Lactose Intolerance

Lactose intolerance is the onset of digestive symptoms — abdominal pain, bloating, wind and diarrhoea — after eating or drinking lactose, the natural sugar in milk, in a person whose small intestine does not fully digest it (Misselwitz et al. 2019). Reviews estimate that about two-thirds of the world's population undergoes a genetically programmed fall in the lactose-digesting enzyme after weaning; one 2017 review puts lactase non-persistence at 65–70% of the world's adults (Deng et al. 2015; Bayless et al. 2017). Being able to digest milk into adulthood is therefore the less common pattern: one review describes most people as following the example of other mammals, whose enzyme falls to about 10% of newborn levels (Szilagyi & Ishayek 2018), and another calls the decline “not diseases but normal variants of human metabolism” (Misselwitz et al. 2019). Lactose intolerance is not the same as a milk allergy, which is an immune reaction (NIDDK). A 2010 NIH consensus panel concluded that most people with lactose malabsorption do not have clinical lactose intolerance and that, in most cases, people do not need to eliminate dairy completely.

Table of Contents

  1. What Is Lactose Intolerance?
  2. Types of Lactose Intolerance
  3. Symptoms
  4. Who Gets It — Ancestry & Genetics
  5. How It Is Diagnosed
  6. Managing It: Diet & Enzymes
  7. Calcium & Vitamin D Without Dairy
  8. Lactose Intolerance vs Milk Allergy vs IBS
  9. Key Points
  10. Key Research Papers
  11. Connections
  12. Featured Videos

What Is Lactose Intolerance?

Lactose is the main sugar in milk. Chemically it is a disaccharide — two smaller sugars, glucose and galactose, joined together. Lactose cannot be absorbed as-is; the two halves must first be split apart by an enzyme called lactase, made by the cells lining the small intestine (Misselwitz et al. 2019). When enough lactase is present, lactose is broken down, the glucose and galactose are absorbed, and milk is digested without symptoms.

When there is not enough lactase, undigested lactose travels on into the large intestine (the colon). Undigested lactose traps water in the bowel by osmosis, and colonic bacteria ferment it, producing hydrogen, carbon dioxide, methane and short-chain fatty acids; one review notes that fermentation raises the osmotic load in the colon about eightfold, and that diarrhoea results when the lactose load exceeds what the bacteria can ferment or the colon can reabsorb (Misselwitz et al. 2019). That fluid and gas produce the bloating, cramping, rumbling, wind and diarrhoea of lactose intolerance.

Two terms are worth separating. Lactose malabsorption means the gut does not fully digest lactose. Lactose intolerance is malabsorption plus symptoms. Not everyone who malabsorbs lactose has symptoms: reviews list the lactose dose, the amount of lactase made, the intestinal bacteria, how fast the gut moves and how sensitive the gut is as factors that decide whether malabsorption causes symptoms (Misselwitz et al. 2013; Deng et al. 2015).

Lactose intolerance is not a milk allergy. Lactose intolerance is a digestive problem — too little of a sugar-splitting enzyme. A milk allergy is an immune reaction to one or more proteins in milk (NIDDK). The two have different causes and different levels of danger: lactose intolerance causes uncomfortable symptoms, while a serious allergic reaction to milk can be life-threatening (NIDDK). The BSACI guideline on cow's milk allergy states that it must be distinguished from primary lactose intolerance (Luyt et al. 2014). The two are compared side by side below.

Types of Lactose Intolerance

Lactose intolerance has several causes, and the cause bears on whether it is permanent, temporary, or present from birth.

1. Primary lactase deficiency (lactase non-persistence)

This is the genetically programmed kind and the most common cause of low lactase levels (NIDDK). In people with lactase non-persistence the small intestine makes less lactase after infancy, and levels fall further with age (NIDDK); one review describes the decrease as happening in the first two decades of life (Misselwitz et al. 2019). People who keep making lactase for life have a genetic trait called lactase persistence, described in the ancestry section. No treatment increases the amount of lactase the small intestine makes in lactase non-persistence (NIDDK).

