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John Eagles is a consultant psychiatrist at Royal Cornhill Hospital (Cornhill Road, Aberdeen AB25 2ZH, UK) and an honorary reader in mental health at the University of Aberdeen. He has been assessing and treating patients with seasonal affective disorder for 10 years. His other research interests include eating disorders and suicide.
| Abstract |
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| Historical perspective on seasonal affective disorder |
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| Symptoms of winter depression |
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Many of the symptoms of winter depression are also characteristic of non-seasonal depressive episodes: low mood (albeit usually without prominent diurnal variation), loss of interest, anhedonia, anergia, poor motivation, low libido, anxiety, irritability and social withdrawal. Other symptoms occur that are much more characteristic of winter depression. About three-quarters of patients experience a significant increase in duration of sleep, while perceiving their sleep to be of poor quality. This is associated with daytime somnolence, which often peaks in the late afternoon. A similar proportion of patients experience an increase in weight and in appetite, during which cravings for carbohydrate and chocolate are frequently prominent. As described below, several of these symptoms often interact, giving rise to further deteriorations in well-being.
Onset is typically between 20 and 30 years of age, although symptoms may often be recalled much earlier in life. Winter depression does occur in children; fatigue, irritability and academic problems at school are often the presenting features.
| Differential diagnosis and comorbidity |
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As with non-seasonal depression, several conditions are not uncommonly comorbid with seasonal affective disorder. Anxiety symptoms are common concomitants of winter depression (Thompson & Isaacs, 1988) and, although estimates have varied, it seems likely that 520% of patients experience panic disorder. Patients with eating disorders, most notably bulimia nervosa, frequently experience a winter exacerbation of their symptoms (Blouin et al, 1992). Women with pre-menstrual depression report increased seasonal fluctuations in well-being, as do patients with chronic fatigue syndrome. Several studies have found high rates of comorbid personality disorders in seasonal affective disorder, although the prevalence of these diagnoses tends to reduce once patients become euthymic (Reichborn-Kjennerud et al, 1997).
| Does seasonal affective disorder exist? |
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| Epidemiology of winter depression |
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Kasper et al(1989) introduced the term sub-syndromal seasonal affective disorder (otherwise known as winter blues) to describe a milder form of the condition; their group felt this to be a useful diagnosis, since symptoms also responded to light therapy in a small trial. Inclusion of this group, however, served to further lower the bar with regard to the prevalence of treatable winter depression, giving rise to usual population rates in the Seasonal Pattern Assessment Questionnaire (SPAQ; Rosenthal et al, 1987), the most widely used screening instrument for seasonal affective disorder, in excess of 20%. That the SPAQ yields an overinclusive estimate of the prevalence of the disorder has since been demonstrated, but much of what we know about the epidemiology of seasonal affective disorder derives from SPAQ screening studies and claims of such high prevalence did little in some quarters to render the diagnosis credible. More recent studies in the UK, utilising interviews and DSMIV criteria after screened patients had fulfilled SPAQ criteria for winter depression, gave rise to estimated adult community prevalence rates of 3.5% in Aberdeen (Eagles et al, 1999) and 2.4% in North Wales (Michalak et al, 2001).
In their large study of seasonal affective disorder among North American children, Swedo et al(1995) found that the low prevalence in young children of both genders increased markedly at puberty in girls but not in boys. Rates of the disorder reach a peak among women in their reproductive years (Fig. 1
), with a decline in old age, so that the genders are again fairly evenly affected.
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| Aetiological considerations |
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Allied to this is the phase-shift hypothesis (as occurs in jetlag) described by Lewy et al(1987). The circadian rhythms of people with winter depression are seen as phase delayed with late onset of melatonin secretion, a pattern that can be corrected with morning light.
At the neurotransmitter level, serotonin has the clearest links with seasonal affective disorder. Various parameters of serotonergic function fluctuate seasonally, serotonin is linked intimately with regulation of appetite and sleep, and tryptophan depletion gives rise to worsening of symptoms in recovered patients. Evidence for the likely importance of noradrenergic mechanisms has also emerged (Neumeister et al, 1998).
Evolutionary factors might play an aetiological role. At one stage, it may have been advantageous to have been energetic and to require little sleep in the summer and to be anergic and sleepy in winter. This may have applied especially to women and their offspring, since it would be optimal to become pregnant in summer, resulting in childbirth in spring, when food is more plentiful and the weather is becoming warmer.
