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Objectives Lactose malabsorption is generally assessed by hydrogen breath testing (HBT). However, this test is not recommended in patients with high baseline hydrogen concentrations (H2B). In addition, breath testing is not recommended in the current situation created by the COVID-19 pandemic, due to the potential infectiveness of the samples. The objective is to assess concordance between HBT and lactose tolerance test (LTT) depending on H2B concentrations. Methods A total of 430 patients (40 years, Q1–Q3 = 28–54 years; 66.7% women) suspected of lactose malabsorption were included in the study. Breath and heparinized blood samples were collected at baseline and sequentially after the intake of 50 g of lactose, to measure hydrogen in breath and glycemia in blood, respectively. Results H2B was 20 ppm in 15.8% of subjects. In patients with H2B 2B levels obtained in HBT. Conclusions LTT emerges as an alternative to HBT to assess lactose malabsorption in the presence of high H2B levels or when breath testing is not recommended by the circumstances. The best concordance was obtained when the cut-off for LTT was set at 15 mg/dL.

Lactose is the most important source in mammalian milk. In normal children, Lactose is hydrolyzed by lactase, and directly absorbed into bloodstream by an active transport mechanism. The term of lactose malabsorption is reserved to patients in whom impaired intestinal lactose hydrolysis and uptake has been proven by an appropriate test. The severity of lactose malabsorption and the extent of symptoms vary widely and are the results of several factors such as the amount of ingested lactose, gastric emptying time, intestinal transit time, and colonic flora. The diagnosis of lactose malabsorption is based on clinical findings and the results of appropriate tests. The breath hydrogen test has obvious advantages for pediatric population because it is painless, non-invasive, sensitive and specific. In the absence of bacterial colonization in the small intestine, the elevation of the concentration of hydrogen in the expired air implies the arrival of lactose in the colon. The increasing respiratory excretion of hydrogen is indicative of a deficit of lactase in enterocyte brush border. This test can also be used to show the existence of bacterial growth. Dietary fiber, some drugs, preparation for colonoscopy, colonic pH, and diarrhea can influence the result of breath hydrogen test.

Background The prevalence of lactose malabsorption varies widely throughout the world. Only people of Caucasian genetic background continue to produce high amount of lactase throughout adulthood. Previous studies in Indonesia revealed that the prevalence of lactose malabsorption was 21-58% in children aged 3-11 years. Objective To determine the prevalence of lactose malabsorption in the older age group and whether a change in milk drinking habit can affect it. Methods A cross sectional descriptive study was conducted on 98 children aged between 12 and 14 years (junior high school) in Jakarta. Lactose malabsorption was evaluated with Lactometer Breath Hydrogen Test (Hoek Loes, Amsterdam). Milk drinking habit was recorded, and drinking at least 1 glass of milk everyday since 6 months or more before the study was considered as regular milk drinking. Results This study showed 73% of the children had lactose malabsorption. Regular milk drinking habit was found in 32 (33%) children and lactose malabsorption occurred in 26. From 66 children who were irregular milk drinkers, lactose malabsorption was found in 46 (70%). Lactose intolerance was about the same in both groups. Conclusion There was an increasing prevalence of lactose malabsorption in older children. Milk drinking habit is a major concern to review the practical implications of lactose malabsorption.

The lactose hydrogen breath test is a commonly used, non-invasive method for the detection of lactose malabsorption and is based on an abnormal increase in breath hydrogen (H₂) excretion after an oral dose of lactose. We use a combined (13)C/H₂ lactose breath test that measures breath (13)CO₂ as a measure of lactose digestion in addition to H₂ and that has a better sensitivity and specificity than the standard test. The present retrospective study evaluated the results of 1051 (13)C/H₂ lactose breath tests to assess the impact on the diagnostic accuracy of measuring breath CH₄ in addition to H₂ and (13)CO₂. Based on the (13)C/H₂ breath test, 314 patients were diagnosed with lactase deficiency, 138 with lactose malabsorption or small bowel bacterial overgrowth (SIBO), and 599 with normal lactose digestion. Additional measurement of CH₄ further improved the accuracy of the test as 16% subjects with normal lactose digestion and no H₂-excretion were found to excrete CH₄. These subjects should have been classified as subjects with lactose malabsorption or SIBO. In conclusion, measuring CH₄-concentrations has an added value to the (13)C/H₂ breath test to identify methanogenic subjects with lactose malabsorption or SIBO.

