Why your genetics change what your supplements should be

Nutrigenomics is the study of how genetic variants influence individual responses to nutrients. It's been peer-reviewed for over 20 years. Here's what it actually says — and how GNLAB applies it.

The problem with standard supplements

Every supplement on the shelf is formulated for a statistical average. "Adults need 600–2000 IU of vitamin D daily." "Recommended magnesium: 300–400 mg." These numbers are population means — useful for public health guidance, not for calibrating an individual's biology.

The variance around those means is enormous. VDR polymorphisms cause a 2–3x difference in effective vitamin D requirements between individuals with identical serum levels. Two people can have the same blood test result and require completely different doses to achieve the same cellular outcome. Generic supplements can't account for that. They don't know which person you are.

The same pattern applies across dozens of nutrient pathways. Your genetics determine not just how much you need, but what molecular forms you can actually use — and that's the gap standard supplements leave entirely unaddressed.


What nutrigenomics actually is

Nutrigenomics examines how genetic variants — single nucleotide polymorphisms (SNPs) in specific genes — affect how your body processes nutrients. It's not a fringe field. The foundational research has been published in journals including Nature Genetics, The American Journal of Clinical Nutrition, and The Journal of Human Genetics, with thousands of peer-reviewed studies documenting specific gene-nutrient relationships.

The key distinction from "DNA diet" services is what the research actually supports. Predicting optimal macronutrient ratios from genetics has weak evidence. Predicting how specific micronutrient pathways function — absorption, conversion, utilisation — has strong, replicable evidence. GNLAB stays in the latter category.


The genetic variants that matter for nutrition

GNLAB analyses 60+ markers. Here are the best-characterised ones and what they mean in practice.

VDR gene — vitamin D receptor

Vitamin D absorption and cellular response

The VDR gene encodes the vitamin D receptor — the protein your cells use to respond to vitamin D. Three well-studied polymorphisms (Bsm1, Fok1, Taq1) affect receptor binding efficiency and downstream signalling. Individuals with the TT genotype at Fok1 have receptors with reduced binding affinity, meaning the same serum 25(OH)D level produces less cellular vitamin D activity. Multiple studies demonstrate that these variants predict 25–40% variation in bone mineral density response to identical vitamin D supplementation protocols. Source: Uitterlinden et al., Nature Genetics, 2004; Gnagnarella et al., Int J Cancer, 2006.

MTHFR gene — methylenetetrahydrofolate reductase

Folate and B12 metabolism (methylation pathway)

MTHFR encodes an enzyme central to the methylation cycle — the process that converts folate and B12 into active forms your body can use. The C677T variant reduces enzyme activity by approximately 35% in heterozygous carriers and 70% in homozygous carriers. Around 10% of Northern Europeans carry two copies. These individuals cannot effectively process folic acid (the synthetic form in most supplements) — they require methylfolate instead. Elevated homocysteine, a cardiovascular risk marker, is the measurable downstream consequence of MTHFR-impaired methylation. Source: Frosst et al., Nature Genetics, 1995; Wald et al., BMJ, 2002.

FADS1 / FADS2 genes — fatty acid desaturases

Omega-3 conversion from plant sources

FADS1 and FADS2 encode the enzymes responsible for converting short-chain omega-3 ALA (found in flaxseed, walnuts, plant sources) into the long-chain EPA and DHA that your brain and cardiovascular system actually require. Variants in these genes reduce conversion efficiency by up to 50% in affected individuals. Someone with these variants eating a plant-based diet with no marine omega-3 sources is unlikely to produce adequate EPA/DHA regardless of how much ALA they consume. Direct supplementation with pre-formed EPA/DHA becomes necessary rather than optional. Source: Schaeffer et al., Nature Genetics, 2006; Tanaka et al., Nature Genetics, 2009.

HFE gene — haemochromatosis protein

Iron absorption efficiency

The HFE gene regulates iron absorption in the gut. The H63D and C282Y variants increase iron absorption efficiency. For carriers, supplementing iron without confirmed deficiency can lead to iron overload and associated oxidative stress — the opposite of the intended benefit. This makes genotyping particularly important before adding iron to a supplement protocol. HFE variants are common in Northern European populations: H63D affects approximately 15–20% of individuals. Source: Feder et al., Nature Genetics, 1996; Adams et al., NEJM, 2005.

