Sleep is imperative for health and wellness with direct impacts on brain function, physiology, emotional well-being, performance and safety when compromised. Adolescents and young adults are increasingly affected by factors affecting the maintenance of regular sleep schedules. College and university students are a potentially vulnerable population to sleep deprivation and sleep insufficiency. Possible factors that could contribute to poor sleep hygiene include, but are not limited to, academic pressures, social activities, and increased screen time. Arguably, students are still experiencing bone mineralization, until the age of 30 or even 40 years old, which makes it more important to understand the effects that altered sleep patterns could have on continued development of bone health. It is our understanding that to date, studies assessing the risk of sleep insufficiency on bone mineral density in college students have not been conducted. We hypothesized that college-aged students, between the ages of 18-25 years, with shorter sleep durations, greater sleep schedule variability, and poorer sleep environments will have significantly lower bone mineral density. ActiGraph monitoring, via a wrist ActiWatch was used to quantitatively measure sleep habits for up to 7 consecutive days. During the week-long study participants also captured their self-reported sleep data through the use of a sleep diary. Participants were measured one time within the study for bone mineral density of the lumbar spine and total hip through a dual energy x-ray absorptiometry. This was a preliminary analysis of a larger cross-sectional analysis looked at 17 participants, of which there were 14 females and 3 males, (n=5, 1 and 11 Hispanic, Black and White, respectively). The mean age of participants was 20.8±1.7 y with an average BMI of 22.9±3.2 kg/m2. ActiWatch measurement data showed a mean daily sleep duration of participants to be 437.5 ± 43.1 (372.5 – 509.4) minutes. Mean sleep efficiency (minutes of sleep divided by minutes of time in bed) and mean number of awakenings were 87.4±4.3 (75.4-93.4) minutes and 32.1±6.4 (22.3-42.7) awakenings, respectively. The median time for wake after sleep onset (WASO) was 34.5±10.5 (18.3-67.4) minutes. The mean bone mineral density (BMD) for the hips was 1.06±0.14 (0.81-1.28) g/cm2 with a mean BMD of the lumbar spine being 1.24±0.12 (0.92-1.43) g/cm2. Age-matched Z-scores of the hips was 0.31±0.96 (-1.6-2.1) and lumbar spine was 0.53 (IQR: 0.13, 0.98; -2.25-1.55). Neither sleep duration nor sleep efficiency was significantly correlated to BMD of either locations. While WASO was positively associated with hip and spine BMD, this value was not statistically significant in this population. Overall, associations between sleep and BMD of the femur and spine were not seen in this cohort. Further work utilizing a larger cohort will allow for control of covariates while looking for potential associations between bone health, sleep duration and efficiency.

Obesity increases the risk for colorectal cancer. In mice, a pro-obesity high-fat-diet (HFD) leads to an intestinal phenotype characterized by enhanced proliferation, numbers, function and tumor-initiating capacity of stem cells, the cell-of-origin for many intestinal cancers. This phenotype is driven by a lipid metabolism program facilitated by an intrinsic Peroxisome Proliferator-Activated Receptor/Fatty Acid Oxidation (PPAR/FAO) axis that senses and utilizes cellular lipids. However, the microbiome is a known regulator of lipid metabolism in the gut, but little is understood about how the gut commensals affect access to the lipids and alter stem cell function. Here, we use the long term HFD-fed mouse model to analyze the phenotypic changes in the intestinal stem cells (ISCs) after depletion of the gut microbiota. We find that the loss of the gut microbiome after four weeks of antibiotic treatment imposes significant changes in ISC function leading to reduced HFD ISC regenerative potential. These results indicate that the gut microbiome plays a crucial role in the lipid metabolic process which regulates and maintains the HFD ISC phenotype, and further suggests that the gut microbiome may augment the diet-induced tumor initiating capacity by altering the stem cell function.