What is SAD?

The purpose of this paper is to describe what SAD is, what causes it, available treatments and why these treatments are effective. It appears that the decreased amount of sunlight occurring in the fall and winter months probably affects some genetically predisposed people to delay sleep and wake cycles and to produce less serotonin (and its precursors) and more melatonin. These changes may lead people to think negatively about themselves and to ruminate about how bad they feel, which then makes them feel even worse. Light therapy tends to be effective for approximately 65% of SAD sufferers; most of the other SAD sufferers may find relief from SSRIs.

Seasonal Affect Disorder
Seasonal Affect Disorder (SAD) is referred to in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), as major depressive disorder, recurrent, with seasonal pattern (American Psychiatric Association, 2000). Essentially, SAD sufferers get depressed in the dark seasons (fall and winter) and feel symptom remission in the light seasons (spring and summer). They get depressed without major psychosocial stressors that could better account for the depression (DSM-IV-TR). People suffering from a major depressive episode have five of the eight symptoms described in the DSM-IV-TR, such as feeling depressed nearly every day, anhedonia (loss of interest in activities that previously caused pleasure), changes in appetite and sleep, lethargy, feeling worthless and guilty, difficulty concentrating, and suicidal ideation. It is important to note that the majority of people suffering from SAD have the opposite depression symptoms of nonseasonal depression sufferers: SAD sufferers usually sleep more and eat excessive amount of carbohydrates whereas nonseasonal depression sufferers tend to eat and sleep too little (Lam & Levitan, 2000). The purpose of this paper is to describe what SAD is, what causes it, available treatments and why these treatments are effective.
It is estimated that less than one percent of Americans (Lam & Levitan, 2000) one to three percent of Canadians (Levitt, Boyle, Joffe, & Baumal, 2000), and Europeans Chotai, Smedh, Johansson, Nilsson & Adolfsson, 2004; Wirz-Justice, Graw, Krauchi, & Wacker, 2003) and less than one percent of Asians suffer from this disorder (Weir, 2001).
This disorder is more prevalent in the northern hemisphere where winters are harsher and darker than the populated areas of the southern hemisphere (Lam & Levitan). As an extreme example, 22.6% of Inuit adults living in the Canadian Arctic, north of 70 degrees latitude, were depressed and 6.3% suffered from SAD, while almost 40% of this population felt at least one effect of the seasons (Haggarty et al., 2002). Although it is more prevalent in the northern hemisphere, it is also found in Australia (Murray, Allen & Trinder, 2001) and South Africa (Kane & Lowis, 1999). It would be intuitively sound to assume that the higher north people live, the higher the prevalence rate. However, this is not the case. There were no significant differences of SAD prevalence between eight degrees of latitude in Ontario, Canada (Levitt & Boyle, 2002), which may simply mean that eight degrees of latitude is not enough of a difference. There were also no differences found between people living in Iceland and their direct descendants living much farther south in Manitoba. These two groups (Icelandic people and their descendants) had lower prevalence rates than east coast Americans (Lam & Levitan, 2000). These findings suggest there are more complicated factors playing a role in the expression of SAD than simply latitude, climate, and photoperiod (amount of light per day) as it is counterintuitive that people living farther north would have lower incidence of this disorder than people living much farther south.
SAD is more common amongst women than men; researchers found ratios ranged from approximately two women to one man (Chotai et al., 2004; Magnusson & Boivin, 2003; Kane & Lowis, 1999) to as high as four women to one man (Rohan, Sigmon, & Dorhofer, 2003). This finding suggests a hormonal and perhaps a cultural influence on SAD. Another possible support for hormonal influences is that this disorder usually expresses itself in young and middle adulthood then usually abates in the senior years (Magnusson & Boivin). SAD also rarely occurs in children (Magnusson & Boivin). Given these prevalence rates, in people living in various geographical locations and cultures, and occurring more in women than in men, it is apparent that the occurrence of SAD has a complicated etiology.

