Seasonal Affective Disorder

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Norman E Rosenthal - One of the best experts on this subject based on the ideXlab platform.

  • a missense variant p10l of the melanopsin opn4 gene in Seasonal Affective Disorder
    Journal of Affective Disorders, 2009
    Co-Authors: Kathryn A Roecklein, Kelly J. Rohan, Norman E Rosenthal, Wallace C Duncan, Mark D Rollag, Robert H Lipsky, Ignacio Provencio
    Abstract:

    Abstract Background Melanopsin, a non-visual photopigment, may play a role in aberrant responses to low winter light levels in Seasonal Affective Disorder (SAD). We hypothesize that functional sequence variation in the melanopsin gene could contribute to increasing the light needed for normal functioning during winter in SAD. Methods Associations between alleles, genotypes, and haplotypes of melanopsin in SAD participants ( n  = 130) were performed relative to controls with no history of psychopathology ( n  = 90). Results SAD participants had a higher frequency of the homozygous minor genotype (T/T) for the missense variant rs2675703 (P10L) than controls, compared to the combined frequencies of C/C and C/T. Individuals with the T/T genotype were 5.6 times more likely to be in the SAD group than the control group, and all 7 (5%) of individuals with the T/T genotype at P10L were in the SAD group. Limitations The study examined only one molecular component of the non-visual light input pathway, and recruitment methods for the comparison groups differed. Conclusion These findings support the hypothesis that melanopsin variants may predispose some individuals to SAD. Characterizing the genetic basis for deficits in the non-visual light input pathway has the potential to define mechanisms underlying the pathological response to light in SAD, which may improve treatment.

  • effects of tryptophan depletion and catecholamine depletion on immune parameters in patients with Seasonal Affective Disorder in remission with light therapy
    Biological Psychiatry, 2003
    Co-Authors: J Stastny, Siegfried Kasper, Norman E Rosenthal, A Konstantinidis, Markus J Schwarz, Oliver Vitouch, Alexander Neumeister
    Abstract:

    Abstract Background Altered immunologic parameters are found in symptomatic depressed patients relative to remitted depressed patients and healthy controls. We investigated whether tryptophan depletion and catecholamine depletion induce alterations in immunologic parameters in patients with Seasonal Affective Disorder remitted on light therapy, and whether these changes are associated with changes in mood. Methods Remitted patients with Seasonal Affective Disorder underwent tryptophan depletion, catecholamine depletion, and sham depletion in a prospective randomized, double-blind crossover design. Measures of depression, plasma levels of tryptophan and catecholamine metabolites, and plasma levels of cytokines (sIL-4, IL-6, neopterin, sTNF-R1 and sTNF-R2) were obtained at baseline, and 7, 24, and 30 hours after monoamine depletion. Results Tryptophan depletion decreased plasma total and free tryptophan levels; catecholamine depletion decreased plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels. Tryptophan depletion and catecholamine depletion, but not sham depletion, induced a transient exacerbation of depressive symptoms ( p p p r = −.61, p Conclusions The monoamine depletion-induced alterations of humoral and cellular immunity suggest a potential role of immunologic parameters in the pathophysiology of Seasonal Affective Disorder; however, the results must be considered preliminary and require further study.

  • serotonin hypothesis of winter depression behavioral and neuroendocrine effects of the 5 ht1a receptor partial agonist ipsapirone in patients with Seasonal Affective Disorder and healthy control subjects
    Psychiatry Research-neuroimaging, 1999
    Co-Authors: Paul J Schwartz, Erick H Turner, Rina G Vetticad, Diego Garciaborreguero, Jan Sedway, Thomas A Wehr, Dennis L Murphy, Norman E Rosenthal
    Abstract:

    Winter depressions in Seasonal Affective Disorder (SAD) are associated with central serotonergic (5-HT) dysfunction. SAD patients demonstrate rather specific, state-dependent, abnormal increases in 'activation-euphoria' ratings following intravenous infusion of the 5-HT receptor agonist meta-chlorophenylpiperazine (m-CPP). Several studies are also consistent with abnormal serotonergic regulation of the hypothalamic-pituitary-adrenal (HPA) axis in SAD. Here, we investigated the effects of the 5-HT1A receptor partial agonist ipsapirone, which produces behavioral effects and HPA-axis activation, to further characterize the 5-HT receptor subtype-specificity of these disturbances in SAD. Eighteen SAD patients and 18 control subjects completed two drug challenges (ipsapirone 0.3 mg/kg and placebo) separated by 3-5 days in randomized order. We measured behavioral responses with the NIMH self-rating scale, and plasma ACTH, cortisol, and prolactin concentrations. Compared with placebo, ipsapirone was associated with significant increases in self-rated 'functional deficit' and 'altered self-reality', and in each of the hormones. There were no differences between groups on any measures. The level of depression in SAD patients was inversely correlated with their ipsapirone-induced cortisol responses. There were significant drug x order effects on baseline 'anxiety' scores, ACTH and cortisol concentrations, such that subjects were significantly more stressed (higher 'anxiety', ACTH and cortisol) prior to their first challenge compared with their second. In conclusion, post-synaptic 5-HT1A receptors appear to function normally in SAD. The previously observed m-CPP-induced behavioral abnormality may be mediated by either 5-HT2C or 5-HT7 receptors.

