What?! What level of clarity could the testing give for a situation like mine, where my dosage, (130 mg), still really seems to low? CYP2D6 Inhibitor + CYP2D6 genetic variant = problems (maybe). CYP2D6: poor metabolizers: Results in higher systemic concentrations. Right now I have to go back to my doctor to ask for a second dosage increase, because the vyvanse has simply never been high enough for me. Copy number and gene re-arrangement determinations may not always be determined. Poor metabolizer • If an activity score (e.g. Therefore, you are failing to reach the dose necessary for beneficial effects, and the drug gets cleared from your system before having had a chance to be converted. Some people may get relief and finally get some sleep. Based on identified CYP2D6 genotypes, individuals can be categorized into 4 phenotypic metabolizer groups as ultrarapid, extensive, intermediate, and poor. I already offered the name of a company in Canada doing gene-testing. Check your genetic data for rs5030656 (23andMe v4, v5): Members: Your genotype for rs5030656 is —. Thank you so much for your thoughtful response, my gosh, as I read my initial message, I sound like such an angry person. If you're not a subscriber, you can: Deconstructing this word’s Greek roots, we have pharmaco (medication) and kinetics (moving, putting in motion). In such cases, we use the pharmacogenomic profile to adjust the dosing only, not the priority. The effect of CYP2D6 genotype on the dose‐exposure relationship for atomoxetine has not been well characterized in children. Of these medications, methylphenidate has been t… 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. (Learn more at Genomics 101: What is a variant?). He told his wife I was an “inappropriate referral”, and not only did I not get to see him, I had been told I had to give up my place on a waitlist, if I wanted to be put on his, after months of waiting to see another specialist. Each scenario rests on whether the drug in the bottle is 1) active (ready to go) or 2) inactive (the body must metabolize it into an active form): 1. A variant that slows down the CYP2D6 isn’t always bad. Working together is fun and productive. - ADHD Roller Coaster with Gina Pera. The medication in the Vyvanse capsule becomes active only when it reaches a certain point in the gut. When someone with ADHD has issues with substance use, OCD, anxiety, severe tics, dyslexia, insomnia, etc., we generally begin with non-stimulants regardless of whether Harmonyx says to use them first or last. It’s worth re-emphasizing: Genetic testing for ADHD medications will not be a “silver bullet.” It is simply a starting point. The main takeaway here is that if you carry a non-functioning variant, you need to be aware that drugs metabolized through CYP2D6 may not work as well for you. Intermediate metabolizers … ~ Clear Your Data ~. This is a table I find useful, that may help other readers: My husband and I are reaching the end of our vacation. Background: Atomoxetine, a selective norepinephrine reuptake inhibitor effective in the treatment of attention-deficit/hyperactivity disorder (ADHD), is metabolized through the cytochrome P-450 2D6 (CYP2D6) enzyme pathway, which is genetically polymorphic in humans. Check your genetic data for rs1135824 (23andMe v4, v5): Members: Your genotype for rs1135824 is —. Then you mention you have. Stay up-to-date with news and events from Gina Pera and ADHD Roller Coaster. If the drug is taken in its active form, the poor metabolizer might require a lower-than-average dosage. In addition, according to initial research, poor metabolizers showed better spatial working memory (144 people) [ 2, 23 ]. Maybe getting the genetic test would solve a lot of problems for you. But armed with information about your genetic factors affecting drug response, you can find the best medication for you or your child. Thanks in advance. ), Enzymes are produced by—you guessed it!—our genes. 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. These changes will be reflected in our pharmacogenetic report. Trouble is, ADHD affects individuals—not clones. You have successfully joined our subscriber list. For example, consider the “lock and key” nature of the way a drug typically works with a cell. When those two antidepressants are used for treatment of Depression and ADHD simultaneously with : Dexedrine, Adderall and Adderall XR, and Vyvanse. I will say that talking to my doctors has never been helpful as I am just as likely to have to explain metabolic issues to them as the other way around. And in your sleep-deprived state, you decide to take some Nyquil (or another cough syrup containing dextromethorphan). Or you may need to discuss alternative medications with your doctor. Stimulants (methylphenidate, amphetamine salts, lisdexamfetamine). I’m wondering if there might be something else going on, more “horse than zebra.”