According to published studies¹², genetic variations influence the absorption, metabolism, and effectiveness of dietary supplements, determining individual needs for vitamins, minerals, and ergogenic compounds. Targeted nutritional support based on a person’s genetic profile can lead to optimal utilization of micronutrients and improved overall health.
The GENOSOPHY® genetic test analyzes specific genetic variants related to how the body processes key dietary elements. The test is conducted using GENOSOPHY®’s award-winning algorithm, ensuring high accuracy in assessing personalized nutritional needs.
The test is recommended for:
Individuals who wish to tailor their supplement intake to their genetic background.
Individuals with deficiencies in vitamins and minerals such as folic acid, vitamin D, and iron.
Those who want to understand their genetic predisposition regarding the metabolism of micronutrients and ergogenic supplements.
GENOSOPHY®’s genetic analysis includes the study of variants associated with the absorption and metabolism of dietary elements. Some of the genes analyzed include:
Gene / Polymorphism | Effect | Association | How We Help |
---|---|---|---|
MTHFR (rs1801133) | Elevated homocysteine levels | Risk of thrombosis, hypertension, increased miscarriage risk | Customized folic acid and/or riboflavin supplementation protocol |
VDR | Disrupted vitamin D levels | Recurrence of polyps | Personalized management strategies |
BCMO1 (rs12934922) | Reduced carotenoid conversion | Vitamin A deficiency | Personalized guidance for optimal absorption |
TMPRSS6 (rs855791) | Reduced iron absorption | Anemia | Customized iron supplementation protocol |
SLC30A8 (rs13266634) | Increased glucose levels | Risk of type 2 diabetes | Personalized zinc supplementation protocol |
APOE (ε4) | Delayed DHA response | Alzheimer’s risk | Personalized solutions for optimal cognitive health |
FTO (rs9939609) | Increased obesity risk | Impact on vitamin D | Customized vitamin D supplementation protocol |
MTNR1B (rs10830963) | Reduced insulin secretion | Type 2 diabetes risk | Customized nutritional guidance protocol |
HFE (rs1800562) | Iron overload | Hemochromatosis risk | Tailored dietary guidance protocol |
GPX1 (rs1050450) | Increased oxidative stress | Prostate cancer risk | Selenium-targeted interventions |
SLC6A6 (C.1196G>T) | Disrupted taurine homeostasis | Retinal degeneration, cardiomyopathy | Specialized recommendations for long-term support |
ACE, ACTN3, AMPD1, CKM, MLCK | Muscle mass and performance, injury prevention | Response to creatine supplementation | Personalized creatine supplementation protocol |
SLC1A4, PPM1K, BCAT1 | Increased circulating short-chain amino acids | Risk of type 2 diabetes | Avoidance of BCAA supplements |
COMT (rs4680) | Catechin metabolism regulation | Body weight management | Targeted dietary interventions for better weight control |
CYP1A2 (rs762551) | Caffeine metabolism | Caffeine sensitivity, increased cardiovascular risk | Personalized caffeine consumption guidance |
According to published studies³, sodium intake significantly affects blood pressure and cardiovascular health. Some individuals have a genetic predisposition to increased sodium retention, which can lead to hypertension, fluid retention, and elevated cardiovascular risk. Early identification of this predisposition can help optimize diet and enable personalized preventive strategies.
The GENOSOPHY® genetic test assesses the body’s ability to excrete sodium and the associated risk of hypertension.
Individuals with a family history of hypertension or cardiovascular disease
Individuals seeking to adjust their diet for optimal sodium balance
Gene / Polymorphism | Effect | Association | How We Help |
---|---|---|---|
UMOD (rs13333226) | Regulation of renal sodium excretion | Increased sodium retention, hypertension | Salt intake adjustment to reduce risk |
AGT (rs699) | Elevated angiotensin levels | Increased blood pressure, cardiovascular risk | Recommendations to reduce sodium and improve heart health |
As shown in published studies⁴, the ability to metabolize alcohol varies greatly among individuals due to genetic differences in enzymes that break down ethanol. Some variants are associated with rapid alcohol breakdown, causing unpleasant reactions, while others result in slower breakdown of acetaldehyde, increasing the risk of toxic effects on the liver and cardiovascular system.
The GENOSOPHY® genetic test evaluates variants affecting alcohol metabolism and the associated risk of adverse effects. The test is performed using GENOSOPHY®’s award-winning algorithm, ensuring high accuracy in assessing genetic risk.
Individuals who experience intense reactions after alcohol consumption (e.g., facial flushing, nausea, headache)
Individuals interested in understanding how alcohol metabolism may impact their health
Gene / Polymorphism | Effect | Association | How We Help |
---|---|---|---|
ADH1B (rs1229984) | Increased alcohol dehydrogenase activity | Rapid alcohol breakdown, increased discomfort | Alcohol reduction recommendations |
ALDH2 (rs671) | Reduced acetaldehyde breakdown | Increased alcohol sensitivity, facial flushing | Avoidance guidance due to toxic effects |
Identification of individuals with increased or reduced capacity to absorb and metabolize specific nutrients, enabling targeted interventions.
Reliable evaluation of how genetic variants influence the manifestation or management of conditions in relation to dietary supplement use.
Assessment of the effects of specific foods like salt, coffee, and alcohol on the body.
Development of personalized preventive strategies, such as tailored vitamin, mineral, and ergogenic supplement intake.
Saliva sample collection
Analysis of >25 genetic variants and risk assessment using GENOSOPHY®’s award-winning algorithm
Results delivered within 5–6 weeks
Based on the genetic test results, GENOSOPHY® offers the following support services for optimal intolerance management:
Genetic counseling
Diet plans tailored to your genetic profile
Nutritional consulting for targeted dietary interventions
Gkouskou et al., Nutr Rev 2020 Dec 27; DOI: 10.1093/nutrit/nuaa132
Patrick, FASEB J 2018 Oct 5; 33(2):1554–1564. DOI: 10.1096/fj.201801412R
Trudu et al., Nat Med 2013;19(12):1655–1660 / DOI: 10.1038/nm.3384
Macgregor et al., Hum Mol Genet 2009;18(3):580–593 / DOI: 10.1093/hmg/ddn372