SAD schmad : Is seasonal affective disorder a valid construct?

The diagnosis of seasonal affective disorder (SAD) refers to a variant of recurrent depression in which episodes reliably fall in a particular season, typically winter. The construct of SAD subsumes multiple hypotheses including the following: (1) a subtype of recurrent depression is caused by decreased environmental light in winter (with the corollary that locales with greater seasonal variation in daylength should show more SAD), (2) this subtype is specifically responsive to artificial bright light, potentially through circadian mechanisms and (3) full-blown SAD is a pathological variant of a community-wide phenomenon of lowered mood in the darker relative to the lighter months.

Empirically, the SAD construct has been challenged from a number of perspectives. Early research brought SAD under the umbrella of psychological models of depression by showing associations between seasonality and neuroticism/external locus of control (Murray et al., 1995). Studies showing that light is not superior to antidepressants or cognitive behavioral therapy (CBT) in the treatment of SAD further challenge the construct’s divergent validity. There is evidence that the key self-report instrument in this area has limited criterion validity and generates inflated prevalence estimates (Murray, 2003). One of the most intriguing deductions from the SAD construct – the latitude hypothesis – has never been strongly supported. SAD/seasonality is sometimes conceptualised as particularly associated with the bipolar disorder diagnosis, but again, the data are not compelling (Murray et al., 2013).

Most recently, Traffanstedt et al. (2016) investigated the SAD construct through a cross-sectional analysis of a large (N = 34,294) general population survey across 36 US states. Taking advantage of the variety of dates and locales of assessment, regression analyses were conducted to investigate links between SAD-related variables and scores on the eight-item Patient Health Questionnaire (PHQ-8) depression scale. Regression analyses found no significant associations for any of season, latitude, season × latitude or daylight hours, nor were these predictors significant in the sub-sample who met criteria for depression on the PHQ-8 (N = 1754). Traffanstedt argue that any clinically significant effects of SAD/seasonality should have been found with such well-powered analyses. Noting some of the issues above, the authors conclude that it is time to consider removing the seasonal pattern modifier of depression.

There are strong a priori grounds for scepticism about the SAD construct. First, entrenched cultural associations with the seasons will tend to skew expectations towards winter pattern mood variation, such that self-report and clinician perspectives are likely unreliable in this area. Second, any depressogenic effect of daylength on mood would have to be remarkably powerful for it to be measureable at the level of individual mood changes, given that (1) the daylength variable is so remote from the putatively proximal variable of light hitting the eyes of the populace in a given locale and (2) it must compete with the world of recognised non-daylength moderators of mood. Indeed, Diagnostic and Statistical Manual of Mental Disorders (DSM) has never recognised a distinct light-related subtype of depression, instead recognising the possibility that seasons may moderate the likelihood of an episode of recurrent depression in some cases.

The author agrees with Traffanstedt and others that the validity of the SAD construct remains questionable. Future research should attend to inherent methodological challenges, including measurement of a multi-year pattern of mood variation, addressing placebo response to light, etc. By parsing the various hypotheses linked to SAD, we may find some ideas more fruitful than others. For example, SAD has encouraged new interest in subcortical mechanisms (circadian function, light pathways, sleep, activation rhythms) in mood disorders (e.g. Malhi and Kuiper, 2013). Arguably, this evolutionary approach offers an important counter-point to dominant cognitivism/corticalism in psychology/neuroscience.

Conclusion

A central motivation for SAD was the observation that human biology remains connected to nature’s rhythms. While this observation is an important reminder that complex behaviours rest on a more primitive ostinato, it is proving difficult to demonstrate in the seasonal distribution of mood episodes.