Personalized Nutrition: When does a multivitamin fit multiple genotypes?‡
By Kelly Heim, Ph.D.
Personalized medicine is aptly defined as the “right intervention for the right patient at the right dose.” In practice, applying this principle using single agents is straightforward – a product with the right ingredient is amenable to easy dosage adjustments. On the other hand, complex formulations such as multivitamins are less flexible. Practitioners can overcome this challenge by selecting multivitamins that are age-, gender- or condition-specific.
The widespread implementation of genetic testing has given rise to a new level of complexity. Every patient has a unique profile of genetic variations known as Single Nucleotide Polymorphisms (SNPs; pronounced “snips”).1 Many SNPs affect nutrient needs by interfering with methylation, a vital biochemical pathway that enables folate, riboflavin, vitamin B6, B12, choline, and other nutrients to maintain cardiovascular, neurocognitive, mental, behavioral and cellular health.2-5‡
A decisive gene in this pathway is MTHFR, which allows the activation of folic acid to the crucial methyl donor, 5-MTHF (Figure 1). Individuals with SNPs in the MTHFR gene cannot efficiently make this conversion to the active form. Consequently, elevated homocysteine and reduced methylation competence are common observations.3-5 Fortunately, the solution is simple: Providing 5-MTHF as a supplement bypasses the SNP by delivering the activated nutrient.
Figure 1. Healthy methylation is maintained by a series of enzymes encoded by genes. (a) The enzyme MTHFR (Methylene Tetrahydrofolate Reductase) converts folic acid and THF into 5-MTHF, a key methyl donor, using riboflavin (vitamin B2) as a cofactor. (b) MTR (Methionine Synthase), using vitamin B12 as a cofactor, transfers the methyl group from 5-MTHF and methylates homocysteine to form methionine. (c) B12 can be used efficiently by virtue of MTRR (MTR Reductase), which regenerates methylcobalamin. (d) COMT (Catechol O-Methyltransferase) is an enzyme that detoxifies stimulant neurotransmitters and estrogens. (e) The enzyme CBS (Cystathionine Beta-Synthase), a decisive step in this process, requires vitamin B6. (f) TCN2 delivers dietary B12 to cells. (g) FUT2 is a major predictor of B12 status in human studies.
How to address SNPs
Many SNPs can be nutritionally addressed using one or more of the following approaches:
- Bypass the SNP. MTHFR can be bypassed by supplementing with 5-MTHF. SNPs in the BCMO1 gene, which partially inhibit the conversion of beta-carotene to vitamin A, can similarly be overcome by including retinol in the diet.6‡
- Provide cofactors. Most medically relevant SNPs alter the function of an enzyme. Providing the cofactor for that enzyme can support its function. For example, daily supplementation with 1.7 mg riboflavin, the cofactor for MHTFR, supports vascular relaxation in patients with the MTHFR C677T genotype.7,8‡
- Provide indirect support. Lithium is an essential mineral for mental health. Although not directly involved in methylation, lithium supports emotional and behavioral health – a common objective in patients with methylation SNPs.9,10 Since lithium moderates norepinephrine levels, it may potentially provide indirect relaxation support for patients with the COMT Val/Met SNP.11‡
- Trust your manufacturer. It is not necessary to open a biochemistry textbook for every SNP you see. A good manufacturer can formulate products using the foregoing strategies so that you don’t have to.
A formulation you can count on
Customized multivitamins for every possible combination of SNPs are neither realistic nor necessary. The following formulation strategies enable broad applicability and efficacy across multiple genotypes without compromising targeted, individualized support:
- Compatibility: The ingredient doses are sufficient for effectiveness, but not so high as to cause toxicity with additional supplementation for specific SNPs.‡
- Universality: The ingredient is metabolized and assimilated by patients regardless of whether the SNP is present. For example, 5-MTHF, retinol, choline and hydroxycobalamin are universally assimilated and utilized, so they are suitable for any patient. Hydroxycobalamin is converted to methylcobalamin in the body, so it “becomes what is needed.”‡
- Bioavailability: Many SNPs reduce nutrient absorption and/or assimilation, but bioavailability is advantageous regardless of genotype.‡
- Evidence: The product is formulated at doses based on published studies documenting efficacy.‡
The PureGenomics® Multivitamin follows this model with precision, delivering a complete foundation of essential vitamins and minerals in bioavailable, universally metabolized forms, such as Metafolin® L-5-methyltetrahydrofolate (L-5-MTHF), retinol and adenosyl/hydroxycobalamin. This once-daily multivitamin also provides riboflavin, vitamin B6, choline, trimethylglycine and lithium to provide multimodal support for common variations in methylation pathway.‡
Test, translate and target SNPs at www.PureGenomics.com.
SNPs are an opportunity for practitioners to objectively comprehend patient individuality and to tailor nutritional support accordingly. Aligning SNPs and supplements is fast and simple with PureGenomics®, a new website application that distills and translates 23andMe® results into a concise profile of key SNPs affecting nutritional needs, along with specific product recommendations. This dynamic tool bridges the historically immense gap between genetic testing and supplement selection, making personalized nutrition easier and more precise than ever before.
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- Ames BN, Elson-Schwab I, Silver EA. Am J Clin Nutr 2002, 75(4):616-58.
- Bousman CA, Potiriadis M, Everall IP, Gunn JM. Am J Med Genet B Neuropsychiatr Genet 2014, 165B(1):68-76.
- Liu NB, Li J, Qi JF, et al. Med Sci Monit 2014, 20:2817-23.
- Hou X, Chen X, Shi J. Gene 2015 Mar 31. doi: 10.1016/j.gene.2015.03.062.
- Lietz G, Oxley A, Leung W, Hesketh J. J Nutr 2012, 142(1):161S-5S.
- McNulty H, Strain J, Ward M. Arch Public Health 2014, 72(Suppl 1):K2.
- Horigan G, McNulty H, Ward M, et al. J Hypertens. 2010, 28(3):478-86.
- Stein MB, Fallin MD, Schork NJ, Gelernter J. Neuropsychopharmacology 2005, 30(11):2092-102.
- Lewis SJ, Lawlor DA, Davey Smith G, et al. Mol Psychiatry 2006, 11(4):352-60.
- Brunton, L; Chabner, B; Knollman, B (2010). Goodman and Gilman’s The Pharmacological Basis of Therapeutics (12th ed.). New York: McGraw-Hill Professional. ISBN 978-0-07-162442-8.