But scientists and doctors are now using new technology to improve drug efficacy. For example, 30 percent or more of depressed patients are not helped by antidepressants. In psychopharmacological therapy, a patient must be on a drug for at least two weeks before the effects can be fully examined and evaluated. For a patient in that 30 percent, this could mean months of trying medications to find an antidote to their pain. Doesn’t it make more sense to determine that patient’s genetic sensitivity to a variety of antidepressants before administering them in a “wait-and-see” sort of way?
Another example is the drug Plavix, which blocks platelet reception and is the second best-selling prescription drug in the world, even though patients have a variety of responses, not all of them good. GWAS studies have linked a single nucleotide polymorphism (SNP) in the gene CYP2C19 to those who cannot normally metabolize Plavix, which is often given to patients after receiving a stent in the coronary artery to prevent clotting.