Lactose intolerance is a common digestive condition often misunderstood as an allergy or a simple sensitivity. The development of lactose intolerance is primarily governed by genetics and physiological changes, though external factors and dietary choices influence the experience of its symptoms. Understanding the underlying biological mechanisms reveals why some people retain the ability to digest milk sugar throughout life, while others naturally lose it.
How Lactose Intolerance Works
Lactose, the primary sugar found in milk, requires the enzyme lactase for proper digestion. Lactase is located on the brush border of the cells lining the small intestine. Its function is to hydrolyze lactose into two simpler, absorbable sugars: glucose and galactose, which are then absorbed into the bloodstream.
When lactase levels are insufficient, undigested lactose continues into the large intestine. Bacteria in the colon ferment this unabsorbed sugar, generating short-chain fatty acids and gases. The resulting osmotic load and gas production cause the common symptoms of lactose intolerance, such as bloating, abdominal pain, flatulence, and diarrhea.
The Difference Between Primary and Secondary Causes
Lactose intolerance is broadly categorized into two main types based on the cause of the lactase deficiency. The most prevalent form is Primary Lactase Non-persistence, which is genetically predetermined. In this type, lactase production naturally declines after infancy or childhood, a process that is normal for most of the world’s population. This decrease is a programmed genetic change and is not triggered by diet or environment.
The second type, Secondary Lactose Intolerance, arises from physical damage to the small intestine’s lining. Injury or inflammation to this area sharply reduces enzyme activity because lactase is produced in the intestinal brush border. This form is often temporary and can be reversed if the underlying cause is successfully treated and the intestinal mucosa heals.
Does Avoiding Dairy Induce Intolerance?
The belief that cutting out dairy will “make” a person lactose intolerant is a common misconception that conflates genetic predisposition with dietary habit. For individuals genetically programmed to maintain high lactase levels (lactase persistence), abstaining from dairy will not cause intolerance. Their genes continue to express the enzyme regardless of lactose intake.
For the majority of adults who already have Primary Lactase Non-persistence, avoiding dairy simply prevents the symptoms. While lactase production is not significantly inducible by diet, the gut microbiome can adapt to the presence or absence of lactose. Regularly consuming lactose promotes the growth of certain colonic bacteria better at breaking down the sugar, a process called colonic adaptation. Stopping dairy may cause the loss of this beneficial bacterial adaptation, making the reintroduction of lactose more symptomatic.
External Factors That Can Trigger Temporary Intolerance
While simple dietary avoidance does not induce permanent intolerance, external factors that physically injure the intestinal lining can trigger the secondary type. Acute gastroenteritis (stomach flu) is a frequent cause, as the infection temporarily damages the cells that produce lactase. Once the infection resolves and the intestinal lining regenerates, lactase production typically returns to normal.
Chronic intestinal diseases also lead to acquired intolerance. Conditions such as Celiac disease, Crohn’s disease, and inflammatory bowel disease cause ongoing inflammation and damage to the small intestine’s surface. Certain medical treatments, including chemotherapy or radiation therapy to the abdomen, can similarly impair the intestinal cells. In these cases, the intolerance is a side effect of the physical damage and is often reversible upon successful treatment of the underlying condition.