Disease relevance of Seasonal Affective Disorder

• The brain neurotransmitter, serotonin, seems to be involved in the abnormal regulation of mood and food intake that underlies diet failures or weight gain in individuals who suffer from carbohydrate craving obesity (CCO), premenstrual syndrome (PMS) and seasonal affective disorder (SAD) [1].
• A Cys 23-Ser 23 substitution in the 5-HT(2C) receptor gene influences body weight regulation in females with seasonal affective disorder: an Austrian-Canadian collaborative study [2].
• In a series of studies, commencing in patients with Cushing's disease, and extending to hyperimmune fatigue states such as chronic fatigue syndrome and examples of atypical depression such as seasonal affective disorder, we have advanced data suggesting hypofunction of hypothalamic CRH neurons [3].
• Serotonin pathways within the brainstem may be implicated in cluster headache with seasonal affective disorder and a subset of cranial nerve neuralgias [4].
• In contrast to patients with bulimia nervosa, hyperphagic patients with seasonal affective disorder failed to show abnormal meal-related CCK secretion [5].

Psychiatry related information on Seasonal Affective Disorder

• Light, vitamin D and psychiatry. Role of 1,25 dihydroxyvitamin D3 (soltriol) in etiology and therapy of seasonal affective disorder and other mental processes [6].
• Psychomotor performance and memory were assessed in 6 patients with seasonal affective disorder following one week of daily administration of oral melatonin [7].
• In several studies we have found that treatment with bright environmental light, capable of suppressing human melatonin, reverses the winter depressive symptoms of patients with seasonal affective disorder (SAD), whereas light too dim to suppress human melatonin is therapeutically ineffective [8].

High impact information on Seasonal Affective Disorder

• Our findings are further evidence for the notion that changes in release of serotonin by the brain underlie mood seasonality and seasonal affective disorder [9].
• Melatonin supersensitivity to dim light in seasonal affective disorder [10].
• CONCLUSIONS: The beneficial effects of light therapy in the treatment of seasonal affective disorder are reversed by both tryptophan depletion and catecholamine depletion [11].
• BACKGROUND: Bright light therapy is the recommended treatment for winter seasonal affective disorder (SAD) [12].
• Hormonal and subjective responses to intravenous m-chlorophenylpiperazine in women with seasonal affective disorder [13].

Chemical compound and disease context of Seasonal Affective Disorder

• METHODS: After at least 2 weeks of clinical remission, 12 drug-free patients who had had depression with seasonal affective disorder underwent tryptophan depletion in a double-blind, placebo-controlled, balanced cross-over design study [14].
• Neuroendocrine response to 5-hydroxytryptophan in seasonal affective disorder [15].
• Effects of meta-chlorophenylpiperazine infusions in patients with seasonal affective disorder and healthy control subjects. Diurnal responses and nocturnal regulatory mechanisms [16].
• OBJECTIVE: We tested the hypothesis that phase-delayed circadian rhythms underlie seasonal affective disorder (SAD) by measuring phase position of 6-sulfatoxymelatonin excretion and comparing antidepressant response to morning or evening light given as a first treatment [17].
• Multicenter, placebo-controlled study of fluoxetine in seasonal affective disorder [18].

Biological context of Seasonal Affective Disorder

• Two naturally occurring amino acid substitutions of the 5-HT2A receptor: similar prevalence in patients with seasonal affective disorder and controls [19].
• BACKGROUND: Conflicting results have been reported in previous association studies of the serotonin transporter promoter repeat length polymorphism (5-HTTLPR), seasonal affective disorder (SAD) and seasonality (seasonal variations in mood and behaviour) [20].
• Intraocular pressure and prolactin measures in seasonal affective disorder [21].

Anatomical context of Seasonal Affective Disorder

• The author further suggests that there may be a fault in the thyroid metabolism in the brain in seasonal affective disorder patients, and that fault cannot be identified by studying the peripheral thyroid hormone metabolism [22].

Gene context of Seasonal Affective Disorder

• INTRODUCTION: Several lines of research point to a possible overlap between seasonal affective disorder (SAD) and attention deficit hyperactivity disorder (ADHD), particularly in females [23].
• Polymorphism of the serotonin-2A receptor gene (HTR2A) associated with childhood attention deficit hyperactivity disorder (ADHD) in adult women with seasonal affective disorder [23].
• BACKGROUND: We recently described a preliminary association between the hypofunctional seven-repeat allele of the dopamine-4 receptor gene (DRD4) and increased maximal lifetime body mass index in women with seasonal affective disorder (SAD) [24].
• Abnormal pituitary-adrenal responses to corticotropin-releasing hormone in patients with seasonal affective disorder: clinical and pathophysiological implications [25].
• Untreated seasonal affective disorder patients showed normal basal plasma cortisol and ACTH levels, but their responses to CRH tended to be delayed and were significantly reduced [25].

Analytical, diagnostic and therapeutic context of Seasonal Affective Disorder

• Phototherapy of seasonal affective disorder. Time of day and suppression of melatonin are not critical for antidepressant effects [26].
• [123I]-beta-CIT SPECT imaging shows reduced brain serotonin transporter availability in drug-free depressed patients with seasonal affective disorder [27].
• Positron emission tomography scans of nine patients diagnosed with summer seasonal affective disorder (SSAD) were compared with scans of 45 normal control subjects to investigate differences in brain glucose metabolism [28].

References