Unfortunately, clinicians are now seeing more and more patients in their 40s with osteoporosis. Importantly, many teenage girls are self-diagnosing milk intolerance and confusing it with milk allergy. The U.S. National Institutes of Health report that most adolescents aren’t getting the recommended 1,300 mg of calcium a day, nor are they benefiting from vitamin D fortification of milk. By age 17, up to 90% of adult bone mass is established.

Milk allergy vs intolerance

Only 2-4% of infants are truly milk allergic, and by three years old, most of these will have outgrown it. Intolerance to milk products, on the other hand, is not related to the immune system at all, but rather to a deficiency of lactase activity. This may be either primary (congenital) or acquired. Congenital lactase deficiency is an extremely rare autosomal recessive disorder characterized by neonatal failure to thrive associated with watery diarrhea. Symptoms resolve with elimination of milk products from the diet.

Premature infants may exhibit transient lactose intolerance, as significant lactase activity only begins in the small intestine around the 34th week of gestation. Within a few weeks of birth, this enzymatic deficiency is reversed as lactase expression increases in the small intestine. In most mammals, intestinal lactase activity is highest in infancy and then declines to low levels during childhood and adulthood.

Most populations of European origin retain their intestinal lactase activity into adulthood, with lactase deficiency being found in only about 15% of Western or Northern Europeans. In African, Hispanic, Aboriginal, Chinese and Mediterranean populations, however, it may exceed 70%. Frequencies of lactose
intolerance reported in Caucasian populations range from around 2% in Scandinavia to about 70% in Sicily.

What are the symptoms?

Clinical symptoms of lactose intolerance include:

• diarrhea — stools voluminous, frothy, watery
• abdominal cramps
• bloating
• borborygmi — increased bowel sounds, rumbling
• excessive flatulence
• nausea and vomiting.

Typically, for 80% of sufferers, ingestion of 50 g of lactose is sufficient to produce symptoms. Looking at the table on the next page, it’s apparent that most lactose-intolerant people should be able to drink a glass of milk (240 mL). Indeed, this was borne out in Suarez’s study of 30 people with severe lactose intolerance, where volumes up to this amount induced hardly any gastrointestinal (GI) problems.

Note the following:

• intensity varies between individuals
• symptoms occur 30 minutes to
  2 hours after eating dairy
• rapid gastric emptying and short transit time in small bowel can
  aggravate symptoms
• full-fat milk may be easier on the system than fat-free.

The enzyme lactase is present in the brush border (apical surface) of the distal villi of the small intestine, particularly in the jejunum. It hydrolyzes lactose to its constituent b-D-galactose and b-D-glucose molecules. In patients with lactase insufficiency, up to 75% of the dietary lactose may pass from the small intestine into the colon. There, bacteria metabolize the remaining lactose to hydrogen gas (producing symptoms if there’s a lot of lactose) and the short-chained fatty acids acetate, butyrate and proprionate.

Diarrhea occurs when lactose in the colon, and bacterial products of lactose fermentation, cause increased intracolonic osmotic pressure. Depending on bowel transit times, a small proportion of lactose malabsorbers will be symptom-free despite consuming large volumes of milk products.

What’s the differential?

Alternate diagnoses

It’s important to consider alternate diagnoses in patients reporting lactose intolerance. Irritable bowel syndrome, celiac disease, and Crohn’s disease may all produce symptoms similar to lactose intolerance. Unlike Crohn’s and celiac disease, however, lactose intolerance isn’t associated with iron deficiency, extraintestinal manifestations or persistent pains in the absence of exposure to dairy. Uncommonly, complaints may be secondary to fructase deficiency or the surreptitious use of laxatives. If there’s any doubt, do diagnostic tests for lactose malabsorption. If these are negative, consider an alternative diagnosis with appropriate investigation.

Secondary malabsorption

Secondary malabsorption of lactose may be reversible. It can occur in the following circumstances:

• generalized functional impairment of intestinal villi — e.g. celiac disease, tropical sprue, Whipple’s disease, giardiasis or acute gastroenteritis
• loss of mucosal surface area — e.g. short bowel syndrome, Crohn’s disease; following abdominal radiation or small bowel ischemic injury
• bacterial overgrowth syndromes — bacteria in the small intestine compete with the intestinal villi for available intra-luminal lactose.

