L-Tryptophan

Cheap, well-evidenced, regulated serotonin → melatonin precursor for sleep onset and mood support. At 1 g 30-60 min pre-bed on an empty stomach (with optional small carb), it reduces sleep latency by ~15-30 min in mild insomnia and shortens wake-after-sleep-onset; flat effect at sub-1g doses. Better fit for Dylan than V4 glycine because tryptophan actually feeds the melatonin pathway a late-chronotype is trying to advance — glycine doesn't.

Tryptophan is one of nine essential amino acids — body cannot make it, must come from diet (turkey, chicken, oats, etc.) or supplements. About 1-3% of dietary/supplement tryptophan is shunted into the serotonin/melatonin pathway; the rest goes down the kynurenine pathway (more on that below). The serotonin path:

1. Tryptophan → 5-HTP via tryptophan hydroxylase (TPH). This is the rate-limiting step in serotonin synthesis. TPH1 lives in pineal/gut, TPH2 lives in CNS serotonergic neurons (raphe nuclei). Requires Fe²⁺, BH4 (tetrahydrobiopterin), and effectively B6/PLP downstream. TPH is inhibited by stress, B6 deficiency, low magnesium, and inflammation.
2. 5-HTP → Serotonin (5-HT) via aromatic amino acid decarboxylase (AAAD). Fast, B6-dependent.
3. Serotonin → N-acetylserotonin → Melatonin via AANAT and HIOMT in the pineal at night. The dark-onset signal turns on melatonin synthesis, so giving substrate (tryptophan) before bed feeds this pathway exactly when it's active.

The BBB bottleneck (LNAA competition). Tryptophan crosses the blood-brain barrier via the LAT1 transporter, which it shares with the other large neutral amino acids: tyrosine, phenylalanine, leucine, isoleucine, valine, methionine. LAT1 is near-saturated at normal plasma concentrations, so brain tryptophan uptake depends on the tryptophan:LNAA ratio, not absolute tryptophan levels. Eating protein floods the bloodstream with all LNAAs and tryptophan loses the competition (because it's a minority component of dietary protein). This is why "turkey makes you sleepy" is mostly false — the protein in turkey actually reduces brain tryptophan uptake. Carbs do the opposite: insulin shunts the branched-chain amino acids (leucine/isoleucine/valine) into muscle tissue, leaving tryptophan with a clearer LAT1 path. Median tryptophan:LNAA shifts +54% between protein-rich and carb-rich meals. Practical upshot: dose tryptophan away from protein meals, optionally with a small carb (a piece of fruit, a few rice crackers).

The kynurenine diversion. Most tryptophan (~95%) flows down the kynurenine pathway via IDO (indoleamine 2,3-dioxygenase, in immune cells / brain) or TDO (tryptophan 2,3-dioxygenase, mostly liver). Inflammation activates IDO (IL-1, IL-6, IFN-γ, TNF-α all upregulate it), which steals substrate from the serotonin pathway and produces downstream metabolites — kynurenic acid (neuroprotective, NMDA antagonist) plus quinolinic acid and 3-hydroxykynurenine (neurotoxic, NMDA agonist). In a chronically inflamed person, more tryptophan → more kynurenines, not necessarily more serotonin. This is mechanistically why depression correlates with inflammation. Relevance for Dylan: MMA training drives transient inflammation; daily subconcussive impact + 10+ hr/wk training = elevated baseline inflammation likely. If hs-CRP comes back high in June bloodwork, address inflammation (sleep, omega-3 dose, curcumin already in V4) before assuming tryptophan dosing is "wrong."

Why not just take 5-HTP? 5-HTP skips the rate-limiting TPH step and the kynurenine diversion — it goes essentially straight to serotonin. Sounds like a feature; it's actually a bug. The TPH bottleneck is physiological quality control — your body decides how much serotonin to make based on need, cofactor availability, and circadian/inflammatory state. Bypassing it can produce serotonin in the wrong tissues at the wrong times. 5-HTP also bypasses the LNAA-transport competition (it crosses BBB more readily), so dosing is harder to titrate. Long-term 5-HTP use is associated with depleted brain dopamine (because AAAD is the same enzyme that converts L-DOPA → dopamine, and 5-HTP saturates it). Conclusion: tryptophan is the regulated precursor; 5-HTP is the override switch. Dylan should use tryptophan.