  • effects of tryptophan depletion vs catecholamine depletion in patients with Seasonal Affective Disorder in remission with light therapy
    Archives of General Psychiatry, 1998
    Co-Authors: Alexander Neumeister, Erick H Turner, Siegfried Kasper, Jefferey R Matthews, Teodor T Postolache, Ronald L Barnett, Manfred Rauh, Rina G Vetticad, Norman E Rosenthal
    Abstract:

    Methods: Sixteen patients with Seasonal Affective Disorder who had responded to a standard regimen of daily 10 000-lux light therapy were enrolled in a doubleblind, placebo-controlled, randomized crossover study. We compared the effects of tryptophan depletion with catecholamine depletion and sham depletion. Ingestion of a tryptophan-free amino acid beverage plus amino acid capsules was used to deplete tryptophan. Administration of the tyrosine hydroxylase inhibitor a-methyl-paratyrosine was used to deplete catecholamines. Diphenhydramine hydrochloride was used as an active placebo during sham depletion. The effects of these interventions were evaluated with measures of depression, plasma tryptophan levels, and plasma catecholamine metabolites. Results: Tryptophan depletion significantly decreased plasma total and free tryptophan levels. Catecholamine depletion significantly decreased plasma 3-methoxy-4hydroxyphenylethyleneglycol and homovanillic acid levels. Both tryptophan depletion and catecholamine depletion, compared with sham depletion, induced a robust increase (P,.001, repeated-measures analysis of variance) in depressive symptoms as measured with the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version. Conclusions: The beneficial effects of light therapy in the treatment of Seasonal Affective Disorder are reversed by both tryptophan depletion and catecholamine depletion. These findings confirm previous work showing that serotonin plays an important role in the mechanism of action of light therapy and provide new evidence that brain catecholaminergic systems may also be involved.

  • prevalence of Seasonal difficulties in mood and behavior among japanese civil servants
    American Journal of Psychiatry, 1995
    Co-Authors: Norio Ozaki, Yuichiro Ono, Akinori Ito, Norman E Rosenthal
    Abstract:

    Objective: Most prevalence studies of Seasonal changes in mood and behavior have come I rom Western countries. The authors ‘goal was to determine the prevalence ofSeasonal changes in mood and behavior in a randomly selected group of ]apanese workers. Method: They administered a ]apanese translation of the Seasonal Pattern Assessment Questionnaire to I ,2 76 civil servants in Nagoya, ]apan. Results: The estimated prevalence of winter Seasonal Affective Disorder was 0.86%, the estimated prevalence of winter subsyndromal Seasonal aff ective Disorder was 0.86%, the estimated prevalence of summer Seasonal Affective Disorder was 0. 94 % , and the estimated prevalence ofsummer subsyndromal Seasonal Affective Disorder was 2.12%. Conclusions: The authors conclude that Seasonal changes in mood and behavior occur in ]apan, but at a lower frequency and with a different profile than in the United States or Europe. (Am J Psychiatry 1995; 152:1225-1227)

Raymond W. Lam - One of the best experts on this subject based on the ideXlab platform.

  • evidence of a biological effect of light therapy on the retina of patients with Seasonal Affective Disorder
    Biological Psychiatry, 2009
    Co-Authors: Mariepier Lavoie, Raymond W. Lam, Guylain Bouchard, Alexandre Sasseville, Marieclaude Charron, Annemarie Gagne, Philippe Tremblay, Mariejosee Filteau, Marc Hebert
    Abstract:

