Omega-3 Fatty Acids are Uncontrolled in the United States.
Addictive Potential: None
Emergency Room Visits Yearly: No recorded hospital visits
Mandatory Minimum Sentence: None
Mechanism of Action: known to have membrane-enhancing capabilities in brain cells
n−3 fatty acids (popularly referred to as ω−3 fatty acids or omega-3 fatty acids) are a family of unsaturated fatty acids that have in common a final carbon–carbon double bond in the n−3 position; that is, the third bond from the methyl end of the fatty acid.
n−3 fatty acids are known to have membrane-enhancing capabilities in brain cells. One medical explanation is that n−3 fatty acids play a role in the fortification of the myelin sheaths. Not coincidentally, n−3 fatty acids comprise approximately eight percent of the average human brain according to Dr. David Horrobin, a pioneer in fatty acid research. Ralph Holman of the University of Minnesota, another major researcher in studying essential fatty acids, who gave Omega-3 its name, surmised how n−3 components are analogous to the human brain by stating that “DHA is structure, EPA is function.”
A benefit of n−3 fatty acids is helping the brain to repair damage by promoting neuronal growth. In a six-month study involving people with schizophrenia and Huntington’s disease who were treated with EPA or a placebo, the placebo group had clearly lost cerebral tissue, while the patients given the supplements had a significant increase of grey and white matter.
In the prefrontal cortex (PFC) of the brain, low brain n−3 fatty acids are thought to lower the dopaminergic neurotransmission in this brain area, possibly contributing to the negative and neurocognitive symptoms in schizophrenia. This reduction in dopamine system function in the PFC may lead to an overactivity in dopaminergic function in the limbic system of the brain which is suppressively controlled by the PFC dopamine system, causing the positive symptoms of schizophrenia. This is called the n−3 polyunsaturated fatty acid/dopamine hypothesis of schizophrenia (Ohara, 2007). This mechanism may explain why n−3 supplementation shows effects against both positive, negative and neurocognitive symptoms in schizophrenia.
Consequently, the past decade of n−3 fatty acid research has procured some Western interest in n−3 fatty acids as being a legitimate ‘brain food.’ Still, recent claims that one’s intelligence quotient, psychological tests measuring certain cognitive skills, including numerical and verbal reasoning skills, are increased on account of n−3 fatty acids consumed by pregnant mothers remain unreliable and controversial. An even more significant focus of research, however, lies in the role of n−3 fatty acids as a non-prescription treatment for certain psychiatric and mental diagnoses and has become a topic of much research and speculation.
In 1998, Andrew L. Stoll, MD and his colleagues at Harvard University conducted a small double-blind placebo-controlled study in thirty patients diagnosed with bipolar disorder. Most subjects in this study were already undergoing psychopharmacological treatment (e.g. 12 out of the 30 were taking lithium). Over the course of four months, he gave 15 subjects capsules containing olive oil, and another 15 subjects capsules containing nine grams of pharmaceutical-quality EPA and DHA. The study showed that subjects in the n−3 group were less likely to experience a relapse of symptoms in the four months of the study. Moreover, the n−3 group experienced significantly more recovery than the placebo group. However, a commentary on the Stoll study notes that the improvement in the n−3 group was too small to be clinically significant. Though Stoll believes that the 1999 experiment was not as optimal as it could have been and has accordingly pursued further research, the foundation has been laid for more researchers to explore the theoretical association between absorbed n−3 fatty acids and signal transduction inhibition in the brain.
“Several epidemiological studies suggest covariation between seafood consumption and rates of mood disorders. Biological marker studies indicate deficits in omega−3 fatty acids in people with depressive disorders, while several treatment studies indicate therapeutic benefits from omega-3 supplementation. A similar contribution of omega-3 fatty acids to coronary artery disease may explain the well-described links between coronary artery disease and depression. Deficits in omega-3 fatty acids have been identified as a contributing factor to mood disorders and offer a potential rational treatment approach.” In 2004, a study found that 100 suicide attempt patients on average had significantly lower levels of EPA in their blood as compared to controls.
In 2006, a review of published trials in the American Journal of Clinical Nutrition found that “the evidence available provides little support” for the use of fish or the n–3 long-chain polyunsaturated fatty acids contained in them to improve depressed mood. The study used results of twelve randomized controlled trials in its meta-analysis. The review recommended that “larger trials with adequate power to detect clinically important benefits” be performed. A further 2007 study published in the British Journal of Nutrition, which was placebo-controlled and used 218 participants, found that increasing EPA and DHA in the diet “was found not to have beneficial or harmful effects on mood in mild to moderate depression,” confirming previous meta-analysis “that there is an overall negligible benefit of n-3 UFA supplementation for depressed mood”.
However, another meta-analysis published in the Journal of Clinical Psychiatry in 2007 found the opposite result: based on 10 clinical trials Omega-3 polyunsaturated fatty acids were found to significantly improve depression in patients with both unipolar and bipolar disorder. However, based upon the heterogeneity of the trials, the authors concluded that “more large-scale, well-controlled trials are needed to find out the favorable target subjects, therapeutic dose of EPA and the composition of omega-3 PUFAs in treating depression”.