With the Fall and Winter seasons on the horizon, many of us will start to notice changes in our mood in the coming months. Seasonality is the term used to describe the mild to moderate decrease in positive mood that a significant number of people in the population experience when daylight hours are reduced. For a select portion of population, this decrease in mood will be significant enough to meet criteria for Seasonal Affective Disorder (SAD) – a form of clinical depression that only occurs with changes in seasons (it almost always occurs during the Fall and Winter period). To help interested readers better understand seasonality and SAD, including the causes and treatment of SAD, I offer the following brief review.
An Overview of SAD
It is believed that Hippocrates first established the connection between mood and season around 4 B.C., and other notable figures in psychology and medicine (e.g., Phillippe Pinel) made similar observations throughout history (Wehr, 1989). However, it is only during the past 25 years that theorists and researchers have considerably expanded our clinical understanding of SAD, through systematic research. Yet, despite a dramatic blossoming of research on this disorder, there continue to remain many unanswered questions, especially with regards to the causes of SAD (Magnusson & Boivin, 2003; Naumeister et al., 2001). In fact, the available empirical evidence suggests that no one theory dominates as a conceptual model, and it is likely the case that several factors interact to affect people’s mood.
The American Psychiatric Association (APA) considers SAD to be a seasonal pattern specifier for the major mood disorders (ex: Major Depression and Bipolar Disorder) listed in the Diagnostic and Statistical Manual – IV (DSM-IV). In other words, SAD is not itself a disorder – it is used to specify a pattern of mood changes. For example, it is used to help distinguish between regular depression, which can occur at any time of the year, and SAD, which reliably occurs during the Fall and Winter (technically speaking, someone can have SAD in the summer, but this is not common). It is certainly debatable whether SAD should be considered a distinct disorder separate from Major Depression and Bipolar Disorder.
People who suffer from SAD often present with both typical and atypical symptoms. Typical symptoms are considered to be those that are commonly found with regular depression -- including poor mood, anhedonia and difficulty with concentration. However, unlike the majority of patients diagnosed with Major Depression, individuals with SAD also experience atypical symptoms such as increases in sleep, appetite and weight. Oftentimes, patients with SAD sleep through the morning and experience problems with drowsiness throughout the day. They also tend to crave carbohydrates, which partly explains the weight gain, and may relate to dysfunctional levels of serotonin (Schwartz et al., 1999).
Although SAD is a specific type of clinical disorder, with a prevalence somewhere between 1 – 9%, the relationship between mood and changes of the season actually reflects a very common phenomenon known as seasonality (Murray, 2005). Nearly everyone experiences changes in mood and behaviour commensurate with SAD to some extent (also known as the winter blues). SAD appears to be an extreme case of seasonality, which is typically triggered by the onset of Fall and Winter.
Potential Causes of SAD
There are several prominent hypotheses about the cause of SAD and seasonality. One of the more popular theories of SAD is the melatonin hypothesis, which argues that decreases in the amount of daylight hours leads to the onset of SAD through a dysregulation in melatonin (Rosenthal, 1986). Melatonin is hormone produced within the brain that is responsible for regulating sleep (Arendt, 2003). The onset and offset of melatonin production is controlled by the rising and setting of the sun, such that melatonin production stops during daylight hours, and then increases during night time. Hence, the melatonin hypothesis postulates that a decrease in the amount of daylight hours either leads to greater melatonin production or a greater sensitivity to melatonin production. In either case, the individual’s sensitivity to changes in daylight is considered to be factor that renders that person at least vulnerable to SAD.
Although the melatonin hypothesis is a fairly popular understanding of SAD and seasonality, the empirical support is rather mixed. There is certainly evidence for the fact that decreased daylight is associated with the onset of SAD. However, there is poor support for the role of melatonin dysregulation being the only factor responsible for the onset of depression symptoms. For example, suppressing melatonin secretion in the brain does not produce the anticipated antidepressant effect in SAD patients (Rosenthal et al., 1986). Also, light therapy has been shown to be effective when administered during the day, despite the fact that melatonin levels are either low or undetectable at this point in time (Magnusson & Boivin, 2003). This suggests that altering the production of melatonin is not necessary for changing the depression symptoms, and therefore calls into question how central a role melatonin plays in seasonality and SAD.
