<b>Conclusions:</b> This report provides initial evidence of normal melanopsin function and environmental light exposures in patients with pre-dominately mid and moderate non-seasonal depression in a subtropical location in the southern hemisphere.
(1) A subgroup of depressed patients have documented circadian abnormalities in mood, sleep, temperature and neuroendocrine secretion; (2) It is also suggested that seasonal affective disorder (SAD) patients may show an abnormality in their ability to shift their daily circadian rhythms in response to seasonal light changes; (3) The dramatic improvements in some depressions in response to three treatment modalities which manipulate circadian rhythms suggest that circadian abnormalities reported in patients may constitute a core component of the pathophysiology in depression; (4) Mutations in clock genes have been discovered that accelerate or delay circadian cycles; (5) It is hypothesized that 24-hour rhythm abnormalities in major depression and SAD may be due to altered clock genes.
(1) A subgroup of depressed patients have documented circadian abnormalities in mood, sleep, temperature and neuroendocrine secretion; (2) It is also suggested that seasonal affective disorder (SAD) patients may show an abnormality in their ability to shift their daily circadian rhythms in response to seasonal light changes; (3) The dramatic improvements in some depressions in response to three treatment modalities which manipulate circadian rhythms suggest that circadian abnormalities reported in patients may constitute a core component of the pathophysiology in depression; (4) Mutations in clock genes have been discovered that accelerate or delay circadian cycles; (5) It is hypothesized that 24-hour rhythm abnormalities in major depression and SAD may be due to altered clock genes.
5-HTT turnover rate, a measure for the number of inward transport events per minute, and tyramine-induced, 5-HTT-mediated outward transport were assessed at baseline, after 4 weeks of bright light therapy, and in summer using a case-control design in a consecutive sample of 73 drug-free depressed patients with SAD and 70 nonseasonal healthy controls.
SLC6A4 provided strong and consistent evidence of association with the PD and PD+SAD groups, with the most significant association in both groups being at rs140701 (chi(2)=10.72, P=0.001 with PD and chi(2)=8.59, P=0.003 in the PD+SAD group).
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.
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.
A multiple regression analysis was performed to examine whether cost/probability biases, BIS/BAS, and their interactions affected SAD symptoms; following this, the main effects of cost bias and BIS were determined for LSAS-Fear (β = 0.64, <i>p</i> < 0.001; β = 0.33, <i>p</i> < 0.01) and LSAS-Avoidance (β = 0.49, <i>p</i> < 0.001; β = 0.35, <i>p</i> < 0.01).
After treatment, children with SAD in the waitlist group differed from children with SAD in the CBT group by showing stronger cortisol reactivity and a higher responder rate, indicative of a possible sensitization to stress.No difference was found for sAA.
After treatment, children with SAD in the waitlist group differed from children with SAD in the CBT group by showing stronger cortisol reactivity and a higher responder rate, indicative of a possible sensitization to stress.No difference was found for sAA.
After treatment, children with SAD in the waitlist group differed from children with SAD in the CBT group by showing stronger cortisol reactivity and a higher responder rate, indicative of a possible sensitization to stress.No difference was found for sAA.
Although we cannot confirm previous findings of an association between SAD and the ARNTL and NPAS2 genes, these genes may influence seasonal variations through metabolic factors such as body weight and appetite.
Among some SAD patients, it is possible that the sustained ingestion of high-fat diet will rather activate the transcription of the neuropeptide Y gene than deactivate it, indicating a defect in macronutrient selection.
An association between the presence of PMDD and family history (P=0.0029) and 5-HTTLPR long/short allele-heterozygosity (P=0.033) was found in females with SAD.
Association between SAD and the shorter allele of the serotonin transporter promoter repeat length polymorphism (5-HTTLPR) has been reported in an American sample.
Behavioral (reaction time and accuracy) and electrocortical measures (P100, N170, EPN, LPP) were assessed during a facial emotion identification task in children (age 10-13) with SAD (n = 32), clinical controls with mixed anxiety disorders (n = 30), and healthy controls (n = 33).
Collectively, these findings reveal a neurobiological mechanism which may relate to the clinical observation that early trauma increases the risk for substance abuse disorder (SAD) in individuals harbouring haplotypic variations in the Gabra2 gene.