Pathophysiology of SAD
There are many factors — such as amount of daylight, serotonin levels, genetic influences, and cognitive factors — that have been proposed to explain the occurrence of SAD. Although they will be explained separately, it is important to note that SAD is better explained by an understanding that all of these factors play contributory roles.

Photoperiod Hypotheses
The photoperiod hypothesis is that SAD is initiated in the fall and maintained in the dark seasons due to decreased daylight (Magnusson & Boivin, 2003). This decreased daylight affects release of melatonin, which is a messenger hormone secreted by the pineal gland (Lam & Levitan, 2000). The pineal gland starts to secrete melatonin in dim light conditions and therefore prepares the body for sleep (Magnusson & Boivin, 2003). As there is more dim light and darkness in fall and winter, it is hypothesized that SAD sufferers release more melatonin and therefore sleep excessively.
Bower (2001) found support for this hypothesis. He found that people without SAD tended to have a steady melatonin release every night for about nine hours throughout the year, however SAD sufferers tended to release melatonin an average of 38 minutes longer in the dark seasons (fall and winter) than in the lighter seasons.
However, studies of melatonin concentrations in saliva have been mixed and the results are confusing. For example, literature reviewers (Magnusson & Boivin, 2003; Lam & Levitan, 2000) reported that some studies did not find differences between the melatonin concentrations in saliva of SAD sufferers versus nonsufferers and other larger studies have found differences. However, it is difficult to determine whether the larger concentrations of melatonin in SAD sufferers are the cause or the product of hypersomnia (Lam & Levitan).
Another photoperiod hypothesis that seeks to explain how decreased sunlight influences the expression of SAD is the Phase Delay Hypothesis. The phase delay hypothesis holds that people get SAD because their personal circadian clock, including the body’s regular sleep wake cycle, is out of synchrony with the external environment (Burgess et al.). People, like most animals, have an internal clock that is entrained (or synchronized) by the 24 hour cycle of light and dark in the environment (Morris, 2002). Light entrains the circadian clock which is thought to be located in the suprachiasmatic nucleus in the hypothalamus (Burgess, Fogg, Young & Eastman, 2004).
In order to control for several other factors that affect circadian rhythms, such as time and amount of food ingested, time and intensity of activities, and light exposure, researchers need to study participants who are subjected to the same constant routine for 36 hours (Lam & Levitan, 2000). When this method was used, it was found that SAD sufferers had phase delays in the secretion of melatonin by the pineal gland in dim light conditions, core temperature rhythm delays, and cortisol rhythm delays (Lam & Levitan, 2000). These SAD sufferers’ melatonin cycle advanced when they experienced either bright light in the morning or bright light in the morning and early evening (Lam & Levitan). Some support for the phase delay hypothesis was found when SAD sufferers were exposed to bright light therapy and had phase advances that synchronized their internal with external clocks. Other studies failed to find this result, however, the researchers did not use the constant routine method (Lam & Levitan, 2000). One problem with the phase delay hypothesis is that some SAD sufferers do not have these phase delays (Lam & Levitan, 2000).
Burgess, Fogg, Young and Eastman (2004) found some support for the phase delay hypothesis. They “continuously monitored “ (p. 759) 26 SAD sufferers’ rectal temperatures to determine the time in which sufferers reached their minimum core body temperature(time of MCBT) (Burgess et al). They found that morning light therapy advanced the time of MCBT, thus reducing symptoms of SAD and evening therapy delayed it, thus exacerbating SAD symptoms (Burgess et al). People in the placebo group did not show differences in their time of MCBT (Burgess et al). As a placebo light box, researchers made a prop in which they told participants it was a negative ion generator (Burgess et al). However, only 46% of the SAD sufferers in this study had a phase delay at baseline (Burgess et al). Approximately 75% of the SAD sufferers who had phase delay as measured by time of MCBT before the study showed synchrony between internal and external clocks after light therapy (Burgess et al).
The visual system can also play a role in SAD (Levitan & Levitt, 2003). Researchers found that 41% of SAD sufferers who were measured using an electroretinogram, were one standard deviation or more below nonsufferers in terms of retinal sensitivity (Levitan & Levitt). The researchers hypothesized that dark eyed SAD sufferers experience more of an evening phase delay that nonsufferers as a result of how much sunlight dark versus light colored eyes take in (Levitan & Levitt). This finding suggests that SAD sufferers are more prone to retinal hyposensitivity (and getting much less needed light) than nonsufferers.
It is apparent that the expression of SAD is a result of a variety of sources, as some SAD sufferers produced more melatonin, and some did not, and some SAD sufferers had phase delays, while some did not. It also seems that sunlight plays an important role in SAD, but that only a small part of the population get SAD despite being exposed to the same photoperiod.

