World Digestive Health Day WDHD – May 29, 2016 CARBOHYDRATE INTOLERANCE (LACTOSE, SUCROSE, AND FRUCTOSE): IDENTIFICATION AND TREATMENT VIPIN GUPTA, MD Senior Resident Department of Gastroenterology and Human Nutrition All India Institute of Medical Sciences Ansari Nagar, New Delhi, India SHEILA E. CROWE, MD, FRCPC, FACP, FACG, AGAF Professor of Medicine Division of Gastroenterology, Department of Medicine University of California San Diego, California, USA GOVIND K. MAKHARIA, MD, DM, DNB, MNAMS Professor Department of Gastroenterology and Human Nutrition All India Institute of Medical Sciences Ansari Nagar, New Delhi, India INTRODUCTION Intolerance to carbohydrates, such as lactose intolerance, is a common type of non-allergic food intolerance.1 The number of patients diagnosed with carbohydrate intolerance has increased during the last few decades mostly as a consequence of increase in carbohydrate consumption, especially added sugar, in the diet. There has been increasing awareness among both general population and physicians about dietary intolerances and hence more and more patients with this disorder are now diagnosed. Carbohydrate intolerance can either be genetic or non-genetic in origin2 (See Table 1). LACTOSE INTOLERANCE The intolerance to lactose is due to either relative or absolute deficiency of lactase enzyme and the deficiency can occur because of three disorders: • Congenital lactase deficiency • Secondary lactase deficiency • Adult type lactase deficiency Table 1: Classification of carbohydrate intolerance Genetic Non-genetic Early onset Congenital lactase deficiency Congenital sucrase-isomaltase deficiency Glucose-galactose malabsorption Late onset Adult type lactose intolerance Functional impairment Fructose intolerance Sorbitol intolerance Trehalose intolerance CONGENITAL LACTASE DEFICIENCY Congenital deficiency of lactase is rare and it is most often described in reports from Finland. There is a severe deficiency of lactase, the enzyme responsible for the digestion of lactose. Premature stop codons and a truncated protein as a result of frame shifts missense mutations in the coding region of lactase enzyme, or exon duplication are the most common genotypes identified. Symptoms occur shortly after birth. Symptoms subside when diet is changed to lactose free substances. The activities of all other disaccharidases remain normal. SECONDARY LACTASE DEFICIENCY Deficiency of lactase occurs secondary to diseases of the intestinal mucosa both during acute settings (such as after an episode of gastroenteritis, or due to chronic diffuse mucosal diseases such as celiac disease or Crohn’s disease). With the healing of the intestinal mucosa, the level of lactase improves with resolution of the symptoms. The recovery of lactase may take a longer time even when mucosa has healed, which reflects the observation that lactase activity is the last to recover in comparison to other disaccharidases activities. ADULT TYPE LACTASE DEFICIENCY This is the most common cause of lactase enzyme deficiency and up to 70% of world’s population has an activity of lactase a level below a critical threshold for the digestion of dietary lactose. 3 It is an autosomal recessive condition in which there is a gradual reduction in the activity of lactase after two years of age. The prevalence of lactase deficiency varies widely in the different geographic locations around the world. In the USA, 20% of Caucasian people have deficiency of enzyme, while 80-100% of Asians have deficiency of lactase enzyme. The prevalence of lactase deficiency is about 70-95% in Africa and 15-70% in Europe. The persistence or non-persistence of the 20 WGO Handbook on DIET AND THE GUT World Digestive Health Day WDHD May 29, 2016
WGO Handbook on Diet and the Gut_2016_Final
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