    Background Retinal sensitivity anomalies have been reported in patients affected by Seasonal Affective Disorder (SAD). We used the electroretinogram (ERG) to assess Seasonal change in retinal function in patients with SAD and healthy participants, as well as in patients following 4 weeks of light therapy. Methods ERG assessments were obtained in 22 SAD patients (2 men, 20 women, mean age 31 ± 9 years) in the fall/winter season before and after 2 and 4 weeks of light therapy and in summertime. Matched healthy participants (2 men, 14 women; mean age 29 ± 8 years) were evaluated once in the fall/winter and once in summer. The 29-item Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorder version was administered. Standard ERG parameters were derived from the photopic and scotopic luminance response functions. Salivary melatonin concentration during ERG was assessed in both groups but during fall/winter assessments only. Results A significantly lower cone ERG maximal amplitude and lower rod sensitivity was found in SAD patients before light therapy compared with healthy participants. Following 4 weeks of light therapy, a normalization of cone and rod ERG function occurred. ERG parameters in the summer and melatonin concentrations in fall/winter were not significantly different between groups. Conclusions Depressed patients with SAD demonstrate ERG changes in the winter compared with healthy comparison subjects with lower rod retinal sensitivity and lower cone maximal amplitude. These changes normalized following 4 weeks of light therapy and during the summer, suggesting that ERG changes are state markers for SAD.

  • a birth season drd4 gene interaction predicts weight gain and obesity in women with Seasonal Affective Disorder a Seasonal thrifty phenotype hypothesis
    Neuropsychopharmacology, 2006
    Co-Authors: Robert D. Levitan, Mario Masellis, Raymond W. Lam, Allan S. Kaplan, Caroline Davis, Bronwyn Mackenzie, Subi Tharmalingam, Vincenzo S. Basile
    Abstract:

    We have recently described an association between the hypofunctional 7-repeat allele (7R) of the dopamine-4 receptor gene (DRD4), weight gain, and obesity in women with Seasonal Affective Disorder (SAD). In the current study, we examined whether season-of-birth might interact with the 7R allele to influence body weight regulation in SAD. In 182 female probands with SAD, we performed an analysis of covariance predicting maximum lifetime body mass index (BMI) with both the exon-3 variable number of tandem repeat polymorphism of DRD4 and season-of-birth as independent variables, and age as the covariate. The overall model was highly significant (F = 4.42, df = 8, 173, p 30 kg/m2) was also significantly higher in the 7R/spring birth group (9/17=52.9% vs 32/165=19.4%; chi2 = 9.94, df = 1, p = 0.002; odds ratio = 4.68, 95% CI = 1.67-13.07). These data may reflect a novel gene-environment interaction, during early brain development, which establishes an increased risk for obesity in women with SAD. Although the mechanism for season-of-birth effects in psychiatric Disorders is unknown, a characteristic pattern of melatonin exposure during the second and third trimesters may be of particular relevance in this study population. We speculate that these data may reflect the vestigial expression of a Seasonal thrifty phenotype that contributed to the positive selection of the 7R allele over the past 40,000 years.

  • the can sad study a randomized controlled trial of the effectiveness of light therapy and fluoxetine in patients with winter Seasonal Affective Disorder
    American Journal of Psychiatry, 2006
    Co-Authors: Raymond W. Lam, Anthony J Levitt, Robert D. Levitan, Murray W Enns, Rachel Morehouse, Erin E Michalak, Edwin M Tam
    Abstract:

    Objective: Light therapy and antidepressants have shown comparable efficacy in separate studies of Seasonal Affective Disorder treatment, but few studies have directly compared the two treatments. This study compared the effectiveness of light therapy and an antidepressant within a single trial. Method: This double-blind, randomized, controlled trial was conducted in four Canadian centers over three winter seasons. Patients met DSM–IV criteria for major depressive Disorder with a Seasonal (winter) pattern and had scores ≥23 on the 24-item Hamilton Depression Rating Scale. After a baseline observation week, eligible patients were randomly assigned to 8 weeks of double-blind treatment with either 1) 10,000-lux light treatment and a placebo capsule, or 2) 100-lux light treatment (placebo light) and fluoxetine, 20 mg/day. Light treatment was applied for 30 minutes/day in the morning with a fluorescent white-light box; placebo light boxes used neutral density filters. Results: A total of 96 patients were rando...

