Yogurt — Lactose Tolerance

Table of Contents

1. Lactose, Lactase, and Lactase Non-Persistence
2. Lactase Persistence — the LCT-13910 Polymorphism
3. Global Distribution of Lactase Persistence
4. Lactose Intolerance Symptoms and Thresholds
5. The Yogurt Mechanism — Bacterial Lactase in the Gut
6. The 1984 Breath-Hydrogen Studies (Kolars; Savaiano)
7. The EU Health Claim (EFSA Opinion, 2010)
8. Live and Heat-Treated Yogurt — Labels and Findings
9. Colonic Microbial Adaptation Over Time
10. What Reviews Report for People With Lactose Intolerance
11. Key Research Papers
12. Connections
13. Featured Videos

Lactose, Lactase, and Lactase Non-Persistence

Lactose is the sugar of milk. The brush-border enzyme lactase-phlorizin hydrolase, encoded by the LCT gene on chromosome 2 (2q21), splits it into glucose and galactose in the small intestine (Enattah 2002).

In most humans, lactase activity declines after weaning as a consequence of the normal maturational down-regulation of lactase expression (Deng 2015). A 2019 review describes this decrease as happening in the first two decades of life and calls lactase non-persistence (LNP) the phenotype of most individuals worldwide (Misselwitz 2019). Because lactase falls gradually, symptoms may not begin until later childhood, the teen years or early adulthood (NIDDK).

When lactose is not digested, it comes into contact with the intestinal bacteria. Bacterial fermentation of lactose produces gases including hydrogen, carbon dioxide and methane, and short-chain fatty acids that affect gut function (Misselwitz 2019); NIDDK describes the bacteria in the colon breaking down lactose and creating fluid and gas, which in some people causes symptoms.

Two terms are kept apart in the research. Lactose malabsorption is any failure to digest or absorb lactose in the small intestine; lactose intolerance is the onset of abdominal symptoms such as pain, bloating and diarrhoea after lactose in a person with malabsorption. Whether symptoms occur depends on the lactose dose, lactase expression and the intestinal microbiome, and people with visceral hypersensitivity linked to anxiety or irritable bowel syndrome are at increased risk independent of how well they digest lactose (Misselwitz 2019).

Lactose intolerance is not a milk allergy. The British Society for Allergy and Clinical Immunology (BSACI) guideline on cow's milk allergy states that cow's milk allergy must be distinguished from primary lactose intolerance (Luyt 2014).

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Lactase Persistence — the LCT-13910 Polymorphism

People whose lactase stays high into adulthood have the lactase persistence (LP) trait. In 2002, analysis of nine extended Finnish families identified a DNA variant, C/T-13910, roughly 14 kilobases upstream of the LCT gene, that was completely associated with biochemically verified lactase non-persistence in those families and in 236 individuals from four populations; because the variant occurs in distantly related populations, the authors concluded that it is very old (Enattah 2002). The variant lies within an intron of a neighbouring gene, MCM6 (Deng 2015; Misselwitz 2019), and the T allele creates a new binding site for a transcription factor that promotes persistent lactase expression; in people of European ancestry, lactase persistence is nearly uniformly mediated by this variant (Misselwitz 2019). Lactase persistence is inherited as a dominant trait in Europeans (Tishkoff 2007).

In a genotype–phenotype study of 470 Tanzanians, Kenyans and Sudanese, three other variants in the same region — G/C-14010, T/G-13915 and C/G-13907 — were associated with lactase persistence, and their derived alleles enhanced transcription from the LCT promoter in laboratory assays. T/G-13915 was associated with persistence in Kenyans, and C/G-13907 was marginally associated with it in the Beja of northern Sudan (Tishkoff 2007).

These variants arose on different haplotype backgrounds from the European variant and from each other, which the authors describe as convergent evolution under strong selective pressure from animal domestication and adult milk drinking. Haplotype homozygosity around C-14010 extending more than 2.0 megabases was consistent with a selective sweep over roughly the past 7,000 years, and the authors describe these chromosomes as carrying one of the strongest genetic signatures of natural selection yet reported in humans (Tishkoff 2007).

