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excerpt from Chapter 8 of
by SYD BAUMEL Rudin's hypothesis was that all or most of these conditions, from irritable bowel syndrome and migraine headache, to depression and bipolar disorder, were at least partially caused by an endemic nutritional imbalance: too much saturated fat and partially hydrogenated oils (as found mostly in factory-farmed meat and commercial baked goods), and not enough of the nutritionally essential fatty acids of the omega-3 family (as found mostly in fatty cold-water fish and dark leafy greens). To test his hypothesis, Rudin had each patient take an ample daily dose of linseed oil - the remarkably omega-3-rich oil of flaxseeds - along with a small amount of vitamin E to prevent rancidity and B vita- mins to facilitate the omega-3's conversion to other important biochemicals in the body. For the two- to three-year span of the study, almost every patient stuck with the plan. And most of them, Rudin reported, gradually enjoyed significant and persistent improvements in both physical and mental health. Twelve patients had suffered primarily from psychiatric conditions. Two dropped out: one for fear of gaining weight on the high-cal supplement; the other, a bipolar patient who developed severe rapid cycling, possibly from the linseed oil. Of the other ten, seven improved substantially. Most dramatic was a twenty-six-year-old woman diagnosed schizophrenic since the age of sixteen. Despite "brief lucid moments each day," nothing had helped "Debi" for long. But within thirty minutes of her first dose of linseed oil she felt calmer. A week later, her daily hallucinations, intrusive thoughts, and "bizarre, sometimes violent, behavior" subsided. Soon they disappeared entirely. "I've been free of schizophrenia ever since," Debi wrote to Dr. Rudin years later. While continuing on an omega-3-rich diet, Debi had outgrown her need for both linseed oil and antipsychotic drugs and had become a registered psychiatric nurse. It wasn't until the late 1990s that the medical establishment began to catch up. In a double-blind, placebo-controlled multicenter trial published in 1999, an extremely high daily dose of fish oil proved so therapeutic for patients with bipolar disorder that the researchers, led by Harvard's Andrew Stoll, felt compelled to end the study early and put everyone on the nautical elixir. By the time the study saw print, virtually all the patients had stuck with the fishy prescription for up to two years "with continued efficacy." Stoll et al. had chosen a particularly unstable group of bipolar I and II patients. Although well or only mildly symptomatic, all thirty had a history of frequent manic or depressive episodes. Roughly one-third were rapid cyclers. Not unexpectedly, of the sixteen randomly assigned to olive oil (the placebo) as an adjunct to medication-as-usual, only 40 percent were still okay or better by the end of the 120-day study. In contrast, of the fourteen randomly assigned to adjunctive fish oil, nearly 90 percent were. The fish oilers fared significantly better by most other measures too. In particular, their depression scores dropped nearly by half. The control group's rose nearly 25 percent. Stoll and colleague Loren Marangell attempted to put their study into perspective: "[Omega-3] fatty acids . . . seem to be deficient in 'western diets.' . . . Thus, this study may represent the first demonstration of an effective nutritional therapy for bipolar disorder." Omega-3 fatty acids are integral components of the brain's cellular membranes, including the crucial synapses where neurons exchange chemical signals. Although the brain can use other essential fatty acids (EFAs) to build its supple neuronal membranes - notably the arachi- donic acid (AA) that abounds in factory-farmed meat - it prefers the highly polyunsaturated and flexible EFAs that abound in fish oil and other wild animals. These long-chain EFAs are called eicosapentanoic acid (EPA) and docosahexanoic acid (DHA). Most people can make them from the patriarch of the omega-3s, alpha-linolenic acid (ALA), the EFA that abounds in linseed oil, but some people (as we'll see) can't. When EPA and DHA are incorporated into neuronal membranes, Stoll and associates point out, the neurons become more electrochemically stable, less liable to "fly off the handle." This is the kind of stabil- ity created by lithium, Depakote, and other successful treatments for bipolar disorder. Stoll et al. might therefore have expected fish oil to work best for the manic pole of bipolar disorder. Yet in the brief course of their study, most of fish oil's advantage over olive oil was in preventing depression. But what about unipolar depression? In 1998, Joseph Hibbeln of the National Institute of Alcohol Abuse and Alcoholism compared the rate of major depression in nine countries to the estimated per-capita fish consumption, and the results were astonishing. At one extreme, a cluster of Western countries including the United States and Canada had an annual prevalence of major depression in the range of 3 to 6 percent and a modest per-capita fish intake of roughly 25 to 70 pounds. At the other extreme, Japan, with a per capita fish intake of nearly 150 pounds, had a paltry major depression rate of 0.12 percent. High fish intake predicted low depression rate to the tune of a whop- ping 84 percent correlation, where 100 percent would have represented a one-to-one correspondence. As scientists say, "correlation is not causation." But in the case of fish intake and depression, there is good evidence that eating more of the former will make you less of the latter. For one thing, rates of major depressive disorder in industrialized countries have risen dramatically in the past 100 years, while modem farming and food processing have gradually stripped most of the highly perishable omega-3 content from the menu. We have gone from an ancient ancestral diet estimated to have contained equal parts omega-6 and omega-3 to one in which omega-6 predominates by between 10 and 25 to I, according to Hibbeln and colleague Norman Salem, Jr. This radical omega shift is already well-implicated as a promoter of coronary heart disease. If it also promotes depression, we would expect to see more CHD among depressives. And we do. "Depression," Rhian Edwards of the University of Sheffield and her associates note, "is the strongest psychological predictor of coronary heart disease." The correlation gets even hotter than that. In all but one of about half-a-dozen controlled studies by the Sheffield group and three others, the red blood cell membranes and/or serum cholesterol of depressives have been significantly shy of omega-3s. In a 1998 study by Edwards et al., there was a remarkably strong tendency - a 75 percent correlation - for major depressives with the least omega-3s in their diets and red blood cell membranes to be the most severely depressed. Several of these studies have found that two of the major omega-6 fatty acids, linoleic acid (LA) and AA, are also higher in depressives than in controls. In one study cited by Hibbeln, there was a powerful correlation between the ratio of AA to EPA and severity of depression. We are getting a very strong hint that too much omega-6 (especially the AA of factory-farmed meat) and too little omega-3 makes Johnny a very depressed boy. Recently Rhian Edwards took the inevitable next step and conducted a placebo-controlled clinical trial of fish oil for patients with unipolar major depression. Her yet-to-be-published results, along with those to come from other researchers, may soon change how psychiatrists treat depression. Copyright
© 2000 by Syd Baumel.
Dealing with Depression
Naturally
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Dealing with Depression Naturally Complementary and Alternative Therapies for Restoring Emotional Health Amazon.com | Chapters.ca
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