All of this is not to say that melatonin plays no role at all in seasonality and SAD. For instance, although artificially increasing melatonin does not induce the onset of depression in those vulnerable to SAD, it does produce a mild increase in depressive symptoms (Rosenthal et al., 1986). Also, research shows that melatonin secretion is longer for SAD patients in winter relative to summer, and that people without SAD do not show a similar discrepancy (Wehr et al., 2001). Thus, melatonin might be related to seasonality, and therefore vulnerability to SAD, but its causal role does not seem to be as prominent as many people think. People should be aware of this fact before purchasing products claiming to affect their melatonin and cure their SAD.
Related to the melatonin hypothesis is the phase-delay hypothesis, which postulates that natural biological rhythms are significantly disrupted during the winter months by the decrease in light (Lewy, Sack, Miller, & Hoban, 1987). This disruption in biological rhythms affects various biological processes, which can affect mood. Specifically, the decreased amount of sun in winter is presumed to caused a delay in terms of when certain biological processes get turned off. For example, melatonin production and other biological processes affected by circadian rhythm (e.g., body temperature) might be delayed with decreases in light, and it is this delay in circadian rhythm that is responsible for the onset of SAD. Unfortunately, details of the specific mechanisms and processes that lead biological rhythm delays to produce clinical symptoms of depression are relatively unknown (Lewy et al., 1998a).
Also, research evidence is not robust – at least not as strong as one might think given the popularity of this theory (see Koorengevel et al., 2002). One of the strongest pieces of evidence used to support this hypothesis is the finding that light therapy is more beneficial when done in the morning than in the evening. Lewy et al. (1998a) demonstrated a two-fold increase in the effectiveness of morning therapy over evening light therapy. Presumably, exposure to bright light in the morning helps to correct for the delay in circadian rhythms. However, a meta-analysis comparing the efficacy of timed treatments and combination treatment (i.e., patients receive bright light therapy in the morning and evening) found that the combination treatment was significantly more effective (Lee, Blashko, Janzen, Paterson, & Chan, 1997). In other words, it is the absolute amount of bright light received throughout the day that is more important, not when the bright light is received. This finding poses some problems for the phase-delay hypothesis, and at the very least, indicates that problems with circadian rhythms are not the sole cause of SAD.
The serotonin hypothesis proposes that changes in serotonin levels are primarily responsible for seasonality and SAD. Serotonin is a neurotransmitter that is well known to affect mood. In fact, the most popular and effective drugs on the market for depression are Selective Serotonin Reuptake Inhibitors (SSRIs), which basically increase the amount of serotonin being used by the brain. For example, Paxil and Effexor are SSRIs.
There is plenty of research support linking SAD and seasonality to decreases in serotonin. In fact, among most people in the general population, serotonin tends to decrease during the winter, whereas serotonin levels are at their highest levels in the summer (Lambert, Reid, Kaye, & Esler, 2002). There are multiple lines of evidence to support the idea that serotonin dysfunction is a causal factor for SAD. First, drugs that enhance serotonin transmission tend to alleviate symptoms in people with SAD (Murray et al., 2005; Naumeister et al., 2001; Schwartz et al., 1999).
A second line of evidence for the serotonin hypothesis comes from examining the effects of administering serotonin agonists (a chemical that mimics the effects of serotonin) to people who are vulnerable to SAD during the winter (i.e., those with a history of the disorder). Research shows that the administration of such an agonist creates a hypo-manic response (ex: people experience a large increase in energy), which does not occur among people without a history of SAD (see Schawartz et al., 1999; see also Naumeister et al., 2001). This suggests that the serotonin systems of people who are vulnerable to SAD may be more sensitive and unstable than the systems of people without SAD. With an unstable serotonin system, people are more vulnerable to factors that affect serotonin levels – such as daylight.
A third line of evidence for the serotonin hypothesis comes from tryptophan depletion studies. Tryptophan is an essential amino acid, and is known to be a precursor of serotonin levels. Hence, when tryptophan levels are experimentally manipulated, serotonin levels are also affected due to their biological relationship. When researchers lower the amount of tryptophan in individuals with SAD, it tends to create increases in depression symptoms (Naumeister et al., 2001).