Neurotransmitters’ Roles in SAD
The neurotransmitters serotonin, dopamine, and norepinephrine and especially the release and uptake of them, are usually involved in mood disorders (Lam & Levitan, 2000). It is interesting to note that there is more research on serotonin and depression than the other neurotransmitters (Lam & Levitan, 2000). Reasons for this emphasis is that serotonin is thought to play a more significant role in depression and because it is difficult to study the effects of dopamine because of its relation to psychosis and addiction (Lam & Levitan, 2000).
Levels of serotonin fluctuate substantially with the seasons in animals and humans (Magnusson & Boivin, 2003). It has been hypothesized that SAD sufferers have lower levels of serotonin than nonsufferers in the dark seasons. The lowest levels of serotonin are found in humans in December and January, which are the darkest months in the northern hemisphere (Lambert, Reid, Kaye, Jennings, & Esler, 2002). Low levels of 5-HIAA, a major metabolite of serotonin, is found in cerebrospinal fluid in spring, which may be because of low levels of serotonin during the dark season (Magnusson & Boivin). Although there is fluctuating levels of the other metabolites of the other neurotransmitters, the largest fluctuation is observed in serotonin (Magnusson & Boivin).
Serotonin is also known to play a significant role in food cravings, satiation, and sleep (Willeit et al., 2003). People with SAD tend to crave carbohydrates (Lam & Levitan, 2000). This may be because the hypothalamus regulates eating and satiation and hypothalamic levels of serotonin are the lowest during December and January (Lam & Levitan, 2000). SAD sufferers tend to report feeling energized after eating carbohydrates, whereas many people without the disorder tend to feel sleepy after the same ingestion (Lam & Levitan, 2000). This could be due to SAD sufferers having different levels of L-tryptophan, which is serotonin’s amino acid precursor (Lam & Levitan, 2000). Nonsufferers have the highest levels of L-trytophan in April and May and the levels drop substantially in early fall. Another study found high levels in spring and low levels in early summer and winter. These findings could not be explained by food consumption alone, although protein consumption affects the ability of plasma tryptophan to cross the blood brain barrier (Lam & Levitan, 2000).
Studies using tryptophan depletion have illuminated differences in SAD sufferers. Plasma tryptophan can be reduced to 20% of normal levels by ingesting a dose of large neutral amino-acids (Magnusson & Boivin, 2003). This produces a large drop in tryptophan and serotonin production (Magnusson & Boivin). When using this method with SAD sufferers who are in remission, their depression and carbohydrate cravings came back (Lam & Levitan, 2000). These tryptophan studies offer good support for the lower serotonin level hypothesis. Several studies conclude that SAD sufferers have different neuroendocrine levels and dysfunction of several of the 5-HT serotonin receptors, notably 2, 7, and 1D (Lam & Levitan, 2000).
Willeit et al. (2003) analyzed genotypes of 138 SAD sufferers as compared to 146 people who showed low seasonality (people who feel little to no fluctuations between the seasons in terms of mood, eating patterns, energy, and gregariousness). They found no significant differences between SAD sufferers and nonsufferers with regard to their genotypes and frequency of s-alleles. However, people who had s-allele were significantly more likely to suffer from SAD than those without the s-allele (Williet et al., 2003) They stated that their data support a hypothesis that SAD is a phenotypic expression of a disease in which 5-HT transmission and 5-serotonin transporter gene promoter region (HTTLPR) contributes to the process.
Although serotonin levels play the most significant role in the neuropsychology of SAD, lower levels of norepinephrine have also been observed in SAD sufferers (Lam & Levitan, 2000). This lower level of norepinephrine may account for sufferers sleeping and eating carbohydrates excessively as they seem to have a central underarousal problem (Lam & Levitan, 2000). The SAD sufferers may be eating carbohydrates excessively in an attempt to feel energized, as a result of under arousal from too little norepinephrine.
Dopamine may also play a minor role in SAD. It is difficult to study the direct effects of dopamine, therefore indirect effects have been speculated. For example, SAD sufferers tend to have low resting prolactin levels, which indicate decreased activity of dopamine as well as the D2 receptors up-regulation to compensate (Lam & Levitan, 2000). Another indirect effect of dopamine depletion is reduced thermoregulation of heat loss. SAD sufferers tend to have problems with thermoregulation of heat loss in the dark season that corrects itself in summer as well as after light therapy (Lam & Levitan, 2000). Light therapy as well as naturally occurring light in the summer months seems to enhance the production of normal levels of dopamine (Lam & Levitan, 2000). Treatment with L-Dopa and carbidopa did not produce remission of symptoms for SAD sufferers (Lam & Levitan, 2000) probably because dopamine only plays a minor role in the production of SAD symptoms.

