Hyperinsulinemia: A Risk Factor For Prostate Cancer And Heart Attacks
Insulin is released, typically after a meal or a snack to remove excess glucose from the blood. When blood glucose levels fall below a certain level, the body begins to use stored sugar as an energy source by breaking down glycogen (glycogenolysis) stored in the liver and muscles. In addition, insulin also has several other anabolic effects throughout the body.
Hyperinsulinemia is a condition in which levels of circulating insulin are greater than expected relative to blood levels of glucose and can result from a variety of metabolic conditions. While hyperinsulinemia is often seen in people with early stage type 2 diabetes, it is only a symptom of the disease. In type 2 diabetes, liver, skeletal muscle and fat cells become resistant to insulin. With a reduced response to insulin, the pancreas secretes increasing amounts of insulin in response to blood glucose levels, resulting in hyperinsulinemia and enhanced insulin resistance. Hyperinsulinemia is believed to play a causal role in high fat diet-induced obesity.
Many recent studies have suggested that hyperinsulinemia and other components of the so-called metabolic syndrome are risk factors for clinical prostate cancer and may be associated with the its aggressiveness and progression. A recent systematic review and meta-analysis assessed the relative risks of prostate cancer, several parameters of prostate cancer aggressiveness and progression associated with metabolic syndrome. While it found no association between metabolic syndrome and prostate cancer risk, men with metabolic syndrome appeared more likely to have high-grade prostate cancer and more advanced disease, were at greater risk of progression after radical prostatectomy and were more likely to suffer prostate cancer-specific death.
In another recent study, the specific clinical, metabolic and insulin profile at baseline in men who had died from clinical prostate cancer during follow-up was compared with those of men who were still alive at follow-up.
This study followed 320 patients in whom clinical prostate cancer, stages T2-3, had been diagnosed. Their height, body weight, waist measurement, hip measurement and blood pressure were determined. Body mass index and waist/hip ratio (WHR) were calculated. Blood samples were collected to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, uric acid, alanine aminotransferase and fasting plasma insulin level. Prostate gland volume was measured and annual benign prostatic hyperplasia (BPH) growth rate calculated to confirm the diagnosis of prostate cancer.
All patients with clinical prostate cancer were followed up until their death or until the study was terminated. At follow-up, 54 patients had died from prostate cancer and 219 were still alive. The results showed that the men who died of clinical prostate cancer during follow-up period were older, had a larger prostate gland volume, a faster BPH growth rate, a higher prevalence of type 2 diabetes - not to mention a higher stage and grade of clinical prostate cancer along with a higher prostate-specific antigen (PSA) level at baseline than men still alive with clinical prostate cancer at follow-up.
On the other hand, the survivors had higher levels of the ‘good’ HDL-cholesterol, lower fasting plasma insulin levels and lower uric acid levels. Eliminating the effect on mortality of higher stage and grade of the clinical prostate cancer and PSA at baseline, men who died of clinical prostate cancer showed higher fasting plasma insulin levels and lower HDL-cholesterol levels.
In conclusion, this study shows that hyperinsulinemia and five other previously established components of metabolic syndrome are prospective risk factors for deaths due to prostate cancer. These findings confirm previous studies indicating that prostate cancer risk is enhanced by metabolic syndrome. Not only that, hyperinsulinemia and other metabolic disorders clearly precede the deaths caused by prostate cancer.
These data suggest that the insulin levels could be used as a marker of prostate cancer prognosis and tumor aggressiveness, regardless of the patient's prostate cancer stage, cancer grade and PSA level.
Based on this and other studies, insulin appears to act as a stimulus for prostate and probably other cancers to grow and become more aggressive. Not only that, higher insulin levels means a greater likelihood of death. In fact, insulin values were seen to be more accurate than microscopic grading of stage of the tumor or PSA values in identifying persons at risk of rapid fatal cancer courses.
Not only hyperinsulinemia, but also obesity and type 2 diabetes are increasingly being recognized as risk factors for more aggressive disease, treatment failure and cancer-specific mortality. Other factors such as dyslipidemia, hypoxia and inflammation associated with having excess fat tissue may also be driving malignant growth.
While some experts have recommended the use of insulin-lowering medications, revising diets in cancer patients toward low insulin stimulating (low-glycemic) foods may be the least invasive and harmful intervention there is - or at least as worthwhile as the drugs, surgery and other treatments administered to treat clinical prostate cancer.