Seasonal Affective Disorders

Said, M, University of Liverpool, UK.

• Introduction
• Diagnostic Assessment
• Features
• Assessment
• Epidemiology
• Pathophysiology
• Treatment
• Future
• Conclusion
• References

Introduction

Physicians recorded seasonal depressions as early as Aretaeus and Hippocrates. More recently, patients with regular seasonal depressions were coined as having Seasonal affective disorder (SAD). SAD is described as a subtype of affective disorder (mood disorder) with a seasonal pattern¹ usually in the winter when sufferers experience clinical depression and has a greater prevalence in countries with greater northern latitude. There is some evidence to suggest the existence of a recurrent depression that occurs in summer².               

Diagnostic Assessment

The term SAD was invented by Rosenthal et al in 1984 with the criteria shown below:

 

Table 1: SAD criteria of Rosenthal et al (1984)3

1) A history of major affective disorder, according to Research Diagnostic Criteria (Spitzer et al 1978)4

2) At least two consecutive previous years in which the depressions developed  during fall or winter and remitted by the following spring or summer

3) Absence of any other Axis I DSM-III psychiatric disorder (American Psychiatric Association 1980)

4) Absence of any clear-cut seasonally changing psychosocial variables that would account for the seasonal variability in mood and behaviour

 

Now the diagnostic term is included in the Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American Psychiatric Association. The DSM-IV is one of two standard diagnostic manuals used by psychiatrists for diagnosis, the other one being the International Classification of Diseases, currently in its 10^th edition (World Health Organisation, 1992). The patient must satisfy certain criteria before a diagnosis of SAD can be made (Table 2).

Table 2: DSM-IV criteria for seasonal pattern specifier

Specify if, with seasonal pattern (can be applied to the pattern of major depressive episodes in bipolar I disorder, bipolar II disorder, or major depressive disorder, recurrent):

a. There has been a regular temporal relationship between the onset of major depressive     episodes in bipolar I or bipolar II disorder or major depressive disorder, recurrent, and a particular time of year (e.g. regular appearance of the major depressive episode in autumn or winter)

b. Full remissions (or a change from depression to mania or hypomania) also occur at a characteristic time of year (e.g. depression disappears in the spring).

c. In the last 2 years, two major depressive episodes have occurred that demonstrate the temporal season relationship defined in criteria a and b, and no non-seasonal major depressive episode has occurred during the same period.

d. Seasonal major depressive episodes (as described above) substantially outnumber the non-seasonal major depressive episodes that may have occurred over the individual’s lifetime.

Note: Do not include cases in which there is an obvious effect of season-related psychosocial stressors (e.g. regularly being unemployed each winter)

Source: American Psychiatric Association (1994).

Typically, winter SAD sufferer would be a patient who has been regularly diagnosed as suffering from major depression during the winter and remits during the summer. Around 30% of patients with SAD also experience a bipolar mood swing from depression to a feeling of elation or ‘high’, usually during spring, which if severe could be diagnosed as a hypomania.

The diagnosis must take into account any psychosocial factors that may be linked to seasonal changes in mood, e.g. unemployment during winter, whereby the effects of the season would not be the causal factor of the mood change. Evidence also shown the existence of a milder form of SAD, ‘subsyndromal SAD’ (S-SAD), which is clinically significant but not severe enough as SAD⁵.

  

Clinical features

Characteristic symptoms of SAD are those of depression, which include dysphoria, feeling low, decreased in energy and activity, increased irritability, concentration difficulties, anxiety, decreased libido and social withdrawal. Unlike classically depressed patients, most SAD patients develop ‘atypical’ symptoms of increased fatigue, increased sleep duration and increased appetite and weight. Not only do SAD patients crave carbohydrates, but also they actually report eating more carbohydrate-rich foods in the winter¹.

A study point out that patients are more disturbed by the lethargy and fatigue than by the mood changes themselves, especially in the early phases of their winter depression, therefore often seeking the help of a physician rather than a psychiatrist⁶. Untreated, SAD episodes generally resolve by springtime, although some do not fully recover before the early summer. Many patients reported that travel to latitudes nearer the equator resulted in remission or diminishing of their symptoms³.

Winter SAD is also seen in children, who present with fatigue, irritability, difficulty getting out of bed in the morning and school problems⁷. The seasonal pattern of summer is opposite to that of winter SAD with reversal of their winter symptoms in summer.

 

Table 3 shows the comparison between SAD and non-seasonal depression.