  • the dopamine 4 receptor gene associated with binge eating and weight gain in women with Seasonal Affective Disorder an evolutionary perspective
    Biological Psychiatry, 2004
    Co-Authors: Robert D. Levitan, Mario Masellis, Vincenzo S. Basile, Raymond W. Lam, Allan S. Kaplan, Caroline Davis, Pierandrea Muglia, Bronwyn Mackenzie, Subi Tharmalingam, Sidney H. Kennedy
    Abstract:

    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). In this study, we examined whether binge eating behavior mediated this putative association. Methods The study sample consisted of 131 women with winter SAD who reported increased intake of high-carbohydrate/high-fat foods during depressive episodes. We compared rates of binge eating behavior in the two genotypic groups defined by the presence or absence of the seven-repeat allele of DRD4. Results Consistent with our working hypothesis, the proportion of binge eaters was significantly greater in probands with the seven-repeat allele (18 of 46, 39.1%) than in probands without this allele (14 of 85, 16.5%) [χ2(1)= 8.32, p = .004; odds ratio = 3.25, 95% confidence interval 1.43, 7.41]. Conclusions Pending replication in other samples, these results point to a genetic factor that could help in the early identification and treatment of women at higher risk for Seasonal weight gain associated with binge eating behavior. At a theoretic level, the current results suggest a novel link between evolutionary models of Seasonal weight gain on the one hand and the DRD4 gene on the other.

  • electroretinography in patients with winter Seasonal Affective Disorder
    Psychiatry Research-neuroimaging, 2004
    Co-Authors: Marc Hebert, Lakshmi N Yatham, Edwin M Tam, Craig W Beattie, Raymond W. Lam
    Abstract:

    A retinal sensitivity abnormality has been hypothesized in Seasonal Affective Disorder (SAD). To explore this hypothesis, the electroretinogram (ERG) was used to assess retinal sensitivity at the level of the rod photoreceptor system. We examined 27 depressed patients who met DSM-III-R criteria for major depression, recurrent, with a Seasonal (winter) pattern and 23 normal control subjects who were age-paired and sex-matched as much as possible with the SAD patients. ERG testing was performed in dark-adapted, dilated eyes in winter between 10:00 and 15:00 h. Retinal sensitivity was based on the light stimulus intensity necessary to reach a 50-μV amplitude threshold. We found that retinal sensitivity was significantly lower (0.21 log units) in SAD patients compared with normal control subjects and that 55% of the patients had a retinal sensitivity value one standard deviation lower than the mean value of the control subjects. These results are consistent with a retinal hyposensitivity hypothesis for SAD, but the explanation for lower rod photoreceptor sensitivity in SAD is not known. We hypothesize that brain neurotransmitter dysregulation may be at the origin of both the mood Disorder and retinal sensitivity change.

Alexander Neumeister - One of the best experts on this subject based on the ideXlab platform.

  • effects of tryptophan depletion and catecholamine depletion on immune parameters in patients with Seasonal Affective Disorder in remission with light therapy
    Biological Psychiatry, 2003
    Co-Authors: J Stastny, Siegfried Kasper, Norman E Rosenthal, A Konstantinidis, Markus J Schwarz, Oliver Vitouch, Alexander Neumeister
    Abstract:

    Abstract Background Altered immunologic parameters are found in symptomatic depressed patients relative to remitted depressed patients and healthy controls. We investigated whether tryptophan depletion and catecholamine depletion induce alterations in immunologic parameters in patients with Seasonal Affective Disorder remitted on light therapy, and whether these changes are associated with changes in mood. Methods Remitted patients with Seasonal Affective Disorder underwent tryptophan depletion, catecholamine depletion, and sham depletion in a prospective randomized, double-blind crossover design. Measures of depression, plasma levels of tryptophan and catecholamine metabolites, and plasma levels of cytokines (sIL-4, IL-6, neopterin, sTNF-R1 and sTNF-R2) were obtained at baseline, and 7, 24, and 30 hours after monoamine depletion. Results Tryptophan depletion decreased plasma total and free tryptophan levels; catecholamine depletion decreased plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels. Tryptophan depletion and catecholamine depletion, but not sham depletion, induced a transient exacerbation of depressive symptoms ( p p p r = −.61, p Conclusions The monoamine depletion-induced alterations of humoral and cellular immunity suggest a potential role of immunologic parameters in the pathophysiology of Seasonal Affective Disorder; however, the results must be considered preliminary and require further study.