Overall, the research evidence seems to strongly support the serotonin hypothesis. However, this is not to say that the serotonin hypothesis is the major cause of SAD. There is research support for the melatonin and phase-delay hypotheses as well, and all three factors may interact to causes depression symptoms. Another possibility is that people differ with respect the primary cause of SAD – some may be susceptible to SAD through problems with circadian rhythms, while others are most vulnerable because of serotonin problems.
Outside of pure biological explanations of SAD, there are various psychological factors that influence people’s mood as well. In the winter, the following psychological factors all have the potential to impact mood:
(1) People tend to spend more time indoors, which limits the number of positive and healthy activities they can engage in. If someone really gets enjoyment and happiness through activities that primarily occur during the summer (ex: surfing), then removal of this source of pleasure (a positive reinforce) could negatively impact someone’s mood and cause depression.
(2) Related to point #1, the winter is often more associated with decreased time spent socializing, which can also lead to sadness – especially when there is isolation.
(3) Because many people are affected by seasonality, being surrounded by others who are not as happy in the winter could affect mood as well.
(4) The physiological effects of decreased daylight (ex: less energy; feeling physically and mentally sluggish) can affect thinking. Specifically, people are more likely to experience negative thoughts in such circumstances.
Overall, conceptualizing SAD as being an interaction between biological and psychological factors is perhaps the most comprehensive and accurate way to understand this problem.
Treatment
In terms of treating SAD, there are different treatment options available. Bright light therapy is widely considered a first-line treatment, with research trials demonstrating its effectiveness. Light therapy typically entails purchasing a light box that is designed specifically for SAD. The person then uses the box daily – it is often recommended that you use the box in the morning, and research suggests that morning and evening combined might be best. Unfortunately, approximately 50% of people who use light therapy will not improve through this form of treatment. As such, alternative treatment options are available. Medication (ex: SSRIs) has been found to be effective in treating SAD. Also, Cognitive-Behavioural Therapy (CBT) is an empirically-supported treatment of depression, and can be successful with SAD specifically. In fact, results from a recent randomized control trial showed that CBT + Light therapy may be the best possible treatment option available (Rohan et al., 2007).
Thus, those who suffer from SAD have options available to them. I recommend consulting a mental health professional to be properly assessed and to receive a professional opinion in terms of a treatment decision.
Dr. Roger Covin
Montreal Psychologist
www.drcovin.ca
Arendt, J. (2003). Importance and Relevance of Melotonin to Human Biological Rhythms. Journal of Neuroendocrinology, 15, 427-431.
Dahl, K. et al. (1993). Dim light melatonin onset and circadian temperature during a constant routine in hypersomnic winter depression. Acta Psychiatrica Scandinavica, 88, 60-66.
Hedge, A.L., & Woodson, H. (1996). Prevalence of seasonal changes in mood and behavior during the winter months in Texas. (1996). Psychiatry Research, 62, 265-271.
Kasper, S., Wehr, T., Bartko, J.J., Gaist, P.A., & Rosenthal, N.E. (1989). Epidemiological findings of seasonal changes in mood and behavior. Archives of General Psychiatry, 46, 823-833.
Koorengevel, K.M., Beersma, D.G.M., den Boer, J.A., & van den Hoofdakker, R.H. (2002). A forced desynchrony study of circadian pacemaker characteristics in seasonal affective disorder. Journal of Biological Rhythms, 17, 463-475.
Lambert, G.W., Reid, C., Kaye, D.M., & Jennings, G.L. (2002). Effect of sunlight and season on serotonin turnover in the brain. The Lancet, 360, 1840-1842.
Lee, T.M.C., Blashko, C.A., Janzen, H.L., Paterson, J.G., & Chan, C.C.H. (1997). Pathophysiological mechanism of seasonal affective disorder. Journal of Affective Disorders, 46, 25-38.
Lewy, A.J., Bauer, V.K., Cutler, B.A., & Sack, R.L. (1998b). Melatonin treatment of winter depression: A pilot study. Psychiatry Research, 77, 57-61.
