Ethanol acute intoxication caused

Foo and Lemon (1997) assessed the acute effects of kava, alone and in combination with alcohol, on subjective measures of impairment and intoxication and on cognitive performance. This was a placebo-controlled study, with ten subjects in each of four conditions placebo, kava, alcohol, and kava plus alcohol. The placebo was pure fruit juice and fruit juice was added to kava and alcohol as well to maintain double blind conditions. A battery of tests was included to measure outcomes, including subjective measures of impairment and intoxication, and visual-motor and cognitive performance. These measures were performed before (time = 0), and 30, 60 and 90 minutes after consumption of the drinks. Each test trial took about 12 minutes. Kava consumption produced no significant effects on perceived or measured competence, while alcohol caused motor and cognitive impairments. However, when kava and alcohol were combined, kava potentiated both the perceived and measured impairment produced by the alcohol alone. This potentiation effect is in accord with the findings of Jamieson and Duffield (1990) on the positive interaction of ethanol and kava resin in mice. 

Acute gout is triggered by the tissue deposition of sodium urate crystals which cause an inllammatory response. In the chronic situation, tophaceous deposits of sodium urate may form in the tissues (Fig. 4). Gout is exacerbated by alcohol. The reason for this is twofold. Ethanol increases the turnover of ATP and urate production. Ethanol in excess may cause the accumulation of organic acids w hich compete with the tubular secretion of uric acitl. Disorders such as ethanol intoxication, diabetic ketoacidosis and starvation lead to elevations of lactic acid. (3-hydroxybutyric acid and acetoacetic acid, and will cause hyperuricaemia. 

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