Lactose Intolerance in Patients with Chronic Functional Diarrhoea: The Role of Small Intestinal Bacterial Overgrowth

J. Zhao; M. Fox; Y. Cong; H. Chu; Y. Shang; M. Fried; N. Dai


Aliment Pharmacol Ther. 2010;31(8):892-900. 

In This Article

Abstract and Introduction


Background Many studies report a high prevalence of lactose intolerance in patients with functional, gastrointestinal disease.
Aim To evaluate the role of small intestinal bacterial overgrowth (SIBO) in condition of lactose intolerance and the mechanism by which SIBO may impact lactose tolerance in affected patients.
Methods Consecutive out-patients with chronic functional diarrhoea (CFD) and healthy controls underwent a validated 20 g lactose hydrogen breath test (HBT). Patients completed also a 10 g lactulose HBT with concurrent assessment of small bowel transit by scintigraphy.
Results Lactose malabsorption was present in 27/31 (87%) patients with CFD and 29/32 (91%) healthy controls (P = 0.708). From the patient group 14/27 (52%) had lactose intolerance and 13/27 (48%) experienced no symptoms (lactose malabsorption controls). Only 5 (17%) healthy controls reported symptoms (P < 0.01). The oro-caecal transit time was similar between patient groups with or without symptoms (P = 0.969). SIBO was present in 11 (41%) subjects and was more prevalent in lactose intolerance than in lactose malabsorption [9/14 (64%) vs. 2/13 (15%), P = 0.018]. Symptom severity was similar in lactose intolerance patients with and without SIBO (P = 0.344).
Conclusions Small intestinal bacterial overgrowth increases the likelihood of lactose intolerance in patients with CFD as a direct result of lactose fermentation in the small intestine, independent of oro-caecal transit time and visceral sensitivity.


Lactase deficiency and malabsorption (LM) is widespread throughout the world because of a genetically determined, age-dependent decline in lactase activity.[1] The prevalence of this condition varies considerably, ranging from 5% in north-west Europe to almost 100% in some Asian populations.[2] Lactose intolerance (LI) refers to gastrointestinal symptoms including pain, bloating and diarrhoea related to bacterial fermentation of undigested lactose in the gastrointestinal tract, usually in the colon.[3] However, the ingestion of lactose by an individual with LM does not always result in LI.[4,5] It is clear that the amount of lactose ingested and the level of lactase activity are associated with the risk of symptoms[6–8] and other factors, including age and gender,[9–12] altered bowel flora,[13] anatomical pathology or dysmotility of the gastrointestinal tract,[14] abnormal small bowel transit,[15,16] heightened visceral sensitivity[17,18] and psychosocial stress[19–21] have also been implicated. Nevertheless, the factors that determine whether an individual with LM will experience LI are rarely established and treatment is usually empiric and not directed at a specific cause.

The relationship between LM, LI and functional gastrointestinal disorders, especially IBS-D, has been extensively investigated because of their similar symptoms and the possibility that these conditions share a common pathophysiology. A majority of studies found the prevalence of LM in IBS subjects to be virtually the same as in the normal population,[22–24] but few studies focused on the difference of LI symptoms in patients with functional gastrointestinal disorders compared with the healthy controls. In general, such studies found that patients with IBS more often reported symptoms following lactose ingestion than healthy subjects;[25] however, the mechanism underlying this interaction has not been studied.

Small intestinal bacterial overgrowth (SIBO) is a condition in which the small bowel is colonized by colonic bacteria, formally defined by the presence of >105 colony forming units on jejunal aspiration. SIBO is more common in the elderly, in patients with underlying gastrointestinal pathology, and has also been implicated in functional gastrointestinal diseases that are characterized by increased visceral sensitivity and psychosocial stress.[26] Thus, SIBO and LI appear to occur in similar population groups. Moreover, the mechanism of disease is thought to be similar in both conditions, with bacterial fermentation of ingested carbohydrates producing gas (e.g. hydrogen, methane) and fatty acids that lead to bloating, abdominal pain and diarrhoea. Increased LM in the presence of SIBO has been reported in IBS patients and others;[13,27,28] however, in populations with a low prevalence of LM, it is difficult to assess whether a positive breath test is due to lactase deficiency or to malabsorption caused by SIBO. This source of confounding is not present in Chinese populations, in which a vast majority of adults have genetically determined lactase deficiency.

This study proposes that fermentation of lactose in the small bowel due to SIBO increases the likelihood of LI symptoms occurring. This hypothesis was tested in a Chinese population with functional diarrhoea because any effect of SIBO on lactose digestion and symptoms is likely to be of particular clinical relevance in this group.[29–31] The results document (i) SIBO prevalence in LM patients with functional diarrhoea (ii) the impact of SIBO on the likelihood of LI symptoms occurring after lactose ingestion. In addition, the underlying mechanism of disease and cause of symptoms was assessed by comparing and contrasting the results of physiological measurements in patients with and without SIBO.


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