SLCO1B1: the gene that decides how much statin stays in your blood
Your liver's statin doorman, and what one letter does to it.
SLCO1B1 makes a protein called OATP1B1. Think of it as a doorman on your liver cells that pulls certain drugs out of the blood and into the liver, where they get used and cleared. Statins are one of its main passengers. One common change in this gene, rs4149056, weakens that doorman. When the door works slower, the statin (specifically the active form, simvastatin acid) hangs around in your bloodstream longer instead of getting tucked into the liver. Higher blood levels are the reason this variant gets attention, because more statin floating around the body is linked to a higher chance of muscle side effects. This page is educational only. It is not a diagnosis, and it is not a reason to change anything on your own. If you take a statin, the right move is a conversation with your doctor or pharmacist, not a tweak you make solo.
What SLCO1B1 does
Builds OATP1B1, a transporter that sits on liver cells and pulls drugs (including statins) out of the bloodstream and into the liver.
Because statins do their cholesterol work in the liver, this transporter is part of how the drug both gets where it's going and gets cleared from the blood.
The rs4149056 C allele swaps one amino acid (valine to alanine) and makes the transporter work slower, so the active statin lingers in the blood at higher levels.
How much this matters depends on the specific statin. The effect is biggest with simvastatin and much smaller with pravastatin or rosuvastatin, which is why doctors often have options.
Your variants, decoded
This is the single best-studied SLCO1B1 variant. The T allele is the normal, full-speed transporter. Each C allele slows the liver doorman down, so the active statin clears more slowly and sits in the blood at higher levels. The direction is consistent: more C, more exposure.
| TT | Normal OATP1B1 function. Your liver pulls statins out of the blood at the usual rate, so blood levels stay in the expected range. This is the reference group in the research. |
| TC | One slowed-down copy, an intermediate effect. In a single-dose simvastatin study, active simvastatin acid in the blood ran higher than in TT carriers but lower than in CC carriers (CC exposure was about 120% above the TC group). A common, real result worth flagging to a prescriber. |
| CC | Two slowed-down copies, the strongest effect. In that same study, active simvastatin acid exposure was about 221% higher than in TT carriers. This is the genotype most associated with elevated statin blood levels and the most reason to discuss statin choice and dose with a clinician. |
Genotypes are shown order-insensitively and on the forward strand; your own export may print the complementary letters — the meaning is the same.
What the research suggests
If you carry a C allele at rs4149056, the active form of simvastatin reaches higher blood levels because the OATP1B1 transporter clears it more slowly. In a controlled single-dose study, simvastatin acid blood exposure was about 221% higher in CC carriers than in TT, and about 120% higher in CC than in the intermediate TC group. Because the effect is statin-specific and largest for simvastatin, the grounded move is letting a clinician match the statin and dose to your genotype. No over-the-counter product changes how this transporter works, and nothing here should replace medical advice.
PubMed 17108811 · single 40-mg simvastatin dose in volunteers grouped by SLCO1B1 c.521 genotype; active simvastatin acid blood exposure (AUC) was 120% and 221% higher in CC carriers than in TC and TT carriers respectively, with no significant change to the inactive parent drug (simvastatin lactone).
Educational only — not medical advice. “General evidence” means the finding is real but the supplement’s benefit isn’t unique to your genotype.
See this matched to your own DNA — free.
Upload your 23andMe or AncestryDNA file and get your actual SLCO1B1 result, plus every other actionable variant — each line cited, your file never stored.
Questions
Does a C allele mean I can't take statins?
No. It means the active form of certain statins, especially simvastatin, tends to reach higher blood levels in you, which is linked to a higher chance of muscle side effects. Plenty of people with a C allele take statins safely, often on a different statin or a different dose. That's a decision for your doctor, who can weigh your full picture.
Should I stop or lower my statin if I find out I'm CC?
Never adjust or stop a statin based on a genetics result alone. Statins are managing real cardiovascular risk, and stopping carries its own danger. Bring the result to your doctor or pharmacist and let them decide whether a switch or dose change makes sense for you.
Why does my 23andMe file show different letters than TT, TC, or CC?
Genotyping reads one strand of the DNA double helix, and your raw export may print the complementary letters. For rs4149056, T and C can appear as A and G respectively (T pairs with A, C pairs with G). So an A/G result is the same as a T/C result here. The biology doesn't change, just the letter the file happened to print.
Does this affect all statins equally?
No, and that's the useful part. The effect is largest for simvastatin, smaller for atorvastatin, and smallest for pravastatin and rosuvastatin. So even if you carry the higher-exposure genotype, there are usually statin options with a gentler interaction. Your prescriber can pick accordingly.
Is this the same as having high cholesterol genes?
No. SLCO1B1 has nothing to do with how much cholesterol you make or carry. It's purely about how your liver handles the drug once you take it, basically a pharmacology gene rather than a cholesterol gene.