Ethnicity and Drug Response: How Genetics Shape Medication Effectiveness

When a doctor prescribes a pill, they assume it will work the same way for everyone. But that’s not true. For some people, a standard dose of blood pressure medicine might do almost nothing. For others, the same dose could cause dangerous side effects. The reason? Genetic differences tied to ethnicity play a huge role in how drugs are processed in the body.

Why Some Drugs Work Better for Certain Groups

It’s not about skin color or where someone’s family is from-it’s about the tiny variations in DNA that affect how enzymes break down medicine. These variations show up more often in certain populations because of shared ancestry. The most studied enzymes are part of the cytochrome P450 family, especially CYP2D6, CYP2C9, CYP2C19, and CYP3A4. Together, they handle about 70% of all cardiovascular drugs.

Take clopidogrel, a common blood thinner. About 15-20% of East Asians carry a gene variant called CYP2C19*2 that makes their bodies unable to activate the drug properly. That means their blood doesn’t thin as it should, raising the risk of heart attack or stroke. In contrast, only 2-5% of African Americans have this variant. So a one-size-fits-all dose can leave some patients unprotected.

Another example is carbamazepine, used for seizures and nerve pain. People with the HLA-B*15:02 gene variant are at 1,000 times higher risk of a life-threatening skin reaction. That variant is found in 10-15% of Han Chinese, Thai, and Malaysian populations-but almost never in Europeans or Africans. Because of this, doctors in Asia now test for this gene before prescribing carbamazepine. In the U.S., it’s still not routine, even though the FDA has known about this risk since 2007.

Heart Medicines and Racial Disparities

One of the clearest cases of ethnicity-based prescribing is BiDil, a combination of isosorbide dinitrate and hydralazine. In 2005, the FDA approved it specifically for self-identified African American patients with heart failure. Why? Clinical trials showed that African Americans on this combo had a 43% lower risk of dying compared to those on standard treatment. The reason? African Americans tend to have lower levels of nitric oxide, a molecule that helps blood vessels relax. This drug combo helps restore that balance.

But here’s the catch: not all African Americans respond to BiDil. In fact, about 35% of them don’t benefit at all. And many non-African Americans who do respond are never offered it because the label says “for African Americans.” That’s the problem with using race as a shortcut. It’s not biology-it’s a social label that sometimes lines up with genetic patterns, but often doesn’t.

The same pattern shows up with ACE inhibitors, used for high blood pressure and heart failure. African Americans, on average, respond 30-50% less than white patients. Beta-blockers also work less effectively in this group. But again, there’s wide variation within the group. About 30-40% of African Americans respond just fine to ACE inhibitors. So if you assume someone won’t respond based on race, you might be denying them a drug that could help.

Warfarin Dosing: A Genetic Puzzle

Warfarin, a blood thinner used after heart attacks or for atrial fibrillation, is another area where genetics matter more than ethnicity. The right dose depends on two genes: CYP2C9 and VKORC1. European Americans typically need lower doses than African Americans because they’re more likely to carry variants that make the drug stay in the body longer. African Americans often have different CYP2C9 variants that aren’t even included in most standard dosing calculators. That’s why a dose that works perfectly for a white patient could cause dangerous bleeding in an African American patient.

Studies show that using genetic testing to guide warfarin dosing reduces hospitalizations for bleeding or clots by up to 30%. Yet only 37% of U.S. hospitals offer pharmacogenetic testing. Most still rely on age, weight, and race-none of which are as accurate as DNA.

Why Race Isn’t a Reliable Genetic Proxy

The biggest myth in this field is that race equals genetics. It doesn’t. Race is a social category. Genetics are inherited. And human genetic diversity doesn’t follow racial lines.

For example, two people classified as “Black” in the U.S.-one with roots in Nigeria, another with roots in South Africa’s Khoisan community-can be more genetically different from each other than either is from a European. That’s because Africa has the most genetic diversity on Earth. Most genetic studies still focus on European populations, meaning we’re missing huge chunks of the picture.

Dr. Sarah Tishkoff from the University of Pennsylvania puts it plainly: “Using race as a stand-in for genetics is like using a country’s flag to predict someone’s height.” It might give you a rough guess, but it’s often wrong.

Even more telling: genetic ancestry testing can predict how someone will respond to asthma drugs better than self-reported race. In one study, African ancestry was linked to a 33% weaker response to albuterol. But if you just asked patients their race, you’d miss the real pattern-because ancestry, not race, drives the biology.

What’s Changing in Medicine Today

The tide is turning. Instead of race-based labels, leading institutions are moving toward genotype-based prescribing.

The FDA now requires drug companies to collect pharmacogenetic data in clinical trials. In 2022, 78% of new drug applications included this data-up from 42% in 2015. Labels are changing too. Ivacaftor, a cystic fibrosis drug, used to be tested only in white patients. Now, the label says: “Test for CFTR mutations. No matter your race.”

Programs like Mayo Clinic’s and Vanderbilt’s PREDICT are genotyping tens of thousands of patients and using the data to adjust prescriptions automatically. In these systems, adverse drug events have dropped by 28-35%. That’s not because they’re using race-it’s because they’re using DNA.

The NIH’s All of Us program is building the largest diverse genomic database ever, with 80% of its 3.5 million participants coming from racial and ethnic minorities. This is critical. Right now, only 19% of genome studies include non-European populations. That means most genetic tests are calibrated for white people. If you’re not white, your test might be less accurate.

What You Can Do Now

You don’t need to wait for the system to catch up. Here’s what you can do:

• If you’re on a drug that’s known to have genetic interactions-like warfarin, clopidogrel, carbamazepine, or certain antidepressants-ask your doctor if pharmacogenetic testing is available.
• Know your family history. If someone in your family had a bad reaction to a drug, tell your doctor. That’s valuable data.
• Don’t assume your race determines how a drug will work. Ask: “Is there a genetic test that could help me get the right dose?”
• If you’re mixed-race or have ancestry from multiple continents, genetic testing becomes even more important. Race-based dosing will likely mislead you.

The Future: Beyond Single Genes

The next big leap isn’t just testing one gene-it’s looking at hundreds. Polygenic risk scores combine dozens, even hundreds, of small genetic variations to predict how someone will respond to a drug. Early studies show these scores are 40-60% more accurate than race-based dosing.

But there’s still a barrier: cost. A full pharmacogenetic panel runs $1,200-$2,500. Insurance rarely covers it unless you’ve had a bad reaction. Until that changes, access will remain unequal.

The goal isn’t to eliminate race from medicine-it’s to stop using it as a substitute for real science. We’re moving toward a future where your medicine is chosen based on your genes, your environment, and your health history-not your skin tone or the box you check on a form.

Why This Matters for Everyone

This isn’t just about African Americans, East Asians, or Europeans. It’s about all of us. You might be the person who needs half the dose. Or the one who needs double. Or the one who shouldn’t take the drug at all.

If we keep using race as a proxy, we’ll keep misprescribing. We’ll keep missing the real cause. And we’ll keep letting people suffer because the system is too lazy to look deeper.

The science is clear: genes matter more than race. The challenge now is making sure the system catches up.