 

Symptom	Seasonal	Non-seasonal
Sleep	Sleep more/difficulty staying awake. Occasionally, disturbed sleep/early morning wakening	Disturbed sleep/early morning wakening
Energy	Fatigue often incapacitating/slump in energy in the afternoon	Tiredness loss of energy
Eating	Craving for carbohydrates and sweet foods	Loss of appetite
Weight	Increase	Decrease
Concentration	Difficult to concentrate often with additional memory impairment	Difficult to concentrate often with additional memory impairment
Mood	Low mood during the winter, often severe. Remitting in the summer. Some experience short period of hyperactivity (hypomania) in the spring.	Persistent low mood, sometimes labile
Feelings	Sense of misery, loss of self-esteem; sometimes hopelessness and despair. Apathy and flat effect (mood)	Sense of misery, loss of self-esteem; sometimes hopelessness and despair. Apathy and flat effect (mood)
Anxiety	Stress and anxiety common	Stress, anxiety and aggitation
Libido	Less interest in sex	Less interest in sex
Social	Irritability, problems relating to people. Withdrawal and isolation	Irritability, problems relating to people. Withdrawal and isolation
The atypical symptoms of depression are marked in bold italic and predict a good response to phototherapy in seasonal affective disorder

 

Table 3: Symptom comparison⁵

Assessment

Rating scales are used to define the course and intensity of the symptoms and as a guide in an assessment interview. Two scales that are most commonly used by researchers are the Seasonal Pattern Assessment Questionnaire (SPAQ) ³, and the Hamilton Depression Scale, SAD version (SIGH-HAD). The SPAQ is a self-rating scale used to determine the seasonal variation and timing of the symptoms, but these self-report is subjective and exposed to over- and under-reporting. The Hamilton scale is used to describe symptoms and measure severity and its advantage lies in its use as an independent rating tool and as a useful measure of response to treatment.

Epidemiology

Early SAD studies indicated that most patients met criteria for bipolar II disorder (depressive and hypomanic episodes), while only a small proportion had bipolar I disorder (depressive and full manic episodes), or unipolar depression⁸. More recent work, however, has found that the majority of patients to have unipolar depression, with a substantial minority of patients having bipolar II disorder and very few having bipolar I disorder⁹. This discrepancy could possibly be explained because of the use of different sets or criteria or due to different climatic conditions between studies.

The prevalence of SAD has been estimated to range from 0 to 9.7% depending on the population that is being sampled⁵. Women are approximately twice as likely to suffer from SAD than men, which is comparable to gender differences reported in non-seasonal depression although they may reflect bias in sampling¹⁰. According to a study, the mean age of onset in SAD appears to be in the thirties¹¹.

Though the geographical distribution of SAD has not been rigorously studied there is evidence to suggest that the prevalence of SAD and S-SAD increases with an increase in northern latitude¹. This led to the view that SAD is linked to the hours of daylight that people are exposed to at different latitudes, where the further north a person lives the fewer hours of sunlight exposure per day. Research in different areas of the USA found there was a correlation between latitude and prevalence of SAD (Table 4).

 

Table 4: The prevalence of SAD and S-SAD in a survey carried out in the USA¹²

 

Location	Latitude (north)	SAD (%)	SAD + S-SAD (%)
New Hampshire	43o	9.7	20.7
New York	40o	4.7	17.1
Maryland	39o	6.3	16.7
Florida	27o	1.4	4.0

 

SAD = seasonal affective disorder; S-SAD = subsyndromal SAD.

However, when compared with the results above, several studies have found lower rates of SAD in Iceland and Manitoba which are located at 63-67^o north and 50^o north respectively¹³. Even among descendants of Icelandic emigrants in Canada, the prevalence was low suggesting genetic adaptation might play an important role¹⁴. This finding seems to emphasize the importance of genetic, psychosocial, cultural and ethnic factors in the development of SAD.

Pathophysiology of SAD

Biological abnormalities have been found in winter SAD patients, including alterations in hormonal profiles, biochemical challenges, immune responses and visual evoked phenomena. Based on the research findings of phototherapy, a number of biological theories have emerged to explain SAD.

The ‘photon-counting’ hypothesis

The short days of winter deprive susceptible patients of sufficient quanta of light for some chemical process responsible for maintaining a euthymic (normal) state. So this ‘photon deficient’ depression is treated by supplementing the deficient light.

This hypothesis is based on initial report in SAD documenting that bright light acted as an antidepressant whereas dim light did not³ and further supported by data indicating that there is a dose-response relationship for light as well as an inverse relationship between duration and intensity of light required¹⁵. A limitation of this hypothesis is that it doesn’t specify what intervening processes are influenced by these varying amounts of lights, which in turn influence the outcome in SAD patients.

