Research paperPrediction of outcome of bright light treatment in patients with seasonal affective disorder: Discarding the early response, confirming a higher atypical balance, and uncovering a higher body mass index at baseline as predictors of endpoint outcome
Introduction
Seasonal affective disorder, winter type (SAD), consists of recurrent Major Depressive episodes that occur primarily in the fall and winter and remit spontaneously in spring and summer (Magnusson, 2000, Rosenthal et al., 1984). It presents predominantly with āatypicalā symptoms of increased sleepiness and appetite, carbohydrate craving, weight gain, and decreased energy. Bright light treatment is a safe and effective treatment for SAD (Eastman et al., 1998, Lewy et al., 1998, Rosenthal et al., 1984, Terman et al., 1998), although there is disagreement regarding its effect size, ranging from small-moderate (Martensson et al., 2015) to large (Golden et al., 2005). For instance, a pooled analysis revealed that nearly half (47%) of all patients with SAD, and 57% of those with moderate to severe symptoms, did not fully remit (Terman et al., 1998). In addition, as we have reported, for a sizable proportion of patients, response to light is incomplete compared with the degree of spontaneous improvement in the summer (Postolache et al., 1998).
SAD appears to be an expression of a dual vulnerability, first for chronobiological dysregulation, and second for mood dysregulation (Lam et al., 2001b, Young et al., 1991). The evidence for chronobiological vulnerabilities in SAD patients includes circadian and photoperiodic dysregulation (Lewy et al., 1998, Lewy et al., 1987b, Roecklein et al., 2009, Wehr et al., 2001, Zhang et al., 2015). Consistent with addressing this chronobiologic vulnerability, light treatment shifts the circadian rhythms (Lewy et al., 1987a) and utilizes the machinery of the circadian system to decrease the duration of nocturnal melatonin (Wehr, 2001). Evidence for mood dysregulation vulnerabilities includes an increased seasonal variation in serotonin transporter binding in patients with SAD (Mc Mahon et al., 2016) returning to baseline following light treatment (Tyrer et al., 2016a, Tyrer et al., 2016b), and the reversal of tryptophan (i.e. serotonin) and catecholamine depletion by the successful antidepressant effect of light in SAD (Neumeister et al., 1998). Furthermore, light treatment has demonstrated an antidepressant effect not only in seasonal, but also in non-seasonal depression (Lam et al., 2016), and has a rapid onset of improvement in the depression scores, perhaps from the first light session (Virk et al., 2009). Thus, light treatment effects are very likely mediated not only by chronobiological mechanisms.
There are certain similarities between seasonal behavioral and physiological changes, particularly concerning metabolic regulation/dysregulation, between patients with SAD and seasonal animals. For instance, many animals show marked seasonal changes in adiposity (Bartness et al., 2002). Similarly, patients with SAD manifest considerable seasonal variation in their body weight (Cizza et al., 2005). As well, timed exposure to light in photoperiodic mammals can alter their seasonal adiposity (Bartness et al., 2002), which is comparable to the decreased appetite and weight-loss that is often associated with bright light treatment (Rosenthal et al., 1987b) and appears to consistently reduce appetite independent of the seasonal changes in mood (Danilenko et al., 2013). Light treatment also improves the control of eating in patients with comorbid bulimia (Lam et al., 2001a), and Night Eating Syndrome (Friedman et al., 2006, McCune and Lundgren, 2015). Conversely, certain atypical symptoms of depression such as hyperphagia and hypersomnia, predict the response to light (Lam, 1994, Nagayama et al., 1991, Terman et al., 1996).
We had previously reported that improvement of atypical depressive symptoms after one hour of bright light treatment correlated with improvements after two weeks of therapy (Sher et al., 2001). However, the study limitations included such taking place with subjects in a Positron Emission Tomography (PET) scanner, lack of controls, short duration (of only two weeks), and a small sample size.
The primary hypothesis was that changes in depression scores after first bright light treatment session, which we previously reported to significantly improve mood (Reeves et al., 2012), and changes in depression scores with a full course of daily bright light treatment will be positively correlated. Given the metabolic issues implicated in SAD, we also hypothesized that atypical depression symptoms and BMI at baseline would predict treatment outcome.
Section snippets
Participants
The participants were 18ā64 years of age with mean age (SD) of 44.5 (10.3) years, with 33 women (42%) and 45 men (58%), who met criteria for current diagnosis of SAD, winter type and the necessary severity of depression criteria by Structured Interview Guide for Hamilton Depression Rating Scale-Seasonal Affective Disorder Version (SIGH-SAD, Williams et al.,1994). Fig. 1 is a flow chart showing the number of participants involved from the initial telephone screening to the end of the study.
We
Results
In response to ads and flyers 925 patients responded, of which 78 patients were included in the analysis, of which 65 completed the study and 13 withdrew (See Fig. 1). Twenty-seven participants were obese (34.6%), 25 participants were overweight (32.1%) and 26 participants' BMI was within normal limits (33.3%).
Discussion
We did not confirm a hypothesized positive association between improvement after first session of bright light exposure and a full course of daily bright light treatment, as Sher et al. (2001) had previously reported (Sher et al., 2001). The most likely explanation is that the high expectations in the PET scanner and the lack of a control light could have led to nonspecific factors of improvement, a component of every antidepressant treatment. These potentially intercorrelated components may
Role of the funding source
This work was supported by the National Institute of Mental Health (NIMH), National Institute of Health (NIH), Bethesda, Maryland (PI Postolache) [1R34MH073797-01A2]. Dr. Reeves was funded by the NIH [1K12RR023250-01]. Additional support was received from the University of Maryland General Clinical Research Center Grant [M01 RR016500], General Clinical Research Centers Program, and National Center for Research Resources (NCRR) NIH.
Institutional review board
Of the University of Maryland School of Medicine.
Acknowledgement
The authors would like to thank the following: Bahar Khabazghazvini, MD, Monika Acharya, MD, and Dipika Vaswani, MD for their contributions to recruitment, data and literature management. Additionally, Aline Dagdag, RN, and Alexandra Realka Dagdag, are acknowledged for their help with the proofs of the article.
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