Rethinking Medications in the Age of Genetic Testing
What would you do if you were told that one of your go-to medicines for mild to moderate days was something you shouldn’t take because of your specific genetics? None of us wants to have that happen. Living with chronic illness means constantly looking for another medicine or treatment to add to our migraine toolkit, not looking to take something out of it.
Of course, we have to remove things sometimes. We get serious or intolerable side effects. The treatment or medicine doesn’t work, or it does but then it stops working. We develop interactions between it and something else we’re taking or doing.
We’re used to these types of removals. We’ve learned to expect them. But what if we’re told to remove a particular drug – one that’s working at least sometimes, at least on the milder days – because our specific genes make it more likely that we’ll experience serious side effects? Even if those side effects haven’t happened yet?
Silent problems with a common drug
That’s what happened to me with ibuprofen.
My go-to mild pain reliever has always been ibuprofen. I don’t take acetaminophen. It doesn’t work well for me, and I don’t consider the liver risks worth the small to no benefit I receive from taking it. I don’t take any medications with it included, either. Even the opioids I’ve prescribed for my severest days have the acetaminophen removed.
Ibuprofen was my first neurologist’s abortive of choice as well. None of the triptans have been beneficial for me, so in the early days of my diagnosis, she told me to take three to four of the liquid ibuprofen capsules at onset (because my migraines come on severely and rapidly). I would tally the number of days I’d taken medications each month, making sure not to go into what would be considered a risk factor for MOH, and I’d treat the ones I needed to treat just as she said.
It turns out I wasn’t supposed to do that. In fact, according to the genetics test my current neurologist had me take, I was never supposed to that.
Pharmacogenetic testing results
My current neurologist had me take a pharmacogenetic test about six months ago. A pharmacogenetic test is intended to personalize medicine and make treatment safer and more effective by taking into account how your personal genetics interact with a variety of specific medications. Included in my test were nearly all of the medications I’ve been prescribed over the years for migraine (and anxiety/panic attacks) including SSRIs, SNRIs, TCAs, anticonvulsants, NSAIDs, opioids, benzodiazepines, triptans, and ergot derivatives.
The results were fascinating. The test indicated that I have a lower response rate to almost every SSRI available, which matched my personal experiences of never experiencing any relief from drugs like fluoxetine or sertraline despite having tried them all. It also indicated that I would have issues with topiramate, which I absolutely did, and that I am an ultra-rapid metabolizer of both caffeine and codeine, which means I need more than other people do of each in order to feel a therapeutic effect. Finally, it said I had a substantially increased risk of toxicity and severe side effects from ibuprofen.
While none of the others surprised me, and many (like the needing more codeine for relief) actually validated my personal experiences, this last one floored me.
I had never had any issues with ibuprofen, and I’d been taking it for years. It didn’t always work, and I always made sure to take it with food, but I hadn’t expected it to be something I should avoid for fear of toxicity. While some people may have continued to take it, I didn’t. After all, the other results were too accurate, and I had recently studied its potential to cause severe bleeding. Instead, I switched to naproxen, which my results said was okay, and I continue to pray for the day that CAMBIA, which works wonders and is on my gene-approved list, becomes more affordable.
What about you? Have any of you taken a pharmacogenetic test? Would you?
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