Clinical Review

Understanding Lactose Intolerance

Clinician Reviews. 2010 November;20(11):17, 18, 20, 21

References

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.

10. Host A. Clinical course of cow’s milk protein allergy and intolerance. Pediatr Allergy Immunol. 1998;9(11 suppl):48-52.

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.

20. Johns A, Leijten P, Yamamoto H, et al. Calcium regulation in vascular smooth muscle contractility. Am J Cardiol. 1987;59(2):A18-A23.

21. Emory University, National Cancer Institute. Calcium/vitamin D, biomarkers, and colon polyp prevention (PPS4B). clinicaltrials.gov/ct2/show/NCT00399607. Accessed October 25, 2010.

The theory of adaptative phenomena suggests that most people with LI can teach themselves to ingest more lactose gradually, leading over time to beneficial changes in the microflora of the gut and in improved colonic function.^11,17 The ultimate result, whether the explanation is reduced hydrogen excretion or increased gas absorption, is less severe gastrointestinal symptoms. This strategy is not a cure for LI, nor has it been found effective for all patients with LI,¹ but it can help manage symptoms to some extent.

Information for the Patient
Patients often need instruction in reading food labels to identify foods that contain milk, milk products, lactose, whey, curds, milk byproducts, dry milk solids, or even nonfat dry milk powder.⁸ Follow-up with the primary care provider should be arranged on an as-needed basis.

Simply excluding all dairy products from the diet does raise some health concerns. Milk and other dairy products are important sources of calcium and vitamin D, which are needed for growth and bone health in patients of all ages. A decrease in calcium consumption is one of the primary risk factors for osteoporosis, although research examining a possible association between LI and osteoporosis has yielded conflicting results. According to Kudlacek et al,¹⁸ even individuals with severe LI do not appear to be at risk for accelerated bone loss. By contrast, other research groups^7,19 studied patients with LI from various age-groups and concluded that low calcium intake and impaired vitamin D status could lead to increased bone turnover and decreased bone mass, especially in men and postmenopausal women. No guidelines have been published regarding screening for osteoporosis in patients with LI.

According to a consensus statement from the NIH,³ both men and women younger than 50 should consume 1,000 mg/d of calcium, and older persons, 1,500 mg/d. In addition to calcium supplements, patients can obtain the necessary calcium through certain foods, including leafy green vegetables (spinach, kale, broccoli), sardines, calcium-fortified cereal bars, calcium-enriched soy or lactose-free milk and other soy products, fruit juices, dried beans, and tuna.

Calcium is absorbed only when enough vitamin D is present; vitamin D intake should be 400 to 600 IU/d for both women and men.³ Foods that contain vitamin D include eggs, liver, vitamin D–enriched soy or lactose-free milk, and vitamin D–fortified cereals and other processed foods. Regular exposure to sunlight helps the body synthesize vitamin D naturally.³

For optimal bone health, the NIH³ continues to recommend a combination of cardiovascular exercise, weight-bearing exercise, smoking cessation, and a well-balanced diet (including foods that are rich in calcium and vitamin D).

In addition to its role in bone health, calcium has been suggested to improve cardiac and vascular smooth muscle contractility,²⁰ and clinical research is under way to investigate the role of calcium in reducing the risk for adenomatous colon polyps.²¹

Conclusion
Primary LI is a common disorder resulting from a deficiency in the enzyme lactase, making affected patients unable to digest lactose. LI is widespread in varying degrees across all races and ethnicities, affecting people of all ages; however, it is more common among older adults due to natural pathophysiologic processes.

In LI-affected patients, consuming lactose leads to troublesome symptoms of diarrhea, abdominal pain, flatulence, and/or bloating, and sometimes nausea and vomiting.

No tool is considered a “gold standard” for making a diagnosis of LI, so it is important to rule out other gastrointestinal conditions first. Oftentimes a diagnosis of LI is confirmed by the effectiveness of a lactose-free trial diet. When diagnosis is uncertain, referral to a gastroenterologist is required.

Without formal treatment guidelines, the primary form of therapy for LI is to adjust the amount of ingested lactose, with careful attention to adequate calcium and vitamin D intake. Patient education is crucial for management of LI and improvement in the patient’s quality of life.