Smoking and exercise patterns and dietary intake of calcium and Vitamin D (Block Calcium/ Vitamin D screener ) were collected via a one-time interviewer-administered questionnaire conducted during or after study participation. Baseline body weight was calculated using whole-body DEXA data as the sum of total lean, fat, and bone mineral content weights. Laboratory testing, including rapid HIV testing, serum creatinine, phosphorus, and alkaline phosphatase, was Rubex Topoisomerase inhibitor performed at each quarterly visit. Creatinine clearance was calculated using the Cockroft-Gault formula. Evaluation of secondary causes was conducted in men with low BMD at screening or during follow-up and those with.5% decrease from baseline at L2-L4 or total hip, including testing for thyroid stimulating hormone, 25-hydroxy vitamin D level, testosterone level, spot urine calcium/creatinine ratio, and serum parathyroid level for participants over age 40. Mean Z-scores of the lumbar spine (L2-L4), total hip, and femoral neck were calculated, and prevalence of low BMD was determined with exact 95% binomial confidence intervals (CIs). The observed number of low BMD cases was compared using a 2- sided exact binomial test to the number that would have been expected based on reference population data (approximately 2.3% would have Z scores below 2 standard deviations of the mean, assuming Z-scores are normally distributed with mean 0 and standard deviation 1 ). The association of sociodemographic variables and risk factors for low bone mass with baseline BMD was examined using univariate logistic regression analysis. Mean percent change in BMD over time was plotted for each anatomic region by treatment arm, and the proportion of men losing.3% and.5% BMD from baseline at 24 months at each site was determined in a pre-specified analysis. These cut-points were BYL719 PI3K inhibitor chosen because a 3% loss represents more than expected BMD loss in a population of healthy men in which BMD should be stable, and a 5% loss corresponds with the approximate BMD loss seen in post-menopausal women over a 2-year period. Linear mixed models with random intercepts were used to assess effects of TDF on percent change in BMD from baseline to 12 and 24 months among immediate arm participants, and from 9 to 24 months among delayed arm participants. Comparison between treatment arms was by intent-to-treat analysis. Preliminary analyses examining potential interactions between treatment assignment (TDF/placebo) and study month, as well as between treatment assignment and arm (immediate/delayed), revealed no interactions.