Omega-3s in over-the-counter or prescription supplements are available in various forms, depending on their extraction, processing methods, or natural occurrence. These forms include:

• ●  Triglycerides: These occur naturally or through the re-esterification of ethyl esters; they have high bioavailability. (this is what we use in our MAINTAIN supplement)
• ●  Phospholipids: These occur naturally; they have high bioavailability.
• ●  Ethyl esters: These are produced via molecular distillation; they have lowbioavailability.Whereas most omega-3 fatty acids in fish are triglycerides and phospholipids, prescription omega-3 supplements are typically ethyl esters. The FDA regulates prescription supplements for safety and quality, but studies suggest they are not absorbed or integrated into cells as efficiently as omega-3s in triglyceride form.

   How Much Omega-3 Should You Take?

  A good approach for determining how much omega-3 you should take is to check your current omega-3 levels – your Omega-3 Index – and tailor the dose based on those results. We do offer this testing in our office. Just contact us for more information.

  There is no established dose for omega-3 supplementation. However, to reach the optimal Omega-3 Index range of 8 to 11 percent from a baseline of 4 percent, experts recommend consuming 1,750 to 2,500 milligrams (1.75 to 2 grams) of omega-3s daily.

  While higher doses of ethyl ester form greater than 2 grams daily may carry a slightly increased relative risk of arrhythmia in older people with cardiovascular risk factors, they may also provide qualitatively unique benefits, including immune system regulation, neurological support, muscle growth promotion, and heart protection.

  In one trial, elite athletes who consumed up to 3.6 grams of supplemental omega-3s daily experienced reduced pro-inflammatory cytokines, including IL-1B, and increased anti-inflammatory cytokines, including IL-10. Another trial demonstrated that 5 grams of supplemental omega-3s daily attenuated muscle disuse atrophy in young women after immobilization. The study’s investigators posited that high-dose fish oil may increase protein synthesis rates in skeletal muscle.

  In a small study in which 33 healthy people with the APOE4 gene variant took at least 2 grams of DHA-rich omega-3 fatty acids daily along with a B-complex vitamin, DHA and EPA levels in their cerebrospinal fluid increased. Authors of a large-scale review found that 2 to 3 grams of omega-3 daily reduced systolic and diastolic blood pressure.

  Omega-3 fatty acids are considered safe, and clinical trials have demonstrated their safety at high intakes, with some trials providing up to 25 grams daily. However, it’s important to note that the safety of consuming these omega-3 megadoses was assessed in a short-term clinical trial, and such high doses should be approached with caution and under medical supervision.

  Note: Your optimal omega-3 dose may differ considerably from that of your partner, friend, or family member. Many people carry genetic variants in the enzymes that metabolize fatty acids, influencing their omega-3 status.

  Frequently Asked Questions

  Are omega-3s from algae the same as those from fish or krill oil?

  Omega-3s from algae raise circulating omega-3 levels as efficiently as those derived from fish oil. However, they differ in terms of their content and cost-effectiveness.

  Algal-derived omega-3 supplements often:

  • ●  Consist mainly of DHA with little to no EPA, potentially diminishing their effectiveness for cardiovascular disease prevention.
  • ●  Have lower concentrations and smaller recommended doses than products derived from fish or krill oil – and end up costing you more in the long run. Is omega-3 from flaxseed or other plant sources such as hemp suitable as a replacement for marine-derived omega-3s? Plants like flaxseed, hemp, and walnuts contain the omega-3 ALA. The body converts ALA to EPA and DHA, but the conversion rate is remarkably low, with 0.2 to 8 percent of ALA converting to EPA and even less converting to DHA. Therefore, ALA might not be a suitable substitute for EPA and DHA. Although algae-based products provide a plant-based option to increase serum DHA levels effectively, they might not boost EPA. In addition, consuming ALA alone doesn’t usually raise the Omega-3 Index above 8 percent. However, certain biological mechanisms may allow people who follow plant-based diets and consume ALA to reach adequate levels of EPA and DHA. For example, some hormones, such as estrogen, can enhance the efficiency of this conversion.

  Is there an optimal time to supplement omega-3 fatty acids?

  There are no guidelines for optimal “timing” of omega-3 fatty acid intake. However, some evidence suggests that EPA and DHA improve sleep quality and reduce the body’s postprandial (post-meal) pro-inflammatory response.

