Depression, together with insulin resistance, is increasingly prevalent among youth. These conditions have traditionally been compartmentalized, but recent evidence suggests that a shared brain motivational network underlies their co-occurrence. We posit that, in the context of depressive symptoms, insulin resistance is associated with aberrant structure and functional connectivity in the Anterior Cingulate Cortex (ACC) and hippocampus. This motivational neural circuit underlies dysfunctional behavioral responses and increased sensitivity to rewarding aspects of ingesting high calorie food that lead to disinhibition of eating even when satiated. To investigate this shared mechanism, we evaluated a sample of forty-two depressed and overweight (BMI > 85th%) youth aged 9 to 17. Using ACC and hippocampus structural and seed-based regions of interest, we investigated associations between insulin resistance, depression, structure (ACC thickness, and ACC and hippocampal area), and resting-state functional connectivity (RSFC). We predicted that aberrant associations among these neural and behavioral characteristics would be stronger in insulin resistant compared to insulin sensitive youth. We found that youth with greater insulin resistance had higher levels of anhedonia and more food seeking behaviors, reduced hippocampal and ACC volumes, and greater levels of ACC and hippocampal dysconnectivity to fronto-limbic reward networks at rest. For youth with high levels of insulin resistance, thinner ACC and smaller hippocampal volumes were associated with more severe depressive symptoms, whereas the opposite was true for youth with low levels of insulin resistance. The ACC-hippocampal motivational network that subserves depression and insulin resistance separately, may represent a critical neural interaction that link these syndromes together.

Abnormal psychology courses introduce undergraduate students to the range, causes, and treatments of psychological disorders. These courses present important opportunities to instruct students about disorders and treatments associated with childhood maltreatment (CM) as well as its prevalence. Little research has examined the adequacy with which abnormal psychology textbooks present information about CM. The present study reviewed the CM content of 10 abnormal psychology textbooks. The content was assessed in terms of the number of times CM was mentioned, the number of psychological disorders linked to CM, and the number of CM-related research citations. In addition, the authors conducted a content analysis to examine the significance, depth of detail, and organizational structure of the information provided within the sections of text addressing CM. There were significant differences in scores and the accuracy of coverage of CM across textbooks. Most of the textbooks lack key information on CM. The information presented in many textbooks is not consistent with current research and is overly focused on controversies. These findings are concerning because research has linked many psychological disorders and problematic outcomes to CM, but this information is not adequately conveyed to students via abnormal psychology textbooks. The authors make recommendations for improving the coverage of CM in abnormal psychology textbooks.

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Objective Patients with cancers frequently experience sleep and circadian dysfunction. To date, only a few studies have used both a questionnaire and actigraphy for concomitant evaluation of sleep and circadian function in patients with cancer. We sought to evaluate objective sleep and circadian parameters in metastatic colon cancer (MCC) patients and their associations with symptoms and quality of life (QOL). Methods Patients reported subjective sleep problems on the EORTC QLQ-C30. Sleep and circadian parameters were calculated using a wrist-actigraph that patients wore for 72 hours. Results 237 Patients with MCC (age: 60.4 years; range: 20.7–77.6; Male/Female ratio: 1.66) participated in this cross-sectional study. Subjective sleep problems were reported by 63.4% of patients (S+). No differences in any sleep parameters (sleep efficiency, sleep latency, total sleep time, total time in bed, wake after sleep onset, activity bathyphase) were observed between S+ and S- patients. However, S+ patients displayed a significantly worse circadian function than S-patients (96.4% versus 98.1%; p=.005). Presence of poor subjective sleep and objective circadian dysfunction negatively affected symptoms and QOL domains (p=.038). Conclusions Subjective report of sleep problems was not associated with worse objectively-measured sleep parameters in patients with MCC although it was associated with disrupted circadian rest-activity rhythm and poorer QOL. These findings coincide with prior research in cancer patients in that an inconsistent relationship exists between subjective and objective sleep measurements on some sleep domains. This study supports the value of coupled evaluation of self-reported and objective measures of sleep and circadian function in cancer patients.

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