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P.1.i.037 Patients with seasonal affective disorder show seasonal fluctuations in their cerebral serotonin transporter binding
... Seasonal pattern disorders occur most frequently in winter although they can also occur in summer. People with seasonal affective disorder have difficulty regulating the neurotransmitter serotonin, a neurotransmitter believed to be responsible for balancing mood [2]. In one study, people with SAD had 5% more SERT, a protein that assists with serotonin transport, in the winter months than in summer [2]. ...
... People with seasonal affective disorder have difficulty regulating the neurotransmitter serotonin, a neurotransmitter believed to be responsible for balancing mood [2]. In one study, people with SAD had 5% more SERT, a protein that assists with serotonin transport, in the winter months than in summer [2]. SERT transports serotonin from the synaptic cleft to the presynaptic neuron, so higher SERT levels lead to lower serotonin activity, thus causing depression [2]. ...
... In one study, people with SAD had 5% more SERT, a protein that assists with serotonin transport, in the winter months than in summer [2]. SERT transports serotonin from the synaptic cleft to the presynaptic neuron, so higher SERT levels lead to lower serotonin activity, thus causing depression [2]. Throughout the summer, sunlight generally keeps SERT levels naturally low [2]. ...
Seasonal affective disorder or SAD is a recurrent major depressive disorder with a seasonal pattern usually beginning in fall and continuing into winter months. A subsyndromal type of SAD, or S-SAD, is commonly known as “winter blues.” Less often, SAD causes depression in the spring or early summer. Symptoms center on sad mood and low energy. Those most at risk are female, are younger, live far from the equator, and have family histories of depression, bipolar disorder, or SAD. Screening instruments include the Seasonal Pattern Assessment Questionnaire (SPAQ). Typical treatment includes antidepressant medications, light therapy, Vitamin D, and counselling. This paper provides an overview of SAD.
... Lewy et al. (1987) introduced their phase-shift hypothesis, which postulates that the endogenous biological clock of people with winter depression is misaligned-mostly delayed-with the natural day-night cycle (Lewy et al., 1987). This circadian misalignment can contribute to, or in turn, is induced by the following changes found in people with SAD: a higher number of serotonin transporters (SERT), the role of melatonin as a biological signal of change of season and more difficulties with its overproduction, and enhanced inflammatory responses as daylight decreases during the winter season (Lewy et al., 2006;McMahon et al., 2014;Song et al., 2015;Wehr et al., 2001). The causal links between circadian misalignment, serotonin system, melatonin, and inflammation remain to be further elucidated (Melrose, 2015). ...
Background
Many mood disorder patients experience seasonal changes in varying degrees. Studies on seasonality have shown that bipolar disorder has a higher prevalence rate in such patients; however, there is limited research on seasonality in early‐onset mood disorder patients. This study estimated the prevalence of seasonality in early‐onset mood disorder patients, and examined the association between seasonality and mood disorders.
Methods
Early‐onset mood disorder patients (n = 378; 138 major depressive disorder; 101 bipolar I disorder; 139 bipolar II disorder) of the Mood Disorder Cohort Research Consortium and healthy control subjects (n = 235) were assessed for seasonality with Seasonality Pattern Assessment Questionnaire (SPAQ).
Results
A higher global seasonality score, an overall seasonal impairment score, and the prevalence of seasonal affective disorder (SAD) and subsyndromal SAD showed that mood disorder subjects had higher seasonality than the healthy subjects. The former subject group had a significantly higher mean overall seasonal impairment score than the healthy subjects (p < .001); in particular, bipolar II disorder subjects had the highest prevalence of SAD, and the diagnosis of bipolar II disorder had significantly higher odds ratios for SAD when compared to major depression and bipolar I disorder (p < .05).
Conclusions
Early‐onset mood disorders, especially bipolar II disorder, were associated with high seasonality. A thorough assessment of seasonality in early‐onset mood disorders may be warranted for more personalized treatment and proactive prevention of mood episodes.
... 30 Additionally, the concentration of 5-HT is closely related to seasonal variation. 31 GABA is the main inhibitory neurotransmitter in the brain and affects regulation of emotion. 32 Some studies have shown that at the brain level, photoperiodic seasonal responses are mediated by several neurotransmitters, including GABA. ...
Objective
The present study aimed to investigate the effect of seasonal variation on neurotransmitter release in the hippocampus of normal rats and rats with pineal excision.
Methods
Two time points, the summer and winter solstice, which are the longest and shortest days of the year, respectively, were selected. Male Sprague–Dawley rats that underwent a sham operation without pineal excision were included as a control group. The concentrations of 5-hydroxytryptamine (5-HT) and γ-aminobutyric acid (GABA) were determined by radioimmunoassays and enzyme linked immunosorbent assays, respectively.