2. Secondary (acquired) lactase deficiency

Here lactase falls because the lining of the small intestine — where the enzyme is made — has been injured or inflamed. A 2019 review lists infectious gastroenteritis, inflammatory bowel disease, celiac disease and systemic sclerosis as conditions that secondary lactose malabsorption can complicate, and names small intestinal bacterial overgrowth and rapid transit as other causes of malabsorption (Misselwitz et al. 2019). NIDDK also lists Crohn's disease (one form of inflammatory bowel disease) and treatments for other conditions — medicines, surgery or radiation therapy. Secondary malabsorption is often transitory: many people newly diagnosed with celiac disease recover the ability to digest lactose after 6–12 months on a gluten-free diet (Misselwitz et al. 2019), and NIDDK states that people may tolerate lactose again once the cause of the injury is treated.

3. Congenital lactase deficiency

This is a very rare genetic disorder in which the small intestine makes little or no lactase from birth (NIDDK; Misselwitz et al. 2019). One review counts about 40 reported cases, mainly in Finland (Deng et al. 2015). Another describes it as caused by recessive mutations, with symptoms developing rapidly once breastfeeding begins — often severe diarrhoea, acidosis and hypercalcaemia — and with all forms of milk withheld as the therapy (Szilagyi & Ishayek 2018).

4. Developmental lactase deficiency

In babies born prematurely, the small intestine may not make enough lactase for a short time after birth (NIDDK); lactase activity rises until about week 34 of pregnancy and peaks by birth (Deng et al. 2015). NIDDK states that the condition usually improves without treatment as the baby gets older.

Symptoms

NIDDK describes symptoms as starting within a few hours of eating or drinking something that contains lactose, and as mild or severe depending on how much lactose was taken (NIDDK). The symptoms listed by NIDDK and by reviews are:

Symptoms are dose-dependent. A systematic review of 36 randomized trials found moderate-quality evidence that 12–15 g of lactose (about 1 cup of milk) is well tolerated by most adults with presumed lactose intolerance or malabsorption (Shaukat et al. 2010), and a 2019 review states that larger doses may be tolerated if taken with food or spread over the day (Misselwitz et al. 2019). In a 1995 double-blind crossover trial of 30 people who reported severe lactose intolerance, a cup (240 ml) of milk a day with breakfast produced minimal symptoms, no different from lactose-hydrolysed milk; the authors concluded that people who identify themselves as severely lactose intolerant may mistakenly attribute a variety of abdominal symptoms to lactose (Suarez et al. 1995). In the irritable bowel syndrome literature, weight loss and rectal bleeding are listed as alarm symptoms that call for investigation rather than a diagnosis from the history alone (Ford et al. 2020) — see Key Points.

Who Gets It — Ancestry & Genetics

Lactase persistence is described as a textbook example of gene–culture coevolution: an adaptation to the domestication of dairy animals and the drinking of their milk (Ségurel & Bon 2017). A 2017 review describes lactase non-persistence — the fall in lactase after childhood that underlies primary lactose malabsorption — as affecting 65–70% of the world's adults (Bayless et al. 2017), but that average hides large differences between populations. A 2017 meta-analysis (Storhaug et al.) that was widely quoted for a worldwide malabsorption figure of 68% received an expression of concern from its journal in 2024 and was retracted in January 2025, so none of its estimates is used on this page.

Earlier surveys summarised by Tishkoff et al. (2007) put lactase persistence (the ability to keep digesting lactose) at more than 90% of Swedes and Danes, about 50% of Spanish, French and pastoralist Arab populations, about 5–20% of West African agriculturalists and about 1% of Chinese people. Malabsorption is therefore the norm in populations such as China's and uncommon in Scandinavian populations. A worldwide comparison of phenotype and genotype data concluded that the known variants cannot yet explain how common persistence is in much of western and southern Africa, southeastern Europe, the Middle East and parts of central and southern Asia (Itan et al. 2010).

