eMedicine Specialties > Gastroenterology > Intestine

Lactose Intolerance

Praveen K Roy, MD, Comments and Criticisms Editor, Cochrane Colorectal Cancer Group
Abhishek Choudhary, MD, Resident, Department of Internal Medicine, University Hospital of Missouri; Mohamed Othman, MD, Staff Physician, Department of Internal Medicine, University of New Mexico School of Medicine; Homayoun Shojamanesh, MD, Former Fellow, Digestive Diseases Branch, National Institutes of Health; Jack Bragg, DO, FACOI, Assistant Professor, Department of Clinical Medicine, University of Missouri School of Medicine; Gautam Dehadrai, MD, Department Chair, Section Chief, Department of Interventional Radiology, Norman Regional Hospital

Updated: Aug 12, 2008

Introduction

Background

Lactose intolerance is a common disorder and is due to the inability to digest lactose into its constituents, glucose and galactose, secondary to low levels of lactase enzyme in the brush border of the duodenum. Lactase deficiency is the most common form of disaccharidase deficiency. Enzyme levels are highest shortly after birth and decline with aging, despite a continued intake of lactose. Within the animal world, nonhuman mammals usually lose the ability to digest lactose as they reach adulthood. Some populations of the human species, including those of Asian, South American, and African descent, have a propensity for developing lactase deficiency. By contrast, races descended from northern Europe or from the northwestern Indian subcontinent are likely to retain the ability to absorb lactose into adulthood.

Symptoms of lactose intolerance include loose stools, abdominal bloating and pain, flatulence, nausea, and borborygmi. A diagnosis or even the suggestion of lactose intolerance leads many people to avoid milk and/or to consume specially prepared food with digestive aids, adding to health care costs.

Pathophysiology

Lactose, a disaccharide, is present in milk and processed foods. Dietary lactose must be hydrolyzed to a monosaccharide in order to be absorbed by the small intestinal mucosa. A deficiency of intestinal lactase prevents hydrolysis of ingested lactose. The osmotic load of the unabsorbed lactose causes secretion of fluid and electrolytes until osmotic equilibrium is reached. Dilation of the intestine caused by the osmosis induces an acceleration of small intestinal transit, which increases the degree of maldigestion. Within the large intestine, free lactose is fermented by colonic bacteria to yield short-chain fatty acids and hydrogen gas. The combined increase in fecal water, intestinal transit, and generated hydrogen gas accounts for the wide range of gastrointestinal symptoms.

Frequency

United States

The prevalence of primary lactose intolerance varies according to race. As many as 25% of the white population (prevalence in those from southern European roots) is estimated to have lactose intolerance, while among black, Native American, and Asian American populations, the prevalence of lactose intolerance is estimated at 75-90%.

International

Of the world's population, 75% is estimated to be lactose-deficient. Lactose intolerance is very common among Asian, South American, and African persons.

Mortality/Morbidity

• Lactose intolerance is not lethal.
• Morbidity is low from lactose intolerance.
• Osteopenia can be a complication of lactose intolerance.

Race

• Persons of all races are affected by lactose intolerance, with higher prevalence among Asian, African, and South American persons.

Sex

• Males and females are equally affected by lactose intolerance.
• Of those women who are lactose intolerant, 44% regain the ability to digest lactose during pregnancy. This is probably due to slow intestinal transit and bacterial adaptation during pregnancy.

Age

• Among adults, the age of presentation of lactose intolerance is 20-40 years.

Clinical

History

• History in patients with lactose intolerance may include abdominal fullness/bloating, nausea, abdominal pain, diarrhea, and flatulence.
• The symptoms of irritable bowel syndrome (IBS) resemble those of lactose intolerance and can easily be confused. Some patients with IBS can also have lactose intolerance. Restriction of milk products in these patients may relieve the symptoms of IBS.

Physical

• Physical examination findings very often are normal.
• Borborygmi may be present.