Eleven chapters in a book edited by Partonen & Magnusson (2001) are devoted to discussion of the pathogenesis of seasonal affective disorder.
| General aspects of the management of winter depression |
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| Symptom interactions |
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| Some principles of management |
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To my knowledge, the efficacy of psychological therapies in winter depression has not been formally evaluated. It seems unlikely, however, that the place of psychological approaches in winter depression is all that different from their place in other recurrent depressive disorders, and many of the general aspects of management already described are designed partly to promote active mastery over, as opposed to passive submission to, recurrent winter symptoms. It is interesting that Rohan et al(2003) have recently reported that trial participants with winter depression tended to have more negative automatic thoughts than controls throughout the year, and that a ruminative thinking style in autumn correlated with severity of winter symptoms. This serves to support the use of a broadly active mastery or a cognitivebehavioural model of management. Reformulating negative thoughts is often helpful. For example, sufferers tend to focus gloomily on the relative certainty with which depressions recur, rather than on the knowledge that they will remit. Most patients can be reassured that they will learn more about the management of their condition each winter, and thus manage it better during the next. It is usually helpful to regard the shortest day as something of a winning post and to know that by Christmas each day is becoming a few minutes longer.
Mild winter depression
It would probably be justifiable to classify more than half of the UK population as experiencing mild symptoms of winter depression, notably a decrease in energy, enhanced appetite and increased duration of sleep. The general principles of management discussed above suffice for what should be seen as normal seasonal fluctuation in physiological functioning at temperate latitudes.
Moderate to severe winter depression
When symptoms are sufficiently severe to interfere markedly with the ability to function socially and/or at work then, in addition to an active mastery strategy, physical treatments are indicated in the form of light therapy and/or antidepressants.
| Light therapy or antidepressants? |
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Antidepressant treatment
There is also a woeful lack of evidence on which to base antidepressant management of winter depression. Given the usual somnolent, anergic symptom profile, sedative antidepressants are usually avoided and selective serotonin reuptake inhibitors (SSRIs) (for which there is a little evidence of efficacy in this population) are the usual first choice. For most patients, SSRIs are non-sedative and, especially when taken over a period of less than 6 months, tend not to exacerbate potential weight gain. There is no logical reason to select one SSRI over another, although the small amount of evidence is for the efficacy of sertraline and fluoxetine (for a review see Thompson, 2001). If SSRIs prove unsuccessful, venlafaxine is a logical alternative, and it sometimes proves more energising. Reboxetine can have a similar effect. Less sedative tricyclics such as imipramine can be used. Counterintuitively, given its sedative properties, an open trial of mirtazapine found it to be efficacious and well tolerated (Hesselmann et al, 1999).
In patients with established winter recurrences, it is usual to instigate treatment as soon as symptoms re-emerge in the autumn and to phase out treatment in spring. For patients who also experience non-seasonal episodes, year-round prophylaxis may be deployed, sometimes regularly increasing the antidepressant dose during the winter months.
Light therapy
Efficacy
Some of the evidence for the efficacy of light therapy in winter depression can be criticised on the grounds that placebo-controlled trials have been conducted on knowledgeable, often self-diagnosed subjects who could not have been blind to treatment allocation and anticipated improvement with bright light. It is also difficult to envisage many interventions more likely to exert a placebo effect than spending time each day sitting in front of a bright light source. Given these considerations, several well-designed trials have found light therapy to be significantly beneficial for winter depression, and the best evidence of efficacy is that bright light in the mornings is more helpful than bright light in the evenings (Lewy et al, 1998). This also underlines the logic of the phase-shift hypothesis mentioned above. Thompsons (2001) meta-analysis concluded that treatment with a lightbox in seasonal affective disorder had a number needed to treat of between 4 and 5, which compares well with many medical interventions.
Predictors of outcome
Features associated with a good response to light therapy include hypersomnia, increased appetite, winter weight gain and complete remission of symptoms in summer. Factors that have been found, less predictably, to correlate with better outcomes include feeling worse in the morning (possibly a phase-shift phenomenon), young age and eating a lot of sweet foodstuffs late in the day.
Timescales of response and treatment
If light therapy is to prove successful, response often commences within days and is usually apparent by the end of week one. In general, if there has been no response in the first 3 weeks (given adequate adherence to treatment), then a subsequent response is unlikely. For this reason, it is appropriate that some lightbox suppliers have a sale or return policy within 3 weeks of initial purchase. If light therapy is effective, then usually it can be discontinued for a few days (e.g. during a weekend away from home) without too many deleterious effects.
