Health Canada outlines daily dietary requirements for vitamins, minerals and macronutrients necessary for Canadians to be healthy. These values are determined according to scientific data to meet adequate nutrient levels for 97-98% of healthy individuals within a particular life stage and gender;¹ however, a 2012 report by Health Canada shows that a large percentage of individuals fail to meet acceptable levels through diet alone, particularly for magnesium, calcium, vitamins D and A.² In addition, values are meant as a general guideline for the healthy population to generally prevent deficiency and fail to provide guidelines for those that require additional amounts. Situations or populations with additional nutrient requirements include:

• Medication use
• Chronic disease
• Poor absorption or chronic digestive complaints
• Alcohol and/or drug abuse
• Athletes
• Pregnancy
• Elderly population
• Genetic susceptibility and predispositions

Genetic predisposition

Most, if not all vitamins must be digested, absorbed into circulation, transported through the blood, delivered to and taken up by the cell, and then metabolized into an active form for the body to use. In each of these steps a protein, receptor or enzyme helps to carry out this process and is susceptible to individual variations due to genetic mutations.

Genetic mutations come in different forms but the most common are single nucleotide polymorphisms, or SNPs (pronounced “Snips”). SNPs are permanent genetic mutations passed down from our parents that alter the genetic code. Changes in the genetic code can modify the function of the gene product. For example, a certain SNP (C677T) in the gene MTFHR, which produces the MTFHR enzyme (methylene tetrahydrofolate reductase), can reduce the efficiency of this enzyme by up to 70%. Since this enzyme is responsible for converting folate into its active form, those who carry this version of the gene are susceptible to low levels of folate in the blood and high homocysteine, a toxin compound linked to heart disease.^3,4

This isn’t the end of the story. For those who are a carrier of this at-risk SNP, studies show that consuming dosages well above the RDA of vitamin B2, B12 and/or active folate (5-MTHF) are beneficial in lowering homocysteine and compensating for the risk for deficiency.⁵

There are numerous other examples of genes that impact individual dosages for nutrients.

Vitamin A – Genetic variations in the BCMO1 gene reduce enzyme function by up to 57%. Studies show that individuals with this variant form only 9% vitamin A from β-carotene versus those with the normal version.⁶

Vitamin C – Up to 19% of the population is missing the GSTT1 gene, important for detoxification and linked to a risk for cardiovascular disease, asthma and certain types of cancer.⁷ These individuals have additional antioxidant needs to protect from DNA damage linked to their increased susceptibility to environmental toxins.^8,9

Vitamin D – Common genetic variants alter circulating levels of vitamin D and more than double the risk of vitamin D insufficiency. Genetically susceptible individuals have a 140% increase risk of severe vitamin D deficiency (<25 nmol/L). Studies suggest that optimal concentrations and dosages of vitamin D necessary to reduce disease outcomes may vary according to genotype.^10,11

Vitamin E – Genetic variations in the protein Factor 5 Leiden increase susceptibility to clotting, particularly to venous thromboembolism (VTE). For genetic carriers, vitamin E reduces the risk by up to 21%.^12,13

Iron – Genetic variants actually increase risk for both iron deficiency anemia and iron overload, a genetic disorder known as hemochromatosis.¹⁴ For those who are susceptible, it is important to have your iron levels tested regularly, avoid iron supplementation and for some, regular blood donation to prevent organ damage from excess iron levels.

Celiac disease is a genetic-based autoimmune disease that can significantly increase risk for multiple nutrient deficiencies. Identifying high-risk individuals early on to implement early treatment can delay the onset of disease and subsequent consequences.¹⁵

Assessing one’s purpose for supplements, as well as the particular form, dose and length of intake are critical aspects to consider when considering investing in health products. Some standard blood tests performed with your medical doctor, such as vitamin D, B12, and ferritin are useful to determine the need for a particular vitamin; however, not all nutrients are accurately assessed through blood tests. Genetic testing can provide further insight into the exact nutrients you may need to overcome deficiencies and optimize your health. It can not only help you determine if you require supplementary vitamins, it can also provide guidance on the appropriate dosage and form. Of course, it is important to work with your healthcare provider to ensure that what you are taking is safe according to your current state of health and medications.

