So what’s so bad about DHA anyway?
DHA is not a bad thing at all. Developing fetuses, infants and young children need sufficient stores of DHA for healthy brain growth. But for optimal neurologic functioning, the latest research points to limiting the amounts of DHA relative to one’s intake of EPA. Here is an interesting take on this issue:
“The common thinking on the various functionality of Omega-3s is this: EPA is for the heart, DHA is for the brain.
There’s a reasonable-sounding argument behind this notion, based on the fact that DHA (docosahexaenoic acid, or 22:6w3) is a major component of the brain, while there’s only a tiny amount of EPA (eicosapentaenoic acid, or 20:5w3) in the nervous system. So when research started to show that countries and individuals who consumed more fish seemed more resistant to depression, schizophrenia, seasonal affective disorder (SAD), and bipolar disorder, almost everyone leapt to the conclusion that the seaborne secret just had to be DHA.
Not that it made any practical difference, of course: after all, nearly all EPA and DHA supplements come in the form of concentrated fish oil softgels with a significant amount of both fatty acids. So, the assumption was, you could get both benefits in one pill by just taking a common fish oil supplement.
Nice-sounding theory. But, as a series of randomized, placebo-controlled, clinical trials have shown, dead wrong.
Running our expectations through the spin cycle, resent research has revealed that DHA is, at best, useless when it comes to supporting the health of your thought patterns and outlook on the world. Worse: DHA may even be counterproductive. Surprisingly, EPA turns out to be the real slayer of the “Noonday Demons.”
DHA: Brain Fat? Or Fat Chance?
In one trial, researchers tested the effects of pure DHA on victims of clinical depression. For six weeks, people suffering with major depression took a supplement containing either pure DHA (two grams (2000 milligrams) a day or an inactive stand-in oil for six weeks. At the end of the trial, DHA had exerted no detectable effect whatsoever.
In an even more pointed failure, researchers ran a trial to see if DHA supplements could prevent the depression and deficits in information processing associated with postpartum depression. This seemed like an especially good opportunity for DHA to strut its stuff, because women’s levels of DHA usually decline late in their pregnancies, and they remain depressed for months after the birth of their child.
Instead, the results were a complete flop. Women taking DHA supplements were no less depressed, and no better able to process information, than were women taking an inert fatty acid softgel, even though their DHA levels were much higher.
A third trial sought to lay plain the differing effects of EPA and DHA on thought patterns and mental functioning – focusing this time on people suffering from schizophrenia. Forty-five people diagnosed with the disease were randomly assigned to begin using either two grams of high-EPA oil, the same amount of high-DHA oil, or a corn oil placebo, with no one knowing who was taking what.
The results in the DHA group were surprising. At best, they had gotten no better than people on the dummy pill. And overall, in fact, the subjects administered DHA appeared to fare worse than in the placebo group. Although the differences did not reach the statistical level of significance, there was actually a higher percentage of people taking DHA who were either treading water or showing further decay at the end of the trial than was seen with the placebo.
On top of this, whereas the severity of so-called “positive” symptoms (delusions, psychoses, etc) had fallen by an average of 13.7% in patients taking the placebo, it was only reduced by 3.3% in DHA-treated subjects. In other words, it appears that patients get more relief from their “positive” symptoms if they take an inactive dummy pill than if they take DHA – suggesting that DHA may even interfere with the progress that they could otherwise make if they just continue with their conventional treatment.
It was a whole different picture in the pure EPA group. Every single one of the people who had taken the EPA-only supplement got better, with an even split between the number of people showing considerable improvements (more than 25%) on their symptom scores and the number showing more minor improvements.
To make sure the results hadn’t been some kind of wild fluke, the same group initiated a second trial to confirm the powers of EPA-only supplements. For three months, 30 relapsing schizophrenia sufferers who were not already taking drugs for their conditions took either straight EPA or placebo capsules as their sole encapsulated support – unless, during the course of the trial, their doctors deemed it clinically imperative to put them on antipsychotics, in which case the patients’ safety came first and medication was permitted. But no one would know who was getting EPA, and who was taking the stand-in oil capsules.
At the end of the trial, 100% of the people taking the dummy pill had been forced to go on an antipsychotic drug – versus only 57% of the EPA users.
The Power of EPA Confirmed
Since then, three more randomized, placebo-controlled trials have been performed using highly purified EPA supplements to help people with schizophrenia – and two such trials have been performed in victims of clinical depression. There have also been an additional two studies in schizophrenics, and an additional one in victims of depression, using either very high doses of omega-3 supplements containing mostly EPA (but still including some DHA), or such a supplement combined with antioxidants.
All but one of these eight trials showed that the EPA-containing supplements brought relief from these mental torments – and in that one trial, the problem seems to have been the use of excessively high doses.
In one trial, for instance, 20 patients with major depressive disorder were randomly given either 2 grams of pure EPA or a matching stand-in for four weeks. Even in this short period, sixty percent of the people taking pure EPA experienced a remarkable 50% or greater reduction in their scores of depression, versus just ten percent of people taking the placebo.
On average, the relief was clocked as a remarkable 12.4 point improvement on the Hamilton depression scale scores in EPA users – versus just a 1.6 point improvement among people stuck with the lookalike pills.
Summarizing the evidence from these reports, the lead researcher in the trial which originally identified the opposing effects of EPA and DHA concluded that “In both schizophrenia and depression, the studies indicate that DHA is, if anything, rather worse than placebo in its effects on symptomology. Only EPA has given significant positive benefits.” Ω
SOURCE: Advanced Orthomolecular Research
References:
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Peet M, Horrobin DF. A dose-ranging study of the effects of ethyl-eicosapentaenoate in patients with ongoing depression despite apparently adequate treatment with standard drugs. Arch Gen Psychiatry. 2002 Oct;59(10):913-9.
Peet M. Eicosapentaenoic acid in the treatment of schizophrenia and depression: rationale and preliminary double-blind clinical trial results. Prostaglandins Leukot Essent Fatty Acids. 2003 Dec;69(6):477-85.
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