Eating Fish May Reduce Multiple Sclerosis Risk

Eating Fish May Reduce Multiple Sclerosis Risk

Summary: A new study reveals eating fish regularly and taking daily fish oil supplements may reduce the risk of developing multiple sclerosis. Researchers report high fish intake is associated with a 45% reduced risk of developing MS.

Source: AAN.

Eating fish at least once a week or eating fish one to three times per month in addition to taking daily fish oil supplements may be associated with a reduced risk of multiple sclerosis (MS), according to a preliminary study released today that will be presented at the American Academy of Neurology’s 70th Annual Meeting in Los Angeles, April 21 to 27, 2018. These findings suggest that the omega-3 fatty acids found in fish may be associated with lowering the risk of developing MS.

Multiple sclerosis is a disease of the central nervous system that affects communication between the brain and other parts of the body. With MS, the body’s immune system attacks myelin, the fatty white substance that insulates and protects the nerves. This disrupts the signals between the brain and the rest of the body. Symptoms of MS may include fatigue, numbness, tingling or difficulty walking. The first episode of MS symptoms, lasting at least 24 hours, is known as clinically isolated syndrome. There is no cure for MS.

“Consuming fish that contain omega-3 fatty acids has been shown to have a variety of health benefits, so we wanted to see if this simple lifestyle modification, regularly eating fish and taking fish oil supplements, could reduce the risk of MS,” said study author Annette Langer-Gould, MD, PhD, of Kaiser Permanente Southern California in Pasadena, Calif., and a member of the American Academy of Neurology.

For this study, researchers examined the diets of 1,153 people with an average age of 36 from a variety of backgrounds, about half of whom had been diagnosed with MS or clinically isolated syndrome.

Participants were asked about how much fish they regularly ate. High fish intake was defined as either eating one serving of fish per week or eating one to three servings per month in addition to taking daily fish oil supplements. Low intake was defined as less than one serving of fish per month and no fish oil supplements. Examples of fish consumed by study participants include shrimp, salmon and tuna.

salmon

The study found that high fish intake was associated with a 45 percent reduced risk of MS or clinically isolated syndrome when compared with those who ate fish less than once a month and did not take fish oil supplements. A total of 180 of those with MS had high fish intake compared to 251 of the healthy controls.

The study also looked at 13 genetic variations in a human gene cluster that regulates fatty acid levels. Researchers found two of the 13 genetic variations examined were associated with a lower risk of MS, even after accounting for the higher fish intake. This may mean that some people may have a genetic advantage when it comes to regulating fatty acid levels.

While the study suggests that omega-3 fatty acids, and how they are processed by the body, may play an important role in reducing MS risk, Langer-Gould emphasizes that it simply shows an association and not cause and effect. More research is needed to confirm the findings and to examine how omega-3 fatty acids may affect inflammation, metabolism and nerve function.

Fish such as salmon, sardines, lake trout and albacore tuna are generally recommended as good sources of omega-3 fatty acids.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The study was supported by the National Institute of Neurological Disorders and Stroke.

Source: Renee Tessman – AAN
Publisher: Organized by NeuroscienceNews.com.

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Suicide deaths of active-duty US military and omega-3 fatty-acid status

Suicide deaths of active-duty US military and omega-3 fatty-acid status: a case-control comparison.

The recent escalation of US military suicide deaths to record numbers has been a sentinel for impaired force efficacy and has accelerated the search for reversible risk factors.

OBJECTIVE:

To determine whether deficiencies of neuroactive, highly unsaturated omega-3 essential fatty acids (n-3 HUFAs), in particular docosahexaenoic acid (DHA), are associated with increased risk of suicide death among a large random sample of active-duty US military.

METHOD:

In this retrospective case-control study, serum fatty acids were quantified as a percentage of total fatty acids among US military suicide deaths (n = 800) and controls (n = 800) matched for age, date of collection of sera, sex, rank, and year of incident. Participants were active-duty US military personnel (2002-2008). For cases, age at death ranged from 17-59 years (mean = 27.3 years, SD = 7.3 years). Outcome measures included death by suicide, postdeployment health assessment questionnaire (Department of Defense Form 2796), and ICD-9 mental health diagnosis data.