  Postprandial (after eating) inflammation

  Blood levels of lipopolysaccharide (LPS), an endotoxin found in the cell membranes of gut microbes and linked to an array of age-related diseases, increase after eating, promoting an immune response and inflammation. In a study where participants received low versus high doses of the prescription omega-3 Lovaza (1 gram EPA + DHA) before LPS exposure, those who took the high dose had a lower temperature increase (corresponding to a more appropriate immune response). These findings suggest that taking an omega-3 supplement during mealtime may blunt post-meal increases in LPS, thereby attenuating postprandial inflammation.

  Note: While there is no strong evidence advocating for an optimal time to take omega-3 supplements, taking them with a fatty meal improves their metabolism.

  Should I refrigerate omega-3 capsules?

  Omega-3 fatty acids are particularly susceptible to oxidation, which accelerates at higher temperatures. Encapsulation provides some protection against oxidation, but non-encapsulated products (liquid forms) may be more vulnerable. Therefore, it is a best practice and good general rule of thumb to refrigerate all omega-3 supplements. Interestingly, research indicates that neither the expiration date nor the manufacture date on omega-3 supplements reliably predicts rancidity levels, probably because of the heterogeneity between products.

  Omega-3 fatty acids frozen or refrigerated are safe, beneficial, and not associated with adverse effects. If you buy an omega-3 oil, refrigerate it immediately to slow oxidation. However, there is little evidence that refrigerating your omega-3 capsules will prolong their shelf life or lower their rancidity.

  Omega-3 Deficiency

  A deficiency of essential fatty acids—either omega-3s or omega-6s—can cause rough, scaly skin and dermatitis. Plasma and tissue concentrations of DHA decrease when an omega-3 fatty acid deficiency is present. However, there are no known cut-off concentrations of DHA or EPA below which functional endpoints, such as those for visual or neural function or for immune response, are impaired.

  Groups at Risk of Omega-3 Inadequacy

  Evidence that higher LC omega-3 levels are associated with a reduced risk of several chronic diseases, including coronary heart disease, suggests that many Americans could benefit from slightly higher intakes. However, classical essential fatty acid deficiency in healthy individuals in the United States is virtually nonexistent. During periods of dietary-fat restriction or malabsorption accompanied by an energy deficit, the body releases essential fatty acids from adipose-tissue reserves. For this reason, clinical signs of essential fatty-acid deficiency are usually only found in patients receiving parenteral nutrition that lacks PUFAs. This was documented in case reports during the 1970s and 1980s, but all current enteral and parenteral feeding solutions contain adequate levels of PUFAs.

  Omega-3s and Health

  The potential health benefits of consuming omega-3s are the focus of a great deal of scientific research. By far, the majority of research has focused on EPA and DHA from foods (e.g., fish) and/or dietary supplements (e.g., fish oil) as opposed to ALA from plant-based foods.

  Many observational studies link higher intakes of fish and other seafood with improved health outcomes. However, it is difficult to ascertain whether the benefits are due to the omega-3 content of the seafood (which varies among species), other components in the seafood, the substitution of seafood for other less healthful foods, other healthful behaviors, or a combination of these factors. Data from randomized clinical trials are needed to shed light on these questions.

  This section focuses on areas of health in which omega-3s might be involved: CVD and its risk factors; infant health and neurodevelopment; cancer prevention; Alzheimer’s disease, dementia, and cognitive function; age-related macular degeneration; dry eye disease; rheumatoid arthritis; and other conditions.

  Cardiovascular disease and cardiovascular disease risk factors

  Many studies have assessed the effects of omega-3s—primarily EPA and DHA—on CVD and CVD risk factors, such as high blood pressure and elevated plasma lipids. This interest was spurred by epidemiological research dating back to the 1970s that found low rates of myocardial infarction and other coronary events among Greenland Inuit and other fish-eating populations, such as those in Japan. Results from observational studies have been consistent with these findings, with several systematic reviews and meta-analyses showing that higher consumption of fish and higher dietary or plasma levels of omega-3s are associated with a lower risk of heart failure, coronary disease, and fatal coronary heart disease.

  Initial clinical research

  Clinical trial data from the 1989 Diet and Reinfarction Trial, the 1999 open-label GISSI-Prevenzione trial, and others supported the hypothesis that LC omega-3s offer protection from CVD by reducing the heart’s susceptibility to arrhythmias, lowering triglyceride levels, lowering blood pressure, and decreasing platelet aggregation. The authors of a systematic review that included six secondary-prevention trials and one primary-prevention trial of omega-3 supplementation published between 1966 and 2005 concluded that consumption of LC omega-3s from fish and fish oil supplements reduces rates of all-cause mortality, cardiac death, sudden death, and stroke. They noted that the evidence of benefit is stronger for secondary than for primary prevention.