Lewy, A.J., Bauer, V.K., Cutler, B.A., Sack, R.L., Ahmed, S., Thomas, K.H., Blood, M.L., & Jackson, J.M.L. (1998a). Morning vs evening light treatment of patients with winter depression. Archives of General Psychiatry, 55, 890-896.
Lewy, A.J., Sack, R.L., Miller, S., & Hoban, T.M. (1987). Antidepressant and circadian phase-shifting effects of light. Science, 235, 352-353.
Mersch, P.A.A., Middendorp, H.M., Bouhuys, A.L., Beersma, D.G.M., & van den Hofdakker, R.H. (1999). Journal of Affective Disorders, 53, 35-48.
Magnusson, A., & Boivin, D. (2003). Seasonal affective disorder: An overview. Chronobiology International, 20, 189-207.
Naumeister, A., Praschal-Reider, N., Hesselman, B., Vitouch, O., Rauth, M., Baroka, A., & Kasper, S. (1998). Effects of tryptophan depletion in fully remitted patients with seasonal affective disorder during summer. Psychological Medicine, 28, 257- 264.
Rohan et al. (2007). A Randomized Controlled Trial of Cognitive–Behavioral Therapy, Light Therapy, and Their Combination for Seasonal Affective Disorder. Journal of Consulting and Clinical Psychology, 75, 489-500.
Rosenthal, N.E., Sack, D.A., Jacobsen, F.M., James, S.P., Parry, B.L., Arendt, J., Tamarkin, L., & Wehr, T.A. (1986). Melatonin in seasonal affective disorder and phototherapy. Journal of Neural Transmission, 21, 257-267.
Sher, L., Goldman, D., Ozaki, N. & Rosenthal, N.E. (1999). The role of genetic factors in the etiology of seasonal affective disorder and seasonality. Journal of Affective Disorders, 53, 203-210.
Schwartz, P.J., Turner, E.H., Garcia-Borreguero, D., Sedway, J., Vetticad, R.G., Wehr,T.A., Murphy, D.L., & Rosenthal, N.E. (1999). Serotonin hypothesis of winter depression: Behavioural and neuroendocrine effects of 5-HT receptor partial agonist ipsapirone in patients with seasonal affective disorder and healthy control subjects. Psychiatry Research, 86, 9-28.
Sohn, C., & Lam, R.W. (2005). Update on the biology of seasonal affective disorder.CNS Spectrums, 10, 635-646.
An Overview of SAD
It is believed that Hippocrates first established the connection between mood and season around 4 B.C., and other notable figures in psychology and medicine (e.g., Phillippe Pinel) made similar observations throughout history (Wehr, 1989). However, it is only during the past 25 years that theorists and researchers have considerably expanded our clinical understanding of SAD, through systematic research. Yet, despite a dramatic blossoming of research on this disorder, there continue to remain many unanswered questions, especially with regards to the causes of SAD (Magnusson & Boivin, 2003; Naumeister et al., 2001). In fact, the available empirical evidence suggests that no one theory dominates as a conceptual model, and it is likely the case that several factors interact to affect people’s mood.
The American Psychiatric Association (APA) considers SAD to be a seasonal pattern specifier for the major mood disorders (ex: Major Depression and Bipolar Disorder) listed in the Diagnostic and Statistical Manual – IV (DSM-IV). In other words, SAD is not itself a disorder – it is used to specify a pattern of mood changes. For example, it is used to help distinguish between regular depression, which can occur at any time of the year, and SAD, which reliably occurs during the Fall and Winter (technically speaking, someone can have SAD in the summer, but this is not common). It is certainly debatable whether SAD should be considered a distinct disorder separate from Major Depression and Bipolar Disorder.
People who suffer from SAD often present with both typical and atypical symptoms. Typical symptoms are considered to be those that are commonly found with regular depression -- including poor mood, anhedonia and difficulty with concentration. However, unlike the majority of patients diagnosed with Major Depression, individuals with SAD also experience atypical symptoms such as increases in sleep, appetite and weight. Oftentimes, patients with SAD sleep through the morning and experience problems with drowsiness throughout the day. They also tend to crave carbohydrates, which partly explains the weight gain, and may relate to dysfunctional levels of serotonin (Schwartz et al., 1999).