RESULTS:

Risk of suicide death was 14% higher per SD of lower DHA percentage (OR = 1.14; 95% CI, 1.02-1.27; P < .03) in adjusted logistic regressions. Among men, risk of suicide death was 62% greater with low serum DHA status (adjusted OR = 1.62; 95% CI, 1.12-2.34; P < .01, comparing DHA below 1.75% [n = 1,389] to DHA of 1.75% and above [n = 141]). Risk of suicide death was 52% greater in those who reported having seen wounded, dead, or killed coalition personnel (OR = 1.52; 95% CI, 1.11-2.09; P < .01).

CONCLUSION:

This US military population had a very low and narrow range of n-3 HUFA status. Although these data suggest that low serum DHA may be a risk factor for suicide, well-designed intervention trials are needed to evaluate causality.

Reduce inflammatory heart disease with Omega 3

Searches rela

Understanding How Omega 3 Dampens Inflammatory Reactions

Understanding How Omega 3 Dampens Inflammatory Reactions

Summary: Researchers from NTNU find new evidence of how omega 3 fatty acids can dampen inflammatory reactions in the body.

Source: Norwegian University of Science and Technology.

Omega-3 supplements may help slow the development of diseases like cancer, Alzheimer’s and multiple sclerosis.

Omega-3 fatty acids, which we primarily get through eating fatty fish, have long been thought to be good for our health. Many dietary studies have suggested that high intake is associated with a reduced risk of various disorders. Clinical trials have also shown beneficial anti-inflammatory effects in patients taking omega-3 supplements.

Recent research from NTNU supports previous discoveries, and has also found new, useful effects of omega-3 supplements and how these lipids dampen harmful inflammatory reactions in the body.

Effects little known

Despite numerous published dietary and clinical studies, we still don’t fully understand how omega-3 fatty acids affect our cells and if this varies from person to person, between healthy and ill individuals, or whether the mechanism of action varies in different tissues and cells. What we are most sure of is that omega-3 fatty acids can dampen inflammatory reactions. Inflammatory reactions are very important in combating infections, but they can be harmful if activated too strongly or in the absence of bacteria and viruses, like in autoimmune diseases and organ transplants.

Macrophages, which are immune cells that live in all tissues and organs, play a key role in coordinating inflammatory reactions in the body and monitor everything that happens in our tissues. The macrophages convert the information they obtain through various sensors or receptor on their surface to secretion of various hormone-like signal substances that control all parts of inflammatory reactions.

Inflammation can be harmful

We have increasingly become aware that macrophages can be more or less potent in activating inflammatory reactions. So-called sterile inflammatory reactions, such as autoimmune diseases, are often directly harmful.

The ability of macrophages to stimulate inflammatory reactions depends on processes within the macrophage.

Autophagy is one of the processes within macrophages that is important for whether a macrophage is calm or hyperactive. Autophagy (meaning “self-eating”) is a key process for degradation of dysfunctional or unnecessary proteins and other components within our cells.

In the last few years, we’ve learned a lot about how important this process is, say the researchers. The Nobel Prize in Physiology or Medicine 2016 was given to Yoshinori Ohsumi for his discovery of the key genes that control autophagy.

Autophagy is constantly going on in all cells and increases if the cells are starving or injured. We hypothesized that omega-3 fatty acids could dampen inflammatory reactions by elevating autophagy in macrophages. If so, we surmised that this effect might change the signal transformation in the macrophage and as a result, suppress activation of inflammatory reactions.

Activates self-cleaning process

By studying macrophages isolated from mice and humans, we found that the omega-3 fatty acids activated the autophagy and specifically affected some proteins that transform the signals from the environment. Furthermore, we found that omega-3 fatty acids dampened many inflammatory mechanisms within the macrophages, but especially reduced what is known as the type 1 interferon response.

Image shows omega 3 pills.

The factor CXCL-10, which macrophages secrete as part of this interferon response following many types of stimuli, was the most clearly reduced factor after adding omega-3 to the cells.

We then examined blood samples from a clinical study in cardiac transplant patients where we knew that omega-3 supplements improved their clinical status. In these cases, we found that omega-3 fatty acids reduced the level of CXCL-10.

Supplements beneficial

Autophagy thus changes in macrophages in response to omega-3 fatty acids and specifically inhibits the secretion of inflammatory factors that belong to the interferon response, with CXCL-10 showing the clearest reduction. The results of this study are being published in the journal Autophagy.

These findings indicate that omega-3 fatty acid supplements may be particularly beneficial in patients who have conditions that are driven or aggravated by a strong interferon response and CXCL-10.

