The principal sugar, lactose present in milk is a disaccharide and is hydrolyzed by an enzyme lactase, which is a constitutive, membrane bound enzyme present in the brush borders of the epithelium of small intestine. When lactose enters large intestine, the microorganisms present there ferment it in to organic acids, hydrogen and carbon dioxide. The products of the fermentation along with excessive water drawn due to osmotic effect in colon are responsible for the characteristic symptoms of lactose intolerance viz. abdominal pain, cramps, loss of appetite, flatulence and diarrhoea.

The symptoms are an indication that the lactose, which is consumed as a part of dairy product is not digested in the small intestine. The term lactose intolerance has other synonyms like lactase deficiency, low lactase activity, lactose malabsorption, and milk intolerance and they are often used interchangeably. The lactose intolerance can be broadly classified into three types viz.

1. Alactasia or congenital lactase deficiency

This is an extremely rare occurrence where there is a complete lacking in secretion of lactase due to congenital anomaly; i.e. no lactase is secreted to digest the disaccharide although histology of intestinal mucosa remains completely normal.

2. Hypolactasia or primary adult lactase deficiency

This type refers to deficiency in the rate of secretion of the enzyme lactase, as the individual ages or becomes older. It is considered apparently normal and the development is age related. Most of the adult population in the world suffers from this condition due to decreased lactase activity and hence it is named as primary adult lactase deficiency or the condition may otherwise be called as “lactase non-persistence”; the opposite term “lactase persistence” may be used to describe those who retain abundant intestinal lactase activity and it is due to an autosomal dominant trait.

3. Lactase deficiency

This is a case of transient state of low lactase activity in an otherwise normal individual who exhibited lactase persistence previously. The condition occurs due to diseases such as infectious gastroenteritis, celiac sprue, or protein malnutrition. Generally malabsorption of lactose occurs when there is incomplete lactose digestion resulting in flat or relatively decrease in the rate of rise in blood sugar level following a lactose intolerance test.  It is an outcome and not the primary cause of the condition.

Lactose Intolerance and Yogurt

Persons with impaired lactose digestibility can ingest a large amount of yogurt without exhibiting any of the symptoms associated with lactose intolerance. The increased tolerance to lactose may be attributed to the improved lactose digestibility in the gastro intestinal tract due to excess secretion of lactase enzyme by the Streptococcus thermophilus and Lactobacillus bulgaricus (ST and LB). The amount of hydrogen released in the intestine is taken as the measure of lactose intolerance and this is significantly lower in the case of yoghurt when compared to milk.  People experiencing symptoms like diarrhea or flatulence while on milk due to lactose intolerance showed virtually no abnormality when yoghurt is consumed. In other words, yoghurt is more gastro-intestinal tract friendly when compared to milk as far as lactose intolerant individual is concerned.

Mechanism of action

Yoghurt containing live and active flora (as in unheated yoghurt) is more beneficial than pasteurized yogurt for the lactose impaired individuals. Both unheated and pasteurized yoghurt contains the same amount of lactase enzyme but heating significantly reduces the lactase activity. Apart from that, pasteurization destroys both the yoghurt bacteria (ST and LB) and thereby their ability to produce more lactase enzyme. Hence, to be effective, the yoghurt cultures must be viable and their lactase enzymes remaining intact to exert their benevolent effect. Other than that, presence of bile salts stimulates the lactase activity due to their disruptive action on the cell wall of the bacteria and in turn releasing the lactase enzyme. It would be better to screen the bacterial cultures for their ability to secrete lactase enzyme before inoculating them in milk to make yoghurt.

There is one more condition that has to be met before the yoghurt and its constituents bring out the desirable effect in the body. That is the yogurt culture and the enzyme lactase must survive in the acidic gastrointestinal tract without getting killed nor denatured by the extremely low pH available in the gastric juice. This is achieved by the excellent buffering mechanism in the dairy constituents of the yoghurt which prevents the destruction of the yoghurt flora as well as protecting the enzyme lactase against the adverse acidic environment. Moreover, the yoghurt cultures are conditioned to grow at low pH and hence their survivability is higher during their transit through gastric mucosa.