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CYP2D6 is responsible for the metabolism and elimination of approximately 25% of clinically used drugs. Which SNPs do I need to check on 23andme in order to determine if I'm a poor or ultrarapid metabolizer of CYP2D6 substrates, and how reliable would the results be?

I've found one article on this topic, but I'm not sure how accurate it is, and it doesn't cite sources.

PS: why isn't this information more readily accessible to 23andme users, given the relatively large risks incurred by not knowing one's reaction to a large number of drugs?

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Unless your polymorphisms have been tested against a particular drug, you can't extrapolate a starting dosage for it based only on your genotype. It's better to actually take the drug, and change dosage based on observations.

See this paper

https://www.ncbi.nlm.nih.gov/pubmed/24935087

CONCLUSIONS AND RELEVANCE: In this meta-analysis of randomized clinical trials, a genotype-guided dosing strategy did not result in a greater percentage of time that the INR was within the therapeutic range, fewer patients with an INR greater than 4, or a reduction in major bleeding or thromboembolic events compared with clinical dosing algorithms.

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why isn't this information more readily accessible to 23andme users, given the relatively large risks incurred by not knowing one's reaction to a large number of drugs?

Because no-way no-how does 23andMe want to be in the business of giving medical advice. Nor should they be, because for most things, we have no idea how to convert genotype knowledge anything medically actionable.

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    $\begingroup$ This is the case for all genotype guided dosing strategies I'm aware of, even if the polymorphisms have been tested against a particular drug. So far, clinical effect is always better. $\endgroup$
    – De Novo
    Jul 10, 2018 at 23:05
  • $\begingroup$ That was my understanding too, but I phrased it like I did lest there be exceptions unknown to me. $\endgroup$
    – swbarnes2
    Jul 10, 2018 at 23:20

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