. I’m sorry to hear of your struggles. Genes are the “instruction manuals of life.” As such, they specify how to make proteins. Atomoxetine, which is indicated for treatment of attention‐deficit hyperactivity disorder (ADHD), is predominantly metabolized by genetically polymorphic cytochrome P450 2D6 (CYP2D6). Proteins include enzymes and various other molecules. (We’ll explain examples of an active and inactive ADHD medication below. Check your genetic data for rs28371725 (23andMe v4, v5; AncestryDNA): Members: Your genotype for rs28371725 is —. Join now. Several adverse events, including decreased appetite and tremor, were more frequent in poor metabolizers (less than 0.05). If you are a poor metabolizer, you are slower at removing the drug from the bloodstream than the average person. Check your genetic data for rs28371706 (23andMe v4; AncestryDNA). Like others, I do understand that generally speaking a Poor Metabolizer of 2D6 may need a lower dosage than the average bear of an “active” form of amphetamine, whether it be Adderall, Dexedrine or any within that family. This non-stimulant was the first drug to receive an FDA-certified indication for adult ADHD. The CYP2D6 gene encodes cytochrome P450 2D6, an enzyme that plays a crucial role in the metabolism of all tricyclic antidepressants, most SSRIs, and about half of all antipsychotics.1 Inter … Studies suggest people with less active CYP2D6 (poor metabolizers) may perform better in cognitive tasks that demand sustained attention or vigilance (144 people) [2, 23]. On the other hand, it also may significantly increase the risk of Parkinson’s disease for those exposed to pesticides. . https://adhdrollercoaster.org/adhd-medications/can-acidic-foods-affect-stimulant-medications-for-adhd/. Other drugs, however, enter the body in an inactive form and require some additional … alterations. 2011;16(7):691-692. Genetic variants only give you part of the picture -- your lifestyle, diet, gut microbes, and environment all interact with your genes. Dosage adjustment is recommended. That’s the Wrong Question. Too low a dose? Following multiple‐dose oral administration, compared with CYP2D6 normal metabolizers, the risperidone dose‐adjusted steady‐state serum/plasma concentration was 2.35‐fold higher in intermediate metabolizers (95% confidence interval [CI] 1.77–3.13, p<0.0001) and 6.20‐fold higher in poor metabolizers … Welcome to the next post in my 7-part series: Genetic Testing for Choosing ADHD Medications — Part 4. If the drug is taken in its inactive form—that is, the drug must be metabolized to become active—a standard dose might not be enough.”. headache and terrible eye pain! No problem. However, I was able once to get sent to a clinical pharmacist who was able to at least shed some light on my genetic PM 2D6 results (which my geneticist and prescribing physician don’t understand). A fast CYP2D6 enzyme function is usually called an ‘extensive metabolizer’. Briefly defined, pharmacogenetics is the study of genetic variations that can influence individual responses to pharmaceuticals. Genetic variation is what makes us all unique—of hair color, skin color, height, or even the shape of our faces. My adult son with ADHD has at least one SNP (COMT val/val) that may require a higher than normal dosage of medication, but if his Intermediate Status on 2D6 is also hampering the conversion of his 70mg of Vyvanse to the active form that could be a fundamental reason why he constantly says he needs a higher dose and only gets about 6Hrs out of his pill. People who are poor metabolizers break down some medicines slowly and are likely to need altered doses or even a different medicine in some cases. As I read, I was wondering if you’d tried Vyvanse, as it is time-release Dexedrine. We will try to answer this in a few days, but I think it’s really best if you ask your physician. Others…  well, they may not react the same way to dextromethorphan! Below is an excerpt from the drug label for Strattera regarding genes that affect its metabolism. I apologize for my tone in the initial message. (Like enzymes, receptors are proteins made according to genetic instructions.). Specifically, you can learn more about how your genes affect how you respond to medications—and how medications respond to you! Can I ask what lab/company you’d recommend for testing the genes implicated in vyvanse/dexedrine IR metabolism? It breaks down about a quarter of all drugs, including: You’ve probably heard people say, “I’m very sensitive to medication.”