For the European variant, ancient DNA shows the −13910*T allele was very rare or absent in early Neolithic central Europeans. A 2009 simulation study inferred that it first underwent selection among dairying farmers around 7,500 years ago in a region between the central Balkans and central Europe, and its results did not support stronger selection in northern latitudes through a greater need for dietary vitamin D (Itan 2009).

A genetic test for the −13910 variant can detect genetic lactase non-persistence in people of European ancestry. A 2019 review notes that the genetics are more complex in people of African or Asian heritage, that genetic tests are not currently advocated in these populations for clinical purposes, and that secondary (acquired) malabsorption is not detected by genetic tests (Misselwitz 2019). A 2015 review describes the hydrogen breath test as the method of choice for assessing lactose malabsorption and intolerance (Deng 2015).

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Global Distribution of Lactase Persistence

Earlier surveys summarised by Tishkoff and colleagues put the frequency of lactase persistence at:

• Swedes and Danes — more than 90%
• Spanish, French and pastoralist Arab populations — about 50%
• West African agriculturalists — about 5–20%
• Chinese — about 1%
• African pastoralist populations — about 90% in Tutsi and about 50% in Fulani

In the same study's own East African sample, lactase persistence was most frequent in the Beja pastoralists of Sudan (88%) and least frequent in the Sandawe hunter-gatherers of Tanzania (26%) (Tishkoff 2007). A 2009 study describes lactase persistence as common among people of European ancestry but, with the exception of some African, Middle Eastern and southern Asian groups, rare or absent elsewhere in the world (Itan 2009).

Worldwide, reviews describe about two-thirds of the population as undergoing a genetically programmed fall in lactase after weaning (Deng 2015), and lactase non-persistence as affecting 65–70% of the world's adults (Bayless 2017). A 2017 meta-analysis of worldwide lactose-malabsorption prevalence was retracted in 2025 (retraction notice: PubMed PMID: 39674208), so its estimates are not used on this page.

Yogurt has a long history among these populations: a 1984 breath-hydrogen study notes that large quantities of yogurt are consumed by some lactase-deficient population groups (Kolars 1984), and a 2014 review describes yogurt as traditionally consumed throughout the world among populations seemingly unable to digest lactose (Savaiano 2014).

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Lactose Intolerance Symptoms and Thresholds

NIDDK lists the symptoms as bloating, diarrhoea, gas, nausea, abdominal pain, stomach “growling” or rumbling sounds and vomiting, appearing within a few hours of eating or drinking something that contains lactose, and mild or severe depending on how much lactose was taken (NIDDK). A 2015 review lists abdominal pain and distension, borborygmi (audible bowel sounds), flatus and diarrhoea (Deng 2015).

What the research reports about thresholds:

• 12–15 g of lactose at a time — a systematic review of 36 randomized trials found moderate-quality evidence that 12 to 15 g of lactose (approximately 1 cup of milk) is well tolerated by most adults with presumed lactose intolerance or malabsorption (Shaukat 2010). A 2019 review states that most people with lactose malabsorption tolerate at least 12 g (corresponding to 250 mL of milk), and that larger doses may be tolerated if taken with food or spread over the whole day (Misselwitz 2019).
• Self-reported severe intolerance — in a randomized, double-blind crossover trial of 30 people who reported severe lactose intolerance, 240 mL of milk daily with breakfast for one week produced minimal symptoms, with no significant difference in bloating, abdominal pain, diarrhoea or flatus from lactose-hydrolysed milk; 21 of the 30 were lactose malabsorbers. The authors concluded that people who identify themselves as severely lactose intolerant may mistakenly attribute a variety of abdominal symptoms to lactose (Suarez 1995).
• Malabsorption without intolerance — the 2010 NIH consensus panel concluded that the majority of people with lactose malabsorption do not have clinical lactose intolerance, and that many individuals who think they are lactose intolerant are not lactose malabsorbers (NIH 2010).
• Who is more susceptible — a 2018 scoping review found that the evidence suggests women, the elderly or specific racial groups are not more susceptible to lactose intolerance; dose, body size and genetic differences in lactase non-persistence were the primary drivers of symptoms (Lapides 2018).
• Hydrogen breath test — a 2019 review describes an intermediate lactose dose of 20–25 g as possibly optimal in clinical practice; a baseline breath hydrogen below 20 ppm is required for a reliable test, and a rise of 20 ppm or more within 3 hours is diagnostic of malabsorption. Gut bacteria that convert hydrogen to methane can produce false-negative results (Misselwitz 2019).

