What your genes can and cannot tell you about your vitamin and mineral status.
Vitamin deficiencies are more common than most people assume, and they are often more persistent than diet alone would explain. Iron deficiency remains the most widespread nutritional deficiency in the UK despite widespread dietary awareness of iron-rich foods. Vitamin D insufficiency affects a substantial proportion of the UK population even in people who take supplements. The reason, in many cases, is genetics.
Your DNA does not predict deficiency with certainty. But specific genetic variants meaningfully increase the risk of insufficiency for particular nutrients by affecting how efficiently your body absorbs, converts, or utilises them. Understanding which variants you carry tells you where you need to be more deliberate than average, and why standard dietary guidance may not be enough for you specifically.
Folate from food, and from most supplements, needs to be converted into its biologically active form, 5-methyltetrahydrofolate (5-MTHF), before the body can use it. This conversion is carried out by the MTHFR enzyme. Two common variants in the MTHFR gene, C677T and A1298C, reduce the activity of this enzyme. People carrying the C677T variant in homozygous form, two copies, have MTHFR enzyme activity reduced to approximately 30 percent of normal.
For these individuals, a standard dietary folate intake may be sufficient by the numbers, but functionally insufficient because so little is converted to the active form. Symptoms of functional folate insufficiency include low energy, poor mood, and elevated homocysteine, a cardiovascular risk marker. The practical response is either substantially higher folate intake or supplementing with methylfolate, the pre-converted form that bypasses the MTHFR enzyme entirely.
Vitamin D works by binding to the vitamin D receptor (VDR) in cells. Variants in the VDR gene affect how effectively this binding occurs and how strongly cells respond to vitamin D. Two people can have identical circulating vitamin D levels but very different functional vitamin D activity at the cellular level depending on their VDR genotype.
This explains why some people experience symptoms of vitamin D insufficiency, low mood, fatigue, muscle weakness, poor immunity, despite blood levels that appear clinically adequate. The vitamin D is present in the blood but the cellular response is reduced. For people with certain VDR variants, maintaining higher circulating vitamin D levels may be necessary to achieve the same functional effect as an average person achieves at lower levels.
TMPRSS6 encodes a protein that regulates hepcidin, the hormone that controls how much iron is absorbed through the gut wall. Variants in TMPRSS6 that reduce its function lead to elevated hepcidin, which suppresses iron absorption. People with these variants absorb a smaller proportion of dietary iron than average, which predisposes them to iron deficiency even on diets that should be adequate.
HFE variants affect iron storage regulation and are associated with both haemochromatosis (excess iron storage) and, in other variants, reduced iron availability. Together these two genes explain a meaningful proportion of the iron deficiency that persists despite adequate dietary intake.
EPA and DHA, the omega-3 fatty acids most relevant to brain, cardiovascular, and immune health, can be obtained directly from oily fish or converted by the body from the plant-based omega-3 ALA. The FADS1 and FADS2 genes encode the enzymes that carry out this conversion. Variants in these genes substantially reduce conversion efficiency. For people with these variants, plant-based omega-3 sources are even less effective than they are for the average person, making direct sources of EPA and DHA significantly more important.
TRPM6 and TRPM7 encode proteins involved in magnesium transport across cell membranes. Variants in these genes affect how efficiently magnesium is absorbed from food and transported into cells. Combined with the fact that dietary magnesium intake is already below recommended levels for a majority of the UK population, genetic variants that further reduce absorption efficiency are a significant risk factor for functional magnesium insufficiency.
The most effective approach combines DNA testing and blood testing. Blood testing tells you your current actual status. DNA testing tells you where your biology creates structural vulnerabilities that diet and supplementation need to account for.
If your DNA results suggest reduced folate conversion efficiency, getting a blood test for serum folate and homocysteine gives you confirmation of whether the genetic tendency is translating into actual insufficiency. If it is, the response is clearer and more targeted: methylfolate supplementation rather than standard folic acid, higher dietary folate from leafy greens and legumes, and regular monitoring.
