In the evolving field of nutrition, the one-size-fits-all model is rapidly being replaced by a more personalized approach. As a nutritionist, you already recognize that each client is unique—with distinct dietary needs, preferences, and health goals. But what if you could go even deeper, tailoring nutrition plans based on a client’s genetic blueprint? Genetic testing offers this transformative potential, providing insights that help you design dietary plans with unparalleled precision. Imagine understanding how a client metabolizes vitamin D, why they might be deficient in B vitamins, or why magnesium is crucial for them—all determined by their genes.

This blog explores the top three ways genetic testing can elevate your approach to personalized nutrition. By identifying how genes influence nutrient metabolism and absorption, you can develop plans that optimize health outcomes and resonate deeply with each client. Let’s dive into how genetics plays a role in nutrient processing and how you can leverage this knowledge to improve your practice.

Vitamin D metabolism: a genetic insight

Vitamin D plays a vital role in bone health, immune function, and overall wellness. Genetic testing can reveal variants in genes such as GC, VDR, and CYP2R1 that influence how vitamin D is metabolized and utilized.

  • GC (Group-Specific Component): this gene produces the vitamin D-binding protein, responsible for transporting vitamin D through the bloodstream. Variants in the GC gene can lower circulating vitamin D levels, necessitating higher dietary intake or supplementation.

  • VDR (Vitamin D Receptor): the VDR gene encodes the receptor for vitamin D. Certain variants can decrease receptor sensitivity, meaning the body may need higher doses of vitamin D to achieve optimal health.

  • CYP2R1: this gene codes for an enzyme that converts vitamin D to its active form. Variants in CYP2R1 can reduce conversion efficiency, affecting overall vitamin D availability.

Dietary sources: fatty fish (salmon, mackerel), fortified dairy products, egg yolks, and mushrooms.

Supplement recommendations

For clients with genetic variants indicating lower vitamin D levels, daily supplementation of vitamin D3 (1,000 to 6,000 IU) may be necessary. Retesting is essential, as some individuals may require alternative solutions like vitamin D injections for optimal absorption. Always consult healthcare professionals for appropriate dosing.

Vitamin B12 absorption and transport

Vitamin B12 is essential for red blood cell formation, neurological function, and DNA synthesis. Since the body cannot produce B12, it must be obtained through diet or supplementation. However, genetic variants can significantly affect B12 absorption, transport, and recycling. Three critical genes influencing B12 metabolism are FUT2, TCN2, and MTRR.

  • FUT2 (Fucosyltransferase 2): FUT2 influences gut microbiota composition, impacting B12 absorption. Non-secretor variants of FUT2 can lead to lower populations of B12-producing bacteria, increasing the risk of deficiency.

  • TCN2 (Transcobalamin II): TCN2 codes for transcobalamin, a protein that transports vitamin B12 to cells. Variants in TCN2 can reduce B12 transport efficiency, potentially leading to intracellular deficiencies.

  • MTRR (Methionine Synthase Reductase): MTRR is involved in recycling vitamin B12 for DNA synthesis and methylation. Variants can impair B12 recycling, resulting in elevated homocysteine levels, a risk factor for cardiovascular issues. Dietary sources: Animal liver, shellfish, fortified cereals, dairy products, and eggs.

Supplement recommendations

Clients with FUT2 or TCN2 variants may benefit from methylcobalamin (a bioavailable form of B12). Regular monitoring of B12 and homocysteine levels can guide supplementation.

Folate Metabolism and MTHFR gene variants

Vitamin B9 (folate) is essential for DNA synthesis, cell division, and methylation. Folate is especially crucial during pregnancy, infancy, and adolescence. However, genetic variants in the MTHFR gene can significantly influence folate metabolism.

  • MTHFR (Methylenetetrahydrofolate Reductase): MTHFR converts folate into its active form (5-MTHF). Variants such as C677T and A1298C can reduce enzyme efficiency by up to 70%, impairing folate metabolism and increasing homocysteine levels. This can lead to cardiovascular risks, neural tube defects, and cognitive issues.

Dietary sources: leafy greens (spinach, kale), legumes, avocados, and fortified grains.

Supplement recommendations

Individuals with MTHFR variants benefit from L-methylfolate, the active form of folate. This bypasses the need for enzymatic conversion, supporting DNA synthesis and reducing homocysteine levels.

Conclusion

Genetic testing unlocks a deeper understanding of nutrient metabolism, absorption, and utilization. By tailoring dietary recommendations and supplement plans based on genetic insights, you can enhance your clients’ health and well-being. This personalized approach not only improves outcomes but empowers individuals to make informed decisions about their nutrition. Embrace the power of genetics to elevate your practice and redefine personalized nutrition for your clients.

References

Wang, T. J., et al. (2010). "Common Genetic Determinants of Vitamin D Insufficiency: A Genome-Wide Association Study." Lancet, 376(9736), 180-188.
Ahn, J., et al. (2010). "Vitamin D-related Genes, Serum Vitamin D Concentrations, and Prostate Cancer Risk." Cancer Epidemiology, Biomarkers & Prevention, 19(11), 2734-2742.
Berry, D. J., et al. (2011). "The Role of Genetic Variation in the Vitamin D Pathway on Vitamin D Levels and Cancer Risk." British Journal of Cancer, 105(4), 557-564.
Hazra, A., et al. (2008). "Common Variants of FUT2 are Associated with Plasma Vitamin B12 Levels." Nature Genetics, 40(10), 1160-1162.
Tanaka, T., et al. (2009). "Genome-Wide Association Study of Vitamin B12 and Folate Levels in Elderly Individuals." Blood, 114(19), 1205-1213.
Molloy, A. M., et al. (2010). "Effects of the Common MTRR Polymorphism on Homocysteine, Folate, and Vitamin B12 Levels." Clinical Chemistry, 55(1), 171-178.
Weisberg, I., et al. (1998). "A Second Genetic Polymorphism in Methylenetetrahydrofolate Reductase (MTHFR) Associated with Decreased Enzyme Activity." American Journal of Human Genetics, 62(5), 1258-1260.
Bailey, L. B., et al. (2002). "Folate Status and Requirements in Women of Reproductive Age: A Review of the Available Evidence." Nutrition Reviews, 60(10), 221-231.
Mutation in the Methylenetetrahydrofolate Reductase Gene: An Additional Risk Factor for Neural-Tube Defects?" American Journal of Human Genetics, 62(5), 1044-1051.