Bernstein J G
Ann N Y Acad Sci. 1987;499:203-15. doi: 10.1111/j.1749-6632.1987.tb36212.x.
Evidence from published studies and clinical experience indicates that neuroleptic drugs, tricyclic and heterocyclic antidepressants, monoamine oxidase inhibitor antidepressants, and lithium all possess varying abilities to increase appetite, stimulate carbohydrate craving, and cause weight gain over prolonged periods of administration. Sedatives and benzodiazepine-type antianxiety drugs fail to stimulate appetite or induce weight gain, and it is unlikely that the sedative or calming effects of other psychotropic drugs contribute significantly to changes in appetite or weight. Studies of the endocrine and metabolic aspects of psychotropic drugs suggest that these mechanisms do not contribute significantly to explaining the observed effects on appetite or weight. Numerous studies indicate that a wide variety of compounds, including the serotonin precursor, tryptophan, the serotonin receptor stimulant, fenfluramine, and the serotonin reuptake inhibitor, fluoxetine, are all capable of decreasing carbohydrate hunger, reducing consumption of carbohydrate-rich foods, and inhibiting weight gain in humans and animals. Widely divergent psychotropic drugs produce antagonistic effects at serotonin receptor sites, and it is likely that this action contributes to their ability to stimulate appetite, carbohydrate craving, and weight gain. Those psychotropic drugs that inhibit serotonin reuptake mechanisms, increasing serotonin activity within the central nervous system, either fail to stimulate carbohydrate hunger and weight gain or are actually capable of decreasing carbohydrate craving and facilitating weight loss. Because many antidepressants, including trazodone and amitriptyline, the neuroleptic, chlorpromazine, and the mood stabilizer, lithium, may all, under some circumstances, inhibit serotonin reuptake mechanisms and may simultaneously block serotonin receptor sites, their effects on appetite and weight gain may represent a balance between serotonergic and antiserotonin activities. Monoamine oxidase inhibitors, which slow the metabolic degradation of monoamines, including serotonin and norepinephrine, allow for increased levels of these neurotransmitters within the brain. It is conceivable that the relative noradrenergic effect related to an amphetamine-like structure of tranylcypromine may explain its lesser ability to stimulate appetite and weight gain than the appetite and weight effects observed with phenelzine. Furthermore, the production of dry mouth and thirst by psychotropic drugs appears to contribute to weight gain, secondary to consumption of high-calorie beverages.(ABSTRACT TRUNCATED AT 400 WORDS)
已发表研究和临床经验的证据表明,抗精神病药物、三环和杂环抗抑郁药、单胺氧化酶抑制剂抗抑郁药以及锂盐在长期给药过程中均具有不同程度增加食欲、刺激对碳水化合物的渴望并导致体重增加的能力。镇静剂和苯二氮䓬类抗焦虑药物不会刺激食欲或导致体重增加,其他精神药物的镇静或安定作用也不太可能对食欲或体重变化有显著影响。对精神药物内分泌和代谢方面的研究表明,这些机制并不能很好地解释所观察到的对食欲或体重的影响。大量研究表明,多种化合物,包括血清素前体色氨酸、血清素受体兴奋剂芬氟拉明以及血清素再摄取抑制剂氟西汀,都能够减少对碳水化合物的饥饿感,减少富含碳水化合物食物的摄入量,并抑制人和动物体重增加。作用差异很大的精神药物在血清素受体部位产生拮抗作用,很可能正是这种作用导致它们具有刺激食欲、对碳水化合物的渴望以及体重增加的能力。那些抑制血清素再摄取机制、增加中枢神经系统内血清素活性的精神药物,要么不会刺激对碳水化合物的饥饿感和体重增加,要么实际上能够减少对碳水化合物的渴望并促进体重减轻。因为许多抗抑郁药,包括曲唑酮和阿米替林、抗精神病药物氯丙嗪以及心境稳定剂锂盐,在某些情况下可能都会抑制血清素再摄取机制,并且可能同时阻断血清素受体部位,它们对食欲和体重增加的影响可能代表了血清素能和抗血清素活性之间的一种平衡。单胺氧化酶抑制剂减缓包括血清素和去甲肾上腺素在内的单胺的代谢降解,使大脑内这些神经递质水平升高。可以想象,反苯环丙胺类似苯丙胺的结构所产生的相对去甲肾上腺素能效应,可能解释了其刺激食欲和体重增加的能力不如苯乙肼的原因。此外,精神药物引起的口干和口渴似乎会导致体重增加,这是由于饮用高热量饮料所致。(摘要截选至400词)