Preliminary research suggests that there are genetic factors that may protect or make people vulnerable to acquiring SAD. Comparing people who live in Iceland who experience long winters, to descendants of the Icelandic people living in Manitoba, Canada, to American citizens living on the east coast, it was found that the American citizens had a higher prevalence rate than the other two groups despite experiencing more daylight than the other two groups (Lam & Levitan, 2000). It is hypothesized that these Icelandic people and their descendants had genetic factors that reduced SAD’s prevalence (Axelsson, Stefansson, Magnusson, Sigvaldson, & Karlsson, 2002).. Axelsson et al. (2002) also compared people living in Winnipeg, Manitoba who were direct descendants from Icelandic people to people living in the same city who did not have Icelandic genes. They found that the Icelandic descendants had lower rates of SAD than the nondescendants (Axelsson et al., 2002). Lam and Levitan (2002) concluded from their literature review of SAD that it is a complex phenotype associated with genes that play a role in production of tryptophan and serotonin. One study involving 4,629 pairs of adult twins in Australia found that genetics in SAD accounted for 29% of the variance (Lam & Levitan, 2000).
One group of researchers did not find a difference in prevalence between the first generation of relatives of a group of people who had SAD versus a group who had other mood disorders, suggesting that the genetic and environmental precursors for SAD are no stronger than that of other mood disorders(Stamenkovic et al., 2001). The researchers found that 16.5% of first generation relatives of SAD sufferers had SAD and 19% of first generation relatives of other mood disorders had mood disorders (Stamenkovic et al., 2001). Weir (2001) found similar results in that the studies she reviewed reported a range of 13% to 17% of first degree relatives of SAD sufferers also experiencing SAD.

