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BACKGROUND/OBJECTIVES: Inner-city Black women may be more susceptible to post-traumatic stress disorder (PTSD) than White women, although mechanisms underlying this association are unclear. Living in urban neighborhoods distinguished by higher chronic stress may contribute to racial differences in women’s cognitive, affective, and social vulnerabilities, leading to greater trauma-related distress including PTSD. Yet social support could buffer the negative effects of psychosocial vulnerabilities on women’s health. METHODS/DESIGN: Mediation and moderated mediation models were tested with 371 inner-city women, including psychosocial vulnerability (i.e., catastrophizing, anger, social undermining) mediating the pathway between race and PTSD, and social support moderating psychosocial vulnerability and PTSD. RESULTS: Despite comparable rates of trauma, Black women reported higher vulnerability and PTSD symptoms, and lower support compared to White Hispanic and non-Hispanic women. Psychosocial vulnerability mediated the pathway between race and PTSD, and social support moderated vulnerability, reducing negative effects on PTSD. When examining associations by race, the moderation effect remained significant for Black women only. CONCLUSIONS: Altogether these psychosocial vulnerabilities represent one potential mechanism explaining Black women’s greater risk of PTSD, although cumulative psychosocial vulnerability may be buffered by social support. Despite higher support, inner-city White women’s psychosocial vulnerability may actually outweigh support’s benefits for reducing trauma-related distress.

The dim light melatonin onset (DLMO) is the most reliable circadian phase marker in humans, but the cost of assaying samples is relatively high. Therefore, the authors examined differences between DLMOs calculated from hourly versus half-hourly sampling and differences between DLMOs calculated with two recommended thresholds (a fixed threshold of 3 pg/mL and a variable “3k” threshold equal to the mean plus two standard deviations of the first three low daytime points). The authors calculated these DLMOs from salivary dim light melatonin profiles collected from 122 individuals (64 women) at baseline. DLMOs derived from hourly sampling occurred on average only 6–8 min earlier than the DLMOs derived from half-hourly saliva sampling, and they were highly correlated with each other (r ≥ 0.89, p < .001). However, in up to 19% of cases the DLMO derived from hourly sampling was >30 min from the DLMO derived from half-hourly sampling. The 3 pg/mL threshold produced significantly less variable DLMOs than the 3k threshold. However, the 3k threshold was significantly lower than the 3 pg/mL threshold (p < .001). The DLMOs calculated with the 3k method were significantly earlier (by 22–24 min) than the DLMOs calculated with the 3 pg/mL threshold, regardless of sampling rate. These results suggest that in large research studies and clinical settings, the more affordable and practical option of hourly sampling is adequate for a reasonable estimate of circadian phase. Although the 3 pg/mL fixed threshold is less variable than the 3k threshold, it produces estimates of the DLMO that are further from the initial rise of melatonin.

Inflammatory bowel disease (IBD) is a waxing and waning disease characterized by diarrhea, abdominal pain and weight loss. Recently, there has been an increased interest in the roles that sleep, circadian rhythms and melatonin could have as regulators of inflammation in the Gl tract. Advances in our understanding of the molecular machinery of the circadian clock, and the discovery of clock genes in the GI tract are opening up new avenues of research for a role of sleep in IBD. Altering circadian rhythm significantly worsens the development of colitis in animal models, and preliminary human studies have shown that patients with IBD are at increased risk for altered sleep patterns. Further research is needed to clarify the role of disturbances in IBD.

Bright light is the recommended treatment for winter seasonal affective disorder (SAD). Previously we showed that the antidepressant effect of morning (but not evening) light was greater than placebo after 3 weeks of treatment. Here, we determined if the magnitude and direction of circadian rhythm phase shifts produced by the bright light in the previous study were related to the antidepressant effects. Twenty-six SAD patients from the original sample of 96 had their rectal temperature continuously monitored while they participated in a placebo-controlled parallel design conducted over six winters. After a baseline week, there were three treatments for 4 weeks-morning light, evening light, or morning placebo. Bright light was produced by light boxes (approximately 6000 lux). Placebos were sham negative ion generators. All treatments were 1.5 h in duration. Depression ratings were made weekly by blind raters. Circadian phase shifts were determined from changes in the timing of the core body temperature minimum (Tmin). Morning light advanced and evening light delayed the Tmin by about 1 h. The placebo treatment did not alter circadian phase. As the sleep schedule was held constant, morning light increased and evening light decreased the Tmin to wake interval, or phase angle between circadian rhythms and sleep. Phase advance shifts and increases in the phase angle were only weakly associated with antidepressant response. However, there was an inverted U-shaped function showing that regardless of treatment assignment the greatest antidepressant effects occurred when the phase angle was about 3h, and that patients who moved closer to this phase angle benefited more than those who moved farther from it. However 46% of our sample had a phase angle within 30 min of this 3 h interval at baseline. So it does not appear that an abnormal phase angle can entirely account for the etiology of SAD. A majority (75%) of the responders by strict joint criteria had a phase angle within this range after treatment, so it appears that obtaining the ideal phase relationship may account for some, but not all of the antidepressant response. In any case, regardless of the mechanism for the antidepressant effect of morning light, it can be enhanced when patients sleep at the ideal circadian phase and reduced when they sleep at a more abnormal circadian phase.

