Thank goodness, we are past those days. Genes are the “instruction manuals of life.” As such, they specify how to make proteins. Meanwhile, in a poor metabolizer, the drug can build up in the body to toxic levels and cause treatment-related adverse reactions. Specifically, you can learn more about how your genes affect how you respond to medications—and how medications respond to you! I don’t want to steer anyone wrong here, but I do think it is important for people to know that their genetic variants impact drug metabolism rates. For example, there are generally three categories that describe the rate at which humans metabolize drugs, based on the enzymes produced by their gene variants: Sometimes these categories are further broken down into smaller gradients, such as ultra-rapid metabolizers and intermediate metabolizers. There are different CYP2D6 gene versions, or variants, and each has a different effect on how well codeine is metabolized in the body. The FDA states that the dose of atomoxetine may need to be adjusted in patients known to be CYP2D6 poor metabolizers . (We’ll explain examples of an active and inactive ADHD medication below. Non-stimulants (atomoxetine, guanfacine, clonidine). Mol Psychiatry. Briefly defined, pharmacogenetics is the study of genetic variations that can influence individual responses to pharmaceuticals. Risperdal, Abilify,). Knowing whether you’re a fast or slow metabolizer may make it easier to find the right dosage of certain medications. Instead, you can follow the wise practice of “start low, titrate slow” (meaning, increase the dose slowly). Substance A can bind to the receptor and an action results. (Learn more at Genomics 101: What is a variant?). Check your genetic data for rs28371706 (23andMe v4; AncestryDNA). Intermediate metabolizers … Now we go into more detail on two key aspects: We’ve all seen those TV commercials for laundry stain-removers with enzymes. I think the genetic testing could, potentially? Therefore, data have been collected to explore any relationship between metabolizer status and therapeutic aspects of this drug. Notify me of follow-up comments by email. CYP2D6 metabolizer status and atomoxetine dosing in children and adolescents with ADHD. About 7% of Caucasians and 1-2% of African-Americans and Asians are poor metabolizers (PMs) of CYP2D6 metabolized drugs. After years of adverse drug reactions I had a physician casually remark that I must be a fast metabolizer. Stimulants (methylphenidate, amphetamine salts, lisdexamfetamine). I suppose the NHS doesn’t pay for the Genesight testing. Some drugs, such as tamoxifen, need to be metabolized to their active form by CYP2D6 in order to work. There is no “best medication” for ADHD. Regardless, the manufacturer of atomoxetine does recommend a dose reduction in patients with hepatic impairment, those on a known CYP2D6 inhibitor or those known to be a "2D6 poor metabolizer".1 References: - ADHD Roller Coaster with Gina Pera, http://medicine.iupui.edu/clinpharm/ddis/, Post 7: Gene-Testing To Inform ADHD Drug Therapy - ADHD Roller Coaster with Gina Pera, Part 6: Gene-Testing To Inform ADHD Drug Therapy - ADHD Roller Coaster with Gina Pera, Part 5: Gene-Testing to Inform ADHD Drug Therapy - ADHD Roller Coaster with Gina Pera, Pharmacokinetics (PK): “What the Body Does to the Medication”, Pharmacodynamics: “What the Medication Does to the Body”, Antipsychotics (e.g. The notion that one should “try this drug” first, next or last based on the pharmacokinetic profile is a bit of an over-reach by Harmonyx. I just said poor metabolizers risk having too much medication in their system, even with an average dose. This CYP2D6 Mutation Detection Panel is the most extensive on the market and covers over 93-97% of poor metabolizer phenotypes. Assuming that the diagnosis is correct and the medications being considered are recommended for it, beneficial effects depend upon identifying the dosage that works best for the individual. By contrast, there are the “nothing phases me” types— and of course plenty of people in between. 2. We also have enzymes in our bodies—but not to break down stains. The enzyme is highly genetically polymorphic. The two patient populations that are likely at the greatest risk for being a CYP2D6 poor metabolizer include African Americans/Black Africans and Asians. Variations in plasma atomoxetine exposures can occur because of genetic variation or as a consequence of … I, too, am most worried about the “try this first/next/last” recommendations being taken literally by patients, as I’ve already heard some parents of children with ADHD report. Just wanted to point out that ‘poor metabolism’ is a double-edged sword. I need to read the rest of your blog! after I took the pill everything I saw suddenly had dimensions like in childhood, I was calm and normal, stopped trying to walk into the walls instead of doorways, galloping down my food instead of chewing it, and was consistently in a good mood even after the meds stopped working. Members: Your genotype for rs28371706 is —. Thank you again for this valuable resource! Is it possible that your son, like many adults with ADHD, suffers sleep deficits, over-uses electronics, has vitamin or mineral deficiencies, consumes caffeine or nicotine, and/or depends on a stimulant to “propel” him through the day rather than to provide the focus that helps to implement strategies to support Executive Functions? Planners. This series has been great with a wealth of information on a complicated but crucial topic. Yes, let’s throw in another factor in medication response: whether the drug is inactive or active. I hope you share if you get more info. I wish I knew exactly what tests I need to take to determine what level of vyvanse and evening dexedrine IR I need. Too high? For this reason, it has been marketed as being less easily abused than other medications in the amphetamine class of stimulants (e.g., Adderall, Dexedrine). I haven’t seen the stimulants on the list of 200 or so medications already documented. Of these medications, methylphenidate has been t… Revised on 4/26/19. P.S. By the way, this is FDA-controlled text. Drug B doesn’t come close. A variant that slows down the CYP2D6 isn’t always bad. For example, stomach enzymes break down the food you ingest into tiny bits that can be converted into energy. I read it at the time, thought about it, and I have no idea. 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