Results
In the winter, the 5-HT and GABA levels in normal rats exhibited a difference compared with those in the operation group (P < .01). A difference was also noted in GABA levels between the normal group and the sham operation group (P < .05). The concentrations of 5-HT and GABA in the hippocampal tissues of the normal group exhibited a seasonal rhythm consisting of elevation during the summer and reduction during the winter (P < .01), while the GABA levels in the sham operation group exhibited a significant difference, with elevation during the summer and reduction during the winter (P < .01). In the operation group, GABA showed the same trend (P < .01).
Conclusion
The seasonal rhythm of neurotransmitter secretion by the hippocampus (5-HT and GABA) consisted of elevation during the summer and reduction during the winter. During the winter, the pineal gland exhibited a reverse regulatory effect on the secretion of 5-HT and GABA in the hippocampus, and it exhibited seasonal selectivity with regard to the regulation of 5-HT.
... The annual shortening of the photoperiod is believed to be the main factor in SAD onset; however, responses to cold temperatures and epigenetic changes have been documented in seasonal mammals and exhibit evolutionary conservation down to lower forms of life [3][4][5][6] , suggesting that many very basic physiologic mechanisms could contribute to SAD. Ultimately, SAD is a complex disease with both chronobiological and neurobiological underpinnings [7][8][9][10][11] , which may include an etiology that for some could even begin in utero [12][13][14][15][16] . ...
There is a growing interest in personalized and preventive medicine initiatives that leverage serious patient engagement, such as those initiated and pursued among participants in the quantified-self movement. However, many of the self-assessments that result are not rooted in good scientific practices, such as exploiting controls, dose escalation strategies, multiple endpoint monitoring, etc. Areas where individual monitoring and health assessments have great potential involve sleep and behavior, as there are a number of very problematic sleep and behavior-related conditions that are hard to treat without personalization. For example, winter depression or seasonal affective disorder (SAD) is a serious, recurrent, atypical depressive disorder impacting millions each year. In order to prevent yearly recurrence antidepressant drugs are used to prophylactically treat SAD. In turn, these antidepressant drugs can affect sleep patterns, further exacerbating the condition. Because of this, possibly unique combinatorial or ‘polypharmaceutical’ interventions involving sleep aids may be prescribed. However, little research into the effects of such polypharmacy on the long-term sleep quality of treated individuals has been pursued. Employing wireless monitoring in a patient-centered study we sought to gain insight into the influence of polypharmacy on sleep patterns and the optimal course of therapy for an individual being treated for SAD with duloxetine (Cymbalta) and temazepam. We analyzed continuous-time sleep data while dosages and combinations of these agents were varied. We found that the administration of Cymbalta led to an exacerbation of the subject’s symptoms in a statistically significant way. We argue that such analyses may be necessary to effectively treat individuals with similar overall clinical manifestations and diagnosis, despite their having a unique set of symptoms, genetic profiles and exposure histories. We also consider the limitations of our study and areas for further research.
... The annual shortening of the photoperiod is believed to be the main factor in SAD onset; however, responses to cold temperatures and epigenetic changes have been documented in seasonal mammals and exhibit evolutionary conservation down to lower forms of life [3][4][5][6] , suggesting that many very basic physiologic mechanisms could contribute to SAD. Ultimately, SAD is a complex disease with both chronobiological and neurobiological underpinnings [7][8][9][10][11] , which may include an etiology that for some could even begin in utero [12][13][14][15][16] . ...
There is a growing interest in personalized and preventive medicine initiatives that leverage serious patient engagement, such as those initiated and pursued among participants in the quantified-self movement. However, many of the self-assessments that result are not rooted in good scientific practices, such as exploiting controls, dose escalation strategies, multiple endpoint monitoring, etc. Areas where individual monitoring and health assessments have great potential involve sleep and behavior, as there are a number of very problematic sleep and behavior-related conditions that are hard to treat without personalization. For example, winter depression or seasonal affective disorder (SAD) is a serious, recurrent, atypical depressive disorder impacting millions each year. In order to prevent yearly recurrence antidepressant drugs are used to prophylactically treat SAD. In turn, these antidepressant drugs can affect sleep patterns, further exacerbating the condition. Because of this, possibly unique combinatorial or ‘polypharmaceutical’ interventions involving sleep aids may be prescribed. However, little research into the effects of such polypharmacy on the long-term sleep quality of treated individuals has been pursued. Employing wireless monitoring in a patient-centered study we sought to gain insight into the influence of polypharmacy on sleep patterns and the optimal course of therapy for an individual being treated for SAD with duloxetine (Cymbalta) and temazepam. We analyzed continuous-time sleep data while dosages and combinations of these agents were varied. We found that the administration of Cymbalta led to an exacerbation of the subject’s symptoms in a statistically significant way. Further, we unmasked and monitored treatment effects on a latent obstructive sleep apnea condition. We argue that such analyses may be necessary to effectively treat individuals with similar overall clinical manifestations and diagnosis, despite their having a unique set of symptoms, genetic profiles and exposure histories. We also consider the limitations of our study and areas for further research.
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