The aim of this study was to compare the impact of whole milk supplementation on gut microbiota and cardiometabolic biomarkers between lactose malabsorbers (LM) and absorbers (LA). We performed a pair-wise intervention study of 31 LM and 31 LA, 1:1 matched by age, sex, body mass index, and daily dairy intake. Subjects were required to add 250 mL/day whole milk for four weeks in their routine diet. At the beginning and the end of the intervention period, we collected data on gut microbiota and cardiometabolic biomarkers. Whole milk supplementation significantly increased Actinobacteria (P &lt, 0.01), Bifidobacterium (P &lt, 0.01), Anaerostipe (P &lt, 0.01), and Blautia (P = 0.04), and decreased Megamonas (P = 0.04) in LM, but not LA. Microbial richness and diversity were not affected. The fecal levels of short-chain fatty acids (SCFAs) remained stable throughout the study. Body fat mass (P &lt, 0.01) and body fat percentage (P &lt, 0.01) reduced in both groups, but the changes did not differ between groups. No significant differences in other cardiometabolic markers were found between LM and LA. When compared with LA, whole milk supplementation could alter the intestinal microbiota composition in LM, without significant changes in fecal SCFAs and cardiometabolic biomarkers.

Background: Sheep milk (SM) is a possible alternate dairy source for those who experience digestive symptoms with cow milk (CM). While both the milks contain lactose, one of the causes for self-reported intolerance to CM, the composition of SM and CM also differs across proteins and fats, which have been shown to impact digestive processes.Objective: To compare the acute digestive comfort and lactose malabsorption of SM to CM in female dairy avoiders.Method: In a double-blinded, randomized cross over trial, 30 dairy-avoiding females (aged 20–30 years) drank 650 mL of SM or CM (each reconstituted from spray dried powder) following an overnight fast, on two separate occasions at least 1 week apart. Blood samples were collected for glucose and insulin assessment, and single nucleotide polymorphisms of the lactase (LCT) gene (C/T13910 and G/A22018). Breath H2 and visual analog scale (VAS) digestive symptom scores were recorded at fasting and regular intervals over 4 h after ingestion.Results: Eighty percentage of study participants were lactase non-persistent (LNP; CC13910 and GG22018 genotype). Digestive symptoms, including abdominal cramps, distension, rumbling, bloating, belching, diarrhea, flatulence, vomiting, and nausea, were similar in response to SM and CM ingestion (milk × time, P > 0.05). Breath H2 was greater after CM than SM (72 ± 10 vs. 43 ± 6 ppm at 240 min, P < 0.001), which may be due to greater lactose content in CM (33 vs. 25 g). Accordingly, when corrected for the lactose content breath H2 did not differ between the two milks. The response remained similar when analyzed in the LNP subset alone (n = 20).Conclusions: Despite a higher energy and nutrient content, SM did not increase adverse digestive symptoms after ingestion, relative to CM, although there was a reduced breath H2 response, which could be attributed to the lower lactose content in SM. The tolerability of SM should be explored in populations without lactose intolerance for whom underlying trigger for intolerance is unknown.

OBJECTIVES: Sheep milk (SM) is compositionally different from cow milk (CM), but maintains the nutritional benefits of CM, making it a potential alternative for CM avoiders. While dairy avoidance is often due to intolerance to lactose, which is also found in SM, there are consumer anecdotal reports that SM is better tolerated than CM. Thus, this clinical trial was undertaken to assess acute digestive comfort and lactose malabsorption comparing SM and CM in female dairy avoiders. METHODS: In a double-blinded, randomized cross over trial, 30 dairy avoiding females (aged 20–30 years) drank 650 mL of SM or CM (reconstituted from spray dried powder) following an overnight fast, on separate occasions at least one week apart. Blood samples were collected for single nucleotide polymorphisms of the LCT gene (lactase gene; C/T(13910) and G/A(22018)). Breath H(2) and visual analog scale (VAS) digestive symptom scores were recorded at fasting and regular intervals over 4 h after ingestion. RESULTS: Genotyping showed 80% of the dairy avoiders were lactase non-persistent (CC(13910) and GG(22018) genotype), hence lactose malabsorbers. Digestive symptoms were similar in response to SM and CM, with increased symptoms; abdominal cramps, rumbling, bloating, belching, flatulence, and nausea, after the ingestion of either milk (P

