How to Choose The Right Medication for Depression and Anxiety

At-Home DNA Testing Can Help You Choose the Right Medication

As an everyday consumer or patient, you have more control over your medication options than you might think. If you’re dealing with anxiety or depression, drugs like citalopram, escitalopram, and sertraline are commonly recommended. The choice often depends on your symptoms, your history with side effects, potential interactions with other medications, or even foods!

For instance, did you know that sertraline can interact with grapefruit juice? Grapefruit juice contains compounds that inhibit cytochrome P450 enzymes, particularly CYP3A4. These enzymes play a role in metabolising sertraline. When CYP3A4 is inhibited, it can increase sertraline levels in your bloodstream, potentially leading to stronger side effects or toxicity.

At AttoDiagnostics and AttoPGx, we’re focused on empowering doctors, medical practitioners, and patients with greater certainty and knowledge when it comes to personalised prescribing. We take it a step further by exploring drug-gene interactions. This science, called pharmacogenomics, examines how your genetic makeup can affect drug metabolism and response.

As part of testing our new product, employees at The AttoGroup tried our Mental Health PGx test. Here’s what one employee learned from their experience with anxiety and depression medications.

When Did You First Take a Prescription for Anxiety?

In my 30s, I was prescribed citalopram, a commonly used selective serotonin reuptake inhibitor (SSRI). I tried it for about a year before moving overseas.

How Did the Medication Work for You?

It worked okay, but when I moved overseas with work, my anxiety increased. I also noticed some weight gain—though that might have been due to the portion sizes in America! My new doctor in the U.S. recommended a drug called Viibryd.

Let’s Check Viibryd: That’s the Brand Name for Vilazodone. How Did It Work?

It worked very well. After a few years in the U.S., I moved to Los Angeles. By then, I wasn’t feeling anxious anymore. Considering the endless sunshine and a healthier lifestyle, I decided to stop taking the medication.

What Happened Next?

In my 40s, I returned to the UK and faced a tough period at work. My doctor prescribed sertraline, which I took for about a year. It worked better than citalopram did the first time around.

The interesting part came later when I got my PGx test results that looked at my DNA.

What Did Your PGx Report Reveal?

Thanks to my expression of the CYP2C19 gene, I’m a rapid metaboliser of citalopram. The report explained:

“Increased metabolism of citalopram and escitalopram to less active compounds compared to normal metabolisers. Resulting in lower plasma concentrations which decrease the probability of clinical benefit at normal dosing.”

For sertraline, the report said:

“Normal metabolism through the CYP2B6 gene pathway. Rapid metaboliser through the CYP2C19 gene pathway."

So being a normal metaboliser there was no need to change my medication based on this gene alone. But through the CYP2C19 gene pathway, I am a rapid metaboliser, therefore I have a small increase in metabolism of sertraline to less active compounds compared with CYP2C19 normal metabolisers. Initiate therapy with the recommended starting dose, but will require an increased dose to achieve clinical effectiveness (per CPIC strong recommendation).

So, Two Genetic Pathways Affect Sertraline Metabolism?

Exactly! CYP2B6 and CYP2C19 both play a role, and I’m a “normal” metaboliser through CYP2B6 (CPIC Level B evidence - genetic information could be used to change prescribing) and a rapid metaboliser through CYP2C19 gene (CPIC Level A evidence - change in prescribing recommended). This probably explains why sertraline worked but didn’t achieve the optimum therapeutic outcome, as the drug wouldn’t have stayed in my system for long due to rapid breakdown to less active compounds by the CYP2C19 gene.

What About Viibryd?

My PGx report didn’t specifically mention Viibryd or vilazodone, but I did some research. I learned that:

• CYP3A4 is the major enzyme responsible for vilazodone metabolism.

• Genetic variations in CYP3A4 can affect drug plasma levels and side effects.

• CYP2C19 and CYP2D6 play minor roles in vilazodone metabolism, but they can still influence individual responses.

According to my PGx report, I’m a normal metaboliser for CYP3A4, which likely explains why Viibryd was effective for me.

What’s Your Takeaway With Regards to PGx Testing?

The AttoDiagnostics PGx test provided strong evidence for why sertraline and Viibryd worked better for me than citalopram, but for sertaline, a guided increased dose would have produced a better outcome. If I ever need prescriptions for mental health or other conditions, I’d definitely share this information with my doctor.

Out of curiosity, I also checked methotrexate (available in the Comprehensive PGx product), which my mother took for rheumatoid arthritis. I recently had a blood test showing elevated Anti-CCP levels—a potential precursor to rheumatoid arthritis. My PGx report lists methotrexate in the “use as directed” column, which is reassuring, should I ever need to embark on that journey.

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