Clinical Review Understanding Lactose Intolerance Clinician Reviews. 2010 November;20(11):17, 18, 20, 21 -- Allison Thorn, FNP-BC, MSN Among US adults, 30 million may be affected by lactose intolerance (LI), and older patients are particularly susceptible. How is LI best investigated in patients who report its troublesome symptoms? And for -- 1. Shaukat A, Levitt MD, Taylor BC, et al. Systematic review: effective management strategies for lactose intolerance. Ann Intern Med. 2010;152(12):797-803. 2. Lomer MC, Parkes GC, Sanderson JD. Review article: lactose intolerance in clinical practice—myths and realities. Aliment Pharmacol Ther. 2008;27(2):93-103. 3. NIH Consensus Development Conference. Lactose intolerance and health: final statement. February 22–24, 2010; Bethesda, MD. 4. Heyman MB; American Academy of Pediatrics Committee on Nutrition. Lactose intolerance in infants, children, and adolescents. Pediatrics. 2006;118(3):1279-1286. 5. Eadala P, Waud JP, Matthews SB, et al. Quantifying the ‘hidden’ lactose in drugs used for the treatment of gastrointestinal conditions. Aliment Pharmacol Ther. 2009;29(6):677-687. 6. Swagerty DL Jr, Walling AD, Klein RM. Lactose intolerance. Am Fam Physician. 2002;65(9): 1845-1850. 7. Wilt TJ, Shaukat A, Shamliyan T, et al. Lactose intolerance and health. Evid Rep Technol Assess (Full Rep). 2010 Feb(192):1-410. 8. National Digestive Diseases Information Clearinghouse, National Institute of Diabetes and Digestive and Kidney Diseases, NIH. Lactose intolerance (2009). http://digestive.niddk.nih.gov/ddiseases/pubs/lactoseintolerance. Accessed October 25, 2010. 9. Pray WS, Pray JJ. Lactose intolerance. US Pharmacist. 2004;29(6). www.medscape.com/viewarticle/482131. Accessed October 25, 2010. -- 11. Montalto M, Curigliano V, Santoro L, et al. Management and treatment of lactose malabsorption. World J Gastroenterol. 2006;12(2): 187-191. 12. Labayen I, Forga L, Gonzalez A, et al. Relationship between lactose digestion, gastrointestinal transit time and symptoms in lactose malabsorbers after dairy consumption. Aliment Pharmacol Ther. 2001;15(4):543-549. 13. Hovde O, Farup PG. A comparison of diagnostic tests for lactose malabsorption: which one is best? BMC Gastroenterol. 2009;9 82-88. 14. Srinivasan R, Minocha A. When to suspect lactose intolerance: symptomatic, ethnic, and laboratory clues. Postgrad Med. 1998;104(3): 109-111,115-116,122-123. 15. Arola H. Diagnosis of hypolactasia and lactose malabsorption. Scand J Gastroenterol Suppl. 1994;202:26-35. 16. Lin MY, Dipalma JA, Martini MC, et al. Comparative effects of exogenous lactase (beta-galactosidase) preparations on in vivo lactose digestion. Dig Dis Sci. 1993;38(11):2022-2027. 17. Hertzler SR, Savaiano DA. Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance. Am J Clin Nutr. 1996;64(2):232-236. 18. 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):1014-1019. 19. Segal E, Dvorkin L, Lavy A, et al. Bone density in axial and appendicular skeleton in patients with lactose intolerance: influence of calcium intake and vitamin D status. J Am Coll Nutr. 2003;22(3):201-207. -- clinicaltrials.gov/ct2/show/NCT00399607. Accessed October 25, 2010. Lactose intolerance (LI), a term closely associated with hypolactasia (lactase deficiency) and lactose malabsorption,^1 is a common syndrome composed of diarrhea, abdominal pain, flatulence and/or bloating, and sometimes nausea and vomiting in severe cases, after ingestion of dairy products.^2 This common disorder results from a deficiency in the enzyme lactase, which makes affected patients unable to digest lactose, a sugar found in milk and other dairy products.^3 Malabsorption of lactose produces the symptoms associated with LI. The level of LI varies among affected individuals, depending on many nutritional and genetic factors, the amount of lactose consumed, the patient’s degree of lactase deficiency, and the substance in which the lactose is ingested.^4 Epidemiology -- and Asian Americans. LI is least common in people of northern European descent (and is unlikely to develop before adulthood^7), although it has been suggested that 30 million American adults experienced lactose malabsorption to some degree by age 20.^3,8 Heyman^4 estimates that approximately 2% of people of northern European descent have LI. -- covered with a membrane that has a brush border composed of microvilli.