Lactose intolerance (LI) is a digestive issue defined by the inability to properly digest lactose, the sugar present in milk and dairy products. This difficulty stems from a deficiency in the enzyme lactase, which is produced in the small intestine. While the common form develops slowly over many years, a seemingly sudden onset is possible. This rapid change in tolerance is usually due to a different underlying mechanism than the gradual form.
The Digestive Mechanism of Lactose
Lactase is a digestive enzyme located on the brush border, the surface layer of cells lining the small intestine. Its function is to break down the disaccharide lactose into two simpler, absorbable sugars: glucose and galactose. These monosaccharides are then easily absorbed into the bloodstream.
When there is not enough lactase, the undigested lactose continues its journey to the large intestine. Bacteria in the colon ferment this unabsorbed sugar, producing gas, including hydrogen and methane. This fermentation, combined with the osmotic effect of lactose drawing water into the bowel, leads to common symptoms like bloating, abdominal pain, and diarrhea.
Lactose intolerance is categorized into two main types based on cause. Primary lactose intolerance is the most common form, involving a genetically programmed, gradual decline in lactase production after childhood. Secondary lactose intolerance results from damage to the small intestine lining, which temporarily reduces the available lactase.
When Onset Appears Sudden
The experience of developing lactose intolerance “overnight” is almost always a manifestation of the secondary form of the condition. Unlike primary LI, which is a slow, lifelong process of declining enzyme activity, secondary LI occurs when the lactase-producing cells in the small intestine are physically compromised.
Because the intestinal lining is highly sensitive, damage from an acute event can quickly impair lactase production. This rapid enzyme reduction means a person who previously tolerated dairy can suddenly experience symptoms after consuming a lactose-containing product. The sudden onset reflects the speed at which the small intestine’s surface layer, the primary location of lactase, can be injured.
The resulting lactase deficiency is often temporary, as the intestinal lining has the potential to heal and restore normal enzyme levels. Since the symptoms appear suddenly, it is important to investigate the underlying cause of the intestinal damage.
Common Triggers for Rapid Change
A variety of common issues can trigger the intestinal damage that leads to secondary lactose intolerance. Acute gastroenteritis, often called the stomach flu, is a frequent culprit, as viral or bacterial infections cause inflammation and temporary damage to the small intestinal lining, impairing lactase production.
Chronic inflammatory conditions, such as Crohn’s disease or undiagnosed Celiac disease, can cause ongoing damage to the intestinal villi where lactase resides. Symptoms may appear suddenly before the underlying condition is diagnosed and treated. Small intestinal bacterial overgrowth (SIBO) can also interfere with lactose absorption and digestion, contributing to a sudden presentation of symptoms.
Some medications, including prolonged courses of antibiotics or certain chemotherapy agents, affect the intestinal mucosa, leading to a temporary drop in lactase activity. Antibiotics can disrupt gut flora, while chemotherapy can directly injure the cells of the intestinal lining. Once the irritant is removed or the underlying disease is treated, the small intestine usually repairs itself, and lactose tolerance returns.
Confirmation and Management of Symptoms
If a sudden change in dairy tolerance occurs, a healthcare professional may suggest testing to confirm lactose intolerance and rule out other conditions. The most widely used diagnostic tool is the hydrogen breath test, which measures the amount of hydrogen gas produced by colonic fermentation after a person ingests a known dose of lactose. An elevated level of hydrogen in the breath indicates that the lactose was not fully digested in the small intestine.
A simple elimination diet, where lactose-containing foods are removed for a period and then reintroduced, can also help confirm the diagnosis based on symptom resolution and recurrence. Management for sudden-onset secondary LI focuses on two tracks: supporting the intestinal lining’s recovery and temporarily reducing symptoms. Since the condition is often temporary, complete, long-term dairy avoidance is usually not necessary.
Reducing dairy intake for a few weeks allows the intestinal lining time to heal and regenerate the lactase-producing cells. Over-the-counter lactase enzyme supplements can be taken immediately before consuming dairy to help break down the lactose in the meal. Treating the underlying cause, such as a gastrointestinal infection or celiac disease, is the primary way to achieve a full resolution of secondary lactose intolerance.