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Adverse Effects in Animals. Several rodent studies have demonstrated that supplementation of low-protein diets with L-tryptophan (5 percent) reduces food intake and weight gain over a 4-day to 4-week period


(reviewed by Benevenga and Steele, 1984; Harper et al., 1970). Funk and coworkers (1991) found that rats given a 20 percent casein diet supplemented with 14.3 percent tryptophan for 4 weeks developed scaly tails and thinning hair. However, no adverse effects were seen when the diets contained 1.4 or 2.9 percent L-tryptophan. No cancers were observed over an 80-week period when rats were fed diets containing 2 percent added L-tryptophan (Birt et al., 1987). Addition of 2.5 or 5 percent L-tryptophan to diets of rats and mice for 2 years resulted in decreased body weights of male and female mice and male (but not female) rats (DHEW, 1978). In pigs, supplementation with 0.1 or 1 percent L-tryptophan for up to 40 days did not affect weight gain, but 2 or 4 percent decreased weight gain and 4 percent also decreased food intake (Chung et al., 1991).

Several developmental studies have shown that maternal weight gain is impaired and fetal weight is reduced when maternal rat diets are supplemented with 1.4 to 6 percent L-tryptophan (Funk et al., 1991; Matsueda and Niiyama, 1982). Decreased brain weights were observed when 1 percent L-tryptophan was added to diets of male and female rats beginning 2 weeks before mating (Thoemke and Huether, 1984). Over three successive generations, brain weights decreased with each generation.

Adverse Effects in Humans. Serotonin and its metabolite 5-hydroxy-indoleacetic acid (5-HIAA) in human blood and brain cerebrospinal fluid (CSF) increase after tryptophan loading, which is similar to the effects of L-tryptophan in animals. For example, Young and Gauthier (1981) found elevations in blood and 5-HIAA and CSF serotonin after single doses of 3 or 6 g of L-tryptophan. However, Benedict and coworkers (1983) conducted a double-blind, placebo-controlled trial in six normal men fed 3 g/d of L-tryptophan in divided doses with meals for 3 days, and found a 113 percent elevation in plasma tryptophan, but no changes in platelet or plasma serotonin or in plasma catecholamines. They also found no changes in urinary catecholamines. Additionally, they found no changes in blood pressure, heart rate, plasma sodium levels or 24-hour sodium excretion in urine.

L-Tryptophan administration (2 g) as a single dose before a meal has been found to decrease subjective hunger ratings, food intake, and alertness in men (Hrboticky et al., 1985), but not women (Leiter et al., 1987). Hrboticky and coworkers (1985) also tested 15 humans only once with 0, 1, 2, and 3 g of L-tryptophan. Individuals receiving 2 and 3 g of L-tryptophan had decreased hunger and alertness and increased faintness and dizziness. Administration of 1 g of L-tryptophan with 10 g of carbohydrates before each meal (3 g L-tryptophan/d) for 3 months did not affect body weight of obese humans (Strain et al., 1985). Wurtman and coworkers (1981) found that daily doses of 2.4 g of L-tryptophan for 2 weeks did not produce a significant reduction in the consumption of carbohydrate snacks in the


majority of the 24 individuals. Ten healthy adults given 5 g of L-tryptophan in a double-blind, placebo-controlled study reported severe nausea and headache and increased drowsiness soon after ingestion (Greenwood et al., 1975).

Smith and Prockop (1962) reported sustained nystagmus and drowsiness in seven adults given 70 and 90 mg/kg of body weight of L-tryptophan orally in single doses, but found that these effects were absent at 30 or 50 mg/kg. However, Lieberman and coworkers (1985) reported decreased self-ratings of vigor and alertness and increased subjective fatigue in 20 men treated with a single oral dose of 50 mg/kg of tryptophan. Yuwiler and coworkers (1981) also reported that five individuals given 50 or 100 mg/kg/d of L-tryptophan as a single dose or 50 mg/kg/d for 14 days experienced prolonged lethargy and drowsiness within 30 minutes of ingestion under all loading conditions.

Newborns (2 to 3 days of age) given infant formula supplemented with L-tryptophan (about 20 mg) were found to enter active and then quiet sleep sooner than those newborns given unsupplemented formula (Yogman and Zeisel, 1983). In a later study, these same investigators found that low doses of L-tryptophan have sleep-inducing properties in full-term infants (Yogman and Zeisel, 1985).

Finally, retrospective studies covering the time prior to the 1989 eosinophilia-myalgia syndrome (EMS) outbreak—thought to be caused by L-tryptophan contaminated with 1,1-ethylidene-bis[tryptophan] (EBT) — indicate that use of L-tryptophan alone may increase risk of eosinophilic fasciitis. Blauvelt and Falanga (1991) examined the history of L-tryptophan use in 49 patients with cutaneous fibrosis. Eleven of 17 patients reported using L-tryptophan prior to onset of eosinophilic fasciitis, as did two of ten patients with localized scleroderma, but use of L-tryptophan was not reported in any of 22 patients with systemic sclerosis. Intakes of L-tryptophan were from 0.5 to 5 g/d for 1 month to 10 years before the onset of symptoms of eosinophilic fasciitis were noted. L-tryptophan use in individuals with localized scleroderma occurred for 3 or 10 months before onset of symptoms, and intake was 1.5 to 2 g/d. Hibbs and coworkers (1992) found that 9 of 45 patients with eosinophilic fasciitis used 0.5 to 2.5 g/d of L-tryptophan for 1 month to 10 years before symptom onset. It is unknown whether or not these results occurred because of impurities in the L-tryptophan supplements.

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