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The incidence of prostate cancer is estimated to continue to increase. However, Prostate cancer is cancer with an aetiology that is still not well understood at present due to the complexity of the factors involved. Obesity has been identified as a contributing factor to at least twelve types of cancer, including prostate cancer. This thesis has been structured with the main objective of providing an overview of how the adipokines (leptin and adiponectin) and lipid profiles contribute to the interaction between obesity and prostate cancer, with each chapter using a different study design and research question in order to get a more complete picture of how obesity is linked to prostate cancer. While obesity has been related to prostate cancer, the results from this thesis have shown the role for adipokines in terms of risk, aggressiveness and progression of prostate cancer is still uncertain, with the work conducted in this thesis systematically reviewing the literature and highlighting weaknesses within that literature, which new analysis of an available prospective cohort study, the PRIME study, attempted to rectify. Ultimately, findings from this survival analysis suggested trends in terms of associations between adipokines and prostate cancer mortality, but results were not statistically significant, likely due to a low number of cases, and therefore further robust studies are required considering the method of assessment of adipokine exposure and development of robust models using appropriate confounders, which will allow conclusions regarding this potential association. Post-hoc analysis of a diet and lifestyle intervention has demonstrated that, although previously analysed anthropometric outcomes and dietary intake were altered, there was no significant effect on lipid profile and CVD risk outcomes, while level of adherence also did not seem to be associated with these secondary outcomes, although adherence was associated with the primary anthropometry outcome. As for the survival analysis, a lack of statistical power is likely to have been an issue for the secondary lipid outcomes, and a retrospective power calculation confirmed this.