Cow's milk allergy is a different condition. The BSACI guideline describes it as presenting in the first year of life with an estimated population prevalence of 2–3%, with clinical manifestations very variable in type and severity; its treatment is advice on cow's milk avoidance and suitable substitute milks, the allergy often resolves, and reintroduction can be achieved by graded exposure using a milk ladder (Luyt 2014). The yogurt studies on this page concern lactose digestion; they did not study milk allergy.

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The Yogurt Mechanism — Bacterial Lactase in the Gut

Under the US standard of identity, yogurt is made with a characterizing bacterial culture that contains Lactobacillus delbrueckii subsp. bulgaricus and Streptococcus thermophilus (21 CFR 131.200). Yogurt still contains lactose: a 2019 review states that yoghurt contains about 50% of the lactose of unprocessed milk, and gives representative values of 3.0 g of lactose per 100 g of fresh yoghurt (9.3 g per typical serving) and 4.0 g per 100 g of “biological” yoghurt (9.5 g per serving), against 4.7 g per 100 g of full milk (15 g per serving) (Misselwitz 2019). Strained and unstrained yogurt are compared on the Greek vs Regular page.

A 2014 review sets out how the yogurt bacteria help digest this lactose (Savaiano 2014):

1. Protection in the stomach — the bacterial lactase survives the acidic conditions of the stomach, apparently physically protected within the bacterial cells and helped by the buffering capacity of yogurt.
2. Activity in the small intestine — the rising pH as yogurt enters the small intestine and a slower gastrointestinal transit time allow the bacterial lactase to be active, digesting lactose from yogurt sufficiently to prevent symptoms in lactose-intolerant people.
3. Commercial yogurts — there is little difference in the lactase capability of different commercial yogurts, which apparently contain L. bulgaricus and S. thermophilus in sufficient quantities (10⁸ bacteria/mL). Flavoured yogurts appear to have somewhat reduced lactase activity compared with unflavoured yogurts but are still well tolerated.
4. Other species — Lactobacillus acidophilus appears to require disruption of its cell membrane to release its lactase.

The 1984 Kolars study attributed the better absorption of lactose from yogurt to digestion of lactose inside the intestine by lactase released from the yogurt organisms (Kolars 1984), and a 2021 review notes that the same study reported active microbial beta-galactosidase in the intestinal contents of its subjects (Savaiano 2021).

In a 1984 study, heat treatment changed the result for lactose digestion but not for symptoms. Pasteurizing yogurt eliminated its enhanced lactose digestion, reduced its lactase activity 10-fold and reduced its cell counts 100-fold; yet all subjects fed pasteurized yogurt were symptom-free, whereas eight of nine had gastrointestinal distress after cultured milk (buttermilk), even though the amount of lactose malabsorbed was similar (Savaiano 1984).

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The 1984 Breath-Hydrogen Studies (Kolars; Savaiano)

Two studies published in 1984 used breath hydrogen — a marker of lactose that reaches colonic bacteria unabsorbed — to test yogurt in lactase-deficient adults.

Kolars, Levitt, Aouji and Savaiano (New England Journal of Medicine, 1984) gave lactase-deficient subjects 18 g of lactose in yogurt, or a similar load in milk or water. The abstract reports:

• Lactose in yogurt produced only about one third as much hydrogen excretion as a similar load in milk or water, indicating much better absorption of the lactose in yogurt.
• Yogurt produced fewer reports of diarrhoea or flatulence than a similar quantity of lactose in milk or water.
• The enhanced absorption appeared to result from digestion of lactose inside the intestine by lactase released from the yogurt organisms. The authors described yogurt as a well-tolerated source of milk for lactase-deficient persons.

The abstract does not state the number of subjects.

Savaiano, AbouElAnouar, Smith and Levitt (American Journal of Clinical Nutrition, 1984) compared yogurt with three other fermented or microbe-containing dairy foods — pasteurized yogurt, cultured milk (buttermilk) and sweet acidophilus milk — in nine lactase-deficient subjects. Yogurt was unique among the products tested in enhancing lactose digestion; pasteurization eliminated that effect, reduced lactase activity 10-fold and cell counts 100-fold. Eight of nine subjects had gastrointestinal distress after cultured milk, whereas all subjects fed pasteurized yogurt were symptom-free, although the amount of malabsorbed lactose was similar (Savaiano 1984).