Lactose is the main source of calories in milk, an essential nutriedigestion, patients with visceral hypersensitivity nt in infancy and a key part of the diet in populations that maintain the ability to digest this disaccharide in adulthood. Lactase deficiency (LD) is the failure to express the enzyme that hydrolyses lactose into galactose and glucose in the small intestine. The genetic mechanism of lactase persistence in adult Caucasians is mediated by a single C→T nucleotide polymorphism at the LCTbo -13'910 locus on chromosome-2. Lactose malabsorption (LM) refers to any cause of failure to digest and/or absorb lactose in the small intestine. This includes primary genetic and also secondary LD due to infection or other conditions that affect the mucosal integrity of the small bowel. Lactose intolerance (LI) is defined as the onset of abdominal symptoms such as abdominal pain, bloating and diarrhoea after lactose ingestion by an individual with LM. The likelihood of LI depends on the lactose dose, lactase expression and the intestinal microbiome. Independent of lactose digestion, patients with visceral hypersensitivity associated with anxiety or the Irritable Bowel Syndrome (IBS) are at increased risk of the condition. Diagnostic investigations available to diagnose LM and LI include genetic, endoscopic and physiological tests. The association between self-reported LI, objective findings and clinical outcome of dietary intervention is variable. Treatment of LI can include low-lactose diet, lactase supplementation and, potentially, colonic adaptation by prebiotics. The clinical outcome of these treatments is modest, because lactose is just one of a number of poorly absorbed carbohydrates which can cause symptoms by similar mechanisms. ispartof: GUT vol:68 issue:11 pages:2080-2091 ispartof: location:England status: published

Background. Insufficient vitamin D and calcium intake associated with the restricted intake of milk and dairy products can lead to poor health outcomes like malnutrition and abnormal bone mineralization. The aim of the study was to estimate the prevalence of primary and secondary lactose intolerance in children with IBD. Methods. The study included 107 patients (mean age 14.07±3.58 years; 46.7% boys) which includes 43 patients with Crohn’s disease (CD), 31 with ulcerative colitis (UC), and 33 children with functional abdominal pain (AP-FGID). We analysed the result of the hydrogen breath test with lactose loading, two single nucleotide polymorphisms of the LCT gene (LCT-13910CC and LCT-22018GG). The results were analysed with MedCalc Statistical Software. Results. Adult-type hypolactasia (ATH) was found in 31% of patients with IBD and 42.4% of AP-FGID (p=0.2). Lactose malabsorption (LM) was found in 27.9% of patients with CD, in 22.6% with UC, and in 24.2% with AP-FGID (p=0.8). Lactose intolerance (LI) was diagnosed in a similar percentage of patients in each group (p=0.9). Secondary LI in IBD patients does not depend on the location, duration, and activity of the disease and the number of relapses (p>0.05). The median time of lactose-free diet in CD was 10 months and in CU 24 months. Conclusions. The incidence of LI, LM, and ATH does not differ among children with IBD from the population.

