Lactase insufficiency affects 70 to 100 % of the World’s population. Only North American, Europe and Australia have lower rates of around 15%.
Lactase insufficiency is characterised by an insufficient production of the β-galactosidase enzyme (lactase) responsible for cleavage of the dietary disaccharide lactose. This enzyme is usually present in the brush border membrane of the enterocytes of the small intestine. The absence of β-galactosidase results in an inability to digest lactose and this causes lactose malabsorption syndrome. lactose malabsorption causes fermentation of the lactose in the colon by microorganisms, and this produces hydrogen gas which can result in bloating, flatulence, diarrhea, and associated discomfort. Lactose malabsorption can be measured clinically and a blood glucose concentration above 1.12 mmol/L or a breath hydrogen over 20 ppm after ingestion of 1 gram per kg weight or 50 grams of lactose. A number of factors are known to affect lactose intolerance including age, sex, ethnic origin and geographical region. The most widely provided solution to lactose intolerance is to avoid the foods that cause lactose malabsorption syndrome.
Lactase insufficiency is not one disorder but a group of closely related conditions. Adult-type lactose malabsorption is characterised by a high β-galactosidase enzyme activity at birth, which decreases in adulthood. This is regarded to be the normal condition for mammals, as lactose is consumed from the milk of the mother when young, but as the offspring ages there is no need to continue producing the lactase enzyme. Around 70 to 100 % of the World’s population have such primary hypolactasia, with only populations from Northern and Central America, Europe and Australasia not fitting this pattern. In Europe for example, prevalence of primary lactasia is closer to 15 %. Other forms of lactose intolerance derive from damage to the gut mucosa and functional loss of small intestinal tissue such as protein deficiency or bacteria infection. However, lactose digestion ability returns to these individuals with proper gut structure. Congential lactose intolerance is an autosomally rare condition that results in no ability to digest lactose from birth.
Those with primary hypolactasia can digest a limited amounts of lactose, which has been estimated to be around 9 to 12 grams equivalent to a 200mL glass of milk. Lactose intolerance is not fully understood, but the malabsorption of lactose is thought to increase the amount of water secreted into the gut through osmosis, accelerate gut transit times, dilate the lumen of the small intestine and disrupt peristalsis. The cramps associated with lactose insufficiency are thought to be caused by contraction of the small intestine smooth muscle, although the mechanism is not known. Bloating and flatulence result from the production of gases such as hydrogen and methane, as the undigested lactose passes to the colon and is fermented by bacteria. Most of the gas produced in lactose fermentation is then subsequently metabolised by other gut bacteria limiting the problem of bloating to a much lesser degree than potentially possible. The main symptoms of lactose intolerance can be lessened by treatment of the lactose maldigestion in the small intestine.
Yoghurt is beneficial in cases of lactose intolerance and can be tolerated in small amounts without discomfort. This may be because yoghurt contains active bacteria that possess the β-galactosidase enzyme that can survive the transit of the stomach to the small intestine, Release of the β-galactosidase enzyme from the bacteria in the small intestine by the bile salts breaking open the cells is a requirement of effective lactose digestion by the β-galactosidase enzyme. Studies comparing the effects of live bacteria and irradiated bacteria on symptoms of lactose malabsorption have shown that the bacteria do not need to be alive to have beneficial effects, but must be intact. Another reason that yoghurt may be effective at preventing symptoms of lactose insufficiency is because yoghurt can delay gastric emptying and this may decrease the osmotic problems caused by the lactose. This is evidence by yoghurt containing non-live cultures of bacteria still being able to inhibit the symptoms of lactose insufficiency somewhat, through delayed gastric emptying.
Some evidence suggests that adaptation to lactose is possible in those with primary hypolactasia intolerance. Because lactose activity in mammals is not inducible, this means that some other mechanisms must be present. One explanation for this is changes to the microbial colonies in the gut resulting in a more favourable environment for the fermentation of lactose in the colon. In particular the fermentation capacity of bifidobacteria and other lactic acid bacteria which can metabolise lactose without hydrogen production may increase. The continual feeding of lactose may shift the composition of the bacterial populations to increase lactic acid production. This may lower the pH of the colon which could have beneficial osmotic effects or could decrease the metabolism of detrimental products by other bacteria. However, some have concluded the effects of continual feeding lactose to lactose insufficient individuals may be a placebo effect. Lactase tablets may also be beneficial, as may the consumption of lactose free milk.
