What genetic single-nucleotide polymorphisms are you assessing in clinical practice?

Very few. It depends what the clinical question is. Probably, sometimes, I’m looking at MTHFR [methylenetetrahydrofolate reductase] C677t and A1298c. Sometimes, kind of looking at the COMT [catechol-O-methyltransferase], the VDR [vitamin D receptor], if I’m thinking about it. Almost everyone, I would say APOE [apolipoprotein E] is the other one that I’m probably looking at, how aggressive do I need to be in terms of thinking about brain health, cardiovascular disease risks, so APOE I probably want to see. That would be the most important one to me. Methylation genetics, we’re still learning so much about it and I don’t “treat SNPs.” If I’m looking at single-nucleotide polymorphisms, I’m thinking about what are the other markers I need to be thinking about or looking at, like, what are the potential downstream effects because of the SNP, but we still can’t look at the epigenetic changes, so I think that genetics are very interesting and we’re learning a lot about them, but because we can’t completely test the epigenetics rate even with APOE 44, exponential increase in the risk of Alzheimer’s disease. But I read a paper that what’s going on with this cohort APOE 44 carriers who don’t go on to get Alzheimer’s disease because of this exponential increase, but they don’t, and this paper [from] a conventional medical journal said this cohort of APOE 44 carriers who do not go on to get dementia, they are coming from a culture a belief system that there is value and wisdom to old age. Our beliefs can turn genes on or off, and we can’t test that. Again, APOE 4 I test because I’m definitely going to think about diet, how aggressive do I want to be in terms of toxins, gut, etc., but my take right now is I’m not going to treat a single-nucleotide polymorphism. I’m just going to take it into account. Think about where else I want to look.