Prostate cancer (PC) is the second most common cancer in men worldwide, with over 1,400,000 new cases per year (Sung et al, CA Cancer J Clin 71:209–249, 2021). The strongest risk factors for PC include age, genetic (Al Olama et al., Nat Genet 46:1103–1109, 2014; Cancel-Tassin, Cussenot, BJU Int 96:1380–1385, 2005), and metabolic factors. Among men with one, two, or three first-degree relatives with PC, the risk of PC is increased 2-, 5-, and 11-fold, respectively. Obese patients (as defined by body mass index) have an increased risk of PC, including a more aggressive phenotype (MacInnis, English, Cancer Causes Control 17:989–1003, 2006). The underlying mechanisms are unclear; prior studies examining serum androgen, estrogen, and insulin levels have provided inconclusive evidence of an association of these hormones with elevated risk of PC. Inhibition of testosterone production and signaling are the backbone of systemic therapy for PC. Although the development of more potent inhibitors of androgen receptor signaling has led to improved outcomes, monitoring for the long-term metabolic side effect of treatment is paramount.