Cognitive Behavioral Factors in Seasonal Affective Disorder
Both biological and psychological factors appear to play roles in how vulnerable, how early, how long, how severe and how well SAD sufferers respond to treatment. Cognitive theories of depression, and the research that supports these theories, state that depressed people process information in a negative, pessimistic, exaggerated way that maintains depression (Dalgleish, Spinks, Golden, & du Toit, 2004). Dalgleish et al. found that people with SAD endorsed more negative adjectives describing themselves and were more likely to have a negative attributional style than did nonsufferers. A negative attributional style refers to thinking they are responsible for all negative circumstances and they have no control over positive outcomes. They believe negative circumstances are pervasive over most situations. A typical statement of a person with a negative attributional style is “why do bad things always happen to me?” These results support the idea that negative thoughts either contribute, maintain or initiate SAD. Risk factors for depression, both seasonal and nonseasonal, are number of negative events experienced in one’s life (such as death of a loved one, divorce, war etc.) and little and poor quality of social support (Michaluk et al., 2004).
Response Style Theory suggests that a person’s reaction to subjective feelings of negative mood, probably caused by biological factors, can change SAD. If SAD sufferers respond by ruminating over how bad they feel and for how long they feel that way, they exacerbate their disorder. If instead of ruminating, they distract themselves from the negative mood, and engage in other more positive thoughts, they can lessen the impact of biological changes (Young & Azam, 2003). Young and Azam found that SAD sufferers who tended to ruminate had more severe symptoms than those that did not. These SAD sufferers tended to increase rumination as their symptoms got worse, thus exacerbating their symptoms. Levitan and Levitt (2003) reported that SAD sufferers reported higher levels of hostility and rumination than a suicidal depressed group.
Rohan et al. (2003) found that one significant correlate of SAD was negative thought patterns. For example, SAD sufferers tended to believe in statements such as “I’m worthless, and I can never succeed,” Other correlates were lower activity levels, lower enjoyment of activities in the fall and winter, and rumination. Goel, Terman, and Terman (2002) found that SAD sufferers who were single or divorced suffered more anxiety and depression than married sufferers. Unemployed SAD sufferers were more likely than employed SAD sufferers to experience anhedonia (loss of pleasure in activities), psychomotor retardation or agitation, reduced desire to eat, and excessive or inappropriate guilt. It is unclear whether these symptoms (anxiety, depression, anhedonia, slowness, eating problems, and guilt) are a result, cause or relation of the marital and employment status (Goel et al., 2002). It seems that there is an important relationship between the biological and psychological bases of this disorder. For example, lower serotonin levels probably contribute to developing a negative attributional style and the lower norepinephrine probably contributes to feeling less energetic, over sleeping, and wanting to feel better by eating carbohydrate-rich comfort foods.

Treatment for SAD
Effective treatments for SAD are light therapy and psychotropic medications (Lam & Levitan, 2000; Magnusson & Boivin, 2003). Some sufferers do not respond to light therapy and therefore may find relief from medication (Yamadera, Masako, & Takahashi, 2001).
Light Therapy
Light is a biological need for all life; without it, people can not survive (Morris, 2002). With very little amounts of sunlight, and the vitamin D the body produces as a result, people become terminally ill and deformed, as in the case of rickets (Morris). It is interesting to note that even blind fish living in caves and mammals living in darkness need some light in order to survive (Morris).
Light therapy usually involves the SAD sufferer sitting at a desk with a light box 50 to 100 centimeters away. The person can do any activity while sitting there as long as s/he occasionally glances at the light box. Light therapy usually is administered for a 30 to 120 hours per day contingent on the intensity of light obtained. Using these methods, the SAD sufferer receives approximately 2,000 to 10,000 lux.
Morris (2002) noted that perhaps it is not the light therapy that produces relief but rather the vitamin D the body produces as a result of sunshine. He reviewed studies in which some light therapies did not produce remission of symptoms but that some SAD sufferers taking high doses of vitamin D did get relief (Morris, 2002).
After reviewing 60 studies of light therapy, Magnusson and Boivin (2003) concluded that light therapy is effective for approximately 65% of SAD sufferers. Sher, Matthews, Turner, Postolache, Katz, and Rosenthal (2001) found a method to predict whether a SAD sufferer will be one of the 65% who will get relief from light therapy. They found that the minor improvement of mood after one hour of light therapy predicted the improvement SAD sufferers would experience after two weeks of one hour sessions of light therapy (Sher et al). This finding saved a lot of researchers’ and participants’ time and money.
It was hypothesized that because there is less light during the morning and evening in the dark seasons, and that consistent with the phase delay theory, the circadian clock needs light at those times to be entrained, that light therapy should be provided morning and evening for a total of two to four hours per day to replace the decreased exposure to sunlight. Although morning and evening light replacement sounds logical, it is not empirically supported.
In reviews of the literature, researchers concluded that light therapy is effective when administered at any time during the day. Some studies and most meta-analyses found morning light therapy superior to late afternoon therapy and that light therapy should not be administered during evening hours as it can have a stimulating effect and can delay sleep onset (Lam & Levitan, 2000; Magnusson & Boivin, 2003). It is also noted that most SAD sufferers will relapse if light therapy is terminated before spring (Magnusson & Boivin, 2003).

