Chronic inflammation may promote the development of prostate cancer.
Inflammation is a sign that the immune system is doing its job in protecting us from infectious agents and injuries. But chronic inflammation has been associated with a wide range of diseases. Today scientists know that inflammatory cells produce free radicals—toxic molecules that can damage cells, especially cellular DNA. This type of DNA damage (also called oxidative damage) can cause genetic alterations (mutations) that lead to the uncontrolled cell division that characterizes cancer. Research conducted at Johns Hopkins now suggests a potential pathway by which inflammation may encourage the development of prostate cancer.
Pathologists at Johns Hopkins have found pockets of inflammation in the midst of cancerous prostate cells and abnormal (probably precancerous) cells known as prostatic intraepithelial neoplasia (PIN). Around the areas of inflammation, they discovered something new—groups of cells that look as if they are dying (atrophying) but are actually dividing (proliferating). The Hopkins researchers named these bizarre groups of cells proliferative inflammatory atrophy (PIA) and believe them to be either the very beginning of cancer formation or perhaps a breeding ground for prostate cancer.
These areas containing PIA show high levels of an enzyme called glutathione S-transferase (GST), a critical substance that helps protect DNA from free radical damage. Ultimately, the gene that produces GST becomes inactivated in these areas of inflammation. GST production is halted, and the surrounding cells lose their DNA protection. Gene mutations may result, and the mutated genes may lead to prostate cancer.
The theory is that inflammation—perhaps triggered by chronic infection, in conjunction with dietary or hereditary factors—leads to the DNA damage and the gene mutations that set prostate cancer in motion. Indirect evidence, gathered over many years, supports this inflammation-prostate cancer link. Some population-based studies, for example, have found a lower risk of prostate cancer among men who take inflammation-reducing medications or follow dietary patterns that are less likely to promote inflammation.
Several population-based studies have suggested that men who take non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, have a lower risk of developing prostate cancer. In one large study of more than 90,000 men participating in the Kaiser Permanente Medical Care program, those who took six aspirin a day had a 24% risk reduction of developing prostate cancer.
Cholesterol-lowering “statin” medications, such as Lipitor (atorvastatin) or Zocor (simvastatin), also have an anti-inflammatory effect. Some research indicates that men who have taken statins for several years are less likely to be diagnosed with advanced prostate cancer. In an analysis conducted by Hopkins researcher Elizabeth Platz, men who took cholesterol-lowering drugs (90% of which were statins) were half as likely to develop advanced prostate cancer as men who had not taken the drugs.
Dietary habits also influence inflammation. The typical American diet— high in saturated fat, sugar, and red meat and low in fiber, fruits, and vegetables—encourages inflammation (not to mention obesity and heart disease). Reducing your intake of saturated fat—found primarily in animal-based products such as meat, poultry, whole milk products, butter, and cheese—and increasing your intake of fruits and vegetables are important first steps to discouraging inflammation and thus reducing your risk of prostate cancer.
