Lactose Intolerance — a trait present in 65% of the global population that in its common form is genetic adaptation, but in its rare congenital form (CLD) is a neonatal emergency requiring immediate formula change.
Whole genome sequencing distinguishes genetic lactase non-persistence (common, benign) from congenital lactase deficiency (rare, neonatal emergency) and sucrase-isomaltase deficiency — providing the clinical precision that symptom presentation alone cannot supply.
Lactose Intolerance — Genetic
Lactose intolerance in its most common form — adult-onset primary lactase deficiency — is caused by the developmental decline in lactase-phlorizin hydrolase (LPH) expression in the small intestinal brush border that occurs in most mammals after weaning. In most humans, LCT gene expression declines after early childhood — a state called lactase non-persistence (LNP). The minority ancestral adaptation, lactase persistence (LP), evolved independently multiple times in populations with a history of dairying cattle — Northern Europeans (LP allele frequency ~90%), some East African pastoralist groups (~50-80%), and certain Middle Eastern and South Asian populations. The genetic basis of LP involves regulatory single-nucleotide variants upstream of the LCT gene in the MCM6 intron, of which c.-13910C>T (rs4988235) is the primary European LP variant.
Primary lactase non-persistence affects approximately 65% of the global adult population and causes symptoms of lactose malabsorption — bloating, abdominal cramps, flatulence, and diarrhea — after lactose consumption exceeding a variable threshold. The condition is not a disease, but rather the ancestral mammalian norm, and its severity and symptom threshold vary widely. Distinguishing primary LNP from the rare but clinically distinct condition of congenital lactase deficiency (CLD), caused by pathogenic variants in the LCT structural gene itself, is clinically important: CLD presents in the neonatal period with profuse watery diarrhea immediately after the first lactose-containing feed, causing severe dehydration. CLD is most common in Finland (LGLS variants) and requires immediate switch to lactose-free formula.
Sucrase-isomaltase deficiency — caused by pathogenic variants in MGAM (maltase-glucoamylase) or SI (sucrase-isomaltase) — produces symptoms indistinguishable from lactose intolerance but requires dietary sucrose restriction rather than lactose restriction, and is treatable with sacrosidase (Sucraid). Trehalase deficiency (TREH variants) similarly causes carbohydrate intolerance superficially resembling lactose intolerance. These mechanistically different conditions are important to distinguish in patients with refractory 'lactose intolerance' symptoms who remain symptomatic despite dairy exclusion. Whole genome sequencing evaluates LCT, MCM6, SI, MGAM, and TREH simultaneously.
Congenital lactase deficiency (CLD), caused by LCT coding variants, is a rare neonatal emergency — presenting within days of first feeding with profuse watery diarrhea, dehydration, and failure to thrive. It is distinct from common adult lactase non-persistence and requires immediate dietary management.
Breath tests diagnose lactose malabsorption. They do not distinguish common genetic LNP from congenital LCT deficiency or sucrase-isomaltase deficiency — conditions with different dietary treatments. Molecular genotyping provides this distinction.
Patients with persistent symptoms after dairy exclusion may have sucrase-isomaltase deficiency — not lactose intolerance
Sucrase-isomaltase (SI) deficiency is estimated to affect 0.2% of Northern Europeans and up to 5% of Greenlandic Inuit, causing disaccharide intolerance with symptoms almost identical to lactose intolerance. Patients with SI deficiency who eliminate dairy often remain symptomatic because sucrose in bread, fruit, and sweetened foods is the actual trigger. SI deficiency is treatable with sacrosidase enzyme supplementation (Sucraid, FDA-approved). A genome-wide analysis evaluating LCT, MCM6, SI, MGAM, and TREH simultaneously can identify the specific genetic cause of carbohydrate intolerance — distinguishing conditions with different dietary exclusions and different treatment approaches from what is presented as 'refractory lactose intolerance.'
The MCM6 regulatory variant determines lifetime dairy tolerance — a permanent trait worth knowing definitively
The MCM6 c.-13910C>T variant — the primary European lactase persistence allele — is a simple Mendelian trait. Homozygous CC (non-persistence) individuals have low adult lactase expression and are typically lactose intolerant as adults. Homozygous TT or heterozygous CT (persistence) individuals maintain lactase expression. Knowing this genotype definitively — rather than inferring it from a hydrogen breath test that can be confounded by rapid transit, small intestinal bacterial overgrowth, and other variables — provides a permanent, unambiguous result that determines the dietary approach without repeat testing. For individuals of non-European ancestry, additional LP regulatory variants (1390G, 14011G) relevant to East African and Middle Eastern populations are also evaluated by whole genome sequencing.
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A patient came to Dante to investigate periodic paralysis. Reading the complete genome identified a concurrent hereditary cardiac finding — Brugada syndrome — that their doctor confirmed with an ECG. The result also explained a family member's unresolved cardiac history. One test. Every answer in it.
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Learn more →When traditional lab tests say you're fine. And you know you're not.
Standard diagnostic tests check for a pre-selected set of answers. We sequence your full DNA — including parts that no test was designed to check. If the answer is in your genome, we will help you find it.
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Your genes determine which treatments are most likely to work — and which are not. We give your doctor the tools and insights to inform your treatment plan.
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Some people don't wait for a diagnosis or a family history to act. Whole genome sequencing gives you the complete genetic picture now — so you and your doctor can make informed decisions before anything becomes urgent.
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Common questions about whole genome sequencing.
What is the difference between whole genome sequencing and a targeted genetic test?
Targeted genetic tests — including standard hereditary cancer panels — read a pre-defined list of known variants in a specific set of genes. They are designed to find what they already know to look for. Whole genome sequencing reads your entire genome: all 6 billion base pairs, every gene, every region between genes. A Mayo Clinic study published in JAMA Oncology found that standard testing guidelines missed more than half of patients with inherited cancer mutations. Genome Test does not have a fixed list.
What will I receive when my results are ready?
Your Dante Genome delivers 200+ physician-ready reports organized by clinical category — hereditary cancer, cardiac conditions, rare diseases, pharmacogenomics, carrier status, and more. Reports are delivered to your secure Genome Manager and are formatted for direct clinical use. Your genome data is permanently retained and re-analyzed automatically as science advances.
What happens if a clinically significant variant is found?
If a pathogenic or likely-pathogenic variant is identified, it will be clearly flagged in your physician-ready report with clinical context, published evidence, and recommended next steps. We recommend sharing any clinically significant finding with your physician or a genetic counselor, who can guide decisions about surveillance, risk reduction, or cascade testing for family members.
How is this different from a consumer DNA test like 23andMe or AncestryDNA?
Consumer DNA tests use genotyping chips that read less than 0.1% of your genome — a tiny pre-selected set of common variants. They are optimized for ancestry and population-level traits, not clinical genetic findings. The Dante Genome Test sequences 100% of your genome at 30X coverage, the same standard used in clinical diagnostic settings. The two tests are not comparable in scope, methodology, or clinical utility.
How long does it take to get results, and how are they delivered?
Your collection kit ships within 48 hours of ordering. Once your sample arrives at our CLIA-certified laboratory, sequencing and analysis takes 6–8 weeks. Results are delivered securely to your Genome Manager, where you can access your reports, share them with your physician, and receive automatic updates as new findings are validated against your genome.
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Ships within 48 hours · Results in 6–8 weeks
