Lactose Intolerance

Lactose intolerance related to primary or secondary lactase deficiency is characterized by abdominal pain and distension, borborygmi, flatus, and diarrhea induced by lactose in dairy products. The biological mechanism and lactose malabsorption is established and several investigations are available, including genetic, endoscopic and physiological tests. Lactose intolerance depends not only on the expression of lactase but also on the dose of lactose, intestinal flora, gastrointestinal motility, small intestinal bacterial overgrowth and sensitivity of the gastrointestinal tract to the generation of gas and other fermentation products of lactose digestion. Treatment of lactose intolerance can include lactose-reduced diet and enzyme replacement. This is effective if symptoms are only related to dairy products; however, lactose intolerance can be part of a wider intolerance to variably absorbed, fermentable oligo-, di-, monosaccharides and polyols (FODMAPs). This is present in at least half of patients with irritable bowel syndrome (IBS) and this group requires not only restriction of lactose intake but also a low FODMAP diet to improve gastrointestinal complaints. The long-term effects of a dairy-free, low FODMAPs diet on nutritional health and the fecal microbiome are not well defined. This review summarizes recent advances in our understanding of the genetic basis, biological mechanism, diagnosis and dietary management of lactose intolerance.

BackgroundCows' milk generally contains two types of β-casein, A1 and A2 types. Digestion of A1 type can yield the peptide β-casomorphin-7, which is implicated in adverse gastrointestinal effects of milk consumption, some of which resemble those in lactose intolerance. This study aimed to compare the effects of milk containing A1 β-casein with those of milk containing only A2 β-casein on inflammation, symptoms of post-dairy digestive discomfort (PD3), and cognitive processing in subjects with self-reported lactose intolerance.MethodsForty-five Han Chinese subjects participated in this double-blind, randomized, 2 × 2 crossover trial and consumed milk containing both β-casein types or milk containing only A2 β-casein. Each treatment period was 14 days with a 14-day washout period at baseline and between treatment periods. Outcomes included PD3, gastrointestinal function (measured by smart pill), Subtle Cognitive Impairment Test (SCIT), serum/fecal laboratory biomarkers, and adverse events.ResultsCompared with milk containing only A2 β-casein, the consumption of milk containing both β-casein types was associated with significantly greater PD3 symptoms; higher concentrations of inflammation-related biomarkers and β-casomorphin-7; longer gastrointestinal transit times and lower levels of short-chain fatty acids; and increased response time and error rate on the SCIT. Consumption of milk containing both β-casein types was associated with worsening of PD3 symptoms relative to baseline in lactose tolerant and lactose intolerant subjects. Consumption of milk containing only A2 β-casein did not aggravate PD3 symptoms relative to baseline (i.e., after washout of dairy products) in lactose tolerant and intolerant subjects.ConclusionsConsumption of milk containing A1 β-casein was associated with increased gastrointestinal inflammation, worsening of PD3 symptoms, delayed transit, and decreased cognitive processing speed and accuracy. Because elimination of A1 β-casein attenuated these effects, some symptoms of lactose intolerance may stem from inflammation it triggers, and can be avoided by consuming milk containing only the A2 type of beta casein.Trial registrationClinicalTrials.gov/NCT02406469.

Lactose intolerance refers to symptoms related to the consumption of lactose-containing dairy foods, which are the most common source for this disaccharide. While four causes are described, the most common is the genetically-determined adult onset lactose maldigestion due to loss of intestinal lactase governed by control of the gene by a 14,000 kb promoter region on chromosome 2. Gastrointestinal symptoms from lactose have expanded to include systemic effects and have also been confounded by other food intolerances or functional gastrointestinal disorders. Partly because lactose maldigestion is often interpreted as lactose intolerance (symptoms), focus of therapy for these symptoms starts with lactose restriction. However, withholding of dairy foods completely is not appropriate due to a more favorable impact on health. Industrial efforts to substitute with plant-based products is not completely successful at this time. This narrative article reviews the complexities of the perception of lactose intolerance, its epidemiology, and pathogenesis. Treatments are discussed, including the inappropriateness of dairy avoidance. In conjunction, effects of dairy products on 19 common diseases are reviewed. Different methods of treatment, lactose-reduced products, plant-based dairy substitutes, adaptation, prebiotics, exogenous lactase, probiotics, and some other dietary interventions are further discussed.

Lactose is a disaccharide found in dairy products, which provide energy and essential nutrients. Digestion of lactose relies on the intestinal enzyme lactase, or lactase-phlorizin hydrolase, located on the brush border of the small bowel mucosa. This enzyme splits lactose into two absorbable monosaccharides: glucose and galactose. When lactase activity is insufficient, undigested lactose proceeds to the colon where it is fermented by the gut flora, generating gas that trigger the uncomfortable symptoms associated with lactose intolerance. Lactase non-persistence is extremely common, affecting approximately 70% of the adult population world-wide. Prevalence varies markedly across geographic regions, typically ranging from 50 to 90% in African, Asian, and South American countries. The subjective diagnosis of lactose intolerance requires the occurrence of symptoms such as abdominal pain, bloating, flatulence and diarrhea following the ingestion of high lactose dairy products. An objective assessment of lactose intolerance may be achieved with a specific breath test that measures hydrogen emission in breath following the ingestion of lactose. Consequently, current international guidelines require concurrent report of typical symptoms and pathologic breath test results in order to diagnose lactose intolerance. Management of lactose intolerance often involves dietary restrictions and the prescription of formulations that contain lactase. However, one should recognize that avoiding dairy products can increase the risk of nutritional deficiencies. Therefore, ongoing research is focused on alternative strategies, notably utilizing gut microbiota in order to improve tolerance to lactose. This review aims to explore the evidence supporting the use of probiotics as a potential treatment strategy to alleviate the symptoms of lactose intolerance by modulating colonic metabolism and enhancing lactose digestion.