  Results from the Japan EPA Lipid Intervention Study in 2007 supported the growing body of evidence that LC omega-3s reduce the risk of heart disease, especially in people with a history of coronary artery disease. In this study, 18,645 people with hypercholesterolemia (total cholesterol of at least 251 mg/dL) with or without coronary artery disease received either 1.8 g/day EPA plus a statin or a statin only. After a mean of 4.6 years, the EPA group had 19% fewer major coronary events than the control group. The EPA group also experienced a significant reduction in rates of unstable angina and nonfatal coronary events but not in rates of sudden cardiac death or coronary death in comparison with the control group.

  In an analysis of the primary prevention subgroup from this study (participants with no history of coronary artery disease), EPA supplementation had no significant effects on any outcome. However, for the secondary prevention subgroup (those with a history of coronary artery disease), the EPA group had a 28% reduction in the rate of unstable angina and a 19% reduction in that of major coronary events. A separate analysis of data from this study found that the EPA supplementation did not affect total stroke incidence but did reduce the risk of recurrent stroke by 20% in patients who had previously experienced a stroke.

  Several subsequent clinical trials, however, had largely null findings. For example, the 2012 Outcome Reduction with an Initial Glargine Intervention (ORIGIN) trial included 12,536 patients who had diabetes or a high risk of diabetes and a high risk of cardiovascular events. Supplementation with 1 g/day omega-3s (375 mg DHA and 465 mg EPA) for about 6 years significantly lowered triglyceride levels but had no effect on risk of myocardial infarction, stroke, or death from cardiovascular causes in comparison with placebo. Similarly, in the 2010 Alpha Omega Trial, low-dose EPA and DHA supplementation (150 mg DHA and 226 mg EPA daily, supplied in a margarine) for 40 months also failed to reduce the rate of major cardiovascular events in comparison with placebo among 4,837 older men and women who had previously experienced a myocardial infarction and were receiving antihypertensive, antithrombotic, and/or lipid-lowering medications .

  Recent clinical trials

  Scientists gained additional insight into the effects of omega-3s for the primary prevention of CVD, including in patients with diabetes, from two 2018 trials: Vitamin D and OmegA-3 TriaL (VITAL) and A Study of Cardiovascular Events in Diabetes (ASCEND). Both trials compared the same 1 g/day omega-3 formulation (460 mg EPA and 380 mg DHA) with placebo, but in different populations. VITAL included 25,871 men age 50 and older and women age 55 and older with no previous heart attacks, strokes, or cancer, whereas ASCEND included 15,480 adults age 40 or older with diabetes but no evidence of CVD. VITAL also tested the omega-3 supplement with and without 2,000 International Units (IU)/day vitamin D.

  In VITAL, the omega-3 supplement did not significantly reduce the rate of major cardiovascular events combined (myocardial infarction, stroke, and cardiovascular mortality) after a median of 5.3 years. However, participants taking the omega-3 supplement did experience a statistically significant 28% reduction in total myocardial infarction rates (including a 77% reduction among African Americans and a 40% reduction among those who consumed less than 1.5 servings of fish per week). Supplement users also had significant reductions in rates of fatal myocardial infarction, total coronary heart disease, and percutaneous coronary intervention (a procedure that widens blocked or narrowed coronary arteries). No significant reductions in stroke or death rates from cardiovascular causes were observed.

  ASCEND had similar findings. After a mean follow-up of 7.4 years, the omega-3 supplement did not significantly affect the risk of a serious vascular event (composite of nonfatal myocardial infarction or stroke, transient ischemic attack, and cardiovascular death, excluding intracranial hemorrhage) or revascularization. However, omega-3 supplementation did significantly reduce the risk of cardiovascular death by 19% in comparison with placebo.

  The 2019 Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial (REDUCE-IT) found significant CVD benefits with Vascepa, a high-dose, prescription form of omega-3s containing EPA in the form of icosapent ethyl (IPE), an ethyl ester. REDUCE-IT included 8,179 participants with CVD age 45 years or older or with diabetes and at least one other risk factor age 50 years or older. All participants had a fasting triglyceride level of 135 to 499 mg/dL even though they were receiving statin therapy, and an LDL cholesterol level of 41 to 100 mg/dL. Participants received either 4 g/day IPE or a placebo of mineral oil for a median of 4.9 years. IPE significantly reduced rates of cardiovascular events (a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, and unstable angina) by 25%. IPE also significantly reduced rates of other outcomes, including cardiovascular death by 20%, fatal or nonfatal stroke by 28%, and fatal or nonfatal myocardial infarction by 31%.

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