  • Changes of clinical pattern in Seasonal Affective Disorder (SAD) over time in a German-speaking sample
    European Archives of Psychiatry and Clinical Neuroscience, 2002
    Co-Authors: D. Winkler, J Stastny, A Konstantinidis, M. Willeit, N. Praschak-rieder, M. J. Lucht, E. Hilger, N. Thierry, E. Pjrek, Alexander Neumeister
    Abstract:

    Objective The goals of this study are to provide estimates of clinical and demographic variables of patients with Seasonal Affective Disorder (SAD) in Germany and Austria, to compare our results with those of previously published SAD studies, and to find out whether the clinical pattern of SAD remained stable over several years. Method We investigated 610 SAD patients from the outpatient clinics in Bonn (n = 190) and Vienna (n = 420). Patients in Bonn were recruited in the fall-winter season of the years 1989–1992, those in Vienna in the years 1993–2001. Results We observed a change in the clinical pattern in our patients: patients from Bonn, who were diagnosed and treated about 5 years earlier, were more likely to suffer from melancholic depression, whereas Viennese patients rather suffered from atypical depression (χ^2 = 54.952, df = 2, p < 0.001). The symptoms of hypersomnia, daytime fatigue, increased eating and carbohydrate-craving were more frequent in the Viennese sample, anxiety and deterioration of patients' capacity to perform at work predominated in Bonn. In addition, patients from Vienna obtained a higher GSS (global Seasonality score, measured by the SPAQ – Seasonal Pattern Assessment Questionnaire) than those from Bonn (15.7 ± 3.3 and 14.6 ± 4.1 respectively; t = 3.104, p = 0.002). Taken together, our results were in good accordance to other published SAD materials, but we were able to demonstrate that our patients reported “feeling worst” (measured by item 13H of the SPAQ) in November and December, whereas SAD patients in the USA clearly had their worst months in January and February. Conclusions We suggest that an increase in awareness of fall-winter depression in the last decade by both doctors, who referred patients, as well as patients or the entire population must have caused patients to sign up for light therapy at the Viennese SAD clinic because of having heard about the atypical symptom profile. This increased awareness of SAD can also be measured by a statistically significant reduction in the diagnostic latency (from the age of onset to the diagnosis of SAD) when comparing the two study locations.

  • effects of tryptophan depletion vs catecholamine depletion in patients with Seasonal Affective Disorder in remission with light therapy
    Archives of General Psychiatry, 1998
    Co-Authors: Alexander Neumeister, Erick H Turner, Siegfried Kasper, Jefferey R Matthews, Teodor T Postolache, Ronald L Barnett, Manfred Rauh, Rina G Vetticad, Norman E Rosenthal
    Abstract:

    Methods: Sixteen patients with Seasonal Affective Disorder who had responded to a standard regimen of daily 10 000-lux light therapy were enrolled in a doubleblind, placebo-controlled, randomized crossover study. We compared the effects of tryptophan depletion with catecholamine depletion and sham depletion. Ingestion of a tryptophan-free amino acid beverage plus amino acid capsules was used to deplete tryptophan. Administration of the tyrosine hydroxylase inhibitor a-methyl-paratyrosine was used to deplete catecholamines. Diphenhydramine hydrochloride was used as an active placebo during sham depletion. The effects of these interventions were evaluated with measures of depression, plasma tryptophan levels, and plasma catecholamine metabolites. Results: Tryptophan depletion significantly decreased plasma total and free tryptophan levels. Catecholamine depletion significantly decreased plasma 3-methoxy-4hydroxyphenylethyleneglycol and homovanillic acid levels. Both tryptophan depletion and catecholamine depletion, compared with sham depletion, induced a robust increase (P,.001, repeated-measures analysis of variance) in depressive symptoms as measured with the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version. Conclusions: The beneficial effects of light therapy in the treatment of Seasonal Affective Disorder are reversed by both tryptophan depletion and catecholamine depletion. These findings confirm previous work showing that serotonin plays an important role in the mechanism of action of light therapy and provide new evidence that brain catecholaminergic systems may also be involved.

Robert D. Levitan - One of the best experts on this subject based on the ideXlab platform.

  • the chronobiology and neurobiology of winter Seasonal Affective Disorder
    Dialogues in clinical neuroscience, 2007
    Co-Authors: Robert D. Levitan
    Abstract:

    This review summarizes research on the chronobiology and neurobiology of winter Seasonal Affective Disorder (SAD), a recurrent subtype of depression characterized by a predictable onset in the fall/winter months and spontaneous remission in the spring/summer period. Chronobiological mechanisms related to circadian rhythms, melatonin, and photoperiodism play a significant role in many cases of SAD, and treatment of SAD can be optimized by considering individual differences in key chronobiological markers. Converging evidence also points to a role for the major monoamine neurotransmitters serotonin, norepinephrine, and dopamine in one or more aspects of SAD. Ultimately, as with other psychiatric illnesses, SAD is best considered as a complex Disorder resulting from the interaction of several vulnerability factors acting at different levels, the various genetic mechanisms that underlie them, and the physical environment. Models of SAD that emphasize its potential role in human evolution will also be discussed.