It is usually advisable, especially if patients are buying their own lightbox, to advocate that light therapy commences for the first time only once symptoms are clearly present; only then can effectiveness be assessed. However, in future winters, patients who respond to light therapy should usually start treatment as soon as the first symptom emerges. Although it has not been evident in my own clinical practice, light therapy prior to the onset of symptoms might prevent a winter episode of depression (Partonen & Lonnqvist, 1996). Light therapy is usually phased out gradually in spring, often round about the time the clocks change, but this will depend on previous timing of symptom offset and current well-being.
Light and exercise
The benefits of winter exercise outdoors have been mentioned already. Leppamaki et al(2002) described a possible adjunctive effect of exercise and bright morning light. For patients with winter depression, this would generally comprise exercising on a treadmill or stationary bicycle while using a lightbox or light visor.
Side-effects of light therapy
Headaches and blurred vision are the most commonly reported adverse effects, occurring in up to 20% of patients. Feeling wired (anxiously energetic as if after too much caffeine) is also fairly common. Rarely, hypomania may be precipitated. If used too late in the day, especially in people who are responders to light therapy, insomnia may well be induced. Light therapy might cause problems for patients on potentially photosensitising medication such as chlorpromazine, lithium or St Johns Wort. People with pre-existing retinitis pigmentosa or macular degeneration are advised to have an opthalmological examination before treatment, although there are no known cases of opthalmological damage attributable to light therapy. There is, however, one recent report (Swiecicki & Szafranski, 2002) of possible serotonin syndrome when used in tandem with SSRIs.
Light therapy in other phase-shifted conditions
The use of light therapy in jetlag, sometimes in combination with melatonin, is quite well accepted. It has also been used effectively in delayed sleep phase disorder (common in adolescence), and timed bright light can enhance adaptation to shift work. In older people with dementia, dawn and/or dusk simulation (see below) can improve disturbed sleep/wake cycles.
| How should a lightbox be used? |
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Box 1 Practical aspects of light therapy for winter depression
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| Which lightbox? |
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Alternatives to lightboxes
Desk lamps and small lightboxes are frequently used at work for those requiring longer or less bright exposure. Two other alternatives to lightboxes are light visors and dawn-simulating alarm clocks.
Rechargeable light visors are similar to baseball caps with small light sources in the brim shining into the wearers eyes. Older versions were rather heavy and cumbersome, but more recent designs are more comfortable to wear. Visors can be useful when it is impractical to sit still in front of a lightbox, perhaps most commonly among mothers of young children. Although anecdotal accounts of the efficacy of light visors are very often positive, the research evidence to support their use is not compelling.
There is more evidence to support the effectiveness of dawn-simulating alarm clocks. These come on at dim illuminance and gradually increase in brightness over a period of 30 to 90 minutes leading up to the persons normal wakening time. A study by Avery et al(2001) found them to be more efficacious in patients with winter depression and hypersomnia than lightboxes or placebo (dim red) dawn-simulating alarm clocks. This may relate partly to the difficulties that depressed, oversleeping patients sometimes encounter in complying adequately with 30 minutes of morning lightbox therapy; dawn-simulating alarm clocks require less energy and commitment. In our own service, we have been lending dawn-simulating alarm clocks to patients with established seasonal affective disorder, usually as an adjunct to lightboxes, and they usually report wakening feeling more refreshed and alert. Some of these alarm clocks also simulate dusk, through a reciprocal dimming down function that can be useful for those who have difficulty falling asleep. Dawn-simulating alarm clocks are of much lower illuminance than lightboxes and, given their use while patients are asleep, a great deal less light enters the eyes. It is hypothesised that they exert their therapeutic effects because the light stimulation occurs at a particularly sensitive point on humans light-phase response curve, as we are especially reactive to changes in light levels around dawn.
| Multiple choice questions |
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| References |
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Avery, D. H., Elder, D. N., Bolte, M. A., et al (2001) Dawn simulation and bright light in the treatment of SAD: a controlled study. Biological Psychiatry, 50, 205216.[CrossRef][Medline]
Blouin, A. G., Blouin, J. H., Aubin, P., et al (1992) Seasonal pattern of bulimia nervosa. American Journal of Psychiatry, 149, 7381.
Eagles, J. M., Wileman, S. M., Cameron, I. M., et al (1999) Seasonal affective disorder among primary care attenders and a community sample in Aberdeen. British Journal of Psychiatry, 175, 472475.
