Nutritional Deficiency

Nutritional Deficiency

Dietary vitamins and minerals are critical for nourishment and healing. Deficiencies in essential nutrients can contribute to many health ailments such as vision loss, osteoporosis, anemia, depression and more. Studies indicate that genetics play a large role in Genetic Nutritional Deficiencies. The information provided in the Nutritional report allows for patients and providers to make informed dietary and supplement choices.

Deficiencies in essential vitamins and minerals can oftentimes go unnoticed and have been associated with risks of many adverse health effects. Recent and reputable scientific research has shown that individuals’ genes play a large role in these deficiencies. Our Genetic Nutritional Deficiencies Panel was assembled by a team of researchers who have identified the scientific studies regarding the specific genes that increase susceptibility to nutritional disorders and deficiencies involving Vitamin A, Vitamin B12, Vitamin D, Folate, and Iron.





Vitamin A – Vitamin A is a fat-soluble vitamin crucial for proper vision, immune response, and cellular differentiation.3 Vitamin A is created from three natural vitamin A precursors called carotenoids essential compounds found mainly in plant-based foods.4 The first step in the metabolic conversion of the three carotenoids is their cleavage by the enzyme beta, beta-carotene 15,15’-monooxygenase 1 (BCMO1) located in the small intestine.5 Unfortunately, about 45 percent of the Western population can be classified as low beta-carotene converters.6 A variant allele of the BCMO1 gene results in the reduction of the BCMO1’s enzyme’s catalytic activity by 48 percent, which can lead to a vitamin A deficient state.


Vitamin B12 – One of eight B vitamins, vitamin B12 plays a key role in brain and nervous system function, and is involved in the metabolism of every cell in the body; particularly in DNA synthesis and regulation.15 A vitamin B12 deficiency, due to low consumption of animal-source foods and/or inadequate absorption, often associated with pernicious anemia, becomes increasingly common as people age.15 Studies have also shown that individuals with reduced intake of vitamin B12 have elevated levels of homocysteine, an established predictor of cardiovascular disease.16 Importantly, clinical research has identified multiple genetic mutations that affect vitamin B12 levels and the risk of deficiency.16,17


Vitamin D – Vitamin D is produced by the body when skin is exposed to sunlight, and can also be found in fish, fish oils, egg yolks, fortified dairy and grain products. Vitamin D is essential for strong bones and deficiencies have been associated with rickets, diabetes, cardiovascular disease, and some cancers.11 Up to half of all adults in the developed world suffer from vitamin D deficiency.12 Researchers have identified variants in four genes that may play a role in vitamin D deficiency: GC, CYP2R1, and DHCR7/NADSYN1. Knowing the status of these gene variants could help healthcare providers identify a patient’s risk for vitamin D deficiency.13,14


Folate – The B vitamin is crucial to the maintenance of red blood cells, methylation of DNA, prevention of neural tube defects, and conversion of homocysteine to methionine.15 Importantly, before it can play a role in maintaining and promoting health, folate must be converted into its active form through a series of enzymatic reactions. The methylenetetrahydrofolate reductase (MTHFR) enzyme is critical in this process. Scientific research has shown that common mutations that decrease MTHFR activity can lead to a reduction in the activated form of folate.18, 19 Carriers of these mutations may be at an increased risk of certain cardiovascular diseases. 20


Iron – Iron is a common nutrient deficiency, resulting in anemia which can lead to fatigue, weakness, pale skin, and shortness of breath.7 Several clinical biomarkers of iron – including serum ferritin concentrations, hemoglobin, and levels of iron-bound transferrin – are strongly heritable, indicating a role for genetics in iron deficiency.7, 8 Scientists have found that a mutation in the gene coding for transmembrane protease serine 6 (TMPRSS6) is associated with several clinical indicators of anemia, including levels of serum iron, transferrin saturation, erythrocyte mean cell volume, and hemoglobin.9,10