Lifetime Prevalence of Psychiatric Disorders in Adolescents with Unexplained Weight Loss, Underweight, or Poor Appetite.

BACKGROUND: When adolescents present with symptoms of unexplained weight loss, underweight, or poor appetite, eating disorders (EDs) are commonly on the list of differential diagnoses. However, the relationship of these symptoms to other psychiatric disorders is often less clear. METHODS: Using the Rochester Epidemiology Project database, a retrospective cohort study of adolescents (13-18 years) with billing diagnoses of weight loss, underweight, or loss of appetite was conducted between January 2005 and December 2017. Patients who presented with conditions commonly associated with weight loss, underweight, or poor appetite (e.g., cancer) were excluded. This study sought to examine the proportion of patients who received ED and psychiatric diagnoses within 5 years of the index visit and patient characteristics associated with these diagnoses. RESULTS: Of 884 patients diagnosed with symptoms of unexplained weight loss, underweight, or poor appetite, 662 patients ( M age = 15.8; SD = 1.6; 66.0% female) met study criteria. Within 5 years of the index visit, the lifetime prevalence of all psychiatric disorders was 70% (n = 461) and of EDs was 21% (n = 141). For both psychiatric disorders and EDs, sex and race were significantly associated with receiving a diagnosis within 5 years. Decrease in body mass index (BMI) percentile was associated with receiving an ED diagnosis, whereas the highest historical BMI percentile was associated with receiving a psychiatric diagnosis. CONCLUSION: Patients presenting with symptoms of unexplained weight loss, underweight, or poor appetite are at risk not only for EDs but also for other psychiatric disorders that may require further assessment and follow-up.

CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels.

Decreased NAD+ levels have been shown to contribute to metabolic dysfunction during aging. NAD+ decline can be partially prevented by knockout of the enzyme CD38. However, it is not known how CD38 is regulated during aging, and how its ecto-enzymatic activity impacts NAD+ homeostasis. Here we show that an increase in CD38 in white adipose tissue (WAT) and the liver during aging is mediated by accumulation of CD38+ immune cells. Inflammation increases CD38 and decreases NAD+. In addition, senescent cells and their secreted signals promote accumulation of CD38+ cells in WAT, and ablation of senescent cells or their secretory phenotype decreases CD38, partially reversing NAD+ decline. Finally, blocking the ecto-enzymatic activity of CD38 can increase NAD+ through a nicotinamide mononucleotide (NMN)-dependent process. Our findings demonstrate that senescence-induced inflammation promotes accumulation of CD38 in immune cells that, through its ecto-enzymatic activity, decreases levels of NMN and NAD+.