Understanding and Managing Lactose Intolerance

US Pharm. 2008;33(12):12-15.

The inability to ingest milk as an adult, known as lactose intolerance (LI), is characteristic of many ethnic groups. The pharmacist must have a full understanding of LI and the various products that can be used to help prevent this condition from producing uncomfortable symptoms.

Lactose Digestion
Lactose in milk is a rich nutrient for infants, who develop the ability to break it down into glucose and galactose by producing lactase in the brush border membrane of the small intestine.¹ Lactase levels remain high during infancy, until weaning from the breast occurs. Then there is a gradual loss in the ability to digest milk, due to a loss of ability to produce lactase. This is called primary LI, also known as hypolactasia or lactase deficiency.^2,3 Some people retain the ability to digest milk as adults; these individuals are referred to as lactase persistent or lactose tolerant.

Prevalence
Approximately 70% of the world's peoples are lactose intolerant.⁴ The incidence of primary LI is about 90% to 100% in Native Americans, Africans, and Asians. It is estimated to be 80% in African Americans, and 55% to 80% in Hispanics. The lowest incidence (10%-15%) occurs in those descended from northern Europeans, residents of the northwestern Indian subcontinent, and desert nomads.⁵

The theory for this sharp difference in prevalence relies on archeological and anthropological evidence suggesting that the ancestors of those with lactase persistence herded cows or camels and learned to ingest their milk as a survival measure. Those who were lactase persistent survived to pass that mutation on, eventually becoming the predominant state in that subculture.

Secondary Lactose Intolerance
Some patients with lactase persistence lose the ability to digest lactose as a result of environmental triggers, a condition known as secondary LI. Lactase production is confined to the upper third of the intestinal villi.⁴ Due to its superficial location, conditions that affect villi often disrupt lactase production. One example is intestinal infection. Rotavirus is a common cause of diarrhea in infants, often contracted in daycare. After the child recovers from the effects of the rotavirus, parents may notice the infant cannot ingest formula or milk like before. Infection with Giardia lamblia or enteropathogenic Escherichia coli may also be causal. Patients who experience secondary LI from an infection may be advised to slowly reintroduce lactose-containing products to ascertain whether lactase is again present. If it is not tolerated, lactose should be withdrawn and reintroduced later.

Secondary LI may also be caused by celiac disease, malnutrition, irritable bowel syndrome (IBS), or intestinal surgery.⁴ Tetracyclines, neomycin, cimetidine, and antithyroid medications have all been implicated as causes.

Manifestations
The manifestations of primary and secondary LI are virtually identical. When a patient with LI ingests milk, lactose that cannot be digested reaches the small and large intestines in intact form. Symptoms usually begin about 30 to 120 minutes postingestion. Lactose is osmotically active and causes the intestines to draw in and retain additional water with a meal. This osmotic activity produces the same type of manifestations as ingestion of saline laxatives, such as magnesium citrate or Fleet Phospho-Soda.

Initial symptoms of the excessive intestinal fluid include nausea, rumbling in the stomach, cramping, and abdominal discomfort or pain.⁶ The excessive fluids are moved through the bowel more rapidly. When they reach the large intestine, resident bacteria ferment the lactose, causing excessive production of hydrogen, short-chain fatty acids, methane, and carbon dioxide.⁷ Thus, the patient also experiences flatulence, bloating, and added abdominal discomfort. The end result is the collection of large amounts of gas and fluids in the distal bowel. The patient usually feels an urgent need to defecate. If the individual is unable to do so, intense pressure may overcome the anal sphincter's ability to retain materials, causing involuntary leakage of stool, staining of undergarments, and incontinence. If the patient is able to defecate, stools will often be diarrheal and watery.

Diagnosis
There are several tests that can be used to diagnose LI. In the lactose tolerance test, blood glucose is examined at several points after lactose ingestion to determine whether it was digested.^8,9 A hydrogen breath test measures intestinal absorption of hydrogen after lactose inges­ tion.¹⁰ The hydrogen level in the breath is normally nil. Elevated levels imply colonic maldigestion of lactose with resultant hydrogen production.

Tolerance Level
Adults who retain the ability to ingest dairy products can take full advantage of their nutrients (i.e., calcium, vitamins A and D). Those whose diets completely restrict milk intake are especially prone to osteoporosis and osteopenia, increasing the risk of bone fractures in later life.⁴ Many Americans lie in the middle of these two extremes in that they can ingest a specific amount of lactose without experiencing symptoms. Unfortunately, they may assume that they are completely lactose intolerant and voluntarily cease ingestion of all dairy products.