. Hope he’s learning the basics now, but I certainly wouldn’t bet my health on it. The effect of CYP2D6 genotype on the dose-exposure relationship for atomoxetine has not been well characterized in children. Log in and select your data file Not a member? I need to read the rest of your blog! Turns out I am a poor metabolizer for 2D6, which explained my adverse reactions to the Beta blockers and tricyclic antidepressants. How can that be? The genetic testing for ADHD medications do not provide the slam-dunk answers many patients and doctors seem to think they do. I see this company. CYP2D6 poor metabolizer: 0: Significantly decreased metabolism of atomoxetine may result in higher concentrations as compared to non‐poor metabolizers. [Gina does an excellent job of explaining this vis a vis ADHD medications in her first book, Is It You, Me, or Adult A.D.D.?]. This series has been great with a wealth of information on a complicated but crucial topic. Thus, many drugs metabolized by CYP2D6 may also be broken down with other enzymes. No spam, just cool stuff. If your body metabolizes a drug too quickly, it can decrease the drug’s efficacy. Receive Gina Pera's award-winning blog posts and news of webinars and workshops. Coming up next: Post 5, The limits of genetic testing for ADHD medications. The genetic factors are highly variable. This is just one example, among many, of medications that are metabolized by the CYP2D6 enzyme. Now let’s consider an ADHD medication in its active form: Strattera. Now we go into more detail on two key aspects: We’ve all seen those TV commercials for laundry stain-removers with enzymes. Variations in plasma atomoxetine exposures can occur because of genetic variation or as a consequence of … Thank goodness, we are past those days. The outstanding question then becomes: how much lower of a dose should you take? P.S. In other words, these genetic variants affect pharmacokinetics (PK). Other drugs are turned into their inactive form by CYP2D6. In addition, accurate copy number calling is critical in determining the CYP2D6 phenotype as the variation in copy number might lead to increased or no function compared to normal. Free weekly newsletter with latest articles and interesting health research. I often will refer such questions to the nearest university-hospital pharmacist. You don’t get a therapeutic benefit (nothing happens). Originally published 6/2015. © Copyright 2021 Genetic Lifehacks | Moon Consulting, Combining 23andMe and AncestryDNA Raw Data Files, Problems with IBS? Note: This post is a little longer than the previous ones. There are lots of enzymes in humans, but here’s a particularly significant one when it comes to drug-response: Cytochrome P450 2D6, an enzyme encoded by the CYP2D6 gene. 2. I wish I knew exactly what tests I need to take to determine what level of vyvanse and evening dexedrine IR I need. Check your genetic data for rs3892097  (23andMe v4; AncestryDNA): Members: Your genotype for rs3892097 is —. 1 CYP2D6 is highly polymorphic. Refer to FDA labeling for specific dosing recommendations. Here in part 4, below, you’ll discover how, when, and why this data might prove helpful. A stimulant such as Adderall or Ritalin interacts with certain receptors with great specificity. With the last post (7), we’ll provide a list of takeaway points. Objective To quantify the difference in the antipsychotic and antidepressant exposure among patients with genetically associated CYP2C19 and CYP2D6 poor (PM), intermediate (IM), and normal (NM) metabolizers. 0 -0.5) indicates the patient MAY be a poor metabolizer, the phenotype assigned will be: CYP2D6 possible poor metabolizer We will be wrapping up with some of the issues you mention, but we figured the incremental approach would work best in explaining these complex factors. Otherwise, my pharmacist has been the most help (at least providing me with a table of the enzyme substrates, etc). I hope you share if you get more info. Peñas-Lledó EM, Dorado P, Agüera Z, et al. The answer:  The medication that works best for the individual. So here is my confusion: would not it make more sense, according to metabolism reaction, that I was supposed to take, and process, Vyvanse even in higher than 10 mg dose? 2 Trzepacz PT et al. I end up taking 60 mg more, then going without for six days at the end of the month, but that won’t get me through five chemistry courses this semester. Members: Your genotype for rs28371706 is —. Of course there was no drug I had taken, except sleeping pills, that was addictive, (I did need them to sleep sometimes), but being a Canadian doctor, he didn’t know enough to understand that ADHD stimulants aren’t addictive. We have already investigated another gene believed to have an impact on dosing with Strattera, the SLC6A2 gene.However, in that earlier post, we alluded to another gene responsible