Although SAD is a specific type of clinical disorder, with a prevalence somewhere between 1 – 9%, the relationship between mood and changes of the season actually reflects a very common phenomenon known as seasonality (Murray, 2005). Nearly everyone experiences changes in mood and behaviour commensurate with SAD to some extent (also known as the winter blues). SAD appears to be an extreme case of seasonality, which is typically triggered by the onset of Fall and Winter.
Potential Causes of SAD
There are several prominent hypotheses about the cause of SAD and seasonality. One of the more popular theories of SAD is the melatonin hypothesis, which argues that decreases in the amount of daylight hours leads to the onset of SAD through a dysregulation in melatonin (Rosenthal, 1986). Melatonin is hormone produced within the brain that is responsible for regulating sleep (Arendt, 2003). The onset and offset of melatonin production is controlled by the rising and setting of the sun, such that melatonin production stops during daylight hours, and then increases during night time. Hence, the melatonin hypothesis postulates that a decrease in the amount of daylight hours either leads to greater melatonin production or a greater sensitivity to melatonin production. In either case, the individual’s sensitivity to changes in daylight is considered to be factor that renders that person at least vulnerable to SAD.
Although the melatonin hypothesis is a fairly popular understanding of SAD and seasonality, the empirical support is rather mixed. There is certainly evidence for the fact that decreased daylight is associated with the onset of SAD. However, there is poor support for the role of melatonin dysregulation being the only factor responsible for the onset of depression symptoms. For example, suppressing melatonin secretion in the brain does not produce the anticipated antidepressant effect in SAD patients (Rosenthal et al., 1986). Also, light therapy has been shown to be effective when administered during the day, despite the fact that melatonin levels are either low or undetectable at this point in time (Magnusson & Boivin, 2003). This suggests that altering the production of melatonin is not necessary for changing the depression symptoms, and therefore calls into question how central a role melatonin plays in seasonality and SAD.
All of this is not to say that melatonin plays no role at all in seasonality and SAD. For instance, although artificially increasing melatonin does not induce the onset of depression in those vulnerable to SAD, it does produce a mild increase in depressive symptoms (Rosenthal et al., 1986). Also, research shows that melatonin secretion is longer for SAD patients in winter relative to summer, and that people without SAD do not show a similar discrepancy (Wehr et al., 2001). Thus, melatonin might be related to seasonality, and therefore vulnerability to SAD, but its causal role does not seem to be as prominent as many people think. People should be aware of this fact before purchasing products claiming to affect their melatonin and cure their SAD.
Related to the melatonin hypothesis is the phase-delay hypothesis, which postulates that natural biological rhythms are significantly disrupted during the winter months by the decrease in light (Lewy, Sack, Miller, & Hoban, 1987). This disruption in biological rhythms affects various biological processes, which can affect mood. Specifically, the decreased amount of sun in winter is presumed to caused a delay in terms of when certain biological processes get turned off. For example, melatonin production and other biological processes affected by circadian rhythm (e.g., body temperature) might be delayed with decreases in light, and it is this delay in circadian rhythm that is responsible for the onset of SAD. Unfortunately, details of the specific mechanisms and processes that lead biological rhythm delays to produce clinical symptoms of depression are relatively unknown (Lewy et al., 1998a).
Also, research evidence is not robust – at least not as strong as one might think given the popularity of this theory (see Koorengevel et al., 2002). One of the strongest pieces of evidence used to support this hypothesis is the finding that light therapy is more beneficial when done in the morning than in the evening. Lewy et al. (1998a) demonstrated a two-fold increase in the effectiveness of morning therapy over evening light therapy. Presumably, exposure to bright light in the morning helps to correct for the delay in circadian rhythms. However, a meta-analysis comparing the efficacy of timed treatments and combination treatment (i.e., patients receive bright light therapy in the morning and evening) found that the combination treatment was significantly more effective (Lee, Blashko, Janzen, Paterson, & Chan, 1997). In other words, it is the absolute amount of bright light received throughout the day that is more important, not when the bright light is received. This finding poses some problems for the phase-delay hypothesis, and at the very least, indicates that problems with circadian rhythms are not the sole cause of SAD.