SOD2 / CAT / GPX — antioxidant enzymes

Oxidative stress response capacity

SOD2 (superoxide dismutase 2), CAT (catalase), and GPX (glutathione peroxidase) encode the primary intracellular antioxidant enzymes. Variants reducing enzyme activity lower your baseline capacity to neutralise reactive oxygen species — which accumulate during exercise, stress, and aging. Individuals with reduced SOD2 activity derive more measurable benefit from exogenous antioxidant supplementation (vitamin C, vitamin E, CoQ10) than those with full enzyme function. For athletes, this directly affects how well you recover between training sessions. Source: Mitrunen et al., Pharmacogenetics, 2001; Devasagayam et al., Curr Sci, 2004.

Additional markers analysed

Magnesium, calcium, B-vitamins, caffeine interactions, and more

GNLAB analyses over 60 markers in total, including variants affecting magnesium retention and excretion, calcium metabolism and bone density pathways, B6 and B2 processing, zinc absorption, and caffeine metabolism (CYP1A2) — relevant because caffeine affects how certain nutrients are absorbed and how micronutrient timing should be structured. The full panel provides a comprehensive picture of your nutritional genetic profile across all major pathways.


What the research supports — and what it doesn't

GNLAB is transparent about where the science is strong and where it continues to evolve.

Strong evidence — what we build from

  • Micronutrient form selection: Which molecular forms (methylfolate vs folic acid, D3 vs D2, magnesium glycinate vs oxide) your variants can effectively use. Well-characterised across hundreds of studies.
  • Direction of effect: Whether a given variant increases or decreases your requirement for a specific nutrient. Consistently replicated in independent cohorts.
  • Nutrient interactions: Which nutrients compete for absorption (calcium + iron, zinc + copper) and which are synergistic — relevant for timing and combining in a sachet.

Emerging — included with caveats

  • Precise dosing thresholds: Most research confirms direction of effect reliably. Exact optimal doses from multi-variant combinations are actively researched. GNLAB uses validated ranges, not single-point doses.
  • Multi-gene interaction modelling: Most published studies are single-gene. Real biology involves multiple interacting variants. Our models are built on published interaction data where available, with conservative defaults where not.

Not supported — what we don't do

  • DNA-based macronutrient ratios ("your genotype suggests low-carb"). Evidence for this is weak and not reproducible in large trials.
  • Disease prediction or diagnostic claims. GNLAB is a nutrition company, not a medical diagnostics company.
  • Guaranteed outcomes. Biology is complex. Your formula is built on the best available evidence, and we update our models as the field advances.

Why the delivery format matters as much as the formula

Getting the right nutrients in the right forms is only half the problem. Getting them into your cells is the other half.

Standard capsules dissolve in the stomach, releasing everything at once. Gastric acid destroys a significant portion of active ingredients before they reach the small intestine where absorption occurs. Competing nutrients — calcium and iron, zinc and copper — block each other's absorption transporters when they arrive simultaneously.

GNLAB uses microencapsulated pellets — individually coated nutrient particles that release at different points in the digestive tract. Synergistic nutrients are timed to arrive together. Competing nutrients are timed apart. Fat-soluble vitamins release in the small intestine where bile acids are available to aid absorption. Water-soluble nutrients release earlier. The result is measurably better delivery compared to standard capsule formats.


The laboratory

DNA analysis is performed by an accredited European genetics laboratory in Austria. The laboratory operates under ISO 15189 accreditation standards for medical laboratories and handles samples under GDPR-compliant data protection protocols.

Your saliva sample undergoes targeted genotyping of 60+ nutritional SNPs using validated genotyping arrays. The analysis produces a genetic report with your specific variant calls for each marker, which GNLAB's formulation engine uses to calculate your supplement formula.

Your genetic data is stored under GDPR, used exclusively for your supplement formulation, and never shared with third parties for research, advertising, or any other purpose. You can request deletion at any time.

Ready to see what your DNA says?

One test. One formula. Built from your actual biology, not a population average.

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