The diagnosis of secondary lactose intolerance should be evident from a careful history and physical examination.

How is the diagnosis established?

The diagnosis of lactose intolerance can be confirmed in several ways.

Hydrogen breath test

Hydrogen gas, a bacterial product of fermentation, is normally absorbed through the intestinal wall and exhaled in the lungs. In the lactose breath hydrogen test, 2 g/kg of oral lactose in solution is ingested, to a maximum of 25 g. The presence of hydrogen gas > 20 ppm in exhaled breath suggests lactose malabsorption. Rapid production of hydrogen may be indicative of small bowel stasis or bacterial overgrowth. False negatives can occur in patients recently treated with antibiotics.

Lactose tolerance test — blood glucose

In this test, the patient is given 2 g/kg lactose to a maximum of 50 g after an overnight fast. Blood glucose levels are determined at 0, 60 and 120 minutes after ingestion. An increase in serum glucose of < 1.1 mmol/L, plus the development of symptoms, are indicative of lactose intolerance. Impaired gastric emptying may influence the results, however — readings may be higher and peak earlier with rapid emptying and be inappropriately low with delayed.

Stool testing

Stool analysis is an instructive tool, particularly in infants and children. The presence of reducing substances indicates that carbohydrates aren’t being absorbed. Acidic stool, with a pH level under 5.5, suggests probable carbohydrate malabsorption, even in the absence of reducing substances.

Management

Once the food hits the colon and symptoms begin, there’s not much to do but “grin and bear it.” In the absence of guidelines, the most commonly used therapeutic approach has traditionally been prevention — to eliminate dairy products from the diet. This strategy may have serious complications though, including malnutrition, vitamin D deficiency and osteoporosis. Children receiving a diet deficient in dairy products can develop osteomalacia and rickets.

Recent studies have advocated alternative approaches:

• dairy products fortified with exogenous yeast-derived b-galactosidase, i.e. lactose-free milk and cheeses
• oral lactase supplements
• yogurts, particularly those containing probiotics with bacterial lactase activity, i.e. Lactobacillus acidophilus
• milk substitutes enriched with
  calcium, e.g. soy or rice milk
• dairy in combination with foods that lengthen GI transit time.

Lactase supplements are added to milk 24 hours ahead of time — 15 mL of solution to a litre of milk will enzymatically hydrolyze the lactose to glucose and galactose. Because the lactose is predigested, the milk actually tastes sweeter.

Alternatively, supplements can be taken orally as a pill just before eating dairy. The enzymes are released in the stomach and small bowel and work as the bolus makes its way down. If remembered only after ingestion of a dairy meal, however, they’re ineffective. The dose varies between individuals and is dependent on the amount and source of lactose consumed. Each person will need to establish for him- or herself the best dose for each situation through trial and error. Usually, 3 regular-strength tablets or 1 ultracaplet will prevent symptoms.

Aged cheeses and ice cream can often be tolerated — the lactose contents of mozzarella, Swiss and cheddar are negligible. Lactobacillus-containing yoghurts are easy on the system as well.

Research shows that it’s helpful to reduce lactose intolerance by allowing more time for the existing lactase in the small intestine to do its job. The strategy is therefore to keep the food there longer. Additionally, if mixed with other ingredients, the lactose in the bolus isn’t as concentrated. Milk products should thus be drunk or eaten in combination with high-fibre foods, whole wheat bread, bran cereal, fruits and vegetables. Fat content may also decrease gastric and small bowel motility, so it’s best to avoid low-fat milk.

Recognizing that patients may be able to tolerate limited dairy products, it’s better to have frequent small volumes rather than large volumes at a single sitting. Cold liquids may be better absorbed than warm, as they can delay gastric emptying.

In patients with secondary lactose intolerance, treatment of the underlying condition should improve lactose absorption. Consider metronidazole in cases of giardiasis. Individuals with celiac disease might be more tolerant to lactose on a gluten-free diet. Patients with possible bacterial overgrowth may benefit from antibiotic therapy.