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High Doses of Omega 3 EPA and Depression

By Keith Fluegge

Major depressive disorder affects approximately 14.8 million Americans aged 18 and older, according to the National Institutes of Mental Health. By definition, major depressive disorder (MDD) is characterized by a combination of symptoms that interfere with your ability to work, sleep, study, eat and enjoy once-pleasurable activities. While there are other forms of depression, major depressive disorder is the most common and affects more women than men, although men tend to have higher suicide rates when afflicted. Research is ongoing on the various treatment modalities, including diet, for MDD.

Eicosapentaenoic acid (EPA)

Eicosapentaenoic acid (EPA) is an omega-3 long-chain fatty acid that is primarily found in fatty fish. Physiologically, EPA acts as a precursor to docosahexaenoic acid (DHA) formation, another omega-3 fatty acid that has a large presence within the central nervous system, including the brain and retina. EPA also acts as a precursor to the production of eicosanoids, which are, essentially, signaling molecules. According to the Inflammation Research Foundation, the eicosanoids derived from EPA seem to exert anti-inflammatory effects. It is this latter role that has been studied as one possible indirect mechanism for the treatment of MDD.

The Omega 6/Omega 3 Ratio

The study of fatty acid physiology cannot be fully understood, however, without studying the interplay among the many fatty acid classes. In addition to the omega-3 fatty acids, there exist omega-6 fatty acids, such as linoleic acid (LA), which is found in plant oils such as soybean oil. “For most of the time humans have been on earth we have eaten foods containing omega-6's and omega-3's in a ratio of about 2:1. However, over the last 50 years in North America, the ratio has changed to from 2:1 to 10-20:1,” says Dr. Gabe Mirkin, author of "The Healthy Heart Miracle" and radio show host. It is thought that these omega-6 fatty acid metabolites tend to favor the production of many pro-inflammatory markers, although this view is an oversimplification, as both pro- and anti-inflammatory chemical mediators are derived from LA metabolites. These inflammatory agents, according to Dr.Mirkin, can predispose you to a variety of health ailments, including cardiovascular disease, obesity, insulin resistance and even cancer. These markers may also have a bearing on hormone and neurotransmitter production directly tied to depressive symptomatology.

High Doses of EPA

Greater consumption of omega-3 fatty acids, and thus EPA, will compete with omega-6 metabolites for residency in the bilayer. Upon apoptosis, or cell death, metabolites of the fatty acids are released and can have a widespread effect. EPA has been shown to decrease these specific pro-inflammatory markers that have been found to be elevated in depressed patients. Researchers reported in 2007 in "The American Journal of Clinical Nutrition" that production of several pro-inflammatory cytokines, including IL-6, was inhibited after treatment with ALA. However, because ALA is the parent omega to EPA in the body, it is difficult to determine the effective dose of EPA metabolized in these patients in order to have induced the observed effect. In the "Archives of General Psychiatry," Peet, et al., discovered that just 1 g of EPA was needed to reduce scores on the Hamilton Depression Rating Scale (HDRS). Higher dosages (2 and 4 g) did not elicit any reduction in depression scores. Likewise, in the "Journal of the American College of Nutrition," Rondanelli, et al., found similar results upon administering 1.67 g EPA and 0.83 g DHA to a sample of depressed, elderly women. Depression scores on the HDRS were lower, and the bilayer composition significantly increased in EPA and DHA concentrations. Researchers in Taiwan found that higher doses of EPA ( > 4 g EPA) did foment a significant decrease in depression scores on the same scale, but lower doses were not included as part of the study.

It seems as though lower doses of EPA might render a beneficial effect, and higher doses do not seem to elicit any greater benefit when treating MDD. Increasing consumption of EPA, by as little as 1 g per day, may reduce the ratio of AA to EPA within cell membranes, enhance cardiovascular functioning and increase neurotransmission within the brain. All of these effects, in tandem, may yield an improvement in symptoms of major depressive disorder.


Since the study of diet as a treatment modality for MDD and other mental health conditions is ongoing, consult with your physician regarding the best medical approach for your condition. Analysis in this article is presented as informative and not as medical authority.

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