Medications For SAD
Approximately 35% of SAD sufferers do not achieve relief from SAD using light therapy. Some sufferers get side effects from light therapy such as sore eyes and severe headaches (Shen, Kennedy, Levitan, Kayumov, & Shapiro, 2005). Others do not engage in light therapy due to time constraints (Yamadera et al.) For these people, medication may provide some relief.
Drugs that act on serotonin, such as serotonin receptor reuptake inhibitors (SSRIs) were hypothesized to be effective treatment for SAD. Possible side effects of SSRIs are gastrointestinal problems (i.e. nausea and diarrhea), insomnia and dry mouth (Muscovitch et al., 2004) which may reside after a couple of weeks.
Shen et al. (2005) studied the effects of Nefazodone (an SSRI). It works by blocking postsynaptic serotonin receptors and by inhibiting reuptake of both serotonin and norepinephrine. In a well-designed study which included objective measures of sleep (polysomnographic measurements were taken before and eight weeks after medication therapy in a sleep lab), as well as self-report measures that include questions that capture seasonality in depression, Shen et al. found that eight female SAD sufferers experienced a remission of symptoms after taking Nefazodone for eight weeks. One of the limitations of this study, like many drug trial studies, was the small number of SAD sufferers involved, which limits the study’s generalizability to other SAD sufferers. Another weakness of the study was that the SAD sufferers who participated in this study did not first fail at light therapy. It is possible that people who can not find relief from light therapy differ significantly from those that do find relief.
Martiny et al. (2004) conducted a large study of 269 SAD sufferers living in Denmark. Martiny et al. first exposed participants to daily light therapy for one week. The 37.5% of participants that did not respond to light therapy were then excluded from the study. The remaining 168 sufferers who responded to light therapy were randomly assigned to citalopram (an SSRI) therapy versus placebo groups in an attempt to maintain the positive effects of light therapy without having to continue light therapy. Sixty five participants completed 15 weeks of medication therapy, while 7.1% of sufferers dropped out because they could not tolerate side effects and 9.5% of the sample dropped out because of lack of improvement. It is interesting to note that 2.3% of the SAD sufferers in the placebo group dropped out stating the side effects were intolerable and 7.1% dropped out due to lack of relief. Their results indicated that citalopram significantly reduced the relapse rate into SAD over placebo.
Muscovitch et al. (2004) conducted a large study involving SAD sufferers from five northern hemisphere countries comparing sertraline (an SSRI) with placebo. All measures were paper and pencil assessments conducted by the sufferer and by physicians. Some of the items were pertaining to quality of sleep. Almost 11% of the participants receiving sertraline quit their involvement in the study due to side effects and 4.3% of the placebo group quit due to side effects. On all measures of depression, scored by participant and physicians, Muscovitch et al. found that sertraline was statistically significantly more effective than the placebo. Participants noted that sertraline decreased their desire to overeat and decreased their carbohydrate cravings, which are hallmarks of SAD. It was hypothesized that the efficacy of SSRI medication gave support for the theory that 5-HT neurotransmission and the effect it has on serotonin plays a significant role in SAD.