Our research group hopes that this one day will benefit patients with different forms of cancer, meningitis, multiple sclerosis, Alzheimer’s disease or jaundice. But we must emphasize that a lot of work remains.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

The work being published by PhD candidate Jennifer Mildenberger and colleagues was conducted at CEMIR and at NTNU’s Department of Biomedical Laboratory Science in the Faculty of Natural Science. In addition, researchers in St. Louis, USA carried out important sub studies. The blood tests were from a clinical trial conducted at Oslo University Hospital.

Article author Geir Bjørkøy is a professor in the Department of Biomedical Laboratory Science at NTNU.

Article author Jennifer Mildenberger works for NTNU-Cemir.

Source: Jennifer Mildenberger – Norwegian University of Science and Technology
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “N-3 PUFAs induce inflammatory tolerance by formation of KEAP1-containing SQSTM1/p62-bodies and activation of NFE2L2” by Jennifer Mildenberger, Ida Johansson, Ismail Sergin, Eli Kjøbli, Jan Kristian Damås, Babak Razani, Trude Helen Flo & Geir Bjørkøy in Autophagy. Published online August 18 2017 doi:10.1080/15548627.2017.1345411

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Norwegian University of Science and Technology “Understanding How Omega 3 Dampens Inflammatory Reactions.” NeuroscienceNews. NeuroscienceNews, 24 August 2017.
<http://neurosciencenews.com/inflammation-response-omega-3-7369/&gt;.

Abstract

N-3 PUFAs induce inflammatory tolerance by formation of KEAP1-containing SQSTM1/p62-bodies and activation of NFE2L2

Inflammation is crucial in the defense against infections but must be tightly controlled to limit detrimental hyperactivation. Our diet influences inflammatory processes and omega-3 polyunsaturated fatty acids (n-3 PUFAs) have known anti-inflammatory effects. The balance of pro- and anti-inflammatory processes is coordinated by macrophages and macroautophagy/autophagy has recently emerged as a cellular process that dampens inflammation. Here we report that the n-3 PUFA docosahexaenoic acid (DHA) transiently induces cytosolic speckles of the autophagic receptor SQSTM1/p62 (sequestosome 1) (described as SQSTM1/p62-bodies) in macrophages.

We suggest that the formation of SQSTM1/p62-bodies represents a fast mechanism of NFE2L2/Nrf2 (nuclear factor, erythroid 2 like 2) activation by recruitment of KEAP1 (kelch like ECH associated protein 1). Further, the autophagy receptor TAX1BP1 (Tax1 binding protein 1) and ubiquitin-editing enzyme TNFAIP3/A20 (TNF alpha induced protein 3) could be identified in DHA-induced SQSTM1/p62-bodies. Simultaneously, DHA strongly dampened the induction of pro-inflammatory genes including CXCL10 (C-X-C motif chemokine ligand 10) and we suggest that formation of SQSTM1/p62-bodies and activation of NFE2L2 leads to tolerance towards selective inflammatory stimuli. Finally, reduced CXCL10 levels were related to the improved clinical outcome in n-3 PUFA-supplemented heart-transplant patients and we propose CXCL10 as a robust marker for the clinical benefits mobilized by n-3 PUFA supplementation.

“N-3 PUFAs induce inflammatory tolerance by formation of KEAP1-containing SQSTM1/p62-bodies and activation of NFE2L2” by Jennifer Mildenberger, Ida Johansson, Ismail Sergin, Eli Kjøbli, Jan Kristian Damås, Babak Razani, Trude Helen Flo & Geir Bjørkøy in Autophagy. Published online August 18 2017 doi:10.1080/15548627.2017.1345411


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Link between fish consumption and cardiovascular (CV) health

This is a summary of a systematic review that evaluated the recent evidence regarding the effects of omega-3 fatty acids (FAs), primarily from marine oil supplements, on clinical and selected intermediate cardiovascular (CV) outcomes (i.e., blood pressure, lipid concentrations) and the association of omega-3 FA dietary intake and biomarkers with CV outcomes.

The systematic review included 147 articles published between 2000 and June 2015. Studies that analyzed levels of fish (or other food) consumption without exact quantification of omega-3 FA intake were excluded from this review.

This summary is provided to assist in informed clinical decisionmaking.

However, reviews of evidence should not be construed to represent clinical recommendations or guidelines.

