Side-effect-pharmacology, so to speak. A basic example is grapefruit juice, among stuff like cimetidine, inhibits certain liver digestive enzymes. Normally causes some medications to have significantly higher effective doses and longer half-lives, which is dangerous. On the other hand, many people are affected less by medications because of higher-than-normal metabolism (to some being nearly completely unaffected at doses that kill another person), and some drugs which are metabolized normally have toxic metabolism effects that could be reduced if you, you know, metabolized it less. Even on a per-person level, the body can upregulate these enzymes over time, causing some medications to become less effective and liver damaging (it would likely sense damage by some process, and upregulate those enzymes in an attempt to clear the "poison" faster). The rapid metabolism affects my family in particular, we are highly insensitive to certain medications, including painkillers, and genetic testing confirms at least I am an over-rapid metabolizer for CYP1A6.
A more specific example is D2 receptor upregulation has been done by genetically modifying rats via viruses:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659016/The same upregulation happens when people are exposed to haloperidol. Even after a week receptors can be 90+% upregulated. A worthy side-note, while smoking, this upregulation is limited to something like 50 or 70%, and a consequence is schizophrenics who take haloperidol AND smoke have fewer hyperdopaminergic side effects.
Reserpine depletes emotion amines peripherally and centrally, and while it's primary effect is lowering blood pressure, it can also cause suicidal depression. In combination with a receptor blocker it makes an effective antipsychotic. In theory, a more brain-acting form or in combination treatment, it could cause more severe depression, the brain could upregulate, and cessation would cause improved mood.
