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Nutrigenomics

Nutrigenomics explained: how gene variants relate to food traits such as lactose, caffeine, vitamin D and folate, what trials show, and a report’s limits.

By the GeneMatrix editorial teamUpdated 6 min read

A breakfast table: hands around a cup of coffee, buttered toast, a glass of milk, a bowl of fruit and a jar of oats.

In short

Nutrigenomics is the study of how differences in your genes relate to the way your body handles food and nutrients. A few links are clear, such as whether you keep digesting lactose as an adult. Most are small. A nutrigenomics report describes traits and what studies link them to; it can’t diagnose anything or set your diet.

On this page
  1. What is nutrigenomics?
  2. How does a nutrigenomics test work?
  3. Four everyday examples
  4. Genes and body weight
  5. What a nutrigenomics report can’t do
  6. How GeneCore fits in
  7. What to do next

What is nutrigenomics?

Nutrigenomics, also called nutritional genomics, studies how your genes and what you eat work together to shape your traits, such as how you digest milk or clear caffeine.[1]

Everyone has the same set of genes, but in slightly different versions, called alleles. A small difference at one spot in your DNA is a variant. A few variants change how well an enzyme works. Most make no difference you would notice.

Knowing your food traits can be interesting. It hasn’t been shown to make a diet work better.

How does a nutrigenomics test work?

  1. 1Your sampleYou collect a saliva sample at home. It carries the DNA you inherited.
  2. 2GenotypingThe lab checks selected variants, chosen in advance, at known places in your DNA. This is called genotyping.
  3. 3Matching to studiesEach result is matched to what genetic association studies of large groups of people have linked it with.
  4. 4Your reportYou read your result on each trait and what it has been linked to.

Four everyday examples

These four come up most often, from the clearest genetics to the most overstated. The table sums them up; the sections below explain each one.

Four nutrigenomics examples at a glance
TraitGenesWhat your genes can sayWhat they can’t say
Digesting lactose as an adultLCT, controlled from inside MCM6Whether you’re likely to keep making lactase after infancy.[2]Whether dairy will give you symptoms.[3]
Clearing caffeineCYP1A2 and AHRA tendency linked with how much caffeine people habitually take in.[6]How fast you clear it now: age, hormones, smoking and diet change that too.[5]
Vitamin D in the bloodGC, DHCR7 and CYP2R1Whether you carry variants linked, on average, with lower blood levels.[7]Your actual level: only a blood test shows it.[8]
Processing folateMTHFRWhich common version you carry.[9]Which form of folate you need. The CDC says carriers can process all forms.[9]

Our nutrition, supplement, athletic and wellbeing reports are for general wellness and information. The evidence behind these associations is less established than for our clinical panels, and these reports are not intended to diagnose, treat, cure or prevent any disease.

Lactose: do you keep making lactase?

Babies make lactase to digest lactose, the sugar in milk. About 65% of people have a reduced ability to digest lactose after infancy.[2]

Whether you keep making lactase is set by a stretch of DNA that controls the LCT gene, inside a neighboring gene called MCM6. Some people inherit changes there that keep lactase production going into adulthood. This is lactase persistence.[2]

It varies a lot by ancestry. Lactase non-persistence affects 70 to 100 percent of people of East Asian descent, but only about 5 percent of people of Northern European descent.[2] Different variants do the job in different populations: the best-known one is common in Europe, and at least three others are linked with lactase persistence in East Africa.[4] A test that reads only the European variant can miss the others.

A gene result isn’t a test for lactose intolerance, which means having symptoms after lactose. Not everyone who digests lactose poorly gets symptoms.[3]

Caffeine: the CYP1A2 enzyme

CYP1A2 makes the enzyme that breaks down about 95% of the caffeine you take in.[5] In a study of 47,341 people of European descent, variants near CYP1A2, and near AHR, a gene that controls it, were linked with how much caffeine people habitually took in.[6]

Your genes are only part of it. Age, sex and hormones, smoking and diet all change how quickly caffeine is cleared.[5]

Vitamin D: GC and the genes that make and carry it

In a study of 33,996 people of European descent, variants in or near three genes were most clearly linked with blood levels of vitamin D: GC, which makes the protein that carries vitamin D in the blood, and DHCR7 and CYP2R1, which are involved in making and processing it. A fourth, CYP24A1, showed up when all the data were combined. People carrying more of the three main variants were more likely to have low levels. Sun exposure and diet shape your level too.[7]

The vitamin D receptor gene, VDR, is sometimes named in DNA tests, but it wasn’t among the genes that large study found.[7] And no gene result can tell you your vitamin D level: a blood test measures it, usually as a form called 25(OH)D.[8]

Folate and MTHFR: much discussed, little clinical use

MTHFR makes a protein that helps your body process folate. Its common C677T variant is so common that more people in the United States carry one or two copies than don’t.[9]

You may have read that carriers can’t use folic acid. The CDC says that isn’t true: people with an MTHFR variant can process all types of folate, including folic acid, and how much folic acid you get matters more for your blood folate level than your MTHFR type.[9]

The American College of Medical Genetics and Genomics has said there is growing evidence that testing for common MTHFR variants has minimal clinical use.[10] And in the Food4Me trial, people told they carried the variant didn’t improve how much folate they ate any more than people told they didn’t.[11] If you are weighing a test anyway, our page on the MTHFR mutation test sets out what it reads and what it can’t tell you.