Background

The first observation of a link between fish consumption and cardiovascular (CV) health was made in the late 1970s in a Greenland Eskimo population. This population exhibited a comparatively low rate of CV mortality and consumed a greater than average amount of fish. Since this original observation, there have been hundreds of studies conducted to evaluate the effect of omega-3 fatty acids (FAs) on cardiovascular disease (CVD), its risk factors, and its biomarkers.

The omega-3 FAs include eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and alpha-linolenic acid (ALA). These are essential long-chain and very-long-chain polyunsaturated fatty acids that have many physiological effects, including inflammation regulation. EPA, DHA, and DPA are found in fish and other seafood (called dietary marine oils), as well as in supplements prepared from these foods (referred to here as marine oil supplements). ALA is found in walnuts, leafy green vegetables, and oils such as canola, soy, and flaxseed.

An original systematic review of omega-3 FAs was prepared by the Agency for Healthcare and Research Quality in 2004.1,2 Based on the observational studies available at that time, several expert panels suggested that regular consumption of fish and seafood is associated with lower risk of coronary heart disease (CHD) and cardiac death. The recommendations were based on assumptions of benefits from EPA and DHA and their content in fish and seafood.

The current systematic review aimed to update the evidence in light of the more recent literature published on the topic and included both randomized controlled trials (RCTs) and observational studies. Studies that analyzed levels of fish (or other food) consumption without exact quantification of omega-3 FA intake were excluded.

Conclusions

Observational studies suggest possible benefits of dietary intake of marine oils (such as through consumption of fish) for CV death and total stroke (mainly ischemic stroke).

In contrast, there is high strength of evidence (SOE) from RCTs that marine oil supplements do not affect the risk of major adverse cardiac events (MACE), all-cause death, sudden cardiac death, revascularization, or high blood pressure (BP). Marine oil supplements also have no effect on the risk of atrial fibrillation (moderate SOE). Importantly, RCTs focused primarily on marine oil supplements, not on food sources.

Marine oil supplements affect several intermediate outcomes. First, they significantly lower triglycerides (TGs)—possibly having greater effects in higher doses and in people with higher baseline TGs. Second, they cause small increases in both high-density lipoprotein cholesterol (HDL-c) and low-density lipoprotein cholesterol (LDL-c). Finally, marine oil supplements produce small changes in the ratio of total cholesterol to HDL-c (high SOE).

Applicability of the Findings of This Review

  • The RCTs of marine oil supplements that focused on clinical CVD outcomes were mostly conducted in populations at increased risk for CVD (e.g., with diabetes, cardiometabolic syndrome, hypertension, dyslipidemia, or nondialysis-dependent chronic kidney disease) or with established CVD (e.g., a history of myocardial infarction, angina, stroke, or arrhythmia).
  • The RCTs of marine oil supplements that focused on intermediate CVD outcomes (e.g., BP, lipid concentrations) were conducted in three populations of interest—generally healthy, at increased risk for CVD, and with established CVD.
  • Most observational studies examined associations between dietary intake of marine oils and biomarkers of various omega-3 FAs individually and in combination with regard to long-term CVD events and were conducted in generally healthy populations.

Overview of Clinical Research Evidence on Dietary Marine Oils and Combined Marine Oil Supplements

