Understanding pharmacogenomic influences on drug response and adverse effects is critical to precision health, a major goal for modern healthcare. The ability to transcend the current trial-and-error process of treatment matching in psychiatry would prevent harm, improve outcomes and enhance patient quality of life.1 Public enthusiasm for using genetic information to guide prescribing is nearly universal and physician support is strong.1 However, although the world is ready for pharmacogenomics, pharmacogenomics is not ready for the world! Our grasp of the mechanism of disease and drug action remains primitive in psychiatry. Genetic risk for mental illness has only recently begun to be mapped to specific variants and pathways. Very large, well-controlled, unbiased studies are needed to identify genetic factors that influence drug response. The small candidate gene studies nominating most proposed pharmacogenomic variants are known to produce unreliable, false-positive results. More research is required before pharmacogenomic testing can identify the best drug for a patient.2 A profoundly uneven knowledge base supports the two classes of genetic variation that influence drug effects. Pharmacokinetic variants that regulate the absorption, metabolism and disposition of drugs impact what the body does to the drug. Pharmacodynamic variants that modify target receptors and mechanistic pathways affect what the drug does to the body. Both types can alter drug efficacy and side effects. A solid evidence base exists for many pharmacokinetic variants that alter drug metabolism.3,4 Common variants in two enzymes that process the majority of psychotropic drugs, CYP2D6 and CYP2C19, have been shown to impact serum levels of serotonin ...
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", language="en", issn="1516-4446", doi="10.1590/1516-4446-2019-0772", url="http://dx.doi.org/10.1590/1516-4446-2019-0772" }