for the metabolism of the non-stimulant ADHD drug Atomoxetine.This gene is called CYP2D6.The CYP2D6 gene codes for an important enzyme of the same name (which is an important enzyme produced in the liver). Accurate prediction of CYP2D6 phenotype from genotype data is important for many clinically relevant drugs. Check your genetic data for rs16947 (AncestryDNA): There are other (rare) variants for CYP2D6 not covered by 23andMe or AncestryDNA. Check your genetic data for rs5030867 (23andMe v4, v5; AncestryDNA): Members: Your genotype for rs5030867 is —. The CYP2D6 (sounds like “sip-2-dee-6”) gene encodes an enzyme that is involved in the metabolism of codeine. That means less stimulant is required to reach a given effect. This in part due to their drug-response gene variants. Many other patients are most likely in the same sitation, and will have to educate themselves and their doctors in order to get the help they need. But, yes, genetic testing for ADHD medications can provide some useful information. These “scrubbing” enzymes find their targeted stains, latch on, and break down the stain. Thank you so much for weighing in—and making such important points. I sent my husband a query and failed to bird-dog it. That is, it interacts only with those receptors. These range from constipation to dizziness, as stated in the drug label. L-Tyrosine). Typically, a drug is taken in its active form; it goes to work “as is.” Think of it as the protein equivalent of “ready to wear”. I just said poor metabolizers risk having too much medication in their system, even with an average dose. Genetic testing for ADHD medications offers one clear benefit: it can help to identify whether you metabolize medications slowly, normally, or very quickly. There are also substances that inhibit the CYP2D6 enzyme. The cytochrome P450 (CYP)1 enzyme debrisoquine 4-hydroxylase known as CYP2D6 is involved in the oxidative metabolism of many different classes of commonly used drugs, including neuroleptics, tricyclic antidepressants, selective serotonin reuptake inhibitors, β-adrenoceptor blockers, and antiarrhythmics (1)(2). Your advice to go slow and low when trialing medications in poor metabolizers is absolutely correct, and I just want to underscore the point you’ve been making that medication selection is very complex, that there are are many factors, not just the gene profile, that have to be considered. You might start encountering unacceptable side effects—despite that medication being an excellent choice for you. Good luck! Being a poor metabolizer may reduce the risk of some cancers such as bladder or lung. At the other extreme, if your body metabolizes the drug too slowly, unacceptable side effects may result. Hi I have 37 years and found out just couple months ago that I have ADHD so my psychiatrist first gave me vyvanse 10 mg to start and try and after 4 hours I start feeling side effects very intense and then I felt like a rush of energy and only lasted 3 hours and then nothing else and later on in the afternoon around 4pm I was completely awake like alert and that night had insomnia and then I went up in the dose until 40 mg and I quitted the side effects were very intense and the other days I didn’t feel anything that can help adhd symptoms and you said that vyvanse and poor metabolism need a higher dose I think I’m going to try vyvanse again and this time go higher in dose after vyvanse I changed to generic adderall and I started 5mg up to 40mg in a day and nothing happened I didn’t see any changes on ADHD symptoms so I switched to generic ritalin instant release methylphenidate and I’m in 20 mg now but only lasted 1 hour and then goes away I started at 5 mg twice a day and nothing then going up until 20 mg and I thought that small dose I was going to start seeing the benefits of the drug but nothing please help me what do you think my Dr. Is also prescribing me wellbutrin but I stopped taking it because I didn’t work at all and I was taking lamotrigine too but I stopping that one too because is not doing anything Attention-deficit hyperactivity disorder (ADHD) is a chronic neurodevelopmental disorder characterized by persistent symptoms of inattention, hyperactivity and/or impulsivity. Hello Gina… The goal: more accurate information for the layperson (and medical professionals) with little background in molecular biology or genetics. But my body could not take it: too much numbness when the meds wore off, blood vessels constricting to the point of pain, and terrible muscle pain around old injuries. And that’s a very helpful table. Approximately 7% of a Caucasian population are PMs. CYP2D6 poor metabolizer: 0: Significantly decreased metabolism of atomoxetine may result in higher concentrations as compared to non‐poor