Young S N
Department of Psychiatry, McGill University, Montreal, Quebec, Canada.
J Psychiatry Neurosci. 1993 Nov;18(5):235-44.
Although one of the first biological treatments of a major psychiatric disorder was the dietary treatment of pellagra, the use of diet and dietary components in the study of psychopathology has not aroused much interest. This article reviews three areas in which the dietary approach has provided interesting information. The tryptophan depletion strategy uses a mixture of amino acids devoid of tryptophan to lower brain tryptophan in order to study the symptoms that can be elicited. One effect of tryptophan depletion is a lowering of mood, the magnitude of which seems to depend on the baseline state of the subject. Therefore, recovered depressed patients often undergo an acute relapse, while normal subjects show more moderate changes of mood. Totally euthymic subjects show no lowering of mood, but subjects with high normal depression scale scores or subjects with a family history of depression show a moderate lowering of mood. These data indicate that low serotonin levels alone cannot cause depression. However, serotonin does have a direct effect on mood, and low levels of serotonin contribute to the etiology of depression in some depressed patients. Folic acid deficiency causes a lowering of brain serotonin in rats, and of cerebrospinal fluid 5-hydroxyindoleacetic acid in humans. There is a high incidence of folate deficiency in depression, and there are indications in the literature that some depressed patients who are folate deficient respond to folate administration. Folate deficiency is known to lower levels of S-adenosylmethionine, and S-adenosylmethionine is an antidepressant that raises brain serotonin levels. These data suggest that low levels of serotonin in some depressed patients may be a secondary consequence of low levels of S-adenosylmethionine. They also suggest that the dietary intake and psychopharmacological action of methionine, the precursor of S-adenosylmethionine, should be studied in patients with depression. Normal meals have definite effects on mood and performance in humans. The composition of the meal, in terms of protein and carbohydrate content, can influence these behaviors. Because protein and carbohydrate meals can influence brain serotonin in rats, these effects in humans have usually been interpreted in terms of altered serotonin functioning. However, the current balance of evidence is against the involvement of serotonin in the acute effects of protein and carbohydrate meals in humans. The underlying mechanisms involved are unknown, but there are a variety of possibilities.(ABSTRACT TRUNCATED AT 400 WORDS)
尽管糙皮病的饮食疗法是对一种主要精神障碍的首批生物治疗方法之一,但饮食及饮食成分在精神病理学研究中的应用并未引起太多关注。本文综述了饮食疗法提供了有趣信息的三个领域。色氨酸耗竭策略使用不含色氨酸的氨基酸混合物来降低大脑中的色氨酸,以研究可能引发的症状。色氨酸耗竭的一个作用是情绪低落,其程度似乎取决于受试者的基线状态。因此,康复的抑郁症患者常经历急性复发,而正常受试者的情绪变化则较为温和。完全心境正常的受试者情绪不会低落,但抑郁量表得分处于高正常范围的受试者或有抑郁症家族史的受试者情绪会有适度低落。这些数据表明,仅血清素水平低不会导致抑郁症。然而,血清素确实对情绪有直接影响,血清素水平低在一些抑郁症患者的病因中起作用。叶酸缺乏会导致大鼠大脑血清素水平降低,以及人类脑脊液中5-羟吲哚乙酸水平降低。抑郁症患者中叶酸缺乏的发生率很高,文献中有迹象表明,一些叶酸缺乏的抑郁症患者对补充叶酸有反应。已知叶酸缺乏会降低S-腺苷甲硫氨酸水平,而S-腺苷甲硫氨酸是一种能提高大脑血清素水平的抗抑郁药。这些数据表明,一些抑郁症患者血清素水平低可能是S-腺苷甲硫氨酸水平低的继发后果。它们还表明,应该研究抑郁症患者中S-腺苷甲硫氨酸的前体蛋氨酸的饮食摄入和精神药理作用。正常饮食对人类的情绪和表现有明确影响。就蛋白质和碳水化合物含量而言,饮食的组成会影响这些行为。因为蛋白质餐和碳水化合物餐会影响大鼠大脑中的血清素,所以这些对人类的影响通常被解释为血清素功能改变。然而,目前的证据平衡表明,血清素不参与蛋白质餐和碳水化合物餐对人类的急性影响。其中涉及的潜在机制尚不清楚,但有多种可能性。(摘要截选至400字)