Background Current literature proposes associations between homocysteine (HCY), folic acid (FA), vitamin B12 metabolism and depression. However, the exact underlying biological mechanisms remain unclear. This study aimed at evaluating a possible link between primary adult-type lactose malabsorption (PALM), HCY, FA and vitamin B12 metabolism and depressive disorder. Methods Plasma levels of HCY, FA and vitamin B12 were determined in 78 patients with PALM and 160 individuals with lactase persistence sub-grouped by the presence or absence of major depression. Results In 78 patients with PALM, the subgroup of 22 individuals with major depression showed significantly higher median (interquartile range) HCY (10.10 [8.46–12.03] vs. 8.9 [7.54–9.86] μmol/L, p = 0.029) and lower plasma FA levels (5.7 [4.68–9.14] vs. 6.95 [5.24–10.56] μmol/L, p = 0.272) compared to the subgroup of 56 individuals without depression, respectively. No such associations could be observed for those 160 individuals without PALM (i.e., lactase persistence) Plasma HCY levels were positively correlated with depressive symptoms (p = 0.052), and showed negative correlations with FA (p = < 0.001) and vitamin B12 (p = 0.029), respectively. Conclusion Depressed individuals with PALM were found with significantly higher HCY and lower FA levels compared to non-depressed individuals with PALM, however, this association was absent in the subgroup of lactase persistent individuals. These findings suggest an association between increased HCY levels, lactose malabsorption and depression.

WOS:000323601900005; International audience; Background: Lactose malabsorption occurs frequently and the variable consequent intolerance may seriously impair quality of life. No reliable and convenient test method is in routine clinical practice. A recent animal study showed that the respiratory quotient changed significantly after ingestion of sucrose and lactose in naturally lactase-deficient rats. Aims: This exploratory study evaluated the relevance of monitoring the respiratory quotient after lactose ingestion to detect malabsorption. Methods: Healthy volunteers were identified and classified lactose absorbers and malabsorbers by a lactose tolerance test (25 g). After an overnight fast, a second lactose challenge was performed to monitor hydrogen excretion and respiratory quotient kinetics over 4 h. Participants also completed questionnaires to score and localise their gastrointestinal symptoms. Results: 20 subjects were enrolled (10 per group, 60% males, mean age 34 +/- 4 years). Respiratory quotient kinetics were different between absorbers and malabsorbers during the first 100 min after lactose ingestion (p \textless 0.01) and during the initial 30-50 min period. Respiratory quotient was significantly, positively correlated to peak glycaemia (R = 0.74) and negatively correlated to hydrogen excretion (R = -0.51) and symptoms score (R = -0.46). Conclusions: Indirect calorimetry could improve the reliability of lactose malabsorption diagnosis. Studies on larger populations are needed to confirm the validity of this test and propose a simplified measurement. (c) 2013 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

The prevalence and duration of lactose malabsorption was studied in 64 Central Australian Aboriginal children requiring hospitalization for acute enteritis. Lactose malabsorption was determined by the breath‐hydrogen test. Sixty‐nine per cent were shown to malabsorb lactose, a figure similar to that for well nourished urban European children, hospitalized for acute enteritis. Whereas 90 per cent of the European children became lactose‐tolerant 1 month later, only three of 32 aboriginal children were lactose‐tolerant after 3 months. Lactose malabsorption was also associated with more frequent hospitalizations in affected children. Coronavirus‐like particles were the commonest agent isolated from Aboriginal children. The majority of the Aboriginal children were malnourished (< 80% standard weight for age) which may have been contributed to by their lactose malabsorption and explain why this failed to recover in the same way as European children. The possibility of lactose malabsorption must be taken into consideration when managing Aboriginal children with acute diarrhoeal disease and undernutrition. The use of the breath‐hydrogen test allows an accurate diagnosis of lactose malabsorption to be made in Aboriginal children with diarrhoea so that appropriate dietary management can be instituted.

Fermentation, the bacterial process of gaining energy from the breakdown of carbohydrates, takes place in the human large intestine as well as that of the animals. This process is important for the health of the colon. Due to changing dietary habits, the available substrates for fermentation in the human colon are scarce, and this fact may contribute to the increased number of colonic diseases in the Western world. Lactose in lactose-maldigesters increase the amounts of fermentable substrate, and may contribute to the health of the colon in these individuals. The symptoms of lactose maldigestion may be reduced by adaptation. Keywords: Bacterial flora, colon, fermentation, lactose, prebiotic