metabolizers. This CYP2D6 Mutation Detection Panel is the most extensive on the market and covers over 93-97% of poor metabolizer phenotypes. But I knew about the CYP enzymes at least 15 years ago. But until such time as my husband responds… (I’ll remind him). Slow (or no) enzyme function is referred to as a ‘poor metabolizer’. Importance Precise estimation of the drug metabolism capacity for individual patients is crucial for adequate dose personalization. Planners. Here’s why: If you’re a poor metabolizer, you are slow at converting the inactive drug into its active form. Guess what? You explained that a vyvanse dose would need to be raised in poor metabolizes to achieve the same effect. To recap: Genetic variation (or variants, sometimes called mutations) describe the tiny variations in the DNA sequence in each of our genomes. Why is it important to know what type of metabolizer you are? There are MANY reasons to explain what you experienced. If the drug is taken in its active form, the poor metabolizer might require a lower-than-average dosage. They are typically very helpful! Doubly rewarding. CYP2D6 metabolizer status and atomoxetine dosing in children and adolescents with ADHD. (You don’t absolutely need genetic testing for this purpose, though. Consider the ADHD medication Vyvanse. Genetic Variant Information. 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: Based on identified CYP2D6 genotypes, individuals can be categorized into 4 phenotypic metabolizer groups as ultrarapid, extensive, intermediate, and poor. Your doc might invite trouble by documenting your need for that dose without any independent support. Clin Pharmacol Ther. My scientist husband (“Dr. Genetics. Instead, picture miscommunications galore, chronic conflict, tempers raising the roof, and few epithets tossed around before we both said, “I give up! We also have enzymes in our bodies—but not to break down stains. Goat and me working together so harmoniously on a project. Personalized solutions based on your genes, Serotonin: How your genes affect this neurotransmitter, tamoxifen (breast cancer, estrogen blocker), risperidone (schizophrenia, bipolar medication), A fast CYP2D6 enzyme function is usually called an ‘extensive metabolizer’. That requires piling more drug (higher dosage) into the “cup holder” to reach the same snug-fitting effect. That is, are you using all the environmental supports to help you structure your time and focus? A guideline from The Dutch … Think of pharmacokinetics as the physiological mechanisms by which the body absorbs, distributes, metabolizes, and removes a drug from the body. The most recent “doctor” I was on a wait list to see, told his wife, who was my GP, after receiving my medical record, awash with misdiagnoses, and failed medication attempts, that I must be suffering from “drug addiction”, never so much as having tried marijuana in my life. The CYP2D6 enzyme metabolizes (breaks down) about 25% of pharmaceutical drugs including SSRIs, opioids, tamoxifen, dextromethorphan, and beta-blockers. These results suggest that CYP2D6 poor metabolizers taking atomoxetine in doses up to 1.8 mg/kg/day are likely to have greater efficacy, greater increases in cardiovascular tone, and some differences in tolerability compared with CYP2D6 extensive metabolizers taking similar doses. Don’t you hate that? The American Academy of Pediatrics recommends the use of pharmacotherapy and/or behavior therapy for children aged 6 to 11 diagnosed with ADHD. tx! Instead, our enzymes break down certain substances and convert them into other substances. 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). It’s said that medical-science information takes about 20 years to trickle down to the clinical level. This may increase the occurrence of side effects, but also a greater improvement of ADHD symptoms as compared with non‐poor metabolizers in those who tolerate treatment. The majority of genetic polymorphisms to the CYP2D6 gene result in either absent or decreased function of the enzyme activity, with CYP2D6*2xn being the only one that increases its activity. I needed about 1/4 the dose of a “normal” person. It had never been done at my clinic, so they were unsure what to order, but I did get 2D6 and one of the other CYP enzymes tested. This also can affect how long the drug stays your body. Now I’ve dropped two of the chemistry courses, so I’m sane again. I know you realize this, but I need to mention: It’s not advised to use the stimulants as “performance drugs”. If there is any references showing Vyvanse uses 2D6 to convert that would be good information. Your email address will not be published. Inactive medications are also called “pro-drugs.”. 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