Total protein fell from 15.0% → ~12.4%, and calculated Trp from 180 → 128 mg per 100 g diet (≈29% drop). Growth dropped accordingly until either 1.0–1.5 mg/100 g nicotinic acid or ~0.05% free L-Trp was added, which rescued growth. That tryptophan added exogenously amount as free-form L-tryptophan did not need to be that high, note. Nonetheless, it was enough.

• Less Trp in the ration + no preformed niacin forces a higher fraction of the smaller Trp pool into kynurenine → NAD⁺, leaving less for protein synthesis and 5-HT→melatonin—and growth stalls.

• Add back enough free crystalline nicotinic acid niacin to meet the NAD⁺ requirement to spare Trp for its other jobs.

• Add back the needed amount of free L-tryptophan exogenously: you increase the substrate enough that some can be diverted to NAD⁺ and still cover protein/5-HT needs.

Corn merely worsens this general problem because (i) maize protein (zein) is Trp-poor, (ii) all “niacin” from diet like maize or anything else is already converted down, so there is no free-form usable actual niacin aka free crystalline nicotinic acid in diet (meanwhile, exogenously more nicotinic acid is needed to be supplemented to counter the streptothrycin in the dye of corn along with L-tryptophan for the sulfa they add on top of the streptothrycin as with “corn grits” which is covered up with the tale that goes something like, “niacin that corn provides is in a non/bioavailable bound form”), however, the core lever is still the combined amount of free-form crystalline nicotinic acid + L-tryptophan available.

Think of two knobs you can turn to keep development/metabolic function intact:

1. Niacin/NAD+ knob (Preiss-Handler pathway-derived NAD⁺): set high enough that NAD⁺ demand is covered so Trp isn’t siphoned off beyond more than that has to be.

2. Tryptophan knob (substrate): ensure sufficient Trp density so its non-NAD⁺ roles (protein, serotonin→melatonin) aren’t insufficiently powered or become compromised.

Many dietary patterns (corn, low-protein, acid-washed proteins) can depress one or both knobs, essentially really in some way manifest the essential-for-life/function requirement for exogenous free-form nicotinic acid and/or L-tryptophan to have to be supplemented to a countering degree (if NAD+ requirement becomes great enough, then both free-form nicotinic acid and L-tryptophan together, as in real-world settings).

We can frame it as: exogenously supplemented relevant amount of free nicotinic acid or free L-tryptophan can rescue to some degree, but the full counter that is the best outcome is achieved by maxing out free crystalline nicotinic acid amount supplemented that covers the NAD+ requirement so Trp is spared best and ideally further; even accumulating in a free pool as storage surplus to feed its need for growth tissue and serotonin/melatonin axis.

Trying to meet NAD⁺ needs only with Trp demands large Trp flux, starving serotonin/melatonin and protein synthesis. Hence the strategy: let NA do the heavy lifting.