In the second century Aretaeus advised that “lethargics are to be laid in the light, and exposed to the rays of the sun for the disease is gloom”.¹ In the region of 90% of the general population experience some degree of seasonal influence on their mood. Feeling a bit miserable, less energetic and eating more during the winter is normal and many would at least partly identify with this. In order to be diagnosed with seasonal affective disorder (SAD) an individual must meet the criteria for a major depressive episode, lasting two or more weeks, which can be categorised as mild, moderate or severe. It is estimated that 4-6% of the population experience SAD.²

Symptoms of SAD include low mood, fatigue and loss of libido. Rather than the typical biological symptoms of insomnia or loss of appetite, a patient with SAD will typically experience hypersomnolence, hyperphagia, carbohydrate craving and weight gain.³ Along with sleep deficits, those with SAD have been shown to have much more frequent nightmares.⁴ Sub-syndromal seasonal affective disorder is a less severe version of SAD. It does not meet the criteria for SAD but nonetheless represents a significant change for the individual. 

Seasonal affective disorder was first recognised as a ‘seasonal pattern’ in mood disorders in the Diagnostic and Statistical Manual of Mental Disorders in 1987.⁵ The operative criteria have changed considerably since then. SAD was included as a specifier for recurrent major depressive disorder in the DSM-4. The DSM-5 working group debated whether SAD should be counted as a disorder in itself or remain as a specifier.⁶ SAD is currently included as a depressive disorder with seasonal pattern in DSM-5. It does not specify whether it is more likely to occur in unipolar or bipolar depression.⁷ In the ICD-10 it is classified under major depressive disorder, recurrent, which includes recurrent episodes of seasonal depressive disorder.⁸ In the past SAD could only be diagnosed in the absence of non-seasonal depression but it has since been accepted that someone may suffer from both at various points in their lifetime.

The Seasonal Pattern Assessment Questionnaire (SPAQ) is a self-rating questionnaire that is sometimes used to assess for seasonal affective disorder.⁹ A global seasonality score is calculated from this. An average score for those without SAD is five. An average score for those with SAD is 16. This questionnaire has been perceived as somewhat over-inclusive and therefore the seasonal health questionnaire has been developed. This is thought to have better sensitivity and specificity that the SPAQ. It uses the four main operational criteria of the SPAQ and is easier for patients to complete.¹⁰

Non-seasonal depression?

SAD is different from non-seasonal depression as it is characterised by the predictable onset of a major depressive episode during a certain season. In some parts of the world it is most common around the winter solstice, from December to February.¹¹ In others it begins in late autumn and extends into the winter months.¹² A much less common form involves patients experiencing recurrent depressive or manic episodes during the summertime.¹³ This pattern of onset and remission of episodes must occur over a two year period at least. In addition, the seasonal depressive episodes must substantially outnumber any non-seasonal depressive episodes over the individual’s lifetime.⁷ This does not apply to those situations in which the pattern is better explained by seasonally-linked psychosocial stressors, such as seasonal unemployment. 

Why should it matter to non-psychiatric physicians?

Seasonal affective disorder results in significant social impairment that is comparable to that of major depressive disorder and is considerably worse than that of community samples. SAD also increases risk of suicide.¹⁴ Cognitive processes may also be affected. A study by the University of Alaska over a five year period showed hospital medication errors to be almost twice as likely in December than in September.¹⁵ In a study by Mersch et al those with SAD were found to be on sick leave or in unemployment much more often than those without SAD.¹⁶ SAD is also associated with an increased risk of physical illness. One Finnish study looked at the relationship between major non-communicable diseases (NCDs) and seasonal affective disorder as Finns are particularly predisposed to SAD given the intense seasonal temperature and daylight fluctuations. A significant relationship between SAD, cardiovascular disease, respiratory disease and diabetes was found.¹⁷

Aetiology

There are several hypotheses regarding the aetiology of SAD. Changing photoperiod can result in circadian phase delay, increased melatonin synthesis and vitamin D deficiency. Melatonin synthesis is triggered by darkness. The pineal gland then uses serotonin to synthesise melatonin. Patients with SAD have higher levels of daytime melatonin in the winter than those without SAD resulting in lethargy.¹⁸ Light therapy has been shown to suppress melatonin synthesis during the day, which in turn can reduce SAD symptoms.¹⁹

The phase-shift hypothesis states that there may be hormonal changes other than melatonin affected by the change in circadian rhythm. This is partly supported by the finding that minimum nocturnal body temperature is delayed by two hours in those with SAD.²⁰ Serotonergic system dysregulation is consistent with theories for other affective disorders and bulimia nervosa. Given that serotonin is involved in melatonin synthesis it is plausible that serotonin depletion results in SAD. Patients with SAD may be self-medicating by eating excessive carbohydrate-rich foods which contain tryptophan, an essential component in the synthesis of serotonin.²¹ Less exposure to daylight may result in vitamin D deficiency,²² which can result in depressive symptoms.²³ Associations between these hypotheses are certainly evident and causal links are still being investigated.

Risk factors

Females are at greater risk of SAD than males.²⁴ A study by Swedo et al on 2,000 children found that there is a divergence in rates of SAD between males and females at puberty.²⁵ SAD is more common in young people.²⁶ Those who live in northern latitudes are at greater risk.²⁷ The prevalence in northern latitudes, which is estimated to be approximately 10%,²⁸ is thought to be much higher due to the sharper contrast between the seasons and lower levels of sunlight in the winter. While the overall prevalence in the US is 5%,²⁹ this varies from 1% of those who live in Florida versus 9% who live in Alaska.³⁰

Those with family histories of depression, bipolar disorder or SAD are at a higher risk.³¹ Evening chronotype is also thought to be a risk factor. Those who are more active in the evening are likely to have more sleep problems and to suffer more from circadian phase delay. 

