A Serious Look at Lactose Intolerance

The dissertation, MILK HYPERSENSITIVITY
Effects of Cow’s Milk and its Processing on Gastrointestinal
Symptoms and Delayed-Type Immune Responses, by Laura Paajanen, that I just wrote about in The Different Types of Dairy Allergy also has some good technical information on lactose intolerance (also called hypolactasia in some of the medical literature.

Paajanen writes:

In lactase deficiency the activity or concentration of the lactose cleaving enzyme β-galactosidase, also called lactase, in the brush border of the small intestinal mucosa is insufficient. This hypolactasia causes insufficient digestion of lactose, the major carbohydrate of milk, a phenomenon called lactose malabsorption or lactose maldigestion. As reviewed by Sahi (1994), lactose maldigestion affects approximately 60% of the world’s adult population, the prevalence varying in Europe from 2% in Scandinavia to 70% in Italy, 70-90% in South America, Africa and Asia, and reaching 100% in some Asian countries.

The forms of lactose maldigestion are 1) lactase non-persistence, 2) secondary lactose maldigestion, and 3) rare congenital lactase deficiency. In lactase non-persistence, also called adult type lactose maldigestion, lactase activity is high at birth, decreases in a genetically programmed way in childhood and adolescence, and remains low in adulthood, which is the normal physiological situation for humans and other mammals. In populations where lactase non-persistence is predominant, the loss of lactase begins soon after weaning, and vice versa – in populations with low prevalence of lactose maldigestion, it develops later in adolescence or even in early adulthood (Sahi et al. 1983, Sahi 1994). Lactase is found at the tip of the intestinal villi, and is therefore vulnerable to intestinal diseases, inflammation and chemotherapy, leading to a secondary form of lactose maldigestion. Typically, lactase activity returns after recovery from the original disease (e.g. celiac disease, Crohn’s disease, enteritis) and after the discontinuation of chemotherapy (Bode & Gudmand-Hoyer 1988, Murphy et al. 2002, Österlund et al. 2004b). A small intestinal resection may cause irreversible secondary lactose maldigestion. Congenital lactase deficiency is an extremely rare inheritable genetic defect, which is apparent immediately after birth (Savilahti et al. 1983).

Hypolactasia accompanied by clinical symptoms such as bloating, flatulence, nausea, diarrhoea, and abdominal pain is called lactose intolerance. The symptoms occur when undigested lactose passes to the large intestine, where it serves as a fermentable substrate for the microbiota and osmotically increases the flow of water into the lumen. The intensity of the symptoms depends on the amount of lactose ingested, on individual sensitivity, the rate of gastric emptying, gastrointestinal transit time, and the pattern of microbiota in the large intestine. Ingestion of 50 g lactose, the amount commonly used in clinical tolerance tests, causes symptoms in 80-100% of lactose maldigesters, whereas the ingestion of a glass of milk (200-250 ml) causes symptoms to only 30- 50% (Vesa et al. 2000). For some unknown reason, a small percentage of maldigesters remain symptom-free even after the ingestion of large amounts of lactose. Symptoms of lactose intolerance can be reduced by food and meal pattern choices and by the consumption of low-lactose and lactose-free dairy products. Total avoidance of dairy products often results in poor calcium intake and an increased risk of fractures; so lactose intolerance is associated with reduced bone mineral density and may predispose to bone fractures (Jackson & Savaiano 2001, Kudlacek et al. 2002, Obermayer-Pietsch et al. 2004). Self-described "lactose-intolerant" individuals may restrict their dairy and calcium intake without real clinical need, and are at risk of osteoporosis and bone fractures (Savaiano 2003).

Lactose digestion can be measured by direct or indirect methods (Arola 1994). The direct methods – the measurement of mucosal disaccharidases, and an intestinal perfusion technique for the exact measurement of lactose digestion – are laborious. The most widely-used indirect tests are the traditional lactose tolerance test (measurement of serum glucose), the lactose tolerance test with ethanol (measurement of serum galactose), the hydrogen breath test and the urinary galactose test. Genotyping for the C/C-13910 variant of lactase persistence/nonpersistence is a new way of determining susceptibility to adult-type hypolactasia; however, it cannot be used as a diagnostic tool to determine lactose intolerance, as the age of reduction of lactase varies (Enattah et al. 2002, Kuokkanen et al. 2003, Rasinperä et al. 2004).

(One important point: the lactose intolerance test with ethanol is not used in the United States.)

Technical, to be sure, but a strong grounding in the technical side will help you to sort out sense from nonsense when reading articles in newspapers, magazines, or online that often are so simplified by people who dion't understand the subject that they can lead to confusion.