Genetic testing is a good predictor of lactase persistence (LP) in specific populations but its clinical utility in children is less clear. We assessed the role of lactose malabsorption in functional gastrointestinal disorders (FGID) in children and the correlation between the lactase non-persistence (LNP) genotype and phenotype, based on exhaled hydrogen and gastrointestinal symptoms, during a hydrogen breath test (HBT). We also evaluate dairy consumption in this sample. We conducted a 10-year cross-sectional study in a cohort of 493 children with suspected FGID defined by Roma IV criteria. Distribution of the C/T-13910 genotype was as follows: CC, 46.0%, TT, 14.4% (LP allele frequency, 34.1%). The phenotype frequencies of lactose malabsorption and intolerance were 36.3% and 41.5%, respectively. We observed a strong correlation between genotype and both lactose malabsorption (Cram&eacute, r&rsquo, s V, 0.28) and intolerance (Cram&eacute, s V, 0.54). The frequency of the LNP genotype (p = 0.002) and of malabsorption and intolerance increased with age (p = 0.001 and 0.002, respectively). In 61% of children, evaluated dairy consumption was less than recommended. No association was observed between dairy intake and diagnosis. In conclusion, we found a significant correlation between genotype and phenotype, greater in older children, suggesting that the clinical value of genetic testing increases with age.

BACKGROUND Lactose malabsorption is a serious issue and since malnutrition is common in our community, it was deemed worthwhile to conduct a study of lactose malabsorption in malnutrition. The problem of malnutrition in India has grown to the extent that it compels the personnel concerned with human health to pause and think for its remedy. We wanted to study the radiological changes of malabsorption syndrome in lactose malabsorbers. METHODS The study was conducted at outpatient department of Paedicatrics in Late Baliram Kashyap Memorial Government Medical College, Jagadalpur, Chhattisgarh. These cases were selected from children visiting the out patient’s department, Pt. J.N.M. Medical College and Associated D.K. Hospital, Raipur, M.P. Total number of children in the present study was 67 who had no history of diarrhoea in past 15 days and in whom there was no history of worm infection. Data was collected in questionnaire. Barium-meal examination of small intestine is done. The study was conducted for a period of six months. Permission from Institutional Ethics Committee was obtained. Initially informed individual consent was taken from all the patients included in the study. RESULTS Radiological changes of malabsorption syndrome were seen in 37 cases out of 45 of lactose malabsorbers. Out of which, 26 cases (57.8 per cent) were having mild to moderate changes and 11 cases (22.44 per cent) showed severe changes. Barium meal was normal in 4 cases (8.88 per cent) of lactose malabsorbers. In the follow up group, out of 32 lactose malabsorbers, 27 cases (84.37 per cent) showed mild to moderate radiological evidence of malabsorption syndrome, and 4 cases (12.9 per cent) showed severe changes, total being 31 out of 32 (97.27 per cent). CONCLUSIONS In this study, varying grades of malnutrition between six months to 3 years of age were included for the evidence of lactose malabsorption by detecting stool pH and by doing a barium meal radiograph for evidence of malabsorption syndrome. In majority of cases, combined radiological changes of malabsorption syndrome were seen. There is no correlation of radiological evidence of malabsorption syndrome between lactose malabsorbers and absorbers.

The breath hydrogen test (BHT) was adapted for use in young infants and children. The diagnostic criterion of sugar malabsorption in the BHT was determined by oral administration of 0.5 g/kg of unabsorbable sugar (lactulose) to 21 healthy infants and children. A maximum increase in breath hydrogen less than 0.05 ml/min per m2 was observed in all subjects. A good correlation between results by the BHT and by the ordinary lactose tolerance test was obtained after oral administration of 2 g/kg lactose to 21 healthy infants and children, 2 congenital lactase-deficient infants, and 7 adults. Using this test, 80 healthy Japanese infants and children (aged between one month and 15 years) and 18 adults were examined for lactose malabsorption after a dose of 1 g/kg lactose. All infants and children under 2-years old absorbed lactose completely. The incidence of lactose malabsorption was 30% in 3-year, 36% in 4-year, 58% in 5-year, and 86% in 6-year-old children, 85% in schoolchildren, and 89% in adults. Thus the incidence of lactase deficiency gradually increases with age from 3 years, and about 90% of all normal Japanese adults are lactase-deficient.