Causes

• Congenital lactose intolerance is inherited as an autosomal recessive trait and is very rare.
• Primary lactose intolerance is due to low levels of lactase, which develop after childhood.
• Secondary, or acquired, lactase deficiency may develop in a person with a healthy small intestine during episodes of acute illness. This occurs because of mucosal damage or from medications. Some causes of secondary lactase deficiency are as follows:
  • Acute gastroenteritis
  • Giardiasis
  • Ascariasis
  • Crohn disease
  • Celiac sprue
  • Tropical sprue
  • Radiation enteritis
  • Diabetic gastropathy
  • Carcinoid syndrome
  • Whipple syndrome
  • HIV enteropathy
  • Kwashiorkor
  • Chemotherapy
  • Gastrinoma

Differential Diagnoses

Gastrinoma
Giardiasis
Inflammatory Bowel Disease
Irritable Bowel Syndrome

Other Problems to Be Considered

Sucrase deficiency
Diabetic diarrhea
Other disorders listed under causes of secondary lactose intolerance

Workup

Laboratory Studies

• Lactose tolerance test
  • Measure serial blood glucose levels after an oral lactose load. A fasting serum glucose level is obtained, after which 50 g of lactose is administered. Measure the serum glucose level at 0, 60, and 120 minutes.
  • The lactose tolerance test has a sensitivity of 75% and a specificity of 96%.
  • False-negative results occur in presence of diabetes and small bowel bacterial overgrowth. Abnormal gastrointestinal emptying can also affect the results of the lactose tolerance test.
  • The diagnosis is confirmed if the serum glucose level fails to increase by 20 g/dL above baseline.
• Milk tolerance test
  • Administer 500 mL of milk and measure the blood glucose level.
  • An increase of less than 9 mg/dL indicates lactose malabsorption.

Imaging Studies

• Imaging tests are not helpful in the diagnosis of primary lactose intolerance, but they may be helpful for excluding secondary causes.

Other Tests

• Breath hydrogen test
  • This is the diagnostic test of choice.
  • Subjects are administered lactose after an overnight fast, after which expired air samples are collected before and at 30-minute intervals for 3 hours to assess hydrogen gas concentrations.
  • A rise in breath hydrogen concentration greater than 20 parts per million over the baseline after lactose ingestion suggests lactase deficiency.
• Dietary elimination: Resolution of symptoms with elimination of lactose-containing food products and resumption of symptoms with the reintroduction are findings suggestive of lactose intolerance.

Procedures

• Small bowel biopsy
  • This is the criterion standard; however, it is invasive and rarely performed. A major advantage is that it provides definitive information.
  • Biopsy samples from the small bowel are assayed for lactase activity. The biopsy results may be normal if deficiency is focal or patchy.
  • This is not readily available and is not usually necessary.

Treatment

Medical Care

• Dietary adjustment is the primary form of therapy for patients with lactose intolerance.  
  • Advise patients to reduce or restrict products containing lactose.
  • Prehydrolyzed milk (LACTAID) is available and is effective.
  • Yogurt and fermented products, such as cheeses, are better tolerated than regular milk.
  • Soy-based milk or food products are well tolerated.
• Commercially available lactase enzyme preparations (eg, LACTAID, Lactrase) are effective in reducing symptoms; however, they may not be effective in some patients, partially due to insufficient dosing.
• Supplemental calcium should also be recommended.
• In secondary lactase deficiency, treatment is directed at the underlying cause.
• See related CME at Updated Recommendations for Lactose Intolerance.

Consultations

• Gastroenterologist
• Nutritionist

Diet

• Avoid or reduce intake of lactose-containing foods.
• Most patients who are lactose intolerant can ingest as much as 240 mL of milk without an exacerbation of their symptoms.
• Certain medications and foods contain hidden lactose, such as breads, margarine, salad dressings, and candies.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Digestive enzymes

Provide necessary enzymes for lactose digestion.

