David Baxter PhD
Late Founder
Seasonal Affective Disorder
Sunday, October 30, 2005
As we turn the clocks back to mark the end of daylight savings, an estimated 1% to 3% of people in North America will experience a DSM IV diagnosable seasonal affective disorder (SAD) and an estimated 15% to 25% of the global population may experience subsyndromal SAD. It is considered a clinical subtype of major depression. The criteria for winter seasonal pattern specify a recurrent pattern of major depressive episodes during winter and remission of symptoms during summer, in the absence of seasonal psychosocial stressors. The symptoms of SAD can include: increased need for sleep, carbohydrate craving with increased appetite and weight, and extreme fatigue.
According to Sohn and Lam (2005), there are four specific aspects to SAD that make it particularly interesting for study. The first is the seasonality of the condition. The predictable onset and offset of winter episodes allow the investigation of biological parameters at different stages of the disorder, from acute illness to natural remission and vice versa. The second aspect is the rapid response to light therapy. This nonpharmacologic treatment allows comparison of the treated state to the natural, untreated summer remission state. The third aspect is the specificity of the neurovegetative symptoms of SAD (eg, extreme fatigue, hypersomnia, and increased appetite). These symptoms contrast to those of other types of mood disorders (eg, melancholic depression) and may be especially important when comparing SAD to other psychiatric conditions in which similar symptoms are prominent, such as atypical depression and certain sleep and eating disorders. Finally, there is a rich abundance of animal models of seasonality to develop and test specific biological hypotheses about SAD.
A study of circadian signal of change of season in patients with seasonal affective disorder showed that patients with SAD generate a biological signal of change of season that is absent in healthy volunteers. While not proving causality, this finding is consistent with the hypothesis that neural circuits that mediate the effects of seasonal changes in day length on mammalian behavior mediate the effects of season and light treatment on seasonal affective disorder.
Genetic Studies
Recent attention has turned to the pursuit of genetic mechanisms via different approaches including family studies, twin studies, and candidate gene association studies. These have provided some preliminary evidence for hereditary factors in both SAD and seasonality. For example, in family history studies,66-70 25% to 67% of patients with SAD had a positive family history of affective illness while 13% to 17% had first-degree relatives with SAD. Obvious candidate genes include genes involved in the 5-HT system with some promising research in the 102T/C allele and the -1438A allele of the 5-HT2A gene.
Bright Light Therapy
Since the 1984 seminal report by Rosenthal and colleagues, which defined the syndrome of SAD and presented the first controlled trial of bright light therapy. Although bright light therapy can be considered the treatment of choice for SAD, with rapid improvement and generally mild side effects, there remains a significant number of nonresponders and partial responders. Some treatment failures undoubtedly result from nonoptimum dosing and timing. Yet, with typical remission rates around 50% and significant partial improvement around 66%, the field has been motivated to search for alternate effective nonpharmaceutical interventions.
Early studies reported that bright light treatment did not benefit non-depressed, healthy individuals without history of seasonal difficulties. However, a recent study found improved mood and vitality over 1 month using 1 hour of bright light exposure daily. The effect appears to be enhanced by combining the light exposure with physical exercise.
Studies have demonstrated the utility of bright light augmentation of antidepressant treatment in drug nonresponders with nonseasonal MDD, and improved antidepressant response relative to placebo in patients with SAD, when initiating treatment with 10 days of light therapy.
A systematic review of epidemiological studies of seasonal affective disorder revealed that in addition to seasonal variations in mood with depressive symptoms usually peaking in winter. SAD was more prevalent at higher northern latitudes, but the prevalence varied across ethnic groups. SAD has also been identified in children and adolescents. This study also had a interesting finding that seasonal exacerbations and remissions are not limited to mood disorders, it has also been found in bulimia nervosa, anxiety disorders and other psychiatric illnesses.
Cognitive-Behavioral Therapy
A study in the Journal of Affective Disorders by Rohan and colleagues, described the need to develop supplementary or alternative treatments for seasonal affective disorder (SAD). Because a significant minority (47%) of SAD patients are refractory to light therapy, there is a persistence of residual symptoms despite light treatment, and poor long-term compliance with light use. Preliminary studies suggest that cognitive and behavioral factors are involved in SAD, cognitive-behavioral therapy (CBT) warrants investigation as a possible treatment option. CBT, particularly in combination with light therapy, appeared to improve long-term outcome regarding symptom severity, remission rates, and relapse rates. No CBT-treated participant, with or without light, experienced a full SAD relapse compared to over 60% of those treated with light alone.
Alcoholism and seasonal affective disorder
Some patients with alcoholism have a seasonal pattern to their alcohol misuse. They may be self-medicating an underlying seasonal affective disorder (SAD) with alcohol or manifesting a seasonal pattern to alcohol-induced depression. Both genetic and environmental factors play a role in the etiology and pathogenesis of alcoholism and SAD, operating, at least in part, through the brain serotonergic system. Family and molecular genetic studies suggest that there may be a genetic link between seasonality and alcoholism.
