Brooks S C, Linn J J, Disney N
Biol Psychiatry. 1978 Dec;13(6):671-84.
Metabolic compensation appears possible within the serotonergic, folate, purine system and it seems possible that clinical illness may result when the system can no longer compensate. For example, elevated serotonin, induced by stress accumulation of tryptophan, could be compensated by a lowered folate ratio, normalizing the beta-carboline index and preventing hallucinations. Conversely, deficient serotonin, induced by a psychological loss or transport deficit, could be compensated by raising the folate ratio, which would normalize the beta-carboline index and prevent further depression. Increased purine turnover would seemingly lower the folate ratio, compensating perhaps for hallucinatory activity or mania. Several genetic defects of enzymes or transport proteins could seemingly preclude normal compensations within the system.
代谢补偿似乎在血清素能、叶酸、嘌呤系统中是可能的，并且当该系统不再能够进行补偿时，临床疾病可能会出现。例如，由色氨酸应激积累诱导的血清素升高，可以通过降低叶酸比率来补偿，使β-咔啉指数正常化并防止幻觉。相反，由心理损失或转运缺陷诱导的血清素缺乏，可以通过提高叶酸比率来补偿，这将使β-咔啉指数正常化并防止进一步的抑郁。嘌呤周转率增加似乎会降低叶酸比率，可能补偿幻觉活动或躁狂。几种酶或转运蛋白的遗传缺陷似乎可能妨碍系统内的正常补偿。
