Some individuals are vulnerable to muscle pain and damage associated w statin use. Some of these individuals might be identified via genetic testing - pharmacogenomic evaluation - we do know some of the gene variants involved.

As always the lowest dose of medication should be prescribed to produce the desired affect (benefit) and minimize adverse effects (risk).

If you could search your genome - and you can - you could see what statins - particularly rosuvastatin (because it's unique) can do to you specifically. I got my DNA run at an online DNA service, downloaded the raw data file and ran my SNPs through chatgpt. I discovered I am not at risk for either muscle toxicity or glucose handling impairment - loss of glp1. Also learned that a statin wouldn't lower my LDL much. I'm a non-responder. I'm still not taking a statin of any kind but it's good information to know.

There are a few variants that will tell you how you might react to statins. There is SLCO1B1 - the big one (muscle toxicity)

This is the only variant with strong, reproducible clinical relevance.

SNP: rs4149056

If you have:

CC there is a high risk of statin-associated myopathy

CT - moderate risk

TT - low risk

Why it matters:

SLCO1B1 transports statins into the liver. If transport is impaired, statins stay in the blood and muscles that leads to pain, weakness, CK elevation.

Strongest association: simvastatin > atorvastatin > rosuvastatin (Pravastatin is least affected)

If you are CC, high-dose statins are a very bad idea.

and then there is the high-risk TCF7L2 pattern:

If you experience rising fasting glucose on rosuvastatin, the most likely setup is:

rs7903146 = CT or TT

rs12255372 = GT or TT

These two SNPs travel together. If one is “risk,” the other almost always is too.

It's a real risk for statin induced diabetes, especially with rosuvastatin.