A total of 308 healthy Italian adults (192 females, 116 males; mean age 29.2 yr) were examined using a field version of the lactose tolerance test with breath hydrogen determination. Two geographical groups were formed according to the birth places of the probands' grandparents: 208 subjects from northern Italy (mainly from the regions of Piemonte, Lombardia, and Veneto) and 100 probands from Sicily. Lactose malabsorption was diagnosed in 106 subjects in group "north" (51%) and in 71 subjects in group "Sicily" (71%). Awareness of milk intolerance was more frequent in lactose malabsorbers. The incidence of diarrhea after the test dose of lactose was significantly higher in "aware" lactose malabsorbers, when compared with persons of the same group who had not experienced milk intolerance. The significant difference in lactose malabsorption frequency between northern Italy and Sicily is further evidence of a north-south gradient of lactase gene frequencies in Europe.

Plasma insulin levels were determined following oral glucose in 12 patients with adult coeliac disease, after oral lactose in four patients with alactasia, and in age-matched control subjects. In coeliac patients the insulin response was greater than expected from the small rise in blood sugar, and no correlation was found between plasma insulin and sugar levels at any period during the test. The separation of the plasma insulin curve from the blood sugar curve after glucose is in keeping with the concept that a factor responsible for stimulating insulin secretion is released from the gut during or after absorption of glucose. In patients with selective lactose malabsorption (alactasia) administration of lactose by mouth failed to elicit any insulin response, indicating that the insulin-releasing effect of the bowel is not activated merely by the presence of intraluminal carbohydrate.

22% of a group of adult Neapolitans were found to have persistent high lactase activity, and 16% were lactose absorbers as indicated by measurement of breath hydrogen concentration and rise in blood glucose after oral lactose administration. Among adults in the same area with idiopathic senile or presenile cataract 49% were identified as lactose absorbers with the breath hydrogen test and 55% by the rise in blood glucose. These results suggest that adults able to absorb galactose from a lactose-containing diet are especially susceptible to senile or presenile cataract.

Whether or not abdominal symptoms occur in subjects with small intestinal lactose malabsorption might depend on differences in colonic fermentation. To evaluate this hypothesis, we collected fecal samples from subjects with lactose malabsorption with abdominal complaints (LM-IT, n = 11) and without abdominal complaints (LM-T, n = 8) and subjects with normal lactose digestion (NLD, n = 15). Lactose malabsorption was diagnosed using a (13)C-lactose breath test. Colonic fermentation was characterized in fecal samples at baseline and after incubation with lactose for 3 h, 6 h and 24 h through a metabolomics approach using gas chromatography-mass spectrometry (GC-MS). Fecal water cytotoxicity was analyzed using a colorimetric assay. Fecal water cytotoxicity was not different between the three groups (Kruskall-Wallis p = 0.164). Cluster analysis of the metabolite patterns revealed separate clusters for NLD, LM-T and LM-IT samples at baseline and after 24 h incubation with lactose. Levels of 5-methyl-2-furancarboxaldehyde were significantly higher in LM-IT and LM-T compared to NLD whereas those of an unidentified aldehyde were significantly higher in LM-IT compared to LM-T and NLD. Incubation with lactose increased short chain fatty acid (SCFA) concentrations more in LM-IT and LM-T compared to NLD. In conclusion, fermentation patterns were clearly different in NLD, LM-IT and LM-T, but not related to differences in fecal water cytotoxicity. ispartof: Nutrients vol:7 issue:9 pages:7505-7522 ispartof: location:Switzerland status: published

Introduction Lactose malabsorption arises from lactase deficiency and may lead to lactose intolerance - gastrointestinal symptoms after lactose ingestion. Occurrence and severity of the symptoms are influenced by many factors, including the dose of lactose and the intensity of its colonic fermentation to short chain fatty acids and gases. Material and methods The hydrogen breath test (HBT) after 30 g or 50 g of lactose was performed in 387 children. Further analysis included children who had a positive HBT result. The HBT parameters were net hydrogen concentration in each breath and total net hydrogen concentration during the HBT. The time of the first hydrogen rise was also calculated. HBT parameters were analyzed according to symptoms occurrence (lack or present), symptoms severity (lack, moderate or severe) and the dose of lactose (30 g or 50 g). Results One hundred and six children (12.1 years, 46 boys) had a positive HBT result. Symptoms occurrence was positively related to net hydrogen concentration at 30 min, 60 min and 90 min (p < 0.001 at each time point), as well as to the total net hydrogen concentration (p < 0.001). There were no differences in hydrogen excretion between subjects with moderate and severe symptoms after lactose ingestion. Symptoms were more frequent in subjects given 50 g of lactose than in those given 30 g of lactose (79% vs. 47%, p = 0.003). In both dose groups symptoms occurrence was related to hydrogen excretion. Conclusions Symptoms occurrence is closely related to hydrogen excretion and to the dose of ingested lactose.

