Small Intestinal Bacterial Overgrowth (SIBO) is defined by an excessive number of bacteria colonizing the small intestine, which should naturally have a low bacterial concentration. Lactose intolerance (LI) is a digestive disorder where the body cannot fully digest lactose, the sugar found in dairy products. SIBO can cause lactose intolerance, specifically a type known as secondary lactose intolerance. This occurs because bacterial overgrowth damages the small intestinal lining, leading to a temporary deficiency of the enzyme required to break down lactose. When a person with SIBO consumes dairy, the resulting symptoms are often a combination of both disorders.
How SIBO Damages Lactase Production
The lining of the small intestine is covered in microscopic, finger-like projections called villi, and the surface of these cells is the brush border. The lactase enzyme, which breaks down lactose into the easily absorbed sugars glucose and galactose, resides directly on this brush border. In a healthy gut, this process ensures lactose is digested and absorbed.
The presence of an abnormal concentration of bacteria in SIBO creates chronic inflammation and irritation in the small intestine. These bacteria produce byproducts and toxins that directly damage the delicate structure of the intestinal brush border. This physical damage results in a reduction in the number of functional lactase enzymes available to process incoming lactose. The resulting lactase deficiency is acquired due to the underlying intestinal injury, classifying it as secondary lactose malabsorption.
When undigested lactose moves past the damaged small intestine, it enters the large intestine or is fermented by the excess bacteria in the small intestine. These bacteria rapidly metabolize the lactose, producing large amounts of gaseous byproducts like hydrogen and methane. This fermentation leads to the symptoms of gas, bloating, abdominal pain, and diarrhea. The symptoms of secondary lactose intolerance are linked to the underlying SIBO, as both the damage mechanism and subsequent fermentation result from the bacterial overgrowth.
This secondary form of lactose intolerance is distinct from primary lactose intolerance, which is a genetic condition where lactase production naturally decreases after early childhood. Because the SIBO-induced deficiency is caused by physical damage, the ability to digest lactose can potentially be restored once the underlying bacterial issue is resolved. This possibility of reversal makes identifying SIBO as the root cause important for treatment planning.
Diagnosing SIBO Related Lactose Intolerance
Confirming that SIBO is the cause of lactose intolerance symptoms requires a two-step diagnostic approach. The initial step is to confirm lactose malabsorption, typically using a hydrogen and methane breath test with a lactose solution. If a significant rise in breath hydrogen or methane is detected, it indicates that the sugar was not properly digested and was instead fermented by gut bacteria.
A positive lactose breath test alone does not distinguish between primary and secondary lactose intolerance. Therefore, the second step, testing for SIBO, becomes necessary. The SIBO test is also a breath test, but it uses a different substrate, typically lactulose or glucose, to detect the abnormal presence of bacteria in the small bowel. An early rise in hydrogen or methane is diagnostic for SIBO.
If a patient tests positive for both lactose malabsorption and SIBO, it strongly suggests the bacterial overgrowth is responsible for the lactase deficiency. Understanding this relationship is important because the treatment approach changes from simply avoiding dairy to addressing the underlying bacterial issue. Treating SIBO offers the potential to heal the intestinal lining and restore lactase function, whereas managing primary lactose intolerance involves lifelong dietary avoidance or enzyme supplementation.
Treating the Underlying Bacterial Overgrowth
The primary treatment for secondary lactose intolerance involves eradicating the bacterial overgrowth in the small intestine. This is typically achieved using targeted antibiotics, such as Rifaximin, which acts locally within the gut. Healthcare providers may also recommend a course of herbal antimicrobial agents as an alternative.
Once the bacterial population is reduced, the inflammatory environment that damaged the small intestinal lining begins to resolve. With the removal of the irritant, the brush border cells have the capacity to regenerate and heal. As the lining recovers, the production of the lactase enzyme can gradually return to normal levels.
This healing process is not immediate and can take several weeks or months following successful SIBO treatment. During this recovery period, the small intestine needs time to repair damaged tissue and restore enzyme function. Healthcare providers often recommend a temporary low-lactose or low-FODMAP diet to minimize symptoms while the gut heals.
The goal is that by treating SIBO, the need for dietary restriction or lactase enzyme supplements becomes unnecessary. A follow-up SIBO breath test is often performed to confirm the eradication of the overgrowth. Patients may then gradually reintroduce lactose-containing foods to assess the return of their digestive tolerance. This focused approach on healing the gut makes treating the underlying SIBO an effective strategy for potentially reversing secondary lactose intolerance.