As the song goes, “The hip bone is connected to the thigh bone…” but it fails to mention a unique relationship between the liver and the prostate. Although they are very different in their composition and function, they are indirectly connected by a blood-circulated fat, and a drug used to control its levels. The fat is cholesterol, and the drug is a statin.
Cholesterol in itself is not bad. It is a lipid, or fat, that is carried by the blood throughout the body. It is a source of energy that cells need, so it has a good reason to exist. While each cell is like a small business with a capacity to produce its own cholesterol, the liver is the megacorporation, producing about 70% of the body’s cholesterol. The rate at which production occurs in the liver is regulated primarily by an enzyme called HMG-CoA.
So what’s so bad about cholesterol? The problem is excess. When there’s too much of it, deposits of cholesterol cling to the inner walls of blood vessels, causing them to narrow and “harden.” One way to reduce cholesterol levels is to take a pharmaceutical called a statin, the most widely prescribed class of drugs that lower levels by inhibiting the action of HMG-CoA. In response, the liver makes less cholesterol. By now, you are probably wondering what liver production and excessive cholesterol levels have to do with the prostate.
Surprisingly, statins have been reported to discourage the growth of prostate cancer cells. Research has shown that prostate cancer (PCa) patients who were already taking statins had a lower risk of their cancer progressing into advanced PCa. No one knows the exact biochemical mechanisms by which this happens; theories are based in complex, often synergistic, interrelationships at the cellular level. Nonetheless, the correlation has been repeatedly made and it may be good news for men who develop PCa after they’ve been on statin drugs for a while. However, there is no compelling evidence that statins prevent PCa from originating in the gland; men who take statins have the same rate of developing PCa as men who don’t. The important thing is, they seem to have less chance that their disease will become more dangerous. Thus, statins may somehow keep prostate cancer at bay once it starts.
Research about statins and PCa focuses on the potential for statins to prevent PCa from starting. Most cell lines appear to have a long, slow period in which they remain “latent,” similar to an idling car engine that never gets put into gear. There is even new thinking that much Gleason 3+3 cancer will never develop beyond that level. So scientists are conducting laboratory tests on prostate cancer cells to find out which components of statins have the potential to put the brakes on PCa—or keep it from happening altogether. So far they don’t have the answers—and even then it will be a long time before human clinical trials can occur.
Statins have a risk of unwanted side effects, so we strongly advise against any temptation to think they could be used as a PCa management strategy! The fact that a correlation has been observed is not a green light to experiment with your own body. They should only be prescribed by a doctor for elevated cholesterol levels, especially if there’s a history of cardiovascular disease in the individual or his family. Perhaps, as researchers get closer to unraveling the mysterious connection between statins as a way to control liver production of cholesterol and its effect on existing prostate cancer, it will lead them to a new medicine that can effectively and reliably control—or even prevent—prostate cancer.