Seasonal Affective Disorder: Practice and ResearchEdited by:
- T. Partonen &
- A. Magnusson
During the dark days of the year in temperate and polar zones, many people would acknowledge that they feel a little sluggish, eat and sleep more than they do in summer, don't feel like socializing and can find it hard to concentrate at work. These symptoms are part of a continuum that ranges in the general population from no effects at all to full-blown SAD — seasonal affective disorder, or winter depression.
SAD was originally defined in 1984 by Norman Rosenthal and colleagues as the occurrence in autumn and/or winter of at least two episodes of serious depression, which disappear in the spring and summer, and where there are no clear-cut, seasonal, psychosocial precipitating factors. The same article also described what has become the treatment of choice — light therapy.
SAD has aroused a great deal of interest both in the general public and among scientists interested in biological rhythms, specifically the influence of the light–dark environment on human physiology and behaviour. Its description has led to a plethora of publications and the creation of a Society for Light Treatment and Biological Rhythms. The field has expanded to include other disorders related to abnormal rhythms and the mechanisms of action of light treatment. Timo Partonen and Andres Magnusson have contributed substantially to the field and are well placed to present the clinical and basic findings.
From a clinical point of view, the book provides clear descriptions of the syndrome, recommends treatment strategies and evaluates the pros and cons of different times and durations of light treatment, the possible influence of the spectral composition of the light and caveats regarding unsuitable patients. Pharmacological treatment of SAD has been successful, particularly with drugs that selectively inhibit the uptake of the neurotransmitter serotonin and the newer dual-action antidepressants, which act on both the serotoninergic and catecholaminergic systems. More interesting, however, are the attempts to summarize current knowledge about the placebo component of light treatment — which is apparently very large — and its mechanisms of action, possibly through new light-receptor systems in the retina.
The original theory about the origin of SAD brought together animal seasonal biology and human psychiatric research. The photoperiod (day length) affects seasonal events such as reproduction and coat growth in many species. In the body, photoperiodic information is translated as changing patterns of the secretion of melatonin. In animals, melatonin, the 'hormone of darkness', is secreted for longer during the long nights of winter than in the summer. Humans exposed to artificially long or short nights and days also show altered patterns of melatonin secretion. Artificially increasing the length of exposure to bright light to match that of a summer day curtails melatonin secretion in winter. Thus, reasoning that extended secretion of melatonin could be the signal for the onset of winter depression, patients were treated with bright white light in the morning and evening, with considerable therapeutic success.
This theory has never been fully upheld, however, as light treatment works when given at other times of day. To date, no one has shown that a shortening of the melatonin profile is the direct cause of therapeutic benefit. An offshoot of this approach has been some very interesting observations on human seasonality and response to exposure to artificial and natural light.
The book describes several other theories about the action of light. Light treatment given in the morning seems to be somewhat more effective than at other times of day and is usually associated with a shift to earlier timing of at least part of the internal circadian clock. This finding has led to the 'phase shift hypothesis'. There is even some evidence that treatment with melatonin itself, in such a way as to advance the clock, can have therapeutic benefit, but this requires confirmation.
Light treatment does not work if serotonin levels in the brain are depleted by reducing the availability of the amino acid tryptophan from which it is synthesized. These recent observations add substance to the presumed involvement of serotonin in SAD. And there seems to be a genetic component to SAD that may be associated with variations in serotoninergic systems. These early data suggest that some aspects of SAD may be shared in part with other psychiatric disorders.
Although light treatment is widely prescribed and the necessary equipment can easily be obtained from recommended suppliers, there remains some doubt as to how much of the result is real, and how much is due to a placebo effect.
Specialists will find much of interest in this compendium. Inevitably, some information is already out of date; however, most chapters have used publications up to 2001. But the controversy regarding whether or not extra ocular light affects human rhythms does not receive sufficient critical attention. As with all multi-author books, the writing style is uneven, and there is frequent repetition of data in different chapters; in places — most notably chapter 18 — there is also evidence of scant attention to proofreading. In general, however, I found it concise, easy to read and useful.