Decrease in Circulating Tryptophan Availability to the Brain After Acute Ethanol Consumption by Normal Volunteers: Implications for Alcohol-Induced Aggressive Behaviour and Depression

Abstract

Acute ethanol consumption by fasting male volunteers decreases circulating trytophan (Trp) concentration and availability to the brain as determined by the ratio of (Trp) to the sum of its five competitors ([Trp]/[CAA]ratio). These effects of alcohol are specific to Trp, because levels of the 5 competitors are not increased. The decrease in circulating (Trp) is not associated with altered binding to albumin and may therefore be due to enhancement of hepatic Trp pyrrolase activity. It is suggested that, under these conditions brain serotonin synthesis is likely to be impaired and that, as a consequence, a possible strong depletion of brain serotonin in susceptible individuals may induce aggressive behaviour after alcohol consumption. The possible implications of these findings in the relationship between alcohol and depression are also briefly discussed.

Moderate whisky consumption in combination with an evening meal reduces tryptophan availability to the brain but does not influence performance in healthy volunteers

“…1·5 h (Badawy et al 1987;Morgan & Badawy, 2001). This effect of whisky consumption on the plasma Trp:LNAA ratio in the present study is consistent with previous findings of a decline in plasma Trp:LNAA after single ethanol ingestion in fasting male volunteers (Badawy et al 1995). In this latter study, the consumption of 0·8 g ethanol/kg significantly decreased the plasma Trp:LNAA by 17 % as compared with control subjects 2 h after consumption.…”

“…Hence, an increase in plasma glucose concentration constitutes a necessary condition for carbohydrate ingestion to cause an insulinmediated increased uptake of the LNAA into the skeletal muscles, causing a consequent rise in the plasma Trp:LNAA ratio and brain 5-HT (Fernstrom & Wurtman, 1972;Curzon, 1985). In a previous study of Badawy et al (1995), the decline in the plasma Trp:LNAA ratio after alcohol consumption has been attributed to an enhanced hepatic Trp pyrrolase, since ethanol intake was accompanied by a decline in both free and total (free and albumin-bound) Trp concentration. Hence, particularly when alcohol is consumed in combination with solid food, first-pass metabolic effects such as increases in hepatic Trp pyrrolase may be most pronounced (Eckardt et al 1998).…”

“…Only a few studies have attempted to reveal whether ethanol consumption may have an effect on total plasma Trp concentrations (Badawy et al 1987;Morgan & Badawy, 2001) and only one has investigated the effect of ethanol on the Trp:LNAA ratio (Badawy et al 1995). In this latter study, it was demonstrated that ethanol consumption decreases the Trp:LNAA ratio over a 2-3 h time interval.…”

Laboratory-Measured Aggressive Behavior of Women Acute Tryptophan Depletion and Augmentation

“…Serotonin dysfunction has been correlated with impulsive and violent criminal behaviors (Brown et al , 1982Lidberg et al 1985;Limson et al, 1991;Virkkunen and Närvänen 1987;Virkkunen et al 1994aVirkkunen et al , 1994b, alcohol abuse and dependence (Badawy et al 1995;Ballenger et al 1979;Banki 1981;Borg et al 1985;Moss 1987;Roy and Linnoila 1989), Gilles de la Tourette's syndrome (Butler et al 1979;Cohen et al 1978Cohen et al , 1979, bulimia (Jimerson et al 1990(Jimerson et al , 1992, and suicide attempts (Asberg et al 1976(Asberg et al , 1986Banki and Arato 1983;López-Ibor et al 1985), as well as with children institutionalized for aggressive behavior (Kruesi 1989;Kruesi et al 1990Kruesi et al , 1992.…”

A review of physiological and metabolic effects of essential amino acids

“…An excess of serotonin in brain tissue is known to increase the mental effort necessary to maintain physical exercise (Newsholme and Blomstrand, 1996;Davis, 1995). Acute ethanol consumption is known to decrease circulating tryptophan availability (Badawy, 1995). One of the major systemic effects of tryptophan is through its 5-hydroxytryptamine metabolite (Newsholme and Leech, 1983).…”