This review focuses on the acquired causes, diagnosis, and treatment of intestinal malabsorption. Intestinal absorption is a complex process that depends on many variables, including the digestion of nutrients within the intestinal lumen, the absorptive surface of the small intestine, the membrane transport systems, and the epithelial absorptive enzymes.Acquired causes of malabsorption are classified by focussing on the three phases of digestion and absorption: 1) luminal/digestive phase, 2) mucosal/absorptive phase, and 3) transport phase. Most acquired diseases affect the luminal/digestive phase. These include short bowel syndrome, extensive small bowel inflammation, motility disorders, and deficiencies of digestive enzymes or bile salts. Diagnosis depends on symptoms, physical examination, and blood and stool tests.There is no gold standard for the diagnosis of malabsorption. Further testing should be based on the specific clinical context and the suspected underlying disease. Therapy is directed at nutritional support by enteral or parenteral feeding and screening for and supplementation of deficiencies in vitamins and minerals. Early enteral feeding is important for intestinal adaptation in short bowel syndrome. Medicinal treatment options for diarrhoea in malabsorption include loperamide, codeine, cholestyramine, or antibiotics. (C) 2016 Elsevier Ltd. All rights reserved.

Milk is a fundamental component of the diet of every mammal; nevertheless, not every individual can tolerate this kind of food, especially in adulthood. However, lactose intolerance has only been recognized in the last 50 years, and currently, lactose intolerance is defined as a clinical syndrome characterized by pain, abdominal distention, flatulence, and diarrhoea that occur after lactose consumption. Lactose is currently a common disaccharide in human nutrition, both in breastfed infants and in adults, but its digestion requires a specialized enzyme called lactase. The genetically programmed reduction in lactase activity during adulthood affects most of the world’s adult population and can cause troublesome digestive symptoms, which may also vary depending on the amount of residual lactase activity; the small bowel transit time; and, especially, the amount of ingested lactose. Several diagnostic tests are currently available for lactose intolerance, but the diagnosis remains challenging. The treatment for lactose intolerance mainly consists of reducing or eliminating the dietetic amount of lactose until the symptoms disappear, but this is hard to achieve, as lactose is present in dairy products and is even commonly used as a food additive. In addition to dietetic restriction of lactose-containing foods, lactase can be administered as an enzymatic food supplement, but its efficacy is still controversial. Recently, probiotics have been proposed for the management of lactose intolerance; certain probiotic strains have shown specific β-galactosidase activity, thus aiding in the digestion of lactose. The aim of this paper was to review the current knowledge about lactose intolerance and to discuss the potential for the use of specific probiotic strains such as dietary supplements in lactose-intolerant patients.

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.

Context: Severe acute malnutrition (SAM) accounts for approximately 1 million child deaths per year. High mortality is linked with comorbidities, such as diarrhea and pneumonia. Objective: The aim of this systematic review was to determine the extent to which carbohydrate malabsorption occurs in children with SAM. Data Sources: The PubMed and Embase databases were searched. Reference lists of selected articles were checked. Data Extraction: All observational and controlled intervention studies involving children with SAM in which direct or indirect measures of carbohydrate absorption were analyzed were eligible for inclusion. A total of 20 articles were selected for this review. Data Synthesis: Most studies reported carbohydrate malabsorption, particularly lactose malabsorption, and suggested an increase in diarrhea and reduced weight gain in children on a lactose-containing diet. As most studies reviewed were observational, there was no conclusive scientific evidence of a causal relationship between lactose malabsorption and a worse clinical outcome among malnourished children. Conclusion: The combined data indicate that carbohydrate malabsorption is prevalent in children with SAM. Additional well-designed intervention studies are needed to determine whether outcomes of SAM complicated by carbohydrate malabsorption could be improved by altering the carbohydrate/lactose content of therapeutic feeds and to elucidate the precise mechanisms involved.

