5-HTP

Updated June 29, 2026

5-HTP (5-hydroxytryptophan) is the immediate precursor to serotonin in the brain, produced endogenously from the amino acid tryptophan by the enzyme tryptophan hydroxylase. As a supplement it is extracted from the seeds of Griffonia simplicifolia, a West African shrub. Unlike tryptophan itself, 5-HTP crosses the blood-brain barrier efficiently and converts to serotonin with minimal competition from other amino acids for transport. This direct conversion pathway makes it more reliably brain-active than tryptophan supplements, which face significant competition at the blood-brain barrier from other large neutral amino acids.

The mood evidence is the most historically established. In the 1970s and 1980s, Swiss researchers conducted controlled trials comparing 5-HTP to early antidepressants and found comparable efficacy in mild to moderate depression. The effect takes two to four weeks to build, mirroring the timeframe of SSRIs, which is expected given both act on serotonin availability. Unlike SSRIs, 5-HTP does not block reuptake — it increases the total amount of serotonin synthesised. The combination of 5-HTP with SSRIs is not recommended and can cause serotonin syndrome in extreme cases, though clinical reports of this with supplements alone at standard doses are rare.

Sleep quality is a well-supported application. 5-HTP converts not only to serotonin but, in the pineal gland at night, to melatonin via the serotonin-to-melatonin pathway. Evening dosing raises melatonin output and shortens sleep onset in multiple trials. The sleep benefit is distinct from supplementing melatonin directly — 5-HTP improves the quality and architecture of sleep across the full night, increasing slow-wave (deep) sleep duration, not just onset speed. Typical doses for sleep are 50 to 100 mg taken 30 to 60 minutes before bed.

Appetite suppression is another consistent finding. 5-HTP increases satiety signalling via serotonergic pathways in the hypothalamus. Several controlled trials in overweight individuals show reduced caloric intake, reduced carbohydrate cravings, and modest weight loss over 6 to 12 weeks at 300 to 600 mg per day. The effect is most pronounced in people who report carbohydrate cravings as a specific issue, consistent with the well-known link between low serotonin and carbohydrate seeking.

Standard doses range from 50 to 100 mg for sleep or mood, taken one to two hours before the target time. For appetite use, 200 to 300 mg before meals has been used in trials. The most common side effect at higher doses is nausea, especially on an empty stomach. Starting at 50 mg and titrating up over two weeks largely avoids this. Extended use above 300 mg per day has raised theoretical concerns about depleting downstream nutrients (dopamine, norepinephrine), suggesting periodic breaks or B6 co-supplementation, which is required as a cofactor in the conversion to serotonin. This is general information, not medical advice.