Speaking against pharmacokinetic porphyrogenicity is the fact that it probaly is unlikely that an essential aminoacid would act as a potent ligand to PXR/CAR, or induce or inhibit irreversibly major drug-metabolizing Cyps. There are no pharmacodynamic actions or side effects of tryptophan or its metabolites, of relevance to acute porphyria.Tryptophan high-dose regimen may augment periheral and central release of 5-H tryptamine (serotonine). In inflammation and under glucocorticoid therapy the importance of the kynurenine pathway of degradation becomes more important. None of these two pathways of tryptophan degradation is accompanied by metabolic effects of relevance in acute porphyria.

Aminoindol propionic acid M= 204. Aminoacid, essential to humans. Contains one linear secondary amine group and one cyclic tertitiary amine function. Present in banana in significant amounts. Used as dietary supplement.

Depression (Insomnia) Scant evidence of clinical effects. Essential aminoacid. Precursor to serotonine and kynurenine. Physiological effects and bye-effects of possible relevance to acute porphyria: Availability of tryptophan is the main factor regulating 5-OH tryptamine (5-HT / serotonine) biosynthesis and it is conceivable that the large therapeutic load of tryptophan may increase its peripheral- and CNS-neuronal uptake in a way to increase 5-HT secetion. Following release, 5-HT is largely recovered by neuronal re-uptake or cleared by monoamine-oxidase and aldehyde dehydrogenase catalyzed degradation. 5-HT interacts with several types of peripheral (nocioceptive afferent, enteric) neurons, and central receptors.The effects of 5-HT include anxiety, hallucinosis, emesis, induction of sleep, exagerated responses to many forms of sensory stimuli, increased gastrointerstinal mobility, platelet aggregation, vasodialation / vasoconstriction, and it may act as an inflammatry mediator. Adverse effects are nausea, drowsness, head ache, lightheadedness. There are no metabolic effects of 5-HT of clear relevance in acute porphyrias. The kynurenine metabolite is depressogenic, anxiogenic, activate oxidative pathways, cause mitochondrial dysfunctions, and have neuroexcitatory and neurotoxic effects that may lead to neurodegeneration. IDO is induced in inflammation by IFNa, IL6 and TNFa, while TDO is induced by corticoides (PMID 20406665, 211843569) , both conditions favouring the kynurenine pathway of trypyophan degradation. Co-factors in the decarboxylation and hydroxylation reactions are pyridoxine and ascorbic acid, respectively, pyridoxine probably preventing accumulation of kynurenine metabolites.

Tryptophan is metabolized by tryptophan pyrollase, and by hydroylase giving rise to hydroxytryptophan, which is precursor to 5-OH tryptamine (serotonine). Some tryptophan is converted to nicotinic acid and nicotinamide. The heme proteins tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dixygenase (IDO) are specific and powerful oxidation catalysts that insert one molecule of dioxygen into trypophan in the first, and rate limiting step in the kynurenine pathway (PMID 19021508).