Årsaken til depresjon

[AnonymBruker]

Det sies ofte at depresjon kommer av ubalanse eller mangler i nevrotransmitterene dopamin, serotonin og noradrenalin. Dette er kjent som monoamin-hypotesen. Det er den mest aksepterte forklaringen, og den forklaringen medisiner baserer seg på. Men merk at det er en hypotese - ikke en teori. Innen vitenskapsteori så er en teori noe som er veldig grundig undersøkt, og som er veldig stor enighet om - f.eks. relativitetsteorien (innen fysikk). En hypotese er ikke like godt undersøkt eller akseptert, men i og med at monoamin-hypotesen ikke er tilbakevist siden den oppstod på 50-tallet, så er det nok den beste forklaringen man per i dag har.

The pharmacology of antidepressants is not entirely clear. The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin, norepinephrine and dopamine).[1] It was originally proposed based on the observation that certain hydrazine anti-tuberculosis agents produce antidepressant effects, which was later linked to their inhibitory effects on monoamine oxidase, the enzyme that catalyses the breakdown of the monoamine neurotransmitters.[1] All currently marketed antidepressants have the monoamine hypothesis as their theoretical basis, with the possible exception of agomelatine which acts on a dual melatonergic-serotonergic pathway.[1] Despite the success of the monoamine hypothesis it has a number of limitations: for one, all monoaminergic antidepressants have a delayed onset of action of at least a week; and secondly, there are a sizeable portion (>40%) of depressed patients that do not adequately respond to monoaminergic antidepressants.[2][3] Further evidence to the contrary of the monoamine hypothesis are the recent findings that a single intravenous infusion with ketamine, an antagonist of the NMDA receptor — a type of glutamate receptor — produces rapid (within 2 hours), robust and sustained (lasting for up to a fortnight) antidepressant effects.[3] To overcome these flaws with the monoamine hypothesis a number of alternative hypotheses have been proposed, including the glutamate, neurogenic, epigenetic, cortisol hypersecretion and inflammatory hypotheses.[2][3][4][5]

https://en.wikipedia.org/wiki/Pharmacology_of_antidepressants

Men merk at hvis monoamin-hypotesen stemmer, så er det bare et kjennetegn ved depresjon. Årsaken er i ytterste forstand "arv og miljø", og monoamin-hypotesen handler ikke om årsaken til depresjon - det er, hvis det stemmer, kun noe som kjennetegner depresjon på biologisk nivå, og noe man kan basere psykofarmaka etter.

Anonymkode: 55e54...d61