CNS Spectrums presented a recent review of SAD which includes:
The Diagnosis, Symptomatology, and Epidemiology of Seasonal Affective Disorder (PDF)
Update on the Biology of Seasonal Affective Disorder (PDF)
Light Therapy for Seasonal and Nonseasonal Depression: Efficacy, Protocol, Safety, and Side Effects (PDF)
Pharmacotherapy of Seasonal Affective Disorder (PDF)
Sunday, October 30, 2005
As we turn the clocks back to mark the end of daylight savings, an estimated 1% to 3% of people in North America will experience a DSM IV diagnosable seasonal affective disorder (SAD) and an estimated 15% to 25% of the global population may experience subsyndromal SAD. It is considered a clinical subtype of major depression. The criteria for winter seasonal pattern specify a recurrent pattern of major depressive episodes during winter and remission of symptoms during summer, in the absence of seasonal psychosocial stressors. The symptoms of SAD can include: increased need for sleep, carbohydrate craving with increased appetite and weight, and extreme fatigue.
According to Sohn and Lam (2005), there are four specific aspects to SAD that make it particularly interesting for study. The first is the seasonality of the condition. The predictable onset and offset of winter episodes allow the investigation of biological parameters at different stages of the disorder, from acute illness to natural remission and vice versa. The second aspect is the rapid response to light therapy. This nonpharmacologic treatment allows comparison of the treated state to the natural, untreated summer remission state. The third aspect is the specificity of the neurovegetative symptoms of SAD (eg, extreme fatigue, hypersomnia, and increased appetite). These symptoms contrast to those of other types of mood disorders (eg, melancholic depression) and may be especially important when comparing SAD to other psychiatric conditions in which similar symptoms are prominent, such as atypical depression and certain sleep and eating disorders. Finally, there is a rich abundance of animal models of seasonality to develop and test specific biological hypotheses about SAD.
A study of circadian signal of change of season in patients with seasonal affective disorder showed that patients with SAD generate a biological signal of change of season that is absent in healthy volunteers. While not proving causality, this finding is consistent with the hypothesis that neural circuits that mediate the effects of seasonal changes in day length on mammalian behavior mediate the effects of season and light treatment on seasonal affective disorder.
Genetic Studies
Recent attention has turned to the pursuit of genetic mechanisms via different approaches including family studies, twin studies, and candidate gene association studies. These have provided some preliminary evidence for hereditary factors in both SAD and seasonality. For example, in family history studies,66-70 25% to 67% of patients with SAD had a positive family history of affective illness while 13% to 17% had first-degree relatives with SAD. Obvious candidate genes include genes involved in the 5-HT system with some promising research in the 102T/C allele and the -1438A allele of the 5-HT2A gene.
Bright Light Therapy
Since the 1984 seminal report by Rosenthal and colleagues, which defined the syndrome of SAD and presented the first controlled trial of bright light therapy. Although bright light therapy can be considered the treatment of choice for SAD, with rapid improvement and generally mild side effects, there remains a significant number of nonresponders and partial responders. Some treatment failures undoubtedly result from nonoptimum dosing and timing. Yet, with typical remission rates around 50% and significant partial improvement around 66%, the field has been motivated to search for alternate effective nonpharmaceutical interventions.
Early studies reported that bright light treatment did not benefit non-depressed, healthy individuals without history of seasonal difficulties. However, a recent study found improved mood and vitality over 1 month using 1 hour of bright light exposure daily. The effect appears to be enhanced by combining the light exposure with physical exercise.
Studies have demonstrated the utility of bright light augmentation of antidepressant treatment in drug nonresponders with nonseasonal MDD, and improved antidepressant response relative to placebo in patients with SAD, when initiating treatment with 10 days of light therapy.
A systematic review of epidemiological studies of seasonal affective disorder revealed that in addition to seasonal variations in mood with depressive symptoms usually peaking in winter. SAD was more prevalent at higher northern latitudes, but the prevalence varied across ethnic groups. SAD has also been identified in children and adolescents. This study also had a interesting finding that seasonal exacerbations and remissions are not limited to mood disorders, it has also been found in bulimia nervosa, anxiety disorders and other psychiatric illnesses.
Cognitive-Behavioral Therapy
A study in the Journal of Affective Disorders by Rohan and colleagues, described the need to develop supplementary or alternative treatments for seasonal affective disorder (SAD). Because a significant minority (47%) of SAD patients are refractory to light therapy, there is a persistence of residual symptoms despite light treatment, and poor long-term compliance with light use. Preliminary studies suggest that cognitive and behavioral factors are involved in SAD, cognitive-behavioral therapy (CBT) warrants investigation as a possible treatment option. CBT, particularly in combination with light therapy, appeared to improve long-term outcome regarding symptom severity, remission rates, and relapse rates. No CBT-treated participant, with or without light, experienced a full SAD relapse compared to over 60% of those treated with light alone.
Alcoholism and seasonal affective disorder
Some patients with alcoholism have a seasonal pattern to their alcohol misuse. They may be self-medicating an underlying seasonal affective disorder (SAD) with alcohol or manifesting a seasonal pattern to alcohol-induced depression. Both genetic and environmental factors play a role in the etiology and pathogenesis of alcoholism and SAD, operating, at least in part, through the brain serotonergic system. Family and molecular genetic studies suggest that there may be a genetic link between seasonality and alcoholism.
CNS Spectrums presented a recent review of SAD which includes:
The Diagnosis, Symptomatology, and Epidemiology of Seasonal Affective Disorder (PDF)
Update on the Biology of Seasonal Affective Disorder (PDF)
Light Therapy for Seasonal and Nonseasonal Depression: Efficacy, Protocol, Safety, and Side Effects (PDF)
Pharmacotherapy of Seasonal Affective Disorder (PDF)