A 2021 systematic review describes later studies along the same lines: in one, among flavoured and frozen yogurts, ice cream and ice milks, lactose digestion improved significantly only with fresh yogurt, which was also the only product that did not cause gastrointestinal symptoms; in another, both yogurts and kefir improved lactose digestion and reduced symptoms of intolerance compared with milk. The review concluded that a causal relationship exists between lactose digestion and tolerance and yogurt consumption (Savaiano 2021).

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The EU Health Claim (EFSA Opinion, 2010)

In 2010 the European Food Safety Authority (EFSA) Panel on Dietetic Products, Nutrition and Allergies published its scientific opinion on the substantiation of health claims related to live yoghurt cultures and improved lactose digestion (ID 1143, 2976) under Article 13(1) of Regulation (EC) No 1924/2006 (EFSA Journal 8(10):1763). The claim was then included in the EU list of permitted health claims, Commission Regulation (EU) No 432/2012, which gives:

• Claim wording — “Live cultures in yoghurt or fermented milk improve lactose digestion of the product in individuals who have difficulty digesting lactose.”
• Conditions of use — “In order to bear the claim, yoghurt or fermented milk should contain at least 10⁸ Colony Forming Units live starter microorganisms (Lactobacillus delbrueckii subsp. bulgaricus and Streptococcus thermophilus) per gram.”

A 2021 systematic review describes this as an approved function claim in the European Union for live cultures in yogurt or fermented milk to aid lactose digestion, and reports that in a review of the dietary recommendations of 13 EU member states, none mentioned yogurt as an alternative for people with lactose intolerance (Savaiano 2021).

The United States labelling rules for live cultures, which use a different threshold, are set out in the next section.

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Live and Heat-Treated Yogurt — Labels and Findings

• US “contains live and active cultures” — the US standard of identity allows this phrase if the yogurt contains at least 10⁷ colony-forming units per gram (CFU/g) at the time of manufacture, with a reasonable expectation of 10⁶ CFU/g through the manufacturer's assigned shelf life (21 CFR 131.200).
• US heat-treated yogurt — to extend shelf life, yogurt may be treated after culturing to inactivate viable microorganisms; it keeps the name “yogurt” but must carry the phrase “does not contain live and active cultures” in letters at least half the height of the name (21 CFR 131.200).
• EU claim — the lactose-digestion claim requires at least 10⁸ CFU of live starter microorganisms per gram (Regulation (EU) No 432/2012).
• Pasteurized yogurt in a study — pasteurization removed yogurt's enhanced lactose digestion, but the subjects who ate pasteurized yogurt were symptom-free (Savaiano 1984).
• Flavoured and frozen products — in one study described by a 2021 review, only fresh yogurt, among flavoured and frozen yogurts, ice cream and ice milks, significantly improved lactose digestion (Savaiano 2021); a 2014 review describes flavoured yogurts as having somewhat reduced lactase activity but still being well tolerated (Savaiano 2014).
• Lactose-free milk — a different approach: lactase is added to the milk, leaving less than 0.1 g of lactose per 100 g. A 2019 review describes these products as widely available and considered safe, although allergic reactions have been reported (Misselwitz 2019).
• Lactase tablets — lactase supplementation by tablets improves both lactose digestion and symptoms, although the effects are modest (Misselwitz 2019).
• Probiotic preparations — the 2010 systematic review found the evidence for probiotics in lactose intolerance insufficient (Shaukat 2010); a 2019 review cites a later systematic review that found an overall positive effect, but not consistently better than lactase supplements and with limited study quality (Misselwitz 2019).

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Colonic Microbial Adaptation Over Time

A slower process studied in people who maldigest lactose is adaptation of the colonic bacteria to regular lactose intake.