Conclusions and Future Directions
In summary, it appears that the decreased amount of sunlight occurring in the fall and winter months probably affects some genetically predisposed people to delay sleep and wake cycles and to produce less serotonin (and its precursors) and more melatonin. These changes may lead people to think negatively about themselves and to ruminate about how bad they feel, which compounds their misery. Light therapy tends to be effective for approximately 65% of SAD sufferers; some of the other SAD sufferers tend to find relief from SSRIs.
The reviewed literature did not elucidate possible hormonal, cultural, or other reasons that would explain the higher incidence of female SAD sufferers (than males). Future research may shed more light on these reasons, such as perhaps women and men have the same incidence but women are more likely to notice (versus deny) the symptoms and ask for help, perhaps women are more likely to feel comfortable talking about the negative emotion and reporting it than men are, or perhaps men are more likely to distract themselves from symptoms than to ruminate and exacerbate the disorder such that the person notices and reports it to his/her physician.

Axelsson, J., Stefansson, J.G., Magnusson, A., Sigvaldson, H., Karlsson, M. (2002).
Seasonal affective disorders: Relevance of Icelandic and Icelandic-Canadian
evidence to etiologic hypotheses. Canadian Journal of Psychiatry, 47(2),
Retrieved from Ebsco Database.
Bower, B. (2001). Winter depression may heed hormonal signal. Science News, 160.
Retrieved  from Ebsco Database.
Burgess, H.J., Fogg, L.F., Young, M.A., & Eastman, C. Bright light therapy for winter
depression: Is phase advancing beneficial. Chronobiology International, 21, 759-
775. Retrieved from Ebsco Database.
Chotai, J., Smedh, K., Johansson, C., Nilsson, L., Adolfsson, R. (2004). An
epidemiological study on gender differences in self-reported seasonal changes in
mood and behaviour in a general population of northern Sweden. Nordic Journal
of Psychiatry, 58, 429-437. Retrieved rom Ebsco Database.
Dalgleish, T., Spinks, H., Golden, A., & du Toit, P. (2004). Processing of emotional
information in seasonal depression across different cognitive measures. Journal
of Abnormal Psychology, 113, 116-127. Retrieved from Ebsco
Enoch, M.A., Goldman, D., Barnett, R., Sher, L., Mazzanti, C.M., and Rosenthal, N.E.
(1999). Association between seasonal affective disorder and the 5-HT2a promoter
polymorphism, -1438G/A. Molecular Psychiatry, 4, 89-92. Retrieved from Ebsco Database.
Goel, N., Terman, M., & Terman, J.S. (2002). Depressive symptomatology differentiates
subgroups of patients with seasonal affective disorder. Depression and Anxiety,
15, 34-41. Retrieved from Ebsco Database.
Haggarty, J.M., Cernovsky, Z., Husni, M., Minor, K., Merskey, H. (2002). Seasonal
affective disorder in an Arctic community. Acta Psychiatrica Scandinavia, 105,
378-384. Retrieved  from Ebsco Database.
Lam, R.W., Levitan, R.D. (2000). Pathophysiology of seasonal affective disorder: A
review. Journal of Psychiatry and Neuroscience, 25, 469-482. Retrieved March
25, 2006, from Ebsco Database.
Lambert, G.W., Reid, C., Kaye, D., Jennings, G.L., Esler, M.D. (2002). Effect of sunlight
and season on serotonin turnover in the brain. Lancet, 360 (9348). Retrieved
March 25, 2006, from Ebsco Database.
Levitan, R.D., & Levitt, A.J. (2003). Highlights of the abstract program of the fifteenth
annual society for light treatment and biological rhythms virtual meeting 2003.
Chronobiology International, 20, 1139-1148. Retrieved from
Ebsco Database.
Levitt, A.J., Boyle, M.H., Joffe, R.T., & Baumal, Z. (2000). Estimated prevalence of the