The ability to keep digesting lactose into adulthood — lactase persistence — is controlled not by changes in the lactase gene's coding sequence but by regulatory DNA nearby. In Finnish families a variant about 14 kb upstream of the lactase gene, C/T−13910, was completely associated with biochemically verified lactase non-persistence (Enattah et al. 2002), and in people of European ancestry persistence is nearly uniformly mediated by this variant (Misselwitz et al. 2019). Pastoralist populations in Tanzania, Kenya and Sudan carry different variants in the same region (G/C−14010, T/G−13915 and C/G−13907) that enhance lactase-gene transcription; the authors describe this as convergent evolution under strong selective pressure from animal domestication and adult milk drinking, with a selective sweep over roughly the past 7,000 years (Tishkoff et al. 2007). Another variant, −13915G, is listed for the Middle East (Misselwitz et al. 2019). Why persistence was so strongly selected for, when milk processing can lower its lactose content, is still described as an open question (Ségurel & Bon 2017).

Because lactase falls gradually, NIDDK notes that symptoms of lactase non-persistence may not begin until later childhood, the teen years, or early adulthood (NIDDK).

How It Is Diagnosed

NIDDK describes diagnosis as starting from symptoms, family and medical history and eating habits, sometimes with a physical exam and tests (NIDDK). A 2019 review lists five tests of lactose digestion, each with different strengths and limits (Misselwitz et al. 2019):

NIDDK lists irritable bowel syndrome, celiac disease, inflammatory bowel disease and small bowel bacterial overgrowth as conditions that can cause symptoms similar to lactose intolerance.

Managing It: Diet & Enzymes

The 2010 NIH consensus panel concluded that, in most cases, people with lactose intolerance do not need to eliminate dairy completely, and that many people with real or perceived lactose intolerance avoid dairy and take in too little calcium and vitamin D (Suchy et al. 2010, NIH statement). A 2019 review notes that, unlike celiac disease or food allergy, a strict lactose-free diet is not required, because people with lactose intolerance often tolerate up to 250 ml of milk (12 g lactose) without symptoms, and more with food (Misselwitz et al. 2019). Reviews describe the clinical results of treatment as modest, partly because lactose is only one of several poorly absorbed carbohydrates that cause symptoms the same way (Misselwitz et al. 2019).

Approaches described in the research

Lactose in other foods and medicines

Lactose powder is a common additive in processed foods such as sausages, gravy, margarines, bread, sauces and many prepared meals (Misselwitz et al. 2019). NIDDK lists breads and baked goods, breakfast cereals, instant potatoes, soups, margarine, salad dressings, flavoured snack foods, processed meats, milk-based meal replacements and protein powders and bars, and non-dairy coffee creamers and whipped toppings. On ingredient lists, NIDDK states that the words milk, lactose, whey, curds, milk by-products, dry milk solids and nonfat dry milk powder mean the product contains lactose (NIDDK). Some prescription and over-the-counter medicines contain a small amount of lactose as a filler (NIDDK); in a controlled breath-test study, the amount in medicines (an average of 400 mg) did not produce a positive breath-hydrogen rise (Szilagyi & Ishayek 2018).

Calcium & Vitamin D Without Dairy

Milk and milk products are some of the main sources of calcium and vitamin D (NIDDK). The 2010 NIH consensus panel found that many people with real or perceived lactose intolerance avoid dairy and take in too little calcium and vitamin D, which may predispose them to decreased bone accrual, osteoporosis and other adverse outcomes (Suchy et al. 2010, NIH statement). A 2019 review notes that these nutrients can also be obtained from other foods (Misselwitz et al. 2019).

The Institute of Medicine's 2011 Recommended Dietary Allowances are 1,000 mg of calcium a day for adults aged 19–50 and men aged 51–70, and 1,200 mg for women aged 51–70 and everyone over 70; for vitamin D, 600 IU a day up to age 70 and 800 IU from 71 (Ross et al. 2011). Non-dairy sources named by NIDDK and in absorption studies include:

NIDDK describes lactose-free and lactose-reduced milk products as just as healthy as regular milk products.

Lactose Intolerance vs Milk Allergy vs IBS

These three are often confused because they can cause overlapping abdominal symptoms, but their causes, risks and management differ.