  • Some evidence based on observational studies indicated that dietary intake of marine oils (including from fish) may be associated with lower risk of CVD death and total stroke (mainly ischemic stroke) in healthy populations (evidence low).
  • In RCTs, marine oil supplements had no effect on the risk of MACE, death from all causes, sudden cardiac death, and coronary revascularization (evidence high) and no effect on atrial fibrillation (evidence medium) in populations with established CVD or at increased risk for CVD (see Table 1).
  • In RCTs, consumption of marine oil supplements was associated with a statistically significant decrease in the concentration of TGs and a small but statistically significant increase in the concentrations of HDL-c and LDL-c (evidence high) in healthy populations and in those with established CVD or at increased risk for CVD (see Table 1).
  • Consumption of marine oil supplements also decreased the ratio of total cholesterol to HDL-c in all three population subgroups—generally healthy, at increased risk for CVD, and with established CVD (evidence high).
Table 1: Summary of Key Findings—Dietary and Supplemented Marine Oil Omega-3 Fatty Acids: Effects on and Associations With Cardiovascular and Intermediate Outcomes
Note: Most RCTs involved evaluations of supplements. Obs-intake represents observational studies of total dietary intake, and Obs-bio represents observational studies of fatty acid biomarkers.
Omega-3 FA [source] Outcome Key Findings Net Change or RCT Hazard Ratio (95% CI) Number and Type of Studies Strength of Evidence
bio = biomarker; BP = blood pressure; CI = confidence interval; DBP = diastolic blood pressure; DHA = docosahexaenoic acid; DPA = docosapentaenoic acid; EPA = eicosapentaenoic acid; HDL-c = high-density lipoprotein cholesterol; intake = total dietary intake; LDL-c = low-density lipoprotein cholesterol; FA = fatty acid; NA = not available; Obs = observational study; RCT = randomized controlled trial; SBP = systolic blood pressure
a Studies that reported combined EPA and DHA were analyzed together with studies that reported combined EPA, DHA, and DPA.
Marine oil (EPA + DHA ± DPA)a [mainly supplements or supplemented food] Major adverse cardiac events
  • No effect in RCTs
  • No association in Obs-intake
  • Unclear association in Obs-bio
0.96 (0.91, 1.02)
  • 10 RCTs
  • 3 Obs-intake
  • 2 Obs-bio
evidence high
All-cause death
  • No effect in RCTs
  • No association in Obs-intake
0.97 (0.92, 1.03)
  • 17 RCTs
  • 3 Obs-intake
evidence high
Sudden cardiac death
  • No effect in RCTs
  • No association in Obs-intake
1.04 (0.92, 1.17)
  • 9 RCTs
  • 1 Obs-intake
evidence high
Coronary revascularization
  • No effect in RCTs
  • No association in Obs-intake
NA
  • 6 RCTs
  • 1 Obs-intake
evidence high
Atrial fibrillation No effect in RCTs Inconsistent findings in Obs-intake NA
  • 3 RCTs
  • 3 Obs-intake
evidence medium
BP (SBP, DBP) No effect
  • SBP: 0.1 mmHg (–0.2, 0.4)
  • DBP: –0.2 mmHg (–0.4, 0.5)
29 RCTs evidence high
Triglycerides Decrease –24 mg/dL (–31, –18) 41 RCTs evidence high
HDL-c Increase 0.9 mg/dL (0.2, 1.6) 34 RCTs evidence high
LDL-c Increase 2.0 mg/dL (0.4, 3.6) 39 RCTs evidence high
Total cholesterol:HDL-c ratio Decrease –0.2 (–0.3, –0.1) 11 RCTs evidence high

Overview of Clinical Research Evidence on Individual Omega-3 Fatty Acid Supplements

  • DHA: DHA supplements had no effect on BP or LDL-c (evidence medium). Evidence is low or insufficient to permit conclusions about the effects of or associations between DHA and any clinical outcome for CVD (see Table 2).
  • EPA or DPA: Evidence was low or insufficient to permit conclusions about the benefit of EPA or DPA, individually, on any clinical or intermediate outcome for CVD.
  • ALA: ALA supplements had no effect on BP or on concentrations of LDL-c, HDL-c, or TGs (evidence medium). Evidence was low or insufficient to permit conclusions about the effects of or associations between ALA and any clinical outcome for CVD (see Table 2).
Table 2: Summary of Key Findings—Individual Omega-3 Fatty Acid Supplements: Effects on and Associations With Intermediate Outcomes
Note: Most RCTs involved evaluations of supplements. Obs-bio represents observational studies of fatty acid biomarkers.
Omega-3 FA [source] Outcome Key Findings Net Change or RCT Hazard Ratio (95% CI) Number and Type of Studies Strength of Evidence
ALA = alpha-linolenic acid; bio = biomarker; BP = blood pressure; CI = confidence interval; DBP = diastolic blood pressure; DHA = docosahexaenoic acid; HDL-c = high-density lipoprotein cholesterol; LDL-c = low-density lipoprotein cholesterol; FA = fatty acid; NA = not available; Obs = observational study; RCT = randomized controlled trial; SBP = systolic blood pressure
Purified DHA [supplements] BP (SBP, DBP) No effect NA 3 RCTs evidence medium
LDL-c No effect NA 3 RCTs evidence medium
ALA [supplements] BP (SBP, DBP)
  • No effect in RCTs
  • No association in Obs-bio
NA
  • 5 RCTs
  • 1 Obs-bio
evidence medium
LDL-c No effect NA 5 RCTs evidence medium
HDL-c No effect NA 5 RCTs evidence medium
Triglycerides No effect NA 5 RCTs evidence medium
Strength of Evidence Scale

High: evidence high
High confidence that the evidence reflects the true effect. Further research is very unlikely to change our confidence in the estimate of effect.