• Hertzler & Savaiano 1996 — in nine lactose maldigesters, faecal beta-galactosidase activity rose threefold after 16 days of lactose feeding. In a blinded crossover study, 20 lactose-maldigesting adults received lactose or dextrose for 10 days each, the dose rising from 0.6 to 1.0 g per kg per day. After the lactose period, flatus frequency and severity after a lactose challenge fell by 50% compared with the dextrose period, and breath hydrogen was significantly lower; symptoms during the feeding periods themselves did not differ significantly. The authors concluded that colonic adaptation to regular lactose ingestion reduces intolerance symptoms (Hertzler 1996).
• Pribila et al. 2000 — 17 African-American girls aged 11 to 15, 14 of them lactose maldigesters, ate a dairy-based diet averaging 33 g of lactose and 1,200 mg of calcium a day for 21 days. Breath hydrogen fell significantly from the start to the end of the period, and gastrointestinal symptoms were negligible throughout; the authors interpreted the fall as suggesting colonic adaptation (Pribila 2000).

The evidence is described more cautiously in reviews: the 2010 systematic review, which found two randomized trials of incremental lactose for colonic adaptation, judged the evidence insufficient (Shaukat 2010), and a 2019 review lists colonic adaptation by prebiotics as a potential treatment (Misselwitz 2019).

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What Reviews Report for People With Lactose Intolerance

• Dairy need not be eliminated in most cases — the 2010 NIH consensus panel concluded that, in most cases, individuals do not need to eliminate dairy consumption completely (NIH 2010). A 2019 review notes that, unlike in celiac disease or food allergy, a strict lactose-free diet is not required (Misselwitz 2019).
• Amounts — most adults with presumed lactose intolerance or malabsorption tolerated 12–15 g of lactose at a time (Shaukat 2010); larger doses may be tolerated with food or spread over the day (Misselwitz 2019).
• Lactose content of dairy foods — representative values per 100 g in a 2019 review: full milk 4.7 g, fresh yoghurt 3.0 g, buttermilk 3.0 g, cream cheese 3.0 g, butter 0.5 g (about 0.1 g per serving), soft cheese such as camembert 0.3 g, hard cheese such as cheddar or gruyère 0.1 g, and lactose-free milk less than 0.1 g; the review notes that long-ripened cheese is especially low in lactose (Misselwitz 2019).
• Yogurt — a 2021 systematic review found a causal relationship between yogurt consumption and lactose digestion and tolerance (Savaiano 2021).
• Calcium and vitamin D — the NIH panel found that many individuals with real or perceived lactose intolerance avoid dairy and ingest inadequate amounts of calcium and vitamin D, which may predispose them to decreased bone accrual, osteoporosis and other adverse health outcomes (NIH 2010). Non-dairy sources are listed on the Lactose Intolerance page.
• Other carbohydrates and look-alike conditions — a 2015 review states that lactose intolerance can be part of a wider intolerance to fermentable carbohydrates (FODMAPs), present in at least half of people with IBS, who need more than lactose restriction to improve symptoms; it also lists small intestinal bacterial overgrowth among the factors on which lactose intolerance depends (Deng 2015). A 2019 review notes that treatment results are modest because lactose is only one of several poorly absorbed carbohydrates that cause symptoms the same way (Misselwitz 2019).
• Milk allergy — cow's milk allergy is managed differently, by cow's milk avoidance and substitute milks under the BSACI guideline (Luyt 2014).

In summary, the studies on this page found that lactose from live-culture yogurt is digested better than lactose from milk, that pasteurization removes that digestive effect, and that most adults with lactose malabsorption tolerate moderate amounts of lactose. Decisions about diet and testing belong with a clinician.