Feature Lactose Intolerance Cow's Milk Allergy Irritable Bowel Syndrome (IBS)
Underlying mechanism Digestive: shortage of the enzyme lactase Immune: a reaction to one or more milk proteins (NIDDK) Functional disorder with disordered gut–brain communication; cause incompletely understood (Ford 2020)
What triggers it The sugar lactose Milk proteins Many factors; lactose is one of several poorly absorbed fermentable carbohydrates (FODMAPs) linked to symptoms (Deng 2015)
Typical symptoms Bloating, gas, abdominal pain, diarrhoea, nausea Very variable in type and severity (BSACI 2014); a serious reaction can be life-threatening (NIDDK) Abdominal pain with a change in stool form or frequency, often relapsing and remitting (Ford 2020)
Life-threatening? No Serious reactions can be No
Dose sensitivity Dose-dependent; small amounts often fine Managed by avoiding cow's milk; reintroduction can be graded, using a milk ladder (BSACI 2014) Varies by person and trigger
Who it affects most Older children and adults; very common worldwide Presents in the first year of life, 2–3% population prevalence; often resolves (BSACI 2014) 5–10% of people at any one time; more common in young adult women (Ford 2020)
How it is diagnosed Hydrogen breath test, diet trial, other tests above History plus milk-specific IgE (skin prick or blood test), elimination diet and oral challenge (BSACI 2014) Usually from the clinical history, with limited tests unless alarm symptoms are present (Ford 2020)
Management Reduced-lactose diet, lactase enzyme tablets or drops, lactose-free dairy (NIDDK) Cow's milk avoidance and substitute milks (BSACI 2014) Education, dietary changes, soluble fibre and antispasmodic drugs as mainstays (Ford 2020)

Lactose intolerance and IBS frequently overlap. A 2015 review states that intolerance of the wider group of fermentable carbohydrates (FODMAPs) is present in at least half of people with IBS, and that this group needs restriction of more than lactose to improve symptoms (Deng et al. 2015). A 2019 review adds that people with visceral hypersensitivity linked to anxiety or IBS are at increased risk of lactose intolerance regardless of how well they digest lactose, and that intolerance of low–moderate lactose doses often indicates IBS (Misselwitz et al. 2019).

Key Points

A summary of what the sources above report:

Key Research Papers

  1. Suchy FJ, Brannon PM, Carpenter TO, Fernandez JR, et al. National Institutes of Health Consensus Development Conference: Lactose Intolerance and Health. Annals of Internal Medicine. 2010;152(12):792-796. — doi:10.7326/0003-4819-152-12-201006150-00248
  2. Shaukat A, Levitt MD, Taylor BC, MacDonald R, et al. Systematic Review: Effective Management Strategies for Lactose Intolerance. Annals of Internal Medicine. 2010;152(12):797-803. — doi:10.7326/0003-4819-152-12-201006150-00241
  3. Misselwitz B, Butter M, Verbeke K, Fox MR. Update on lactose malabsorption and intolerance: pathogenesis, diagnosis and clinical management. Gut. 2019;68(11):2080-2091. — doi:10.1136/gutjnl-2019-318404
  4. Storhaug CL, Fosse SK, Fadnes LT. Country, regional, and global estimates for lactose malabsorption in adults: a systematic review and meta-analysis. The Lancet Gastroenterology & Hepatology. 2017;2(10):738-746. — doi:10.1016/S2468-1253(17)30154-1 — Retracted; no figure on this page rests on this paper (retraction notice: PubMed PMID: 39674208; expression of concern, 2024: PubMed PMID: 39127069)
  5. The Editors of The Lancet Gastroenterology & Hepatology. Expression of concern — Country, regional, and global estimates for lactose malabsorption in adults: a systematic review and meta-analysis. The Lancet Gastroenterology & Hepatology. 2024;9(9):784. — PubMed PMID: 39127069
  6. The Editors of The Lancet Gastroenterology & Hepatology. Retraction — Country, regional, and global estimates for lactose malabsorption in adults: a systematic review and meta-analysis. The Lancet Gastroenterology & Hepatology. 2025;10(1):13. — PubMed PMID: 39674208
  7. Enattah NS, Sahi T, Savilahti E, Terwilliger JD, et al. Identification of a variant associated with adult-type hypolactasia. Nature Genetics. 2002;30(2):233-237. — doi:10.1038/ng826
  8. Tishkoff SA, Reed FA, Ranciaro A, Voight BF, et al. Convergent adaptation of human lactase persistence in Africa and Europe. Nature Genetics. 2007;39(1):31-40. — doi:10.1038/ng1946
  9. Itan Y, Jones BL, Ingram CJ, Swallow DM, et al. A worldwide correlation of lactase persistence phenotype and genotypes. BMC Evolutionary Biology. 2010;10:36. — doi:10.1186/1471-2148-10-36
  10. Suarez FL, Savaiano DA, Levitt MD. A Comparison of Symptoms after the Consumption of Milk or Lactose-Hydrolyzed Milk by People with Self-Reported Severe Lactose Intolerance. New England Journal of Medicine. 1995;333(1):1-4. — doi:10.1056/NEJM199507063330101
  11. Deng Y, Misselwitz B, Dai N, Fox M. Lactose Intolerance in Adults: Biological Mechanism and Dietary Management. Nutrients. 2015;7(9):8020-8035. — doi:10.3390/nu7095380
  12. Misselwitz B, Pohl D, Frühauf H, Fried M, et al. Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment. United European Gastroenterology Journal. 2013;1(3):151-159. — doi:10.1177/2050640613484463
  13. Szilagyi A, Ishayek N. Lactose Intolerance, Dairy Avoidance, and Treatment Options. Nutrients. 2018;10(12):1994. — doi:10.3390/nu10121994
  14. Bayless TM, Brown E, Paige DM. Lactase Non-persistence and Lactose Intolerance. Current Gastroenterology Reports. 2017;19(5):23. — doi:10.1007/s11894-017-0558-9
  15. Suchy FJ, Brannon PM, Carpenter TO, Fernandez JR, et al. NIH consensus development conference statement: Lactose intolerance and health. NIH Consensus and State-of-the-Science Statements. 2010;27(2):1-27. — PubMed PMID: 20186234
  16. Ross AC, Manson JE, Abrams SA, Aloia JF, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. Journal of Clinical Endocrinology & Metabolism. 2011;96(1):53-58. — doi:10.1210/jc.2010-2704
  17. Heaney RP, Weaver CM, Recker RR. Calcium absorbability from spinach. American Journal of Clinical Nutrition. 1988;47(4):707-709. — doi:10.1093/ajcn/47.4.707
  18. Heaney RP, Weaver CM. Calcium absorption from kale. American Journal of Clinical Nutrition. 1990;51(4):656-657. — doi:10.1093/ajcn/51.4.656
  19. Luyt D, Ball H, Makwana N, Green MR, et al. BSACI guideline for the diagnosis and management of cow's milk allergy. Clinical & Experimental Allergy. 2014;44(5):642-672. — doi:10.1111/cea.12302
  20. Ford AC, Sperber AD, Corsetti M, Camilleri M. Irritable bowel syndrome. The Lancet. 2020;396(10263):1675-1688. — doi:10.1016/S0140-6736(20)31548-8
  21. Ségurel L, Bon C. On the evolution of lactase persistence in humans. Annual Review of Genomics and Human Genetics. 2017;18:297-319. — doi:10.1146/annurev-genom-091416-035340

PubMed Topic Searches

These links open live PubMed searches for the listed keywords — results update as new studies are indexed.

  1. Lactose intolerance — PubMed search
  2. Lactase persistence genetics — PubMed search
  3. Hydrogen breath test for lactose — PubMed search
  4. Lactase enzyme supplements — PubMed search
  5. Lactose malabsorption diagnosis — PubMed search
  6. Lactose-free diet, calcium & bone — PubMed search
  7. Lactose intolerance & IBS — PubMed search

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Connections

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