References

1. Canada H. Dietary Reference Intakes Tables. Aem. https://www.canada.ca/en/health-canada/services/food-nutrition/healthy-eating/dietary-reference-intakes/tables.html. Published July 20, 2005. Accessed August 2, 2019.
2. Canada H. Do Canadian Adults Meet Their Nutrient Requirements Through Food Intake Alone? Aem. https://www.canada.ca/en/health-canada/services/food-nutrition/food-nutrition-surveillance/health-nutrition-surveys/canadian-community-health-survey-cchs/canadian-adults-meet-their-nutrient-requirements-through-food-intake-alone-health-canada-2012.html#a33. Published January 27, 2012. Accessed August 2, 2019.
3. Yang Q-H, Botto LD, Gallagher M, et al. Prevalence and effects of gene-gene and gene-nutrient interactions on serum folate and serum total homocysteine concentrations in the United States: Findings from the third National Health and Nutrition Examination Survey DNA Bank. Am J Clin Nutr. 2008;88(1):232-246. doi:10.1093/ajcn/88.1.232
4. Raina JK, Sharma M, Panjaliya RK, et al. Methylenetetrahydrofolate reductase C677T and methionine synthase A2756G gene polymorphisms and associated risk of cardiovascular diseases: A study from Jammu region. Indian Heart J. 2016;68(3):421-430. doi:10.1016/j.ihj.2016.02.009
5. Willems FF, Boers GHJ, Blom HJ, Aengevaeren WRM, Verheugt FWA. Pharmacokinetic study on the utilisation of 5-methyltetrahydrofolate and folic acid in patients with coronary artery disease. Br J Pharmacol. 2004;141(5):825-830. doi:10.1038/sj.bjp.0705446
6. Leung WC, Hessel S, Méplan C, et al. Two common single nucleotide polymorphisms in the gene encoding β-carotene 15,15′-monoxygenase alter β-carotene metabolism in female volunteers. FASEB J. 2009;23(4):1041-1053. doi:10.1096/fj.08-121962
7. Arruda VR, Grignolli CE, Gonçalves MS, et al. Prevalence of homozygosity for the deleted alleles of glutathione S-transferase mu (GSTM1) and theta (GSTT1) among distinct ethnic groups from Brazil: Relevance to environmental carcinogenesis? Clin Genet. 1998;54(3):210-214.
8. Block G, Shaikh N, Jensen CD, Volberg V, Holland N. Serum vitamin C and other biomarkers differ by genotype of phase 2 enzyme genes GSTM1 and GSTT1. Am J Clin Nutr. 2011;94(3):929-937. doi:10.3945/ajcn.111.011460
9. Michels AJ, Hagen TM, Frei B. Human Genetic Variation Influences Vitamin C Homeostasis by Altering Vitamin C Transport and Antioxidant Enzyme Function. Annu Rev Nutr. 2013;33:45-70. doi:10.1146/annurev-nutr-071812-161246
10. McGrath JJ, Saha S, Burne THJ, Eyles DW. A systematic review of the association between common single nucleotide polymorphisms and 25-hydroxyvitamin D concentrations. J Steroid Biochem Mol Biol. 2010;121(1-2):471-477. doi:10.1016/j.jsbmb.2010.03.073
11. Wang TJ, Zhang F, Richards JB, et al. Common genetic determinants of vitamin D insufficiency: A genome-wide association study. The Lancet. 2010;376(9736):180-188. doi:10.1016/S0140-6736(10)60588-0
12. Glynn RJ, Ridker PM, Goldhaber SZ, Zee RYL, Buring JE. Effects of random allocation to vitamin E supplementation on the occurrence of venous thromboembolism: Report from the Women’s Health Study. Circulation. 2007;116(13):1497-1503. doi:10.1161/CIRCULATIONAHA.107.716407
13. Simone B, De Stefano V, Leoncini E, et al. Risk of venous thromboembolism associated with single and combined effects of Factor V Leiden, Prothrombin 20210A and Methylenetethraydrofolate reductase C677T: A meta-analysis involving over 11,000 cases and 21,000 controls. Eur J Epidemiol. 2013;28(8):621-647. doi:10.1007/s10654-013-9825-8
14. de Tayrac M, Roth M-P, Jouanolle A-M, et al. Genome-wide association study identifies TF as a significant modifier gene of iron metabolism in HFE hemochromatosis. J Hepatol. 2015;62(3):664-672. doi:10.1016/j.jhep.2014.10.017
15. Lionetti E, Castellaneta S, Francavilla R, et al. Introduction of Gluten, HLA Status, and the Risk of Celiac Disease in Children. N Engl J Med. 2014;371(14):1295-1303. doi:10.1056/NEJMoa1400697