Lactase enzymes (LACTAID, Dairy Ease, Lactrase)

For patients with lactase enzymatic deficiency. Prevent osmotic diarrhea in patients deficient in lactase enzymes who consume milk.

Dosing

Adult

Add to milk or milk products

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Persistent diarrhea should be evaluated

Follow-up

Complications

• Osteopenia

Prognosis

• The prognosis of patients with lactose intolerance is excellent with dietary restrictions.

Patient Education

• Instruct patients to read labels on commercial products.
• Whole milk and chocolate milk may be better tolerated than skim milk.

Miscellaneous

Medicolegal Pitfalls

• Lactose intolerance is not lethal and morbidity is low, although osteopenia can be a complication of this disorder. Failure to adequately counsel the patient and to provide proper treatment could lead to medicolegal liability.

References

1. Arola H. Diagnosis of hypolactasia and lactose malabsorption. Scand J Gastroenterol Suppl. 1994;202:26-35. [Medline].

2. Auricchio S, Rubino A, Landholt M. Isolated lactase deficiency in the adult. Lancet. 1963;2:324-6.

3. Bayless TM, Rothfeld B, Massa C, et al. Lactose and milk intolerance: clinical implications. N Engl J Med. May 29 1975;292(22):1156-9. [Medline].

4. Beja-Pereira A, Luikart G, England PR, et al. Gene-culture coevolution between cattle milk protein genes and human lactase genes. Nat Genet. Dec 2003;35(4):311-3. [Medline].

5. Beyerlein L, Pohl D, Delco F, et al. Correlation between symptoms developed after the oral ingestion of 50 g lactose and results of hydrogen breath testing for lactose intolerance. Aliment Pharmacol Ther. Apr 2008;27(8):659-65. [Medline].

6. Born P, Sekatcheva M, Rosch T, et al. Carbohydrate malabsorption in clinical routine: a prospective observational study. Hepatogastroenterology. Sep-Oct 2006;53(71):673-7. [Medline].

7. Carroccio A, Montalto G, Cavera G, et al. Lactose intolerance and self-reported milk intolerance: relationship with lactose maldigestion and nutrient intake. Lactase Deficiency Study Group. J Am Coll Nutr. Dec 1998;17(6):631-6. [Medline].

8. Di Stefano M, Miceli E, Mazzocchi S, et al. Visceral hypersensitivity and intolerance symptoms in lactose malabsorption. Neurogastroenterol Motil. Nov 2007;19(11):887-95. [Medline].

9. Di Stefano M, Veneto G, Malservisi S, et al. Lactose malabsorption and intolerance and peak bone mass. Gastroenterology. Jun 2002;122(7):1793-9. [Medline].

10. Hermans MM, Brummer RJ, Ruijgers AM, et al. The relationship between lactose tolerance test results and symptoms of lactose intolerance. Am J Gastroenterol. Jun 1997;92(6):981-4. [Medline].

11. Järvinen RM, Loukaskorpi M, Uusitupa MI. Tolerance of symptomatic lactose malabsorbers to lactose in milk chocolate. Eur J Clin Nutr. May 2003;57(5):701-5. [Medline].

12. Kern F Jr, Struthers JE Jr. Intestinal lactase deficiency and lactose intolerance in adults. JAMA. Mar 14 1966;195(11):927-30. [Medline].

13. Kudlacek S, Freudenthaler O, Weissboeck H, et al. Lactose intolerance: a risk factor for reduced bone mineral density and vertebral fractures?. J Gastroenterol. 2002;37(12):1014-9. [Medline].

14. Lomer MC, Parkes GC, Sanderson JD. Review article: lactose intolerance in clinical practice--myths and realities. Aliment Pharmacol Ther. Jan 15 2008;27(2):93-103. [Medline].

