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A Family Affair: Essential Fatty Acids More chemical clues to the nature of alcoholism come from research focusing on alcoholics with at least one grandparent who was Welsh, Irish, Scottish, Scandinavian, or native American. Typically, these alcoholics have a history of depression going back to childhood and close relatives who suffered from depression or schizophrenia. Some may have relatives who committed suicide. There also may be a family history of eczema, cystic fibrosis, premenstrual syndrome, diabetes, irritable bowel syndrome, or benign breast disease. The common denominator here is a genetic abnormality in the way the body handles certain essential fatty acids (EFAs) derived from foods. Normally, these EFAs are converted in the brain to various metabolites such as prostaglandin E1 (PGE1), which plays a vital role in the prevention of depression, convulsions, and hyperexcitability. When the EFA conversion process is defective, brain levels of prostaglandin E1 are lower than normal, which results in depression. In affected individuals, alcohol acts as a double-edged sword. It activates the PGE1 within the brain, which immediately lifts depression and creates feelings of well-being. Because the brain cannot make new PGE1 efficiently, its meager supply of PGE1 is gradually depleted. Over time, the ability of alcohol to lift depression slowly diminishes. Several years ago, researchers hit upon a solution to this problem. They discovered that a natural substance, oil of evening primrose, contains large amounts of gamma-linolenic acid (GLA), which can help the brain convert EFAs to PGE1. The results are quite dramatic. In a recent study in Scotland, researcher David Horrobin, M.D., matched two groups of alcoholics whose EFA levels were 50 percent below normal. The first group got EFA replacement, the second, a placebo. Marked differences between the two groups emerged in the withdrawal stage. The group that got EFA replacement had far fewer symptoms, while the placebo group displayed the full range of withdrawal symptoms associated with prostaglandin deficiency: tremors, irritability, tension, hyperexcitability, and convulsions. At the outset of the study, members of both groups had some degree of alcohol-related liver damage. Three months later, the researchers found that liver function among the EFA replacement group was almost normal. There was no significant improvement among the placebo group. A year later, the placebo group was still deficient in the natural ability to convert essential fatty acids into PGE1. Whatβs more, only 28 percent of this group had remained sober; the rest had resumed drinking. Results were dramatically better among the EFA replacement group: 83 percent remained sober and depression free.
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Joan Mathews Larsen (Seven Weeks to Sobriety: The Proven Program to Fight Alcoholism through Nutrition)