Saturday, February 19, 2011


People tend to laugh when a scientist proclaims that if the length of your index finger is longer than your ring finger your risk of prostate cancer is lower than other men. But that was recently in the news. Can it be true? What about the data? Does it substantiate such a conclusion?

Well sort of, but not very convincingly. For one thing the data are taken from men who judged their own finger lengths from pictures which showed examples of various finger lengths, and then they returned this information to the investigators by mail.

Can you imagine Grandpa looking at those finger lengths examples and exclaiming “Mine is bigger than his.” or “What did cousin Homer put on his report? I can beat him any day.” The possible sources for inaccurate measurements are endless. Feel free to make up your own and after you check out your own finger lengths send them to me for publication.

Although the whole idea of finger length and risk of prostate cancer seems almost frivolous there is some basis for the belief that there might be a relationship. It turns out that the growth and pattern of the fingers and gonads (testes and ovaries) are controlled by the same genes and that the male hormone, testosterone, may control finger length.

Therefore, it is possible that in the male fetus the testes may produce relatively high testosterone and this in turn results in a short index finger. Whereas, if testosterone were relatively low the index finger would be longer. This guess work is based on some very squeaky data from another laboratory which attempts to show that fetal testosterone is correlated with length of the index finger. These data are shown on a scatter plot which looks like Wild Bill shot it with his 12 gauge shotgun.

So, my conclusion is there may be something to the finger story but better studies need to be done before any valid conclusions can be drawn.

Monday, February 14, 2011


As I explained in my blog on cholesterol and heart disease (posted on 8/14/2010), although dietary and blood levels of cholesterol were declared the enemy years ago it is now clear that for the vast majority of people cholesterol is not the enemy. Other highly touted villains in our diet like total saturated fat and animal fat have also bitten the dust. The latest epidemiologist’s horse by the name of trans fats has stumbled and has falling.


These findings have not deterred the statin drug industries who make Crestor, Lipitor etc. from continuing to propagate the false claims that cholesterol is your enemy and if you take our drugs you can lower your blood cholesterol and decrease your chances of heart disease. There is truth in these claims because these statin drugs will lower blood levels of cholesterol and they do lower the risk of heart disease, BUT it is not because of the lowered cholesterol. IF NOT, --WHAT?


So if the positive effects of statins on heart disease are not due to lowered cholesterol, then what are they due to? Recently it has become clear that statins block the inflammatory responses associated with heart disease. These inflammatory responses decrease the opening in the arteries and results in plaque formation. Some investigators believe that these responses occur as a result of infection by bacteria.

These inflammatory responses are spelled out in a little more detail below:

1. Endothelial malfunction.

The endothelium is the lining of the arteries where plaques are formed. Plaques are nodular accumulation of a soft, flaky, yellowish material and in larger plaques the center is composed of macrophages nearest the lumen of the artery. All of these things can be viewed as improper function of the endothelial lining due to an inflammatory response which is inhibited by statins.

2. Reduce remodeling of the arteries and heart muscle.

The smooth muscle cells in arteries increase in number during inflammatory episodes and this contributes to narrowing of the blood vessels and reduced blood flow. Also statins decrease production of smooth muscle cells seen after transplants.

3. Inhibit vascular inflammation and stabilize atherosclerotic plaques.

Statins decrease immune activation and exert anti-inflammatory
effects on the vascular wall by decreasing the number of inflammatory
cells in atherosclerotic plaques. They do this by decreasing the expression
of adhesion molecules so blood cells do not stick to the lining of the artery


You can bet that the drug companies are clamoring to come up with a
statin-like drug that is even better than the current statins at inhibiting inflammatory responses. But, it is not easy because statins all act the same way: 1. By blocking the synthesis of cholesterol and 2. By blocking the synthesis of compounds which act as inflammatory agents. Both of these actions have undesirable consequences.

Many people do not know that “Cholesterol is Us” as Pogo would have put it. We could not exist without it. The cells in our bodies can and do make their own cholesterol. It is a major component in our membranes and without it we would all be just be a blob on the floor. So it is obvious that blocking the making of cholesterol by the liver or any other organs in the body has many potential dangers. Some of these show up as reported side effects.

The clinical trials which test these drugs usually indicate the side effects are rare; however, in the real world that we live in side effects occur more often. These include muscle pain, muscle tissue loss, liver damage, nerve damage and memory loss to name a few. It is clear that these are dangerous drugs and prudent use is warranted.

The blocking of inflammatory responses appear to be the good side of the statin-coin; however, inflammatory responses are important and necessary in healing of wounds and infections. So blocking these may lead to troubles which are still lurking in the shadows.