The pharmacist can provide advice on determining the individual lactose tolerance level, allowing patients to still obtain the nutrients found in dairy products. Patients should be advised to identify all milk-containing foods and avoid them scrupulously for about three weeks. If symptoms persist, there are two possibilities.⁴ Either they are still ingesting lactose, or they have another condition such as IBS. If further lactose restriction does not cause symptoms to abate, they must seek a physician diagnosis. If the symptoms do remit, they should remain on the lactose-free diet for three more weeks. Then, adhering to the same diet, the patient should ingest one-quarter cup of milk with breakfast. If symptoms recur, the patient is highly lactose intolerant and should adhere to the diet without introducing milk. However, if they tolerate the milk without symptoms, they should repeat the diet and milk for several days. They should then increase the amount of milk to one-half cup and repeat the cycle. Eventually, they will come to a level that is comfortable for them.

OTC Lactase Products
Pharmacists can also aid patients by suggesting that they purchase lactase-containing tablets. The most well-known product is Lactaid.⁴ It is available in two strengths. Lactaid Original Strength Caplets contain 3,000 FCC units of lactase. The suggested dose is three caplets swallowed or chewed with the first bite of a dairy product. Lactaid Fast Act is available as caplets or chewable vanilla tablets. Each dosage form contains 9,000 FCC units, with a suggested dose of one caplet/tablet with the first bite of dairy. Generic products are also available.

Milk Substitutes
Patients may also be advised by the pharmacist on nonpharmacologic methods to prevent LI. The major thrust is to substitute normal dairy products with lactose-free versions. There are a wide variety of milk substitutes on the market. They include the Lactaid brand, real milk products to which lactase has been added, producing altered milk that is useful for those with LI.⁴ All require refrigeration. The Dairy Ease line of products includes whole milk, reduced-fat, and fat-free options. Consumers can also try a line of soy substitutes, such as Silk Soymilk products, or rice-based milk substitutes, such as Rice Dream.

Milk Allergy
Some patients with LI mistakenly believe that they have developed a milk allergy. It is critical to differentiate LI from a milk allergy.¹¹ Patients with a true allergy to cow's milk must scrupulously avoid it to prevent a constellation of allergic reactions, including fatal anaphylaxis. However, LI is not due to an allergic reaction--it is a food intolerance.¹² With proper advice from pharmacists, patients with LI can still ingest milk and gain the benefits of its nutrients.

REFERENCES
1. Harrington LK, Mayberry JF. A re-appraisal of lactose intolerance. Int J Clin Pract. 2008;62:1541-1546.
2. Seppo L, Tuure T, et al. Can primary hypolactasia manifest itself after the age of 20 years? Scand J Gastroenterol. 2008;43:1082-1087.
3. Shrier I, Szilagyi A, et al. Impact of lactose containing foods and the genetics of lactase on diseases. Nutr Cancer. 2008;60:292-300.
4. Pray WS. Nonprescription Product Therapeutics. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2006.
5. Lomer M, Parkes G, et al. Lactose intolerance in clinical practice--myths and realities. Aliment Pharmacol Ther. 2008;27:93-103.
6. Beyerlein L, Pohl D, 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. 2008;27:659-665.
7. He T, Venema K, et al. The role of colonic metabolism in lactose intolerance. Eur J Clin Invest. 2008;38:541-547.
8. Lactose intolerance. http://digestive.niddk.nih.gov/ddiseases/pubs/lactoseintolerance/. Accessed October 27, 2008.
9. Krawczyk M, Wolska M, et al. Concordance of genetic and breath tests for lactose intolerance in a tertiary referral centre. J Gastrointest Liver Dis. 2008;17:135-139.
10. Mottes M, Belpinati F, et al. Genetic testing for adult-type hypolactasia in Italian families. Clin Chem Lab Med. 2008;46:980-984.
11. Ahrens B, Beyer K, et al. Differential diagnosis of food-induced symptoms. Pediatr Allergy Immunol. 2008;19:92-96.
12. Montalto M, Santoro L, et al. Adverse reactions to food: allergies and intolerances. Dig Dis. 2008;26:96-103.

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