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The state of an individual's mental health depends on many factors. Determination of the importance of any particular factor within a population needs access to unbiased data. We used publicly available data-sets to investigate, at a population level, how surrogates of mental health covary with light exposure. We found strong seasonal patterns of antidepressant prescriptions, which show stronger correlations with day length than levels of solar energy. Levels of depression in a population can therefore be determined by proxy indicators such as web query logs. Furthermore, these proxies for depression correlate with day length rather than solar energy.
People with severe depressive illness have raised levels of cortisol and reduced glucocorticoid receptor function.
To obtain a physiological assessment of hypothalamic–pituitary–adrenal (HPA) axis feedback status in an in-patient sample with depression and to relate this to prospectively determined severe treatment resistance.
The prednisolone suppression test was administered to 45 in-patients with depression assessed as resistant to two or more antidepressants and to 46 controls, prior to intensive multimodal in-patient treatment.
The patient group had higher cortisol levels than controls, although the percentage suppression of cortisol output after prednisolone in comparison with placebo did not differ. Nonresponse to in-patient treatment was predicted by a more dysfunctional HPA axis (higher cortisol levels postprednisolone and lower percentage suppression).
In patients with severe depression, HPA axis activity is reset at a higher level, although feedback remains intact. However, prospectively determined severe treatment resistance is associated with an impaired feedback response to combined glucocorticoid and mineralocorticoid receptor activation by prednisolone.
The metabolism of the amino acid l-tryptophan is a highly regulated physiological process leading to the generation of several neuroactive compounds within the central nervous system. These include the aminergic neurotransmitter serotonin (5-hydroxytryptamine, 5-HT), products of the kynurenine pathway of tryptophan metabolism (including 3-hydroxykynurenine, 3-hydroxyanthranilic acid, quinolinic acid and kynurenic acid), the neurohormone melatonin, several neuroactive kynuramine metabolites of melatonin, and the trace amine tryptamine. The integral role of central serotonergic systems in the modulation of physiology and behaviour has been well documented since the first description of serotonergic neurons in the brain some 40 years ago. However, while the significance of the peripheral kynurenine pathway of tryptophan metabolism has also been recognised for several decades, it has only recently been appreciated that the synthesis of kynurenines within the central nervous system has important consequences for physiology and behaviour. Altered kynurenine metabolism has been implicated in the pathophysiology of conditions such as acquired immunodeficiency syndrome (AIDS)-related dementia, Huntington's disease and Alzheimer's disease. In this review we discuss the molecular mechanisms involved in regulating the metabolism of tryptophan and consider the medical implications associated with dysregulation of both serotonergic and kynurenine pathways of tryptophan metabolism.
Increased central serotonin (5-HT) function has been hypothesised to be a vulnerability trait in anorexia nervosa.
Eighteen women with a history of DSM–III–R anorexia nervosa and 18 female controls were examined. The subjects had recovered weight and menstrual function. A placebo-controlled d-fenfluramine test was used. Subjects ingested d-fenfluramine or placebo and after three hours were offered a ‘free’ meal. The amounts eaten were recorded and plasma Cortisol and prolactin levels were measured. Questionnaires related to eating attitudes and behaviour, to personality, and to mood were administered.
Unlike the control subjects, those recovered from anorexia nervosa did not show the expected appetite-suppressing responses to d-fenfluramine; their eating attitudes and behaviour were more restrained, ‘negative’ perfectionism was more pronounced, and post-meal plasma Cortisol levels did not rise as expected.
Our results do not suggest that increased central 5-HT function is a trait marker in anorexia nervosa, but dysregulation in part of the central 5-HT system may be a vulnerability factor. The flattened post-meal response to Cortisol in the subjects who had recovered from anorexia nervosa suggests that their hypothalamic–pituitary–adrenal axis may be altered and deserves further investigation.
Twelve chronic in-patients with primary polydipsia were studied, during free drinking and after fasting, by concurrent measurements of plasma AVP, serum sodium and osmolality, and urine volume, AVP, osmolality, and creatinine. A majority of the patients showed inappropriately high levels of AVP: plasma AVP estimations demonstrated that seven had Type I SIADH and two had Type II SIADH. Urinary AVP estimations confirmed inappropriately raised AVP in seven of the subjects tested, and there was a significant agreement between the plasma and urine diagnoses. Although able to concentrate their urine in response to fluid deprivation, the patients showed a decreased renal sensitivity to AVP. Despite the mitigating effect of decreased renal sensitivity to AVP, the SIADH seen in these patients appears to contribute to the development of water intoxication caused by polydipsia.
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