^9 The microvilli produce lactase, the enzyme necessary to split and hydrolyze dietary lactose into glucose and galactose for transport across the cell membrane^.6 Unfortunately, lactase is produced in the upper, most shallow section of the villi, which is -- osmotically attract fluid into the bowel lumen. The amount of fluid influx into the bowel is approximately triple the normal amount, based on the osmolality of sugar alone. In addition, the unabsorbed lactose entering the colon is fermented by bacteria, producing gas and resulting in the cleavage of lactose into monosaccharides. Monosaccharides cannot be absorbed by the colonic mucosa; as a result, osmotic pressure increases, and fluid levels rise in the bowel. This -- onset can also be relatively acute.^4 Lactose Malabsorption The three main types of lactose malabsorption are primary, secondary, and congenital. The latter is a rare, genetic form of LI in which the lactase enzyme is entirely absent; for the purposes of this article, congenital lactose malabsorption will not be discussed. Primary lactase deficiency is the most common form and the focus of this article. It is the normal, gradual reduction in lactase enzyme that a maturing individual experiences through adulthood, and the rate of reduction is genetically determined. Secondary lactose malabsorption occurs following an insult to the small bowel, as in severe diarrhea, infection (eg, rotavirus), chemotherapy, or acute gastroenteritis.^4 In -- LI is not considered life threatening, but its symptoms can severely affect a person’s quality of life and productivity. In addition to ethnicity and age, the type and amount of lactose ingested and the amount that the patient is unable to digest all affect the severity of LI symptoms.^13 Lactose makes up between 2% and 8% of the solids in milk; 1 mL of milk (0.03 fl oz) contains 47.2 mg of lactose. No amount of lactose has been specified to produce symptoms, but most adults can tolerate as much as 8 fl oz of milk without problems,^1 and patients can tolerate more lactose if the food containing it is consumed with a meal.^11 Some adults may be able to ingest only 2 to 4 fl oz before symptoms appear^4; in highly sensitive adults, as little as 200 mg of lactose (0.13 fl oz of milk) can produce symptoms.^5 -- 1. Shaukat A, Levitt MD, Taylor BC, et al. Systematic review: effective management strategies for lactose intolerance. Ann Intern Med. 2010;152(12):797-803. 2. Lomer MC, Parkes GC, Sanderson JD. Review article: lactose intolerance in clinical practice—myths and realities. Aliment Pharmacol Ther. 2008;27(2):93-103. 3. NIH Consensus Development Conference. Lactose intolerance and health: final statement. February 22–24, 2010; Bethesda, MD. 4. Heyman MB; American Academy of Pediatrics Committee on Nutrition. Lactose intolerance in infants, children, and adolescents. Pediatrics. 2006;118(3):1279-1286. 5. Eadala P, Waud JP, Matthews SB, et al. Quantifying the ‘hidden’ lactose in drugs used for the treatment of gastrointestinal conditions. Aliment Pharmacol Ther. 2009;29(6):677-687. 6. Swagerty DL Jr, Walling AD, Klein RM. Lactose intolerance. Am Fam Physician. 2002;65(9): 1845-1850. 7. Wilt TJ, Shaukat A, Shamliyan T, et al. Lactose intolerance and health. Evid Rep Technol Assess (Full Rep). 2010 Feb(192):1-410. 8. National Digestive Diseases Information Clearinghouse, National Institute of Diabetes and Digestive and Kidney Diseases, NIH. Lactose intolerance (2009). http://digestive.niddk.nih.gov/ddiseases/pubs/lactoseintolerance. Accessed October 25, 2010. 9. Pray WS, Pray JJ. Lactose intolerance. US Pharmacist. 2004;29(6). www.medscape.com/viewarticle/482131. Accessed October 25, 2010. -- 11. Montalto M, Curigliano V, Santoro L, et al. Management and treatment of lactose malabsorption. World J Gastroenterol. 2006;12(2): 187-191. 12. Labayen I, Forga L, Gonzalez A, et al. Relationship between lactose digestion, gastrointestinal transit time and symptoms in lactose malabsorbers after dairy consumption. Aliment Pharmacol Ther. 2001;15(4):543-549. 13. Hovde O, Farup PG. A comparison of diagnostic tests for lactose malabsorption: which one is best? BMC Gastroenterol. 2009;9 82-88. 14. Srinivasan R, Minocha A. When to suspect lactose intolerance: symptomatic, ethnic, and laboratory clues. Postgrad Med. 1998;104(3): 109-111,115-116,122-123. 15. Arola H. Diagnosis of hypolactasia and lactose malabsorption. Scand J Gastroenterol Suppl. 1994;202:26-35. 16. Lin MY, Dipalma JA, Martini MC, et al. Comparative effects of exogenous lactase (beta-galactosidase) preparations on in vivo lactose digestion. Dig Dis Sci. 1993;38(11):2022-2027. 17. Hertzler SR, Savaiano DA. Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance. Am J Clin Nutr. 1996;64(2):232-236. 18. 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):1014-1019. 19. Segal E, Dvorkin L, Lavy A, et al. Bone density in axial and appendicular skeleton in patients with lactose intolerance: influence of calcium intake and vitamin D status. J Am Coll Nutr. 2003;22(3):201-207.