The ‘melatonin’ hypothesis

The hormone melatonin plays a role in the secretion and regulation of various hormones and seasonal changes in behaviour. Studies have demonstrated that melatonin is inhibited by bright light and therefore is increased in the darker winter months. So suppression of melatonin by light should induce an antidepressant effect.

The results of several studies have argued against this hypothesis. Firstly, administration of melatonin to successfully treated SAD patients did not induce them to relapse¹⁶. Secondly, SAD patients treated with atenolol (beta-adrenergic blocker) that reduces night-time melatonin levels failed to improve their condition¹⁷. These and other results suggest that the suppression of pineal melatonin secretion may account for some symptoms that resolve during light therapy, but there is no convincing evidence that it is central to the disorder.

The ‘phase shift’ hypothesis

This concept was built on the capacity of bright light in the evening to delay the nocturnal rise of melatonin and in the morning to advance the rhythm¹⁸. So the association between phase-advancing and antidepressant effects of phototherapy suggested a connection between delayed circadian rhythms and depression.

This theory postulates that time of day of phototherapy is critical to the antidepressant response. Few studies rejected this theory because it could be argued that evening light treatment should make patients worse whereas, in fact, the reverse happened¹⁹. Nevertheless, circadian rhythms may be linked since the eye may be more sensitive to light in the early morning than at other times. Unanswered questions includes are rhythms really delayed in winter SAD and whether they are the central abnormality.

The ‘amplitude’ hypothesis

This theory was developed from endogenous circadian amplitudes of variables such as temperature, melatonin and heart rate that can be markedly suppressed or enhanced depending upon the timing of light exposure. This suggests that increased circadian amplitude induced by phototherapy may result in the antidepressant effect of light²⁰.

Neurotransmitter hypothesis

Two neurotransmitters may be playing the central roles in the pathophysiology of winter SAD: Dopamine and Serotonin.

Dopamine

Dopamine might play a role in SAD by modulating a ‘behavioural facilitation system’ where evidence of reduced prolactin secretion in SAD patients compared with normal volunteers in both winter and summer suggests that it might be a trait marker of the condition²¹. This finding might indicate a dopaminergic secretion in SAD, since low basal prolactin secretion may result from compensatory up-regulation of D₂-receptors in the anterior pituitary gland associated with low functional activity of dopamine.

     Bright light allows dopamine to be produced in the retina and suppresses the production of retinal melatonin thereby improving mood by mechanisms such as resetting the circadian ocular clock or triggering dopaminergic impulses affecting central neuronal structures²².

Serotonin

This neurotransmitter was nominated as one whose functional deficiency might be responsible for depressive disorders in general because the therapeutic effects of some antidepressant drugs may be dependent on serotonin availability²³.

Carbohydrate craving may also reflect a functional serotonin deficiency, which would be consistent with the serotonin theory of SAD, given the eminent symptom of carbohydrate cravings in winter depression³.

Hormones

Winter SAD patients were shown to have normal basal plasma cortisol and Adrenocorticotrophin Hormone (ACTH) levels, but reduced ACTH responses to infusions of Corticotrophin Hormone that may occur in hypercortisolaemic patients, such as melancholic depressives²⁴.

Other explanation include an underactive Hypothalamus-Pituitary-Adrenal axis associated with the lethargy, hypersomnia and hyperphagia compared to the agitation, insomnia and anorexia seen in melancholic depression.

Treatment

There are three main courses of treatment although phototherapy has been the mainstay of treatments for winter depressions. If any single treatment proves insufficient, a combination regimen are often used, the most common being phototherapy and medication.

Phototherapy

Phototherapy is a treatment involving daily exposure to high-intensity, broad-spectrum light. The discovery that human melatonin production can be suppressed by bright light led to the initial test of bright light in treating winter depression. The therapeutic effects of phototherapy may involve a serotonergic mechanism since rapid tryptophan (dietary amino acid precursor of serotonin) depletion appears to reverse the antidepressant effect of phototherapy²⁵.

     The efficacy of phototherapy has been demonstrated in over 20 placebo-controlled studies around the world^26,27. It is difficult to control for the placebo effect in phototherapy studies, since the patients often believe that light will be helpful and the ideal standard of a double-blind design is not possible. Many attempts have been made to control for placebo effects of light by varying intensity, colour and timing of treatment, as well as directing the light to different parts of the body. Several parameters have emerged for optimal use of phototherapy.