Differential diagnosis and overlap

There has been much debate as to whether SAD is a bipolar variant. Similarities between bipolar affective disorder (BPAD) and SAD include atypical depressive symptoms, high recurrence rate, predictable season of recurrence and the need to assess for mania in both disorders.³² Some studies have found patients with BPAD to have an intermediate seasonality score on the SPAQ.³³ Studies of depressed patients have found that those with more severe forms of SAD are more likely to have bipolar affective disorder, particularly BPAD type 2.^34,35,36

Depressive symptoms are common in chronic fatigue syndrome (CFS).³⁷ While SAD and CFS have mutually exclusive criteria, one study showed that almost a quarter of patients with CFS show a SAD-like pattern.³⁸ A study by Terman et al found that a subgroup of patients with CFS showed high seasonality, low mood, hypersomnia and hyperphagia. These patients may benefit from similar treatments to SAD.³⁹ A study by Lam found that two patients diagnosed with CFS actually had SAD and subsequently benefited from light therapy.⁴⁰

SAD can be comorbid with other psychiatric illnesses including bulimia nervosa, depression, generalised anxiety and panic disorder.^41,42 SAD is particularly over represented in those with bulimia nervosa and serotonergic dysfunction and is thought to be the underlying cause for both disorders.⁴³

Management

Selective serotonin reuptake inhibitors (SSRIs) are the first-line treatment in seasonal affective disorder. Patients have been found to respond particularly well to fluoxetine, which has equal tolerability and cost-effectiveness as compared to light therapy.⁴⁴ Winter depression responds well to monoamine oxidase inhibitors (MAOIs)⁴⁵ including moclobemide⁴⁶ and tranylcyromine,⁴⁷ while summer depression responds better to first-line antidepressants. The effectiveness of bupropion has also been demonstrated in SAD.⁴⁸ Despite SAD being understood as a possible bipolar II variant, there is little evidence for mood stabilisers apart from lamotrigine, which is a useful augmentation agent.⁴⁹ In terms of adjunctive treatments melatonin supplementation may be useful in improving sleep by advancing the circadian phase delay.⁵⁰ Vitamin D supplementation may be useful in alleviating depressive symptoms.⁵¹ Tryptophan is useful in slowing down rates of relapse when added to light therapy.⁵²

Light therapy acts as a form of rhythm therapy in advancing circadian phase delay and thereby resetting the abnormal sleep/wake pattern of melatonin release in those with SAD. Typically the patient is expected to sit in front of a 10,000-lux light box starting at 10-15 minutes per session and increasing this to 30 minutes. The recommended maximum duration is 90 minutes.⁵³ Improvements should be seen within three to four weeks. The main side-effects include eye strain, headache and rarely hypomania. The main limitation in proving the efficacy of light treatment is the lack of a credible placebo treatment. The most compelling evidence stems from trials that have found bright light to be more effective when administered in the morning than in the evening.⁵⁴ This supports the idea that those with SAD have circadian phase delay and that bright morning light promotes a phase advance.⁵⁵

A study by Avery et al found that dawn-simulating alarm clocks out-performed 30 minutes of bright early morning light with a standard light box. However, this was most likely related to treatment adherence with the light box.⁵⁶ This year, a group of high school students in Cambridge, Massachusetts, one of whom suffers with SAD, developed Lifelight, a form of phototherapy that looks like a normal window covering and therefore feels more natural for the user.⁵⁷ A vacation to somewhere sunny in the winter may of course be of benefit as well and this should be encouraged prophylactically in those with established SAD.⁵⁸

Cognitive behavioural therapy (CBT) has somewhat less of an evidence base in seasonal affective disorder than light therapy. CBT can help those with SAD to reinterpret their feelings of low mood and fatigue. A randomised trial by Rohan et al looked at the difference in outcomes between six weeks of twice weekly 90 minute CBT-SAD in group format versus six weeks of light therapy for 30 minutes each morning. Scores improved significantly and comparably with CBT-SAD and light therapy on both scales.⁵⁹ Interpersonal psychotherapy also has an evidence base for SAD.⁶⁰ Interpersonal and social rhythm therapy is a treatment developed for bipolar affective disorder that looks at how the circadian rhythm is affected by daily routine and social roles. Given the overlap with chronic fatigue syndrome, somatic therapy combined with psychotherapy has also been found to be useful.⁶¹ This essentially involves recognition and release of physical tension through different techniques. Morning exercise is also thought to be beneficial in SAD. Wirz-Justice et al found improvement in SAD sufferers after only one week of outdoor walks for an hour each morning.⁶²

Conclusion

Seasonal affective disorder requires the diagnosis of a major depressive episode that recurs during a certain season over a period of at least two years. While SAD is still categorised as a specifier for major depressive disorder, there has been much debate as to whether SAD should be counted as a separate disorder in its own right. More research on SAD as a bipolar variant is also being conducted. SAD has significant associations with other psychiatric and physical illnesses as well as social implications for the patient. There is no definite aetiology as yet but there are numerous hypotheses which may indeed be linked. Management includes traditional treatments for non-seasonal depression such as antidepressant therapy and CBT. However, there is also a good evidence base for light therapy, supplementation agents, social rhythm and somatic therapy.

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