Moderate: evidence medium
Moderate confidence that the evidence reflects the true effect. Further research may change our confidence in the estimate of effect and may change the estimate.

Low: evidence low
Low confidence that the evidence reflects the true effect. Further research is likely to change our confidence in the estimate of effect and is likely to change the estimate.

Insufficient:evidence insufficient
Evidence is either unavailable or does not permit a conclusion.

 The overall evidence grade was assessed based on the ratings for the following domains: study limitations, directness, consistency, precision, and reporting bias. Other domains that were considered, as appropriate, included dose-response association, plausible confounding, and strength of association (i.e., magnitude of effect). For additional details on the methodology used to assess strength of evidence, please refer to: Owens DK, Lohr KN, Atkins D, et al. AHRQ series paper 5: grading the strength of a body of evidence when comparing medical interventions—Agency for Healthcare Research and Quality and the Effective Health-Care Program. J Clin Epidemiol. 2010 May;63(5):513-23. PMID: 19595577.

Gaps in Knowledge and Limitations of the Evidence Base

  • Numerous differences exist between RCTs and observational studies, making comparisons across the two study designs difficult. For example, the doses of marine oil supplements (EPA + DHA) in RCTs were often much higher than the highest dietary intake of marine oils reported for observational studies. Additionally, few RCTs of omega-3 FA supplements attempted to control for background dietary fish or omega-3 FA intake. The response to supplementation may be modified by the background intake.
  • Studies assessed in this review used heterogeneous definitions for most CVD outcomes (e.g., MACE, CVD death, CHD death, CHD), which prohibited direct comparisons across studies in several instances.
  • Few studies compared the dose, formulation, or source of omega-3 FAs, which are all factors that may influence their effectiveness.
  • Long-term RCTs of marine oil supplements would need to be done to determine whether they can influence CV outcomes.
  • Evidence on the effects of or associations with omega-3 FAs based on population, demographic features, or cointerventions (e.g., patients also taking cholestrol-lowering statins, aspirin, or diabetes medications) was insufficient.

What To Discuss With Consumers

  • Dietary intake of marine oils (including from fish) appears to be associated with lower risk of CVD death and stroke in healthy populations.
  • Consumption of marine oil supplements has no effect on health outcomes such as all-cause death, sudden cardiac death, MACE, coronary revascularization, or atrial fibrillation in patients with established CVD or at increased risk for CVD.
  • Consumption of marine oil supplements lowers TG concentrations, raises HDL-c concentrations, and improves lipoprotein ratios (i.e., total cholesterol:HDL-c ratio) but also raises LDL-c concentrations.
  • Consumers considering a marine oil supplement are advised to check the labels for information on quality and purity. The U.S. Pharmacopeial Convention (USP) seal verifies a supplement’s quality.

Source

The information in this summary comes from Balk EM, Adam GP, Langberg V, Halladay C, Chung M, Lin L, Robertson S, Yip A, Steele D, Smith BT, Lau J, Lichtenstein AH, Trikalinos TA. Omega-3 Fatty Acids and Cardiovascular Disease: An Updated Systematic Review. Evidence Report/Technology Assessment No. 223. (Prepared by the Brown Evidence-based Practice Center under Contract No. 290-2012-00012-I.) AHRQ Publication No. 16-E002-EF. Rockville, MD: Agency for Healthcare Research and Quality; August 2016.

This summary was prepared by the John M. Eisenberg Center for Clinical Decisions and Communications Science at Baylor College of Medicine, Houston, TX. It was written by Michelle Swick, Ph.D., Geetha Achanta, PhD., Frank Domino, M.D., and Michael Fordis, M.D.

References

  1. Balk E, Chung M, Lichtenstein A, et al. Effects of omega-3 fatty acids on cardiovascular risk factors and intermediate markers of cardiovascular disease. Evid Rep Technol Assess (Summ). 2004 Mar;(93):1-6. PMID: 15133887.
  2. Wang C, Chung M, Lichtenstein A, et al. Effects of omega-3 fatty acids on cardiovascular disease. Evid Rep Technol Assess (Summ). 2004 Mar;(94):1-8. PMID: 15133888.
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