  • a birth season drd4 gene interaction predicts weight gain and obesity in women with Seasonal Affective Disorder a Seasonal thrifty phenotype hypothesis
    Neuropsychopharmacology, 2006
    Co-Authors: Robert D. Levitan, Mario Masellis, Raymond W. Lam, Allan S. Kaplan, Caroline Davis, Bronwyn Mackenzie, Subi Tharmalingam, Vincenzo S. Basile
    Abstract:

    We have recently described an association between the hypofunctional 7-repeat allele (7R) of the dopamine-4 receptor gene (DRD4), weight gain, and obesity in women with Seasonal Affective Disorder (SAD). In the current study, we examined whether season-of-birth might interact with the 7R allele to influence body weight regulation in SAD. In 182 female probands with SAD, we performed an analysis of covariance predicting maximum lifetime body mass index (BMI) with both the exon-3 variable number of tandem repeat polymorphism of DRD4 and season-of-birth as independent variables, and age as the covariate. The overall model was highly significant (F = 4.42, df = 8, 173, p 30 kg/m2) was also significantly higher in the 7R/spring birth group (9/17=52.9% vs 32/165=19.4%; chi2 = 9.94, df = 1, p = 0.002; odds ratio = 4.68, 95% CI = 1.67-13.07). These data may reflect a novel gene-environment interaction, during early brain development, which establishes an increased risk for obesity in women with SAD. Although the mechanism for season-of-birth effects in psychiatric Disorders is unknown, a characteristic pattern of melatonin exposure during the second and third trimesters may be of particular relevance in this study population. We speculate that these data may reflect the vestigial expression of a Seasonal thrifty phenotype that contributed to the positive selection of the 7R allele over the past 40,000 years.

  • the can sad study a randomized controlled trial of the effectiveness of light therapy and fluoxetine in patients with winter Seasonal Affective Disorder
    American Journal of Psychiatry, 2006
    Co-Authors: Raymond W. Lam, Anthony J Levitt, Robert D. Levitan, Murray W Enns, Rachel Morehouse, Erin E Michalak, Edwin M Tam
    Abstract:

    Objective: Light therapy and antidepressants have shown comparable efficacy in separate studies of Seasonal Affective Disorder treatment, but few studies have directly compared the two treatments. This study compared the effectiveness of light therapy and an antidepressant within a single trial. Method: This double-blind, randomized, controlled trial was conducted in four Canadian centers over three winter seasons. Patients met DSM–IV criteria for major depressive Disorder with a Seasonal (winter) pattern and had scores ≥23 on the 24-item Hamilton Depression Rating Scale. After a baseline observation week, eligible patients were randomly assigned to 8 weeks of double-blind treatment with either 1) 10,000-lux light treatment and a placebo capsule, or 2) 100-lux light treatment (placebo light) and fluoxetine, 20 mg/day. Light treatment was applied for 30 minutes/day in the morning with a fluorescent white-light box; placebo light boxes used neutral density filters. Results: A total of 96 patients were rando...

  • the dopamine 4 receptor gene associated with binge eating and weight gain in women with Seasonal Affective Disorder an evolutionary perspective
    Biological Psychiatry, 2004
    Co-Authors: Robert D. Levitan, Mario Masellis, Vincenzo S. Basile, Raymond W. Lam, Allan S. Kaplan, Caroline Davis, Pierandrea Muglia, Bronwyn Mackenzie, Subi Tharmalingam, Sidney H. Kennedy
    Abstract:

    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). In this study, we examined whether binge eating behavior mediated this putative association. Methods The study sample consisted of 131 women with winter SAD who reported increased intake of high-carbohydrate/high-fat foods during depressive episodes. We compared rates of binge eating behavior in the two genotypic groups defined by the presence or absence of the seven-repeat allele of DRD4. Results Consistent with our working hypothesis, the proportion of binge eaters was significantly greater in probands with the seven-repeat allele (18 of 46, 39.1%) than in probands without this allele (14 of 85, 16.5%) [χ2(1)= 8.32, p = .004; odds ratio = 3.25, 95% confidence interval 1.43, 7.41]. Conclusions Pending replication in other samples, these results point to a genetic factor that could help in the early identification and treatment of women at higher risk for Seasonal weight gain associated with binge eating behavior. At a theoretic level, the current results suggest a novel link between evolutionary models of Seasonal weight gain on the one hand and the DRD4 gene on the other.