seasonal subtype of major depression in a Canadian community sample. Canadian
Journal of Psychiatry, 45, 650-654. Retrieved from Ebsco
Levitt, A.J., & Boyle, M.H. (2002). The impact of latitude on the prevalence of seasonal
depression. Canadian Journal of Psychiatry, 47(4). Retrieved from Ebsco Database.
Magnusson, A., & Boivin, D. (2003). Seasonal affective disorder: An overview.
Chronobiology International, 20, 189-207. Retrieved from Ebsco
Martiny, K., Lunde, M., Simonsen, C., Clemmensen, L., Poulsen, C., Solstad, K. et al.
(2004). Relapse prevention by citalopram in SAD patients responding to 1 week
of light therapy. Acta Psychiatrica Scandinavia, 109, 230-234. Retrieved  from Ebsco Database.
Michaluk, E.E., Tam, E.M., Manjunath, C., Yatham, L., Levitt, A.J., Levitan, R.D. et al.
(2004). Hard times and good friends: Negative life events and social support in
patients with seasonal and nonseasonal depression. Canadian Journal of
Psychiatry, 49, 408-411. Retrieved from Ebsco Database.
Moscovitch, A., Blashko, C.A., Eagels, J.M., Darcourt, G., Thompson, C., Kasper, S. et
al. (2002). A placebo-controlled study of sertraline in the treatment of outpatients
with seasonal affective disorder. Psychopharmacology, 171, 390-397. Retrieved
from Ebsco Database.
Morris, D.B. (2002). Light as environment: Medicine, health, and values. Journal of
Medical Humanities, 23(1), 7-29. Retrieved  from Ebsco
Murray, G., Allen, N.B., and Trunder, J. (2001). A longitudinal investigation of seasonal
variation in mood. Chronobiology International, 18(5) 875-891. Retrieved
from Ebsco Database.
Rohan, K.J., Sigmon, S.T., Dorhofer, D.M. (2003). Cognitive-behavioral factors in
seasonal affective disorder. Journal of Consulting and Clinical Psychology, 71,
22-30. Retrieved from Ebsco Database.
Shen, J., Kennedy, S.H., Levitan, R., Kayumov, L., Shapiro, C.M. (2005). He effects of
nefazodone on women with seasonal affective disorder. Journal of Psychiatry and
Neuroscience, 30, 11-16. Retrieved  from Ebsco Database.
Sher, L., Matthews, J.R., Turner, E.H., Postolache, T.T., Katz, K.S., Rosenthal, N.E.
(2001). Early response to light therapy partially predicts long-term antidepressant
effects in patients with seasonal affective disorder. Journal of Psychiatry and
Neuroscience, 26(4). Retrieved  from Ebsco Database.
Stamenkovic, M., Aschauer, H.N., Riederer, F., Schindler, S.D., Leisch, F., Resinger, E.,
Neumeister, A., Hornik, K., and Kasper, S. (2001). Study of family history in
seasonal affective disorder. Neuropsychology, 44. 65-69. Retrieved from Ebsco Database.
Weir, E. (2001). Winter needn’t be the SAD season. Canadian Medical Association
Journal, 164. Retrieved from Ebsco Database.
Willeit, M., Prashek-Rieder, N., Neumeister, A., Zill, P., Leisch, F., Stastny, J. et al.
(2003). A polymorphism (5-HTTLPR) in the serotonin transporter promoter gene
is associated with DSM-IV depression subtypes in seasonal affective disorder.
Molecular Psychiatry, 8, 942-946. Retrieved from Ebsco
Wirz-Justice, A., Graw, P., Krauchi, K., & Waker, H.R.. (2003). Seasonality in affective
disorders in Switzerland. Acta Psychiatrica Scandinavia, 108, 92-95. Retrieved
from Ebsco Database.
Yamadera, H., Masako, O., Takahashi, K. (2001). Open study of effects of alprazolam on
seasonal affective disorder. Psychiatry and Clinical Neurosciences, 55, 27-30.
Retrieved  from Ebsco Database.
Young, M.A., & Azam, O.A. (2003). Ruminative response style and the severity of
seasonal affective disorder. Cognitive Therapy and Research, 27, 223-232.
Retrieved  from Ebsco Database.

Seasonal Affect Disorder


Leave a Reply

Your email address will not be published. Required fields are marked *

BizStudio-lite Theme by SketchThemes