Protection against ethanol-induced embryonic damage by administering gamma-linolenic and linoleic acids.

Many reports have now confirmed the teratogenic potential of alcohol in humans and in laboratory animals. A characteristic pattern of congenital anomalies is present in infants born to mothers suffering from chronic alcoholism. The pathogenesis of this condition is unclear. Chronic consumption of ethanol causes a depletion of essential fatty acids, partly by blocking gamma-linolenic acid formation and partly by depleting dihomogammalinolenic acid. Whether this action of ethanol on essential fatty acid and prostaglandin metabolism may account for its teratogenic potential was investigated in the rat. Treatment of pregnant rats with ethanol and evening primrose oil (efamol), a rich source of gammalinolenic acid, led to a significant reduction in the embryopathic activity of ethanol.