Before lactose can be absorbed by the body it needs to be broken into its two component sugars. This process requires lactase. In most mammals, lactase activity decreases after weaning but, in some human ethnic groups, lactase activity can persist into adult life, enabling total digestion of large quantities of dietary lactose. This is the case in white Caucasians, for example, who comprise a large proportion of the UK population.

There are two ways by which lactose intolerance can be acquired. Primary lactase deficiency/non-persistence is a genetically inherited, age-related decrease in lactase activity, which normally becomes apparent between the ages of 5-20 years. It is not a condition of early childhood. The loss of lactase activity is rarely total, but decreases to 10-30% of the initial level of the enzyme activity. In primary lactase deficiency, the decrease in enzyme activity is permanent and cannot be induced by large quantities of lactose (by lactose ingestion). Secondary lactase deficiency is a transient state of lactase deficiency due to damage to the lining of the intestine where the lactase is produced. This damage can be caused by a severe bout of gastroenteritis, malnutrition, uncontrolled coeliac disease, inflammatory bowel disease (IBS), cancer or toxins. Although lactose intolerance is mainly present in the adult population, temporary secondary lactose intolerance can occur in babies and young children following gastroenteritis or other forms of infection affecting the intestinal tract. The symptoms of secondary lactose intolerance normally disappear when the intestinal wall has recovered from the injury, normally within 2-4 weeks.

Lactose intoleranceThe genetically-programmed and partial post-weaning loss of intestinal lactase activity affects up to 70% of the world’s population. The prevalence of high lactase activity levels in adulthood (and hence the ability to readily digest lactose) is most common among people of Northern European countries, where the climate is conducive to dairy farming and consequently milk and dairy products have been part of the adult daily diet for centuries. For example, in the UK, Sweden, Holland, Belgium and Ireland, only 5% of the population are thought to suffer any degree of lactose maldigestion. In other European countries, the prevalence of low levels of the lactase enzyme is higher, ranging from 15-75%, although the exact figures are difficult to determine. In the rest of the World, especially among Black and Asiatic communities where milk is not traditionally consumed as part of the typical adult diet, lactase deficiency (low levels of the enzyme) can be almost 100%.

If lactose is thought to be the cause of digestive problems, a diet without milk, milk products and other lactose-containing foods can be tried for 2-3 weeks; if symptoms disappear with a milk-free diet and appear again after reintroduction of milk into the diet, lactose intolerance is likely. The activity of intestinal lactase can be measured either directly or indirectly. Direct methods include intestinal biopsy and intestinal perfusion. Indirect methods comprise giving a standard dose of lactose, normally 50g in liquid form (equal to 1 litre of milk), and the subsequent measurement of blood glucose or breath hydrogen. A small increase or no increase in blood glucose after lactose ingestion indicates that lactose has not been hydrolysed and absorbed in the small intestine. An increase in hydrogen concentration in expired air after lactose ingestion is the result of bacterial fermentation of lactose in the colon. However, decreased activity of intestinal lactase does not necessarily mean that the person will suffer from lactose intolerance when consuming the typical diet of the country, which is unlikely to provide such high concentrations of lactose (a glass of milk typically provides about 8g).

In principle, the symptoms of lactose intolerance are dose-dependent: the larger the amount of lactose administered, the more pronounced the symptoms are likely to be. However, the gastrointestinal symptoms caused by lactose maldigestion can vary between individuals and other factors can also affect the degree of intolerance. Slow gastric emptying and long intestinal transit time have been shown to improve lactose absorption. Therefore, for sufferers, it helps to have lactose as a part of a meal rather than between meals. The metabolic activity of colonic flora varies greatly between individuals and is thought to play an important role in the appearance or absence of intolerance symptoms, which are independent of lactase activity in the intestine. Unabsorbed lactose increases the acidity of the colon contents, causing changes in the composition of the colonic bacteria and their metabolic activities. Over time, some adaptation of bacterial flora might lead to improved tolerance of lactose, despite maldigestion.

Because the symptoms of lactose intolerance and irritable bowel syndrome (IBS) are very similar, misdiagnosis between the conditions is likely. In double-blind controlled studies, self-diagnosed lactose intolerant individuals were not found to suffer significantly more from intolerance symptoms whether they were consuming ordinary milk containing 15g lactose per day or lactose hydrolysed milk (i.e. low lactose milk). Other studies have demonstrated that not all patients with suspected lactose intolerance improve with a lactose-free diet, and therefore are more likely to suffer from IBS than lactose intolerance. However, an individual can have lactase deficiency and suffer from IBS, in which case the symptoms of lactose consumption can be aggravated.