 

Parameters for phototherapy

Brightness

Illuminance, measured in terms of quanta of light sensed over time by a certain surface area or Lux, was the first treatment variable studied systematically. Light boxes delivering 100-850 lux were less effective than brighter units in a series of controlled crossover studies²⁶. Later studies indicated that an overall remission rate of 75% could be achieved using fluorescent light fixtures positioned to produce

10 000 lux²⁸.

Timing

Some researches have found that morning is the most effective time for phototherapy, whereas others have found patients to respond well to light at other times of day²⁹. In accordance to the phase-shift hypothesis for winter depression, morning light that causes a circadian phase advance should be more antidepressant than evening light which causes a delay. Since no studies have found that evening light to be more antidepressant than morning light, investigations have shown either no difference³⁰ or morning light to be superior³¹.

Duration

Few studies indicated that the greater the daily duration, the greater the antidepressant effect, however, there is little published evidence that increased antidepressant effects may be achieved using greater than 2-hour light periods/day¹⁵.

Duration may also be inversely related to intensity in determining efficacy of treatment³²

Spectrum

Original studies use full-spectrum fluorescent lights, which largely reproduce the distribution and range of visible and ultraviolet light. Recent studies has discussed the comparative merits of different brands of white fluorescent lamp emitting different amounts of ultraviolet radiation but to no avail³³ although different wavelengths were demonstrated to have an effect where green light shown to be superior to others. Incandescent light sources may also be effective in the treatment of SAD³⁴.

Route of delivery

Light appears to have its therapeutic effect through the eyes and not the skin in SAD patients³⁵, even though a case report has documented the efficacy of phototherapy in a blind individual³⁶.

When properly administered, phototherapy has no known irreversible side effects. Nevertheless, overexposure to ultraviolet light might adversely affect the eyes or the skin e.g. cortical cataract as a result of excessive long-term exposure to ultraviolet light. Some patients complain of eyestrain, mild headaches, insomnia or hypomanic irritability³⁷.

Pharmacotherapy

Medications may have a role in the treatment of SAD, even though psychiatrist are aware that it is quite easy to misdiagnose SAD and treatment with conventional antidepressants often exacerbate the atypical symptoms of hypersomnia and carbohydrate craving. There have been few studies to assess how effective antidepressant drugs are in the treatment of SAD, however, the serotonin-agonist d-fenfluramine³⁸ and the Selective Serotonin Reuptake Inhibitor (SSRI) sertraline³⁹ has been found to be a promising treatment. SSRIs are used because of the close association between SAD symptoms and serotonergic neurotransmission. Recently another SSRI, fluoxetine usually used in the treatment of non-seasonal major depression⁴⁰ also found to be effective after being compared with phototherapy⁴¹.

Psychotherapy

Cognitive behaviour therapy (CBT) helps patients regain a degree of control over their symptoms consequently managing their illness more effectively. Although it may provide some long-term benefit⁴², CBT alone may not be sufficient to overcome the biological effect experienced by patients in the winter.

Treatment of summer SAD

Patients with summer depression appear to respond to traditional antidepressant medications but manipulations of the environmental stresses in summer, e.g. heat and humidity, have not yet been demonstrated to be as effective as phototherapy for winter SAD⁴³. It would be more difficult technically to perform controlled studies on the effects of environmental temperature as compared to light.

Limitations and future research

Despite the development of several theories on the aetiology of SAD and its treatment, all these have theories have limitations. The biological causes of SAD might benefit from proper family studies exploring possible genetic or familial environmental factors that might contribute the illness and their impact on society. The controversy of phototherapy still stands but as new technologies allow the delivery of light through devices other than light boxes, more sophisticated placebo controls will probably confirm the clinical and research data that already suggests that phototherapy works by more than simply a placebo effect. Formal studies of its safety, especially with long term use, may also be desirable. Summer SAD has been defined but has yet to be fully explored and whether this is a distinct diagnostic syndrome remains debatable. Lastly, more clinical trials on the potential roles of diet and cognitive therapy and the efficacy of various antidepressants in SAD have yet to be undertaken.

Conclusions

SAD is a recurrent depressive disorder occurring at particular times of the year with some atypical symptoms which include hypersomnia, hyperphagia, carbohydrate cravings and increased weight. The specific aetiology of SAD remains unclear although the neurotransmitter serotonin may play a significant part. Both phototherapy and some SSRIs (fluoxetine) produced a good antidepressant effect and were well tolerated, either alone or in combination; however, a larger sample is required to confirm an apparently better response to phototherapy.

 

References

 

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