The serotonin hypothesis proposes that changes in serotonin levels are primarily responsible for seasonality and SAD. Serotonin is a neurotransmitter that is well known to affect mood. In fact, the most popular and effective drugs on the market for depression are Selective Serotonin Reuptake Inhibitors (SSRIs), which basically increase the amount of serotonin being used by the brain. For example, Paxil and Effexor are SSRIs.
There is plenty of research support linking SAD and seasonality to decreases in serotonin. In fact, among most people in the general population, serotonin tends to decrease during the winter, whereas serotonin levels are at their highest levels in the summer (Lambert, Reid, Kaye, & Esler, 2002). There are multiple lines of evidence to support the idea that serotonin dysfunction is a causal factor for SAD. First, drugs that enhance serotonin transmission tend to alleviate symptoms in people with SAD (Murray et al., 2005; Naumeister et al., 2001; Schwartz et al., 1999).
A second line of evidence for the serotonin hypothesis comes from examining the effects of administering serotonin agonists (a chemical that mimics the effects of serotonin) to people who are vulnerable to SAD during the winter (i.e., those with a history of the disorder). Research shows that the administration of such an agonist creates a hypo-manic response (ex: people experience a large increase in energy), which does not occur among people without a history of SAD (see Schawartz et al., 1999; see also Naumeister et al., 2001). This suggests that the serotonin systems of people who are vulnerable to SAD may be more sensitive and unstable than the systems of people without SAD. With an unstable serotonin system, people are more vulnerable to factors that affect serotonin levels – such as daylight.
A third line of evidence for the serotonin hypothesis comes from tryptophan depletion studies. Tryptophan is an essential amino acid, and is known to be a precursor of serotonin levels. Hence, when tryptophan levels are experimentally manipulated, serotonin levels are also affected due to their biological relationship. When researchers lower the amount of tryptophan in individuals with SAD, it tends to create increases in depression symptoms (Naumeister et al., 2001).
Overall, the research evidence seems to strongly support the serotonin hypothesis. However, this is not to say that the serotonin hypothesis is the major cause of SAD. There is research support for the melatonin and phase-delay hypotheses as well, and all three factors may interact to causes depression symptoms. Another possibility is that people differ with respect the primary cause of SAD – some may be susceptible to SAD through problems with circadian rhythms, while others are most vulnerable because of serotonin problems.
Outside of pure biological explanations of SAD, there are various psychological factors that influence people’s mood as well. In the winter, the following psychological factors all have the potential to impact mood:
(1) People tend to spend more time indoors, which limits the number of positive and healthy activities they can engage in. If someone really gets enjoyment and happiness through activities that primarily occur during the summer (ex: surfing), then removal of this source of pleasure (a positive reinforce) could negatively impact someone’s mood and cause depression.
(2) Related to point #1, the winter is often more associated with decreased time spent socializing, which can also lead to sadness – especially when there is isolation.
(3) Because many people are affected by seasonality, being surrounded by others who are not as happy in the winter could affect mood as well.
(4) The physiological effects of decreased daylight (ex: less energy; feeling physically and mentally sluggish) can affect thinking. Specifically, people are more likely to experience negative thoughts in such circumstances.
Overall, conceptualizing SAD as being an interaction between biological and psychological factors is perhaps the most comprehensive and accurate way to understand this problem.
Treatment
In terms of treating SAD, there are different treatment options available. Bright light therapy is widely considered a first-line treatment, with research trials demonstrating its effectiveness. Light therapy typically entails purchasing a light box that is designed specifically for SAD. The person then uses the box daily – it is often recommended that you use the box in the morning, and research suggests that morning and evening combined might be best. Unfortunately, approximately 50% of people who use light therapy will not improve through this form of treatment. As such, alternative treatment options are available. Medication (ex: SSRIs) has been found to be effective in treating SAD. Also, Cognitive-Behavioural Therapy (CBT) is an empirically-supported treatment of depression, and can be successful with SAD specifically. In fact, results from a recent randomized control trial showed that CBT + Light therapy may be the best possible treatment option available (Rohan et al., 2007).
Thus, those who suffer from SAD have options available to them. I recommend consulting a mental health professional to be properly assessed and to receive a professional opinion in terms of a treatment decision.