Background Lactose malabsorption occurs in around 68% of the world’s population, causing lactose intolerance (LI) symptoms, such as abdominal pain, bloating, and diarrhea. To alleviate LI, previous studies have mainly focused on strengthening intestinal β-galactosidase activity while neglecting the inconspicuous drop in the colon pH caused by the fermentation of non-hydrolyzed lactose by the gut microbes. A drop in colon pH will reduce the intestinal β-galactosidase activity and influence intestinal homeostasis. Results Here, we synthesized a tri-stable-switch circuit equipped with high β-galactosidase activity and pH rescue ability. This circuit can switch in functionality between the expression of β-galactosidase and expression of L-lactate dehydrogenase in response to an intestinal lactose signal and intestinal pH signal, respectively. We confirmed that the circuit functionality was efficient in bacterial cultures at a range of pH levels, and in preventing a drop in pH and β-galactosidase activity after lactose administration to mice. An impact of the circuit on gut microbiota composition was also indicated. Conclusions Due to its ability to flexibly adapt to environmental variation, in particular to stabilize colon pH and maintain β-galactosidase activity after lactose influx, the tri-stable-switch circuit can serve as a promising prototype for the relief of lactose intolerance.

Lactose is the main source of calories in milk, an essential nutriedigestion, patients with visceral hypersensitivity nt in infancy and a key part of the diet in populations that maintain the ability to digest this disaccharide in adulthood. Lactase deficiency (LD) is the failure to express the enzyme that hydrolyses lactose into galactose and glucose in the small intestine. The genetic mechanism of lactase persistence in adult Caucasians is mediated by a single C→T nucleotide polymorphism at the LCTbo -13'910 locus on chromosome-2. Lactose malabsorption (LM) refers to any cause of failure to digest and/or absorb lactose in the small intestine. This includes primary genetic and also secondary LD due to infection or other conditions that affect the mucosal integrity of the small bowel. Lactose intolerance (LI) is defined as the onset of abdominal symptoms such as abdominal pain, bloating and diarrhoea after lactose ingestion by an individual with LM. The likelihood of LI depends on the lactose dose, lactase expression and the intestinal microbiome. Independent of lactose digestion, patients with visceral hypersensitivity associated with anxiety or the Irritable Bowel Syndrome (IBS) are at increased risk of the condition. Diagnostic investigations available to diagnose LM and LI include genetic, endoscopic and physiological tests. The association between self-reported LI, objective findings and clinical outcome of dietary intervention is variable. Treatment of LI can include low-lactose diet, lactase supplementation and, potentially, colonic adaptation by prebiotics. The clinical outcome of these treatments is modest, because lactose is just one of a number of poorly absorbed carbohydrates which can cause symptoms by similar mechanisms.

Taking into account the reported incidence of hypolactasia in cystic fibrosis (CF) and the possible impact of milk products on nutritional status we aimed to assess the genetic predisposition to adult-type hypolactasia (ATH) and its incidence in CF. Single nucleotide polymorphism upstream of the lactase gene (LCT) was assessed in 289 CF patients. In subject with −13910C/C genotype (C/C) predisposing to ATH, hydrogen-methane breath test (BT) with lactose loading was conducted and clinical symptoms typical for lactose malabsorption were assessed. The percentage of CF patients with C/C was similar to that observed in healthy subjects (HS) (31.5 vs 32.5% ). Eleven out of 52 (24.5%) CF C/C patients had abnormal BT results. The recalculated frequency of lactose malabsorption was similar for the entire CF and HS populations (6.9 vs 7.2%). Similarly as in the control group, few CF patients have identified and linked to lactose consumption clinical symptoms. The frequency of LCT polymorphic variants in CF patients having and not having severe mutations of CFTR gene showed significant differences. The C allele was more frequent in homozygotes of the severe mutations than in patients carrying at least one mild/unknown mutation (P