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Background Adolescent intake of animal products has been proposed to contribute to prostate cancer (PCa) development because of its potentially carcinogenic constituents and influence on hormone levels during adolescence. Methods We used data from 159,482 participants in the NIH-AARP Diet and Health Study to investigate associations for recalled adolescent intake of red meat (unprocessed beef and processed red meat), poultry, egg, canned tuna, animal fat and animal protein at ages 12-13 years with subsequent PCa risk and mortality over 14 years of follow-up. Cox proportional hazard regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of total (n = 17,349), advanced (n = 2,297) and fatal (n = 804) PCa. Results Suggestive inverse trends were observed for adolescent unprocessed beef intake with risks of total, advanced and fatal PCa (multivariable-adjusted P-trends = 0.01, 0.02 and 0.04, respectively). No consistent patterns of association were observed for other animal products by PCa outcome. Conclusion We found evidence to suggest that adolescent unprocessed beef intake, or possibly a correlate of beef intake, such as early-life socioeconomic status, may be associated with reduced risk and mortality from PCa. Additional studies with further early-life exposure information are warranted to better understand this association.

PURPOSE: Although a growing body of evidence supports an early-life contribution to prostate cancer (PCa) development, few studies have investigated early-life diet, and only three have examined early-life dairy product intake, a promising candidate risk factor because of its known/suspected influence on insulin-like growth factor levels and height. METHODS: We used recalled dietary data from 162,816 participants in the NIH-AARP Diet and Health Study to investigate associations for milk, cheese, ice cream, total dairy, and calcium intake at ages 12–13 years with incident total (n=17,729), advanced (n=2,348), and fatal PCa (n=827) over 14 years of follow-up. We calculated relative risks (RRs) and 95% confidence intervals (CIs) by Cox proportional hazards regression. RESULTS: We observed suggestive positive trends for milk, dairy, and calcium intake with total and/or advanced PCa (p-trends=0.016–0.148). These trends attenuated after adjustment for additional components of adolescent diet, particularly red meat and vegetables/potatoes. In contrast, suggestive inverse trends were observed for cheese and ice cream intake with total and/or advanced PCa (p-trends=0.043–0.153), and for milk, dairy, and calcium intake with fatal PCa (p-trend=0.045–0.117). CONCLUSION: Although these findings provide some support for a role of adolescent diet in increasing PCa risk, particularly for correlates of milk intake or overall dietary patterns, our protective findings for cheese and ice cream intake with PCa risk and mortality, and for all dairy products with PCa mortality suggest alternative explanations, such as the influence of early-life socioeconomic status, and increased PCa screening, earlier detection, and better PCa care.

Polychlorinated biphenyls (PCBs) are a group of persistent organic pollutants that are carcinogenic, neurotoxic, and endocrine disrupting in humans. Although diet is the primary source of exposure, there is no consensus on the association between dietary intake and serum PCBs. Additionally, body mass index (BMI) – with its inverse association with serum PCBs – may play a role in the association, which has never been studied. Therefore, we aimed to examine the association between dietary intake and serum levels of PCBs, and whether the association was modified by BMI. We used data from the National Health and Nutrition Examination Survey (NHANES) 2003–2004, including 1531 participants. We estimated dietary intake of PCBs using the 24-hour diet recall, USDA Food Composition Intake Database, and PCB content in foods from the Canada Total Diet Study. Serum PCBs were measured by high-resolution gas chromatography-mass spectrometry (HRGC-HRMS). We used linear regression to examine the associations of dietary PCB intake with serum levels of seven PCB congeners and six PCB metrics. Further, we explored the role of BMI in the associations. We found that participants who were older and non-Hispanic tended to have a higher serum level of ∑37-PCB. In addition, we observed positive associations between dietary intake and serum PCBs for: PCB 105, 118, 126, 138 + 158, and 153 (P value ranges 0.005–0.03); seven PCB indicators (P value = 0.03) and the sum of 37 PCBs (P value = 0.04). Furthermore, we observed an effect modification by BMI (P for interaction = 0.01 for ∑37-PCBs), with stronger associations in underweight or normal-weight individuals, and no association in overweight and obese individuals. In conclusion, within a cross-sectional, nationally representative sample of the US population, dietary PCB intake was positively associated with serum PCBs and the association was modified by BMI. Additional studies are warranted to replicate and confirm this effect modification.