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Review
, 7 (9), 8020-35

Lactose Intolerance in Adults: Biological Mechanism and Dietary Management

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Review

Lactose Intolerance in Adults: Biological Mechanism and Dietary Management

Yanyong Deng et al. Nutrients.

Abstract

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.

Keywords: FODMAP; genetic test; hydrogen breath test; irritable bowel syndrome; lactase deficiency; lactose intolerance; lactose malabsorption.

Figures

Figure 1
Figure 1
Map of the lactase (LCT) and minichromosome maintenance 6 (MCM6) gene region and location of genotyped single nucleotide polymorphisms (SNPs). (a) Distribution of 123 SNPs included in genotype analysis; (b) map of the LCT and MCM6 gene region; (c) map of the MCM6 gene; and (d) location of lactase persistence-associated SNPs within introns 9 and 13 of the MCM6 gene in African and European populations [12].
Figure 2
Figure 2
Small bowel water content (SBWC) and breath hydrogen (H2) concentrations after drinking each of the drinks: glucose and fructose. The time of drinking (t = 0 min) is highlighted in the chart. Values of SBWC are mean volume (mL) ± s.e.m (standard error of mean). Values of H2 are mean concentration (p.p.m.) ± s.e.m. Figure modified from Murray et al. [21].
Figure 3
Figure 3
Prevalence of lactose malabsorption (LM) and lactose intolerance (LI) in patients with diarrhea predominant irritable bowel syndrome (IBS-D) and controls at 10-, 20-, and 40-g lactose hydrogen breath test (HBTs). * p < 0.05; ** p < 0.01 [31].
Figure 4
Figure 4
Representative photomicrographs showing tryptase positive mast cells (MCs) in the colonic mucosa of a healthy control (HCs) (ac); an diarrhea predominant irritable bowel syndrome (IBS-D) patient with lactose malabsorption (LM) (df) and a patient with lactose intolerance (LI) (gi). IBS-D patients with LI had increased mucosal MCs compared with LM and HCs [36].
Figure 5
Figure 5
Lack of agreement between objective and subjective assessment of lactose intolerance [9].

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