Aims: Previous studies have shown that non-insulin-dependent diabetes mellitus (NIDDM), hypertension, atherosclerotic disease manifestations, tallness, obesity, dyslipidaemia, hyperuricaemia, hyperinsulinaemia and high alanine aminotransferase (ALAT) levels are risk factors for development of benign prostatic hyperplasia (BPH). This indicates that BPH is a component of the metabolic syndrome. In a subsequent study, we found that there was an association between the BPH growth rate and the development of clinical prostate cancer. These findings generated a hypothesis that clinical prostate cancer also was a component of the metabolic syndrome. In the present study, this hypothesis was tested on 299 patients with recently diagnosed clinical prostate cancer. If this hypothesis is true, patients with clinical prostate cancer of high stage and grade would have a larger prostate gland volume, a faster BPH growth rate and a more pronounced clinical, haemodynamic, anthropometric, metabolic and insulin profile than patients with clinical prostate cancer of low stage and grade have. Methods: Two hundred and ninety-nine patients in whom clinical prostate cancer was diagnosed were consecutively included. The prevalence of NIDDM, treated hypertension and atherosclerotic manifestations was provided by the respective patient's medical history. Body length, body weight, waist measurement, hip measurement and blood pressure were determined. Body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-ensity lipoprotein (LDL)-cholesterol, uric acid, ALAT and the fasting plasma insulin level. The prostate gland volume was measured using transrectal ultrasound. The annual BPH growth rate was calculated. The prostate cancer diagnosis was established. Results: Patients with clinical prostate cancer, prostate-specific antigen (PSA) < 50 ng/ml, stage T3, had a bigger prostate gland volume (p < 0.001), a faster BPH growth rate (p < 0.001), were more obese, as measured by body weight (p = 0.062), BMI (p = 0.003), waist measurement (p = 0.011) and hip measurement (p = 0.051) and showed a higher systolic blood pressure (p < 0.070) than patients with T2 clinical prostate cancer. When patients with clinical prostate cancer, PSA > 50 ng/ml, were included at the comparison, T3 tumour patients showed a higher prevalence of treated hypertension (p = 0.026) than patients with T2 tumours. Patients with clinical prostate cancer, PSA < 50 ng/ml, G3, had a greater prostate gland volume (p = 0.004), a faster BPH growth rate (p = 0.005) and were more obese as determined by waist measurement (p = 0.044) and WHR (p = 0.073). Moreover, subjects with a G3 tumour were more dyslipidaemic, as shown by a higher triglyceride level (p = 0.019) and a lower HDL-cholesterol level (p = 0.005), and were more hyperuricaemic (p = 0.023), showed a higher plasma insulin level (p = 0.019) and a higher ALAT level (p = 0.061) than those with a G1 tumour. When patients with clinical prostate cancer, PSA > 50 ng/ml, were included at the comparison, G3 patients had a greater prostate gland volume (p = 0.002) and a faster BPH growth rate (p = 0.003) than patients with G1 tumours. Conclusions: The results of the present study suggest that the prostate gland volume, the BPH growth rate, hypertension, obesity, dyslipidaemia, hyperuricaemia, hyperinsulinaemia and high ALAT levels are risk factors for the development of clinical prostate cancer. Thus, our results support the hypothesis that clinical prostate cancer is a component of the metabolic syndrome. Patients with clinical prostate cancer may have the same metabolic abnormality of a defective insulin-stimulated glucose uptake and secondary hyperinsulinaemia as patients with the metabolic syndrome. Our data also support the hypothesis that hyperinsulinaemia is a promoter of clinical prostate cancer.