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Key Research Papers

1. Kolars JC, Levitt MD, Aouji M, Savaiano DA (1984). Yogurt — an autodigesting source of lactose. New England Journal of Medicine — PubMed PMID: 6417539
2. EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) (2010). Scientific Opinion on the substantiation of health claims related to live yoghurt cultures and improved lactose digestion (ID 1143, 2976) pursuant to Article 13(1) of Regulation (EC) No 1924/2006. EFSA Journal 8(10):1763 — doi:10.2903/j.efsa.2010.1763
3. Enattah NS et al. (2002). Identification of a variant associated with adult-type hypolactasia. Nature Genetics. — PubMed PMID: 11788828 (LCT-13910 discovery)
4. Tishkoff SA et al. (2007). Convergent adaptation of human lactase persistence in Africa and Europe. Nature Genetics. — PubMed PMID: 17159977 (independent African mutations)
5. Suarez FL, Savaiano DA, Levitt MD (1995). A comparison of symptoms after the consumption of milk or lactose-hydrolyzed milk by people with self-reported severe lactose intolerance. NEJM 333(1):1-4 — PubMed PMID: 7776987
6. Hertzler SR, Savaiano DA (1996). Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance. American Journal of Clinical Nutrition — PubMed PMID: 8694025
7. Savaiano DA (2014). Lactose digestion from yogurt: mechanism and relevance. American Journal of Clinical Nutrition — PubMed PMID: 24695892
8. Lapides RA, Savaiano DA (2018). Gender, age, race and lactose intolerance: is there evidence to support a differential symptom response? A scoping review. Nutrients 10(12):1956 — PubMed PMID: 30544891
9. Pribila BA, Hertzler SR, Martin BR, Weaver CM, Savaiano DA (2000). Improved lactose digestion and intolerance among African-American adolescent girls fed a dairy-rich diet. Journal of the American Dietetic Association — PubMed PMID: 10812376
10. Bhatnagar S, Aggarwal R (2007). Lactose intolerance (editorial). BMJ 334(7608):1331-2 — PubMed PMID: 17599979
11. Misselwitz B et al. (2019). Update on lactose malabsorption and intolerance: pathogenesis, diagnosis and clinical management. Gut — PubMed PMID: 31427404
12. Itan Y et al. (2009). The origins of lactase persistence in Europe. PLOS Computational Biology — PubMed PMID: 19714206
13. Savaiano DA, AbouElAnouar A, Smith DE, Levitt MD (1984). Lactose malabsorption from yogurt, pasteurized yogurt, sweet acidophilus milk, and cultured milk in lactase-deficient individuals. American Journal of Clinical Nutrition 40(6):1219-23 — PubMed PMID: 6439026
14. Savaiano DA, Hutkins RW (2021). Yogurt, cultured fermented milk, and health: a systematic review. Nutrition Reviews 79(5):599-614 — PubMed PMID: 32447398
15. Shaukat A, Levitt MD, Taylor BC, et al. (2010). Systematic review: effective management strategies for lactose intolerance. Annals of Internal Medicine 152(12):797-803 — PubMed PMID: 20404262
16. Suchy FJ, Brannon PM, Carpenter TO, et al. (2010). NIH consensus development conference statement: Lactose intolerance and health. NIH Consensus and State-of-the-Science Statements 27(2):1-27 — PubMed PMID: 20186234
17. Deng Y, Misselwitz B, Dai N, Fox M (2015). Lactose intolerance in adults: biological mechanism and dietary management. Nutrients 7(9):8020-35 — PubMed PMID: 26393648
18. Bayless TM, Brown E, Paige DM (2017). Lactase non-persistence and lactose intolerance. Current Gastroenterology Reports 19(5):23 — PubMed PMID: 28421381
19. Luyt D, Ball H, Makwana N, et al. (2014). BSACI guideline for the diagnosis and management of cow's milk allergy. Clinical & Experimental Allergy 44(5):642-72 — PubMed PMID: 24588904
20. Commission Regulation (EU) No 432/2012 of 16 May 2012 establishing a list of permitted health claims made on foods, other than those referring to the reduction of disease risk and to children's development and health (Annex: live yoghurt cultures) — legislation.gov.uk: Regulation (EU) No 432/2012, Annex (as in force 31 December 2020)
21. U.S. Food and Drug Administration. 21 CFR 131.200 — Yogurt (standard of identity) — eCFR: 21 CFR 131.200

PubMed Topic Searches

1. PubMed: Yogurt and lactose digestion
2. PubMed: Lactase persistence genetics
3. PubMed: Bacterial beta-galactosidase delivery
4. PubMed: Hydrogen breath testing
5. PubMed: Colonic adaptation to lactose

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Connections

• All Food
• Yogurt Overview
• Yogurt Benefits Hub
• Probiotic Strains
• Greek vs Regular
• Bone Density and Calcium
• Milk
• Probiotics
• Irritable Bowel Syndrome
• SIBO
• Lactose Intolerance
• Calcium
• Vitamin D3
• Crohn's Disease
• Celiac Disease
• History
• Nutrients

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