Lactose Intolerance is a common ‘cause’ of bloating, flatulence, pain and diarrhoea. This is usually assumed to be due to deficiency of lactase or beta galalactosidase, the enzyme secreted by the small intestine that normally breaks down lactose sugar to glucose and galactose, both of which are rapidly absorbed by active, carrier-mediated transport mechanisms on the intestinal villi. When lactase is deficient, lactose cannot be digested. It retains fluid in the small intestine and enters the colon, where it may overwhelm the salvage capacity and be evacuated as diarrhoea although much is fermented by colonic bacteria yielding large quantities of gas. Indeed the man, who is reputed to be the gassiest ever recorded, the eponymous Mr Sutalf (Sutalf is Flatus spelt backwards), once farted 144 times in a single hour and evacuated 800ml in a four hour period of measurement, enough to launch a small weather balloon.
Nearly all of us have lactase in our small intestine at birth. It is what enables us to digest milk. Infants retain their lactase enzyme until after weaning when in 80% of the world’s population, it declines. However, some races retain their lactase until long after weaning, probably because of the epigenetic effect of the continued presence of milk in the diet. These include people living in North Western Europe and those living around the Horn of Africa. For example only 20% of people living in the UK lose their lactase enzyme and are considered lactase deficient.
Not everybody who is lactase deficient is lactose intolerant. Most can tolerate a cupful of milk with no diarrhoea presumably because the bacteria in the colon turn the unabsorbed lactose into short chain fatty acids which are absorbed through the colonic epithelium, though they may experience an increase in flatulence. People with IBS do not necessarily have more lactase deficiency than the normal population. After all, IBS is no more common in lactase deficient regions of the world. The reason why some of them have symptoms of lactose intolerance may be because their colons are more ‘sensitive’ to unabsorbed lactose.
Disease of the small intestine can cause a ‘secondary’ lactase deficiency. This occurs, for example, in people with coeliac disease, gastroenteritis and small intestinal bacterial overgrowth (SIBO) and clears up once the underlying disease disappears or is treated effectively.
But milk intolerance is not all about lactose. Some people with sensitive guts may not be able to tolerate the amount of fat in full fat milk. About 2 to 3% of children may have an allergy to cows milk proteins (alpha caseins, or beta lactoglobulin), which may in a few cases last into or reappear in adulthood.
It gets more completed. A recent randomised double blind cross over study from Shanghai indicated another variable. The scientists compared the effects of milk that contained a mixture of A1 and A2 beta-caseins with milk that contained just A2 beta-casein in 45 Han Chinese subjects, who were all lactase deficient as diagnosed by an absent galactose in the urine after a 50g load of lactose. The milk containing the mix of caseins caused an increase in inflammatory cytokines and increased symptoms of bloating, flatulence, abdominal pain and stool frequency, compared with the milk that contained A2 beta-caseins. Strangely they also showed longer whole gut transit times, perhaps because alpha 1 casein contains beta-caseomorphin-7, an exogenous opiate which inhibits colonic motility. Similar differences were seen in subjects who were not lactase deficient, though these were less pronounced.
This suggests that people with milk intolerance do much better on milk from cows bred to be homozygous for alpha 2 beta-casein. A2 Milk is licensed and marketed by the a2 Milk Company and sold mostly in Australia, New Zealand, China, United States and the United Kingdom.