  • Childhood Inattention and Dysphoria and Adult Obesity Associated with the Dopamine D4 receptor Gene in Overeating Women with Seasonal Affective Disorder
    Neuropsychopharmacology, 2004
    Co-Authors: Robert D. Levitan, Mario Masellis, Vincenzo S. Basile, Raymond W. Lam, Allan S. Kaplan, Pierandrea Muglia, Subi Tharmalingam, Sidney H. Kennedy, U Jain, J L Kennedy
    Abstract:

    There is significant evidence that altered dopamine activity plays a role in Seasonal Affective Disorder (SAD). The current study examined three separate genetic hypotheses for SAD related to the 7-repeat allele (7R) of the dopamine-4 receptor gene (DRD4), a variant associated with decreased affinity for dopamine. We examined the possible contribution of 7R to the overall expression of SAD, attention deficit Disorder (ADD) comorbidity, and body weight regulation. As part of an ongoing genetic study of increased eating behavior and mood in female subjects, 108 women with winter SAD and carbohydrate craving/weight gain were administered the Wender-Utah Rating Scale to measure childhood ADD symptomatology, and a questionnaire to assess maximal lifetime body mass index (BMI). To test for an association between 7R and the categorical diagnosis of SAD, the transmission disequilibrium test (TDT) was used in a subsample of probands providing familial DNA. Standard parametric tests were used to compare childhood ADD symptoms and maximal lifetime BMI across the two genotypic groups defined by the presence or absence of 7R. The TDT found no initial evidence for an association between 7R and the categorical diagnosis of SAD. However, 7R carriers reported significantly greater inattention and dysphoria in childhood ( p =0.01 and 0.001, respectively) and a higher maximal lifetime BMI ( p =0.007) than did probands without this allele. Furthermore, excluding probands with extreme obesity (maximal BMI >40), a strong correlation was found linking childhood inattentive symptoms and maximal lifetime BMI ( r =0.35, p =0.001). In overeating women with SAD, the 7R allele of DRD4 may be associated with a unique developmental trajectory characterized by attentional deficits and dysphoria in childhood and mild to moderate obesity in adulthood. This developmental course may reflect different manifestations of the same underlying vulnerability related to central dopamine dysfunction. Given the possibility of population stratification when studying genotype/phenotype relationships, future use of genomic controls and replication of our findings in other overeating and/or ADD populations are needed to confirm these initial results.

Siegfried Kasper - One of the best experts on this subject based on the ideXlab platform.

  • Implementing prevention of Seasonal Affective Disorder from patients’ and physicians’ perspectives – a qualitative study
    'Springer Science and Business Media LLC', 2018
    Co-Authors: Barbara Nussbaumer-streit, Siegfried Kasper, E. Pjrek, Christina Kien, Gerald Gartlehner, Lucie Bartova, Michaela-elena Friedrich, Dietmar Winkler
    Abstract:

    Abstract Background Seasonal Affective Disorder (SAD) is a Seasonally recurrent type of major depression that has detrimental effects on patients’ lives during winter. Little is known about how it affects patients during summer and about patients’ and physicians’ perspectives on preventive SAD treatment. The aim of our study was to explore how SAD patients experience summers, what type of preventive treatment patients implement, which preventive treatment methods, if any, physicians recommend, and what factors facilitate or hinder implementation/recommendation of SAD prevention. Methods We conducted 15 semi-structured interviews, ten with adult patients with a history of SAD and five with physicians. Transcripts were analyzed by two researchers using an inductive thematic analysis approach. Results One group of patients was able to enjoy summer and ignore thoughts of the upcoming winter. The other group feared the impending depressive episode in winter, and this fear negatively impacted these patients’ well-being during the summer. Preventive treatment was a relevant issue for all patients, and all but one person implemented SAD prevention during summer. We identified six factors that influenced patient use of preventive treatment of SAD. Four factors occur on an individual level (knowledge about disease and preventive treatment options, experience with treatment in acute phase, acceptability of intervention, willingness to take responsibility for oneself), one on an interpersonal level (social and work environment), and one on a structural level (healthcare system). All psychiatrists recommended some kind of preventive intervention, most commonly, lifestyle changes. Four factors influenced psychiatrists in recommending prevention of SAD (patient expectations, disease history and stability, risk/benefit ratio, lack of evidence). Conclusions Success in the implementation of SAD prevention does not solely depend on the willingness of the patients, but is also influenced by external factors. Raising awareness of SAD among general practitioners and low-level access to mental-health support could help patients find appropriate help sooner. To better guide the optimal treatment choice, comparative effectiveness research on treatments to prevent a new onset in patients with a history of SAD and clinical practice guidelines on SAD are needed