Genes and body weight

Body weight is shaped by many genes, each with a small effect, of which FTO is the best known.[12][13] In trials, people carrying its higher-BMI version lost as much weight as others, and diets or advice matched to people’s genes worked no better than advice that ignored them, as Is there a DNA test for weight loss? explains.[14][15][16]

What a nutrigenomics report can’t do

  • Diagnose. It can’t tell you whether you have a health condition or whether a food causes your symptoms.
  • Set your diet or choose supplements. Trials haven’t shown that gene-based advice works better.[15][16]
  • Measure your levels. Blood tests do that, for vitamin D and much else.[8]
  • Speak for everyone equally. Much of the research is in people of European descent, and the variants that matter can differ by ancestry.[7][4]
  • Find what it doesn’t look for. A genotyping test reads selected variants, so it can miss others.

How GeneCore fits in

A plate, a fork and a spoonA plate divided into three portions that fill in one by one, with a fork and a spoon beside it.
Food traits are one part of the picture, beside what you eat now, how active you are and how you sleep.
  • The all-in-one. GeneCore reads diet, fitness and everyday health traits from one saliva sample and sets them side by side in one report.
  • The diet part. Selected variants studied in carbohydrates and fats, appetite, fullness and taste, caffeine and lactose.
  • Traits, not instructions. Each line gives your result and what research associates with it. It won’t tell you what to eat.

Our nutrition, supplement, athletic and wellbeing reports are for general wellness and information. The evidence behind these associations is less established than for our clinical panels, and these reports are not intended to diagnose, treat, cure or prevent any disease.

To compare it with the single-area tests, see all our DNA nutrition tests on one page.

What to do next

See how a report reads in the sample report, look up any term in the glossary, or find the test that fits you.

Sources

  1. [1]Position of the Academy of Nutrition and Dietetics: nutritional genomics. Journal of the Academy of Nutrition and Dietetics, 2014. Accessed .
  2. [2]Lactose intolerance. MedlinePlus Genetics, U.S. National Library of Medicine. Accessed .
  3. [3]Definition & Facts for Lactose Intolerance. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Accessed .
  4. [4]Convergent adaptation of human lactase persistence in Africa and Europe. Nature Genetics, 2007. Accessed .
  5. [5]Interindividual differences in caffeine metabolism and factors driving caffeine consumption. Pharmacological Reviews, 2018. Accessed .
  6. [6]Genome-wide meta-analysis identifies regions on 7p21 (AHR) and 15q24 (CYP1A2) as determinants of habitual caffeine consumption. PLoS Genetics, 2011. Accessed .
  7. [7]Common genetic determinants of vitamin D insufficiency: a genome-wide association study. The Lancet, 2010. Accessed .
  8. [8]Vitamin D Test. MedlinePlus, U.S. National Library of Medicine. Accessed .
  9. [9]MTHFR Gene Variant and Folic Acid Facts. U.S. Centers for Disease Control and Prevention (CDC). Accessed .
  10. [10]ACMG Practice Guideline: lack of evidence for MTHFR polymorphism testing. Genetics in Medicine, 2013. Accessed .
  11. [11]The impact of MTHFR 677C → T risk knowledge on changes in folate intake: findings from the Food4Me study. Genes & Nutrition, 2016. Accessed .
  12. [12]Genetic studies of body mass index yield new insights for obesity biology. Nature, 2015. Accessed .
  13. [13]A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science, 2007. Accessed .
  14. [14]FTO genotype and weight loss: systematic review and meta-analysis of 9563 individual participant data from eight randomised controlled trials. The BMJ, 2016. Accessed .
  15. [15]Effect of personalized nutrition on health-related behaviour change: evidence from the Food4Me European randomized controlled trial. International Journal of Epidemiology, 2017. Accessed .
  16. [16]Effect of low-fat vs low-carbohydrate diet on 12-month weight loss in overweight adults and the association with genotype pattern or insulin secretion: the DIETFITS randomized clinical trial. JAMA, 2018. Accessed .

How we write and source these pieces: our editorial policy.

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WellnessOur nutrition, supplement, athletic and wellbeing reports are for general wellness and information. The evidence behind these associations is less established than for our clinical panels, and these reports are not intended to diagnose, treat, cure or prevent any disease.

LabOur genetic tests are laboratory-developed tests performed in our own CLIA-certified laboratory. New York is the exception: orders shipped there are completed through a physician order or a reference laboratory permitted in New York. Our genetic tests have not been cleared or approved by the FDA. Results describe inherited traits and risks and are meant to inform decisions you make with your clinician. They are not a diagnosis.