Why do people with diabetes have a lower risk of prostate cancer?

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Cancer risk increases in diabetic patients, but several studies have shown that people with diabetes have a reduced risk of prostate cancer.There are currently some hypotheses related to testosterone (T) concentration, insulin-like growth factor 1 (IGF1), advanced glycation end products (AGEs) and lower risk of prostate cancer.An Australian researcher’s article published in J Clin Endocrinol Metab in July 2019 explored the above hypotheses. Are these factors a factor that reduces the risk of prostate cancer in patients with diabetes?Can these factors reduce the risk of prostate cancer in patients with DM?1. Hormonal prostate is sensitive to androgens, and lower testosterone (T) concentrations can be observed in patients with type 2 diabetes. Similar hormone concentration changes are considered to be one of the factors affecting the risk of diabetic prostate cancer.Therefore, low T concentrations may reduce the risk of prostate cancer in men with type 2 diabetes.Insulin-like growth factor 1 (IGF1) binds to IGF-binding proteins (IGFBPs) in the circulation.Insulin increases the synthesis of IGF1 and reduces the production of free IGFBPs.Long course type 2 diabetes is associated with hypoinsulinemia, which may reduce the production of IGF1, increase the concentration of IGFBPs, and reduce the availability of IGF1 in the blood circulation.Since IGF1 is closely related to the development of prostate cancer, it has also been speculated that this may be another mechanism associated with type 2 diabetes and reduced prostate cancer risk.However, the association between hormonal factors and prostate cancer is not completely clear. Some meta-analysis and prospective research results on the relationship between testosterone, IGF1, IGFBPs and prostate cancer have not found its protective effect or contradicted the conclusions mentioned above, but these studiesThe method used and the test object may have an impact on the analysis.2. AGEs Advanced glycation end products (AGEs) are proteins or lipids that undergo non-enzymatic oxidation in a hyperglycemic environment and are associated with vascular complications related to diabetes.It has not been extensively studied in prostate cancer risk, but studies have shown that it can promote the spread of prostate cancer and increase the risk of prostate cancer.In this study, the effects of aging and other chronic diseases on AGEs were excluded.In addition, factors related to the pathophysiology of type 2 diabetes, including glucose, insulin resistance, and stabilizing compounds methyllysine (CML) and factors related to the risk of primary cancer, may have additional effects on the disease.Research Methodology The study was based on a male health study in Perth, Western Australia.After excluding men with a history of prostate cancer (n = 388), men with testectomy (n = 56), baseline androgen / anti-androgen therapy (n = 98), and lack of hormone data (n = 557), the study included3149 men.The average age of the included samples was 76.96 years, and 450 men (14.3%) had diabetes.Compared with non-diabetic men, they have higher body mass index and lower T, DHT and SHBG concentrations.Insulin-like growth factor 1 is higher in diabetic patients, while IGBFP3 is lower.CML was higher in diabetic patients than in non-diabetic patients, but this difference was not statistically significant.In addition, patients with diabetes have higher blood glucose levels and higher HOMA2-IR values.A fasting blood sample was collected from the subject, and plasma was prepared and tested.Results were statistically analyzed using Stata version 13.1.Taking death as a competitive factor, a proportional-risk competitive-risk analysis method was used for longitudinal analysis.Adjustment factors included age, body mass index, physical activity (≥150 minutes / week of vigorous physical activity), alcohol intake, smoking status, and previous cancer history.The factors used to assess whether diabetes and prostate cancer risk were hormonal variables including T, SHBG, IGF1, and IGFBP1 / IGFBP3, which were individually added to the fully adjusted model.Researchers also tested CML, glucose, and HOMA2-IR (calculated based on available fasting insulin measurements) related to the pathophysiology of type 2 diabetes as potential regulators of the study.Findings and Discussion In the study, 450 men had diabetes at baseline and 315 men were diagnosed with prostate cancer during follow-up.Of the 2,440 men with fasting insulin and blood glucose data, 253 were diagnosed with prostate cancer.After analysis of the competitive risk model, it was found that diabetes is indeed associated with a lower risk of prostate cancer, with a subgroup hazard ratio (SHR) of 0.66; 95% CI: 0.46-0.98; P = 0.028).After inclusion of testosterone, dihydrotestosterone (DHT), estradiol, sex hormone-binding globulin (SHBG), IGF1, IGFBP1, IGFBP3, or glucose, the correlation persisted.In addition, additional corrections to CML in the fully adjusted model did not change the inverse association between diabetes and prostate cancer risk, so CML was not related to prostate cancer risk.Among men with fasting insulin data, diabetes was negatively correlated with prostate cancer risk, but it was not statistically significant (SHR, 0.67; 95% CI, 0.43-1.04; P = 0.071).Adding HOMA2-IR to the fully adjusted model did not change this connection.Based on this, researchers believe that after adjusting for potential confounding factors, elderly diabetic patients do have a lower risk of prostate cancer, but this negative correlation is not mediated by sex hormones, SHBG, IGF1 or its binding protein, or glucose concentration.Moreover, insulin resistance is not related to this connection, but it needs to be further confirmed in larger studies.In addition, CML is not associated with prostate cancer risk in older men.These results also need to be validated in other age groups.Researchers hope to have further research to explore the potential factors that reduce the risk of cancer in diabetic men, and this study also needs to assess whether traditional statistical methods for dealing with competitive risk can explain the bias of current epidemiological research results.The above content is only authorized by for exclusive use, please do not reprint without authorization of the copyright party..


The author ouyangshaoxia