  • effects of tryptophan depletion and catecholamine depletion on immune parameters in patients with Seasonal Affective Disorder in remission with light therapy
    Biological Psychiatry, 2003
    Co-Authors: J Stastny, Siegfried Kasper, Norman E Rosenthal, A Konstantinidis, Markus J Schwarz, Oliver Vitouch, Alexander Neumeister
    Abstract:

    Abstract Background Altered immunologic parameters are found in symptomatic depressed patients relative to remitted depressed patients and healthy controls. We investigated whether tryptophan depletion and catecholamine depletion induce alterations in immunologic parameters in patients with Seasonal Affective Disorder remitted on light therapy, and whether these changes are associated with changes in mood. Methods Remitted patients with Seasonal Affective Disorder underwent tryptophan depletion, catecholamine depletion, and sham depletion in a prospective randomized, double-blind crossover design. Measures of depression, plasma levels of tryptophan and catecholamine metabolites, and plasma levels of cytokines (sIL-4, IL-6, neopterin, sTNF-R1 and sTNF-R2) were obtained at baseline, and 7, 24, and 30 hours after monoamine depletion. Results Tryptophan depletion decreased plasma total and free tryptophan levels; catecholamine depletion decreased plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels. Tryptophan depletion and catecholamine depletion, but not sham depletion, induced a transient exacerbation of depressive symptoms ( p p p r = −.61, p Conclusions The monoamine depletion-induced alterations of humoral and cellular immunity suggest a potential role of immunologic parameters in the pathophysiology of Seasonal Affective Disorder; however, the results must be considered preliminary and require further study.

  • effects of tryptophan depletion vs catecholamine depletion in patients with Seasonal Affective Disorder in remission with light therapy
    Archives of General Psychiatry, 1998
    Co-Authors: Alexander Neumeister, Erick H Turner, Siegfried Kasper, Jefferey R Matthews, Teodor T Postolache, Ronald L Barnett, Manfred Rauh, Rina G Vetticad, Norman E Rosenthal
    Abstract:

    Methods: Sixteen patients with Seasonal Affective Disorder who had responded to a standard regimen of daily 10 000-lux light therapy were enrolled in a doubleblind, placebo-controlled, randomized crossover study. We compared the effects of tryptophan depletion with catecholamine depletion and sham depletion. Ingestion of a tryptophan-free amino acid beverage plus amino acid capsules was used to deplete tryptophan. Administration of the tyrosine hydroxylase inhibitor a-methyl-paratyrosine was used to deplete catecholamines. Diphenhydramine hydrochloride was used as an active placebo during sham depletion. The effects of these interventions were evaluated with measures of depression, plasma tryptophan levels, and plasma catecholamine metabolites. Results: Tryptophan depletion significantly decreased plasma total and free tryptophan levels. Catecholamine depletion significantly decreased plasma 3-methoxy-4hydroxyphenylethyleneglycol and homovanillic acid levels. Both tryptophan depletion and catecholamine depletion, compared with sham depletion, induced a robust increase (P,.001, repeated-measures analysis of variance) in depressive symptoms as measured with the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version. Conclusions: The beneficial effects of light therapy in the treatment of Seasonal Affective Disorder are reversed by both tryptophan depletion and catecholamine depletion. These findings confirm previous work showing that serotonin plays an important role in the mechanism of action of light therapy and provide new evidence that brain catecholaminergic systems may also be involved.

  • evidence for a Seasonal form of recurrent brief depression rbd Seasonal
    European Archives of Psychiatry and Clinical Neuroscience, 1994
    Co-Authors: Siegfried Kasper, Stephan Ruhrmann, Thomas Haase, Hans-jürgen Möller
    Abstract:

    We have established a relationship between recurrent brief depression (RBD) and Seasonal Affective Disorder (SAD) in a cohort of 42 outpatients who presented themselves at a clinic for Seasonal Affective Disorder at the Psychiatry Department of the University of Bonn, Germany. Our preliminary data indicate that 31% of the patients who were diagnosed as suffering from either SAD or its subsyndromal form (S-SAD) can also be categorized as RBD (RBD-Seasonal) for a 1-year observation period. During the time span of 1 year, RBD-Seasonal patients had a mean number of 20±9 episodes, which were accentuated in fall/winter, outnumbering the ones in spring/ summer significantly (P<0.001). The mean duration of each episode was 4.6±2.6 days in the RBD-Seasonal group. RBD-Seasonal patients experienced Seasonal changes as more of a problem and reported a lower percentage of first-degree relatives with a history of depression than the non-RBD-Seasonal group.