Dr. Roger Covin
Montreal Psychologist
www.drcovin.ca
References
Arendt, J. (2003). Importance and Relevance of Melotonin to Human Biological Rhythms. Journal of Neuroendocrinology, 15, 427-431.
Dahl, K. et al. (1993). Dim light melatonin onset and circadian temperature during a constant routine in hypersomnic winter depression. Acta Psychiatrica Scandinavica, 88, 60-66.
Hedge, A.L., & Woodson, H. (1996). Prevalence of seasonal changes in mood and behavior during the winter months in Texas. (1996). Psychiatry Research, 62, 265-271.
Kasper, S., Wehr, T., Bartko, J.J., Gaist, P.A., & Rosenthal, N.E. (1989). Epidemiological findings of seasonal changes in mood and behavior. Archives of General Psychiatry, 46, 823-833.
Koorengevel, K.M., Beersma, D.G.M., den Boer, J.A., & van den Hoofdakker, R.H. (2002). A forced desynchrony study of circadian pacemaker characteristics in seasonal affective disorder. Journal of Biological Rhythms, 17, 463-475.
Lambert, G.W., Reid, C., Kaye, D.M., & Jennings, G.L. (2002). Effect of sunlight and season on serotonin turnover in the brain. The Lancet, 360, 1840-1842.
Lee, T.M.C., Blashko, C.A., Janzen, H.L., Paterson, J.G., & Chan, C.C.H. (1997). Pathophysiological mechanism of seasonal affective disorder. Journal of Affective Disorders, 46, 25-38.
Lewy, A.J., Bauer, V.K., Cutler, B.A., & Sack, R.L. (1998b). Melatonin treatment of winter depression: A pilot study. Psychiatry Research, 77, 57-61.
Lewy, A.J., Bauer, V.K., Cutler, B.A., Sack, R.L., Ahmed, S., Thomas, K.H., Blood, M.L., & Jackson, J.M.L. (1998a). Morning vs evening light treatment of patients with winter depression. Archives of General Psychiatry, 55, 890-896.
Lewy, A.J., Sack, R.L., Miller, S., & Hoban, T.M. (1987). Antidepressant and circadian phase-shifting effects of light. Science, 235, 352-353.
Mersch, P.A.A., Middendorp, H.M., Bouhuys, A.L., Beersma, D.G.M., & van den Hofdakker, R.H. (1999). Journal of Affective Disorders, 53, 35-48.
Magnusson, A., & Boivin, D. (2003). Seasonal affective disorder: An overview. Chronobiology International, 20, 189-207.
Naumeister, A., Praschal-Reider, N., Hesselman, B., Vitouch, O., Rauth, M., Baroka, A., & Kasper, S. (1998). Effects of tryptophan depletion in fully remitted patients with seasonal affective disorder during summer. Psychological Medicine, 28, 257- 264.
Rohan et al. (2007). A Randomized Controlled Trial of Cognitive–Behavioral Therapy, Light Therapy, and Their Combination for Seasonal Affective Disorder. Journal of Consulting and Clinical Psychology, 75, 489-500.
Rosenthal, N.E., Sack, D.A., Jacobsen, F.M., James, S.P., Parry, B.L., Arendt, J., Tamarkin, L., & Wehr, T.A. (1986). Melatonin in seasonal affective disorder and phototherapy. Journal of Neural Transmission, 21, 257-267.
Sher, L., Goldman, D., Ozaki, N. & Rosenthal, N.E. (1999). The role of genetic factors in the etiology of seasonal affective disorder and seasonality. Journal of Affective Disorders, 53, 203-210.
Schwartz, P.J., Turner, E.H., Garcia-Borreguero, D., Sedway, J., Vetticad, R.G., Wehr,T.A., Murphy, D.L., & Rosenthal, N.E. (1999). Serotonin hypothesis of winter depression: Behavioural and neuroendocrine effects of 5-HT receptor partial agonist ipsapirone in patients with seasonal affective disorder and healthy control subjects. Psychiatry Research, 86, 9-28.
Sohn, C., & Lam, R.W. (2005). Update on the biology of seasonal affective disorder.CNS Spectrums, 10, 635-646.
1 comment:
This provides a wonderfully thourough and accurate insight into SAD. I'm studying for my final year exams and this has helped me so much! Thank you!
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