15. Mishkin S. Dairy sensitivity, lactose malabsorption, and elimination diets in inflammatory bowel disease. Am J Clin Nutr. Feb 1997;65(2):564-7. [Medline].

16. Newcomer AD, McGill DB, Thomas PJ, et al. Tolerance to lactose among lactase-deficient American Indians. Gastroenterology. Jan 1978;74(1):44-6. [Medline].

17. Patel YT, Minocha A. Lactose intolerance: diagnosis and management. Compr Ther. Winter 2000;26(4):246-50. [Medline].

18. Suarez FL, Savaiano D, Arbisi P, et al. Tolerance to the daily ingestion of two cups of milk by individuals claiming lactose intolerance. Am J Clin Nutr. May 1997;65(5):1502-6. [Medline].

19. 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. N Engl J Med. Jul 6 1995;333(1):1-4. [Medline].

20. Suarez FL, Savaiano DA, Levitt MD. Review article: the treatment of lactose intolerance. Aliment Pharmacol Ther. Dec 1995;9(6):589-97. [Medline].

21. Upton J, Mackay R, George P. A simple gene test for lactose intolerance/adult hypolactasia. N Z Med J. Nov 9 2007;120(1265):U2817. [Medline].

22. Vesa TH, Marteau P, Korpela R. Lactose intolerance. J Am Coll Nutr. Apr 2000;19(2 Suppl):165S-175S. [Medline].

23. Vonk RJ, Priebe MG, Koetse HA, et al. Lactose intolerance: analysis of underlying factors. Eur J Clin Invest. Jan 2003;33(1):70-5. [Medline].

24. Zhong Y, Priebe MG, Vonk RJ, et al. The role of colonic microbiota in lactose intolerance. Dig Dis Sci. Jan 2004;49(1):78-83. [Medline].

Keywords

lactose intolerance, lactose intolerant, milk, milk allergy, lactase, lactose allergy, lactase deficiency, milk products, dairy allergy, dairy allergies, dairy products, food allergy, food allergies, lactose malabsorption, lactose maldigestion, lactose deficient, lactose tolerance test, milk tolerance test, glucose, galactose, hypolactasia, osteopenia, osteoporosis, disaccharidase deficiency

Contributor Information and Disclosures

Author

Praveen K Roy, MD, Comments and Criticisms Editor, Cochrane Colorectal Cancer Group
Praveen K Roy, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and Canadian Association of Gastroenterology
Disclosure: Nothing to disclose.

Coauthor(s)

Abhishek Choudhary, MD, Resident, Department of Internal Medicine, University Hospital of Missouri
Abhishek Choudhary, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Mohamed Othman, MD, Staff Physician, Department of Internal Medicine, University of New Mexico School of Medicine
Disclosure: Nothing to disclose.

Homayoun Shojamanesh, MD, Former Fellow, Digestive Diseases Branch, National Institutes of Health
Homayoun Shojamanesh, MD is a member of the following medical societies: American Gastroenterological Association, American Medical Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Jack Bragg, DO, FACOI, Assistant Professor, Department of Clinical Medicine, University of Missouri School of Medicine
Jack Bragg, DO, FACOI is a member of the following medical societies: American College of Osteopathic Internists and American Osteopathic Association
Disclosure: Nothing to disclose.

Gautam Dehadrai, MD, Department Chair, Section Chief, Department of Interventional Radiology, Norman Regional Hospital
Gautam Dehadrai, MD is a member of the following medical societies: American College of Radiology, Medical Council of India, and Radiological Society of North America
Disclosure: Nothing to disclose.

Medical Editor

Ronnie Fass, MD, Director of GI Motility Laboratory, Tucson VA Medical Center, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of Arizona School of Medicine
Ronnie Fass, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Motility Society, American Society for Gastrointestinal Endoscopy, and Israel Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Douglas M Heuman, MD, FACP, Director of Hepatology, McGuire Veterans Affairs Medical Center, Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Douglas M Heuman, MD, FACP is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)