New Beginnings

Understanding the Basics

Pharmacogenomics (phar·ma·co·ge·no·mics) may be a multisyllabic. However, the relatively
new field already has helped many, many people.

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How do my genes affect how medications may work for me?

Some medications may work better with your unique genetic profile and some medicines might not work at all for you. Your genes can affect how quickly your body breaks down (metabolizes) medicine and gets medicine into your bloodstream.

When a medication doesn’t work well with your genes, you may not get the relief you need and you may have unwanted side effects. By gathering information about your genetic profile, you and your healthcare provider can make better informed decisions regarding your treatment. Medicines that align well with your genes may work better and with fewer side effects.

Are genomics and genetics the same thing?

No, though it is a common mistake to use genetics and genomics interchangeably. Genetics is the study of a single gene and its role in how conditions are passed from one generation to the next. Genomics is the study of all parts of an organism’s genes.1

What is pharmacogenomics?

Pharmacogenomics uses information about a person’s genetic makeup, or genome, to choose the medication and dosage that are likely to work best for that person.2

The field of pharmacogenomics has revolutionized how medications are prescribed and taken. Until recently, drugs have been developed in a “one size fits all” kind of approach. Pharmacogenomic tests evaluate a person’s DNA to determine how they may metabolize or respond to medications. This type of testing helps guide healthcare providers in choosing medications and dosing.  While it cannot confirm which medications or doses will work for a patient, it can point out which medications to avoid.

There are two types of genes studied in pharmacogenomics:

Pharmacodynamic: these genes make proteins that affect how a medication works and what it does to the body

Pharmacokinetic: these genes make proteins that affect the movement of the medication through the body (i.e., enzymes in the liver that break down the medications)

Ultra Rapid Metabolizers (UM)

Increased risk of toxicity from a prodrug due toexcessive formation of active metabolites. Consider reducing the starting dose and monitor for ADE.

Increased risk of treatment failure from nonprodrugs, consider starting at a higher dose and monitor for lack of efficacy

Intermediate Metabolizers (IM)

Avoid inhibitors, which would functionally result in poor metabolizer ability

Inducers may improve metabolism

Inconclusive and varied data, often a reduced dose is suggested with close monitoring for ADE

Extensive Metabolizers (EM)

Normal drug metabolism should be expected

Poor Metabolizers (PM)

Unlikely to benefi t from a prodrug, consider an alternative drug

Increased risk of toxicity from non-prodrugs, consider reducing the starting dose and monitor for ADE