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Abstract
Metabolic detoxification (detox)—or biotransformation—is a physiological function that removes toxic substances from our body. Genetic variability and dietary factors may affect the function of detox enzymes, thus impacting the body’s sensitivity to toxic substances of endogenous and exogenous origin. From a genetic perspective, most of the current knowledge relies on observational studies in humans or experimental models in vivo and in vitro, with very limited proof of causality and clinical value. This review provides health practitioners with a list of single nucleotide polymorphisms (SNPs) located within genes involved in Phase I and Phase II detoxification reactions, for which evidence of clinical utility does exist. We have selected these SNPs based on their association with interindividual variability of detox metabolism in response to certain nutrients in the context of human clinical trials. In order to facilitate clinical interpretation and usage of these SNPs, we provide, for each of them, a strength of evidence score based on recent guidelines for genotype-based dietary advice. We also present the association of these SNPs with functional biomarkers of detox metabolism in a pragmatic clinical trial, the LIFEHOUSE study.
Highlights
We are exposed to hundreds of toxic substances of endogenous and exogenous origin, including radical oxygen species produced during cellular respiration and foreign compounds known as xenobiotics such as environmental toxicants, food additives, and drugs
We explored the association of the genetic variants presented with functional biomarkers of detox metabolism within the Lifestyle Intervention and Functional Evaluation—Health Outcome Survey (LIFEHOUSE), a real-world pragmatic clinical trial (PCT) conducted at the Personalized Lifestyle Medicine Center (PLMC) by Metagenics Inc
Only six variants in genes encoding Phase I and Phase II detox enzymes have been tested in clinical studies: Cytochrome P-450 1A2 (CYP1A2) rs762551; Cytochrome P450 1B1 (CYP1B1) rs1056836; segmental deletions of Glutathione S-transferase theta 1 (GSTT1) and Glutathione S-Transferases Mu 1 (GSTM1); COMT rs4680-A; and insertion variants of UGTA1 (TA/-)
Summary
We are exposed to hundreds of toxic substances of endogenous and exogenous origin, including radical oxygen species produced during cellular respiration and foreign compounds known as xenobiotics such as environmental toxicants, food additives, and drugs. We have selected these SNPs based on their association with inter-individual variability of detox metabolism in response to certain nutrients in the context of human clinical trials. For each of these SNPs, we provide a strength of evidence score based on recent guidelines for the interpretation and classification of nutrigenetic variants [3]. We have selected these SNPs based on their association with inter-individual variability of detox metabolism in response to certain nutrients in the context of Nutrients 2022, 14, 768 human clinical trials For each of these SNPs, we provide a strength of evidenc3eofs1c6ore based on recent guidelines for the interpretation and classification of nutrigenetic variants [3]. CYP1A2: Cytochrome P-450 1A2; CYP1B1: Cytochrome P-450 1B1; GST: Glutathione Stransferase; GSTM1: Glutathione S-transferase mu 1; GSTT1: Glutathione S-transferase theta 1; COMT: CatecholO-methyltransferase; UGT1A1: UDP-glucuronosyltransferase A-1; ROS: Radical Oxygen Species
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