Eagles, J. M., Howie, F. L., Cameron, I. M., et al (2002) Use of health care services in seasonal affective disorder. British Journal of Psychiatry, 180, 449454.
Hesselmann, B., Habeler, A., Praschak-Reider, N., et al (1999) Mirtazapine in seasonal affective disorder (SAD): a preliminary report. Human Psychopharmacology, 14, 5962.
Kasper, S., Rogers, S. L. B., Yancey, A., et al (1989) Phototherapy in individuals with and without subsyndromal seasonal affective disorder. Archives of General Psychiatry, 46, 837844.[Abstract]
Leppamaki, S., Partonen, T. & Lonnqvist, J. (2002) Bright-light exposure combined with physical exercise elevates mood. Journal of Affective Disorders, 72, 139144.[Medline]
Lewy, A. J., Sack, R. L., Miller, L. S., et al (1987) Antidepressant and circadian phase-shifting effect of light. Science, 253, 352354.
Lewy, A. J., Bauer, B. K., Cutler, N. L., et al (1998) Morning vs evening light treatment of patients with winter depression. Archives of General Psychiatry, 55, 890896.
Magnusson, A. (2000) An overview of epidemiological studies on seasonal affective disorder. Acta Psychiatrica Scandinavica, 101, 176184.[CrossRef][Medline]
Magnusson, A. & Stefansson, J. G. (1993) Prevalence of seasonal affective disorder in Iceland. Archives of General Psychiatry, 50, 941946.[Abstract]
Mersch, P. P. A., Middendorp, H. M., Bouhuys, A. L., et al (1999) Seasonal affective disorder and latitude: a review of the literature. Journal of Affective Disorders, 53, 3548.[CrossRef][Medline]
Michalak, E. E., Wilkinson, C., Dowrick, G., et al (2001) Seasonal affective disorder: prevalence, detection and current treatment in North Wales. British Journal of Psychiatry, 179, 3134.
Michalak, E. E., Wilkinson, C., Hood, K., et al (2003) Seasonality, negative life events and social support in a community sample. British Journal of Psychiatry, 182, 434438.
Neumeister, A., Turner, E. H. Matthews, J. R., et al (1998) Effects of tryptophan depletion vs catecholamine depletion in patients with seasonal affective disorder in remission with light therapy. Archives of General Psychiatry, 55, 524530.
Partonen, T. & Lonnqvist, J. (1996) Prevention of winter seasonal affective disorder by bright-light treatment. Psychological Medicine, 26, 10751080.[Medline]
Partonen, T. & Magnusson, A. (eds) (2001) Seasonal Affective Disorder: Practice and Research. Oxford: Oxford University Press.
Reichborn-Kjennerud, T., Lingjaerde, O. & Dahl, A. A. (1997) DSMIII personality disorders in seasonal affective disorders: change associated with depression. Comprehensive Psychiatry, 38, 4348.[Medline]
Rohan, K. J., Sigmon, S. T. & Dorhofer, D. M. (2003) Cognitive-behavioral factors in seasonal affective disorder. Journal of Consulting and Clinical Psychology, 71, 2230.[Medline]
Rosenthal, N. E., Sack, D. A., Gillin, J. C., et al (1984) Seasonal affective disorder: a description of the syndrome and preliminary findings with light therapy. Archives of General Psychiatry, 41, 7280.[Abstract]
Rosenthal, N. E., Genhart, M., Sack, D. A., et al (1987) Seasonal affective disorder: relevance for treatment and research of bulimia. In Psychology of Bulimia (eds J. I. Hudson & H. G. Pope), pp. 205208. Washington, DC: APA.
Swedo, S. E., Pleeter, J. D., Richter, D. M., et al (1995) Rates of seasonal affective disorder in children and adolescents. American Journal of Psychiatry, 152, 10161019.
Swiecicki, L. & Szafranski, T. (2002) Side effects after phototherapy implementation in addition to fluoxetine or sertraline treatment: a report of two cases. World Journal of Biological Psychiatry, 3, 109111.
Thompson, C. (2001) Evidence-based treatment. In Seasonal Affective Disorder: Practice and Research (eds T. Partonen & A. Magnusson), pp. 151158. Oxford: Oxford University Press.
Thompson, C. & Isaacs, G. (1988) Seasonal affective disorder in a British sample: symptomatology in relation to mode of referral and diagnostic sub-type. Journal of Affective Disorder, 14, 111.[CrossRef][Medline]
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