The comments,here presented,brings us back to the big argument:Are medications good for you?.Medications are altered molecules,introduced into the body,for it to benefit from.Being foriegn to the body,the body reacts.These are the side effects that damage and ,sometimes,kill the body.When it happen we say:"Ouch.I am sorry".Well it does not have to be that way.There are a lot of alternative medication that not only do a good job,but,as it is not a foreign body,the body does not react against it.

In the case of Cardiovsculr Diseases,we have the Statins,claimed to be a "Smart bomb",but it ain't!.It is a "Cluster bomb".We are witnessing a repetetive "Ouch".

What is the alternative? Niacin.Pure Niacin,immediate release,supervised by U.S.P.No side effects except the Flush.Too much noise about the Flush,scares everyboby.With minimal education Flush stops to be an issue.Who says that LDL is the target.Maybe the HDL?(HDL,the good,the bad and the ugly).

It is about time that Niacin will stop being:An Orphane Drug to many Non-Orphane diseases.

It is difficult to practice medicine and carry so many:"Black boxes"

I concur with the below comment regarding the low risk of biochemically evident myopathy. I personally avoid simvastatin 80 due to a higher risk suggested in the A to Z trial. I would like a reference regarding the HPS and the gene-myopathy connection. I do think validation in the case of other statins would be helpful. I am skeptical regarding routine use of this test unless its discriminatory value for myopathy (ROC curves) is demonstrated for simva 40, atorva 40, and/or rova20/40 is established.

On a related issue, I am interested in your opinion regarding the already marketed KIF6 genotyping.

Some important comments here. ApoA1  must have some unusual patients since mucle aches/pain is the most common side effect of statins, and in fact set up the ezetimibe market.  I have treated patients with statins for over 20 years and the incidence of this side ffect becoming an issue for patients is at least 5-10%, many stimate much higher. This is not an academic issue. Ceruvastatin (Baychol) was taken off the market since it induced rhabdomyolysis and deaths---likely indexed to the same gene. The story is not just about marked CK rise 10 fold or greater. There are series of patients who have muscle biopsy proven myositis without CK blood level excess.

Agree with D. Powell that we need more data on all statins. I think the KIF6 story in intriguing but we need more info on that marker as well. The reference in NEJM July 31 has all the related HPS info.

The amioadorone-statin interaction is yet another example of the problem, with many clinicians not aware of the need to go to lower statin doses when using amiodarone concurrently.  Learning the pathway for this myopathy unintended yet frequent effect sets up the potential to prevent it in the future.

ApoA1,

 Dr. Topol was not recommending muscle biopsy. He was referring to the following series of studies:

 Ann Intern Med. 2002 Oct 1;137(7):581-5. Statin-associated myopathy with normal creatine kinase levels.

Genetic risk factors associated with lipid-lowering drug-induced myopathies. Muscle Nerve. 2006 Aug;34(2):153-62.

 Incidentally, I would echo the 5-10% risk of significant myalgias from everyday clinical practice.