The endogenous melatonin onset in dim light (DLMO) is a marker of circadian phase that can be used to appropriately time the administration of bright light or exogenous melatonin in order to elicit a desired phase shift. Determining an individual's circadian phase can be costly and time-consuming. We examined the relationship between the DLMO and sleep times in 16 young healthy individuals who slept at their habitual times for a week. The DLMO occurred about 2 hours before bedtime and 14 hours after wake. Wake time and midpoint of sleep were significantly associated with the DLMO (r = 0.77, r = 0.68 respectively), but bedtime was not (r = 0.36). The possibility of predicting young healthy normally entrained people's DLMOs from their sleep times is discussed.

Patients with inflammatory bowel disease (IBD) complain of poor sleep [1,2], specifically of prolonged sleep latency, repeated awakenings, and poorer sleep quality than healthy controls, even in remission [1]. Possible contributors to this poor sleep include abdominal pain, diarrhea, bathroom trips, stress about future flare-ups, conditioned insomnia, altered immune function, and/or systemic inflammation [1,2]. Circadian disruption can also disturb sleep [3] and is linked to increased incidence of ulcers [4], colorectal cancer [5], and IBD [6]. We recently showed that chronic circadian disruption significantly exacerbates chemically induced colitis in mice, leading to greater weight loss, intestinal tissue injury, and colonic inflammation [7]. To date, circadian state has not been assessed in IBD patients. The gold standard measure of the circadian clock in humans is the melatonin rhythm [8]. This pilot study had two aims: (1) to determine if there was any circadian disruption in asymptomatic IBD patients (by examining the relationship between the timing of the melatonin rhythm and sleep) and (2) to determine if circulating melatonin levels were abnormally low, potentially contributing to the chronic inflammation and poor sleep in IBD. This is the first report of comprehensively measured melatonin rhythms in IBD patients. Four patients (two males, 22–39 years), three with Crohn’s disease and one with ulcerative colitis (clinical and histologically proven) participated. All were symptom free for at least 1 month prior. Patients were of normal weight and were not taking melatonin supplements, sleep aids, or nonsteriodal anti-inflammatory drugs (prescribed medications listed in Figure 1). All patients were nonsmokers and passed a drug screen, except Patient 2 who quit smoking at enrollment (at his own volition) and tested positive for marijuana. All patients had not worked night shifts or crossed time zones in the previous month. The patients wore wrist monitors (Actiwatch-L, Phillips) and followed their habitual sleep schedules for 8–9 days at home before their dim light salivary endogenous melatonin profiles were assessed as per standard procedures [9]. The protocol was approved by the Rush University Medical Center Institutional Review Board and was in accordance with the Declaration of Helsinki. Figure 1 Salivary melatonin profiles of four patients with asymptomatic inflammatory bowel disease. Each patient’s habitual sleep times are represented by a black rectangle. Patients stopped consuming alcohol and caffeine three days before the melatonin ... The wrist actigraphy data revealed that three patients had longer wake time after sleep onset than eight age and sex matched controls recruited online [10] (Table I). The patients’ sleep onset latency was significantly longer and sleep efficiency significantly lower than controls (Table I, both p < 0.05). These data are consistent with previous reports of poor sleep in patients with IBD. Table I The sleep parameters of the four IBD patients and eight matched control subjects during 7 days of baseline sleep. Three of the four patients had circadian rhythms in their melatonin secretion. The variability in the timing and amount of melatonin secreted was similar to a large sample of healthy controls [9]. The patients’ various medications did not abolish the melatonin rhythm in three patients. The lack of circadian rhythm in Patient 2’s melatonin secretion may have been due to his recent smoking and marijuana use. Nonetheless, the results indicate that the circadian rhythm in melatonin excretion can be abnormal in some patients with IBD and this should be studied in a larger cohort.