisons that used dietary ALA as the exposure (pooled RR: 0.90; 95% CI: 0.81, 0.99; I² = 49.0%), with similar but nonsignificant trends in 17 comparisons in which ALA biomarkers were used as the exposure (pooled RR: 0.80; 95% CI: 0.63, 1.03; I² = 79.8%). An evaluation of mean participant age, study design (prospective compared with retrospective), exposure assessment (self-reported diet compared with biomarker), and outcome [fatal coronary heart disease (CHD), nonfatal CHD, total CHD, or stroke] showed that none were statistically significant sources of heterogeneity.
CONCLUSIONS
In observational studies, higher ALA exposure is associated with a moderately lower risk of CVD. The results were generally consistent for dietary and biomarker studies but were not statistically significant for biomarker studies. However, the high unexplained heterogeneity highlights the need for additional well-designed observational studies and large randomized clinical trials to evaluate the effects of ALA on CVD.
Topics: Biomarkers; Cardiovascular Diseases; Diet; Humans; Reproducibility of Results; Risk; alpha-Linolenic Acid
PubMed: 23076616
DOI: 10.3945/ajcn.112.044040 -
Heart (British Cardiac Society) Feb 2006To determine whether dietary supplementation with alpha linolenic acid (ALA) can modify established and emerging cardiovascular risk markers. (Meta-Analysis)
Meta-Analysis Review
OBJECTIVE
To determine whether dietary supplementation with alpha linolenic acid (ALA) can modify established and emerging cardiovascular risk markers.
DESIGN
Systematic review and meta-analysis of randomised controlled trials identified by a search of Medline, Embase, Cochrane Controlled Trials Register (CENTRAL), and the metaRegister of Controlled Trials (mRCT).
PATIENTS
All human studies were reviewed.
MAIN OUTCOME MEASURES
Changes in concentrations of total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, triglyceride, fibrinogen, and fasting plasma glucose, and changes in body mass index, weight, and systolic and diastolic blood pressure.
RESULTS
14 studies with minimum treatment duration of four weeks were reviewed. ALA had a significant effect on three of the 32 outcomes examined in these studies. Concentrations of fibrinogen (0.17 micromol/l, 95% confidence interval (CI) -0.30 to -0.04, p = 0.01) and fasting plasma glucose (0.20 mmol/l, 95% CI -0.30 to -0.10, p < 0.01) were reduced. There was a small but clinically unimportant decrease in HDL (0.01 mmol/l, 95% CI -0.02 to 0.00, p < 0.01). Treatment with ALA did not significantly modify total cholesterol, triglycerides, weight, body mass index, LDL, diastolic blood pressure, systolic blood pressure, VLDL, and apolipoprotein B.
CONCLUSIONS
Although ALA supplementation may cause small decreases in fibrinogen concentrations and fasting plasma glucose, most cardiovascular risk markers do not appear to be affected. Further trials are needed, but dietary supplementation with ALA to reduce cardiovascular disease cannot be recommended.
Topics: Blood Glucose; Blood Pressure; Body Weight; Cardiovascular Diseases; Cholesterol; Dietary Supplements; Fibrinogen; Humans; Risk Factors; Triglycerides; alpha-Linolenic Acid
PubMed: 15890766
DOI: 10.1136/hrt.2004.053538