Abstract
There is a growing interest in personalized and preventive medicine initiatives that leverage serious patient engagement, such as those initiated and pursued among participants in the quantified-self movement. However, many of the self-assessments that result are not rooted in good scientific practices, such as exploiting controls, dose escalation strategies, multiple endpoint monitoring, etc. Areas where individual monitoring and health assessments have great potential involve sleep and behavior, as there are a number of very problematic sleep and behavior-related conditions that are hard to treat without personalization. For example, winter depression or seasonal affective disorder (SAD) is a serious, recurrent, atypical depressive disorder impacting millions each year. In order to prevent yearly recurrence antidepressant drugs are used to prophylactically treat SAD. In turn, these antidepressant drugs can affect sleep patterns, further exacerbating the condition. Because of this, possibly unique combinatorial or 'polypharmaceutical' interventions involving sleep aids may be prescribed. However, little research into the effects of such polypharmacy on the long-term sleep quality of treated individuals has been pursued. Employing wireless monitoring in a patient-centered study we sought to gain insight into the influence of polypharmacy on sleep patterns and the optimal course of therapy for an individual being treated for SAD with duloxetine (Cymbalta) and temazepam. We analyzed continuous-time sleep data while dosages and combinations of these agents were varied. We found that the administration of Cymbalta led to an exacerbation of the subject's symptoms in a statistically significant way. Further, we unmasked and monitored treatment effects on a latent obstructive sleep apnea condition. We argue that such analyses may be necessary to effectively treat individuals with similar overall clinical manifestations and diagnosis, despite their having a unique set of symptoms, genetic profiles and exposure histories. We also consider the limitations of our study and areas for further research.
Highlights
Winter depression or seasonal affective disorder (SAD) is an atypical depressive disorder that in most cases has onset in fall or winter with remission in spring or summer
The dataset was not balanced in the sense that we had different numbers of observations while the subject was on different dosages of a drug
Similar figures for the number of times the subject was awakened, time to REM sleep, percent time after sleep onset that the subject was awake and percent time in REM sleep during 5-minute intervals detected by the Zeo Sleep Monitor are presented in the Supplementary Material (Figure S1–Figure S4, respectively)
Summary
Winter depression or seasonal affective disorder (SAD) is an atypical depressive disorder that in most cases has onset in fall or winter with remission in spring or summer. It is estimated that approximately 5–10 percent of people in the U.S (i.e., 10–20 million people) experience varying degrees of SAD in a given year[1]. While full syndromal SAD (frequently dependent on additional external negative stressors) is not reached every year, subsyndromal symptoms can be seen[2]. These symptoms are multiple, and include varying degrees of hypersomnia, carbohydrate-craving and jet-lagged physical and mental states (what is known as “brain fog”) resulting in fatigue and irritability. SAD is a complex disease with both chronobiological and neurobiological underpinnings[7,8,9,10,11], which may include an etiology that for some could even begin in utero[12,13,14,15,16]
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