Explore the vast range of titles available.

Functional gastrointestinal symptoms are frequent, and may be driven by several pathogenic mechanisms. Symptoms may persist in lactose intolerant (LI) patients (i.e., subjects with intestinal lactase deficiency, lactose malabsorption producing symptoms), after a lactose-free diet. Our hypothesis was that probiotic and vitamin B6 treatment may be useful to alleviate symptoms in LI patients through a positive modulation of gut microbial composition and relative metabolism. We aimed to test the efficacy of a novel formulation of Bifidobacterium longum BB536 and Lactobacillus rhamnosus HN001 plus vitamin B6 (ZR) in 23 LI subjects with persistent symptoms during a lactose-free diet. Symptoms, microbiome, and metabolome were measured at baseline and after 30 days in a crossover, randomized, double-blind study of ZR versus placebo (PL). Compared with PL, the administration of probiotics and vitamin B6 significantly decreased bloating (p = 0.028) and ameliorated constipation (p = 0.045). Fecal microbiome differed between ZR and PL. ZR drove the enrichment of several genera involved in lactose digestion including Bifidobacerium. Moreover, the relative abundance of acetic acid, 2-methyl-propanoic acid, nonenal, and indolizine 3-methyl increased, while phenol decreased. Our findings highlight the importance of selected probiotics and vitamin B6 to alleviate symptoms and gut dysbiosis in lactose intolerant patients with persistent functional gastrointestinal symptoms.

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.

Lactose intolerance is a common but poorly understood cause of gastrointestinal symptoms. Contrary to popular belief, there is much more to its diagnosis beyond symptoms with exposure and management beyond milk- and dairy-product avoidance. In this article, we review definitions, genetic basis, pathogenesis, clinical signs, as well as diagnostic and management strategies.

INTRODUCTION:We aimed to explore the prevalence of carbohydrate (lactose and fructose) intolerance in patients with disorders of gut-brain interaction (DGBI) and to characterize those patients regarding gastrointestinal and nongastrointestinal symptoms.METHODS:Patients with DGBI who were referred to the physiology unit of our hospital between May 2022 and December 2023 for lactose (25 g) and fructose (25 g) breath tests were prospectively included. Patients were required to have a negative glucose breath test, before lactose and fructose breath tests, and to have completed the adult carbohydrate perception questionnaire during each breath test. Intolerance was defined as an increase of ≥20 mm in the Visual Analog Scale score from baseline in at least 1 of the 5 symptoms (pain, nausea, bloating, flatulence, and diarrhea) assessed with the adult Carbohydrate Perception Questionnaire.RESULTS:Among the 301 patients with DGBI included in our analysis, 178 (59.1%) had carbohydrate intolerance. Carbohydrate-intolerant patients were significantly more likely to be female (P value < 0.001), to have 2 or more DGBI (P value = 0.001), to have lactose maldigestion (P value< 0.001) and fructose malabsorption (P value = 0.023), higher irritable bowel syndrome and somatic symptom severity, and lower quality of life (P value < 0.001) compared with patients without carbohydrate intolerance. The binary logistic regression showed that lactose maldigestion (P value = 0.001), as well as somatic symptoms (P value = 0.025), were independently associated with carbohydrate intolerance (Nagelkerke R Square = 0.206).DISCUSSION:Carbohydrate intolerance affects a substantial group of patients with DGBI, affecting their quality of life and symptom severity. Further research is needed to explore the underlying mechanisms in patients who do not have carbohydrate malabsorption/maldigestion.

Lactose-free dairy is able to provide the essential nutrients present in regular dairy products, like calcium and vitamins, to those that are not able to digest lactose. This product category currently has a wide and growing health appeal to consumers. In recent years, the quality and product variety in the lactose-free dairy segment has been increasing significantly, giving consumers more tempting products to decide from. As a result, lactose-free dairy is now the fastest growing market in the dairy industry. This review discusses the market developments and production possibilities and issues related to the wide variation of lactose-free dairy products that are currently available. Additionally, the health benefits that lactose-free dairy may offer compared to dairy avoidance are illustrated.

IntroductionFood intolerances are prevalent in Europe and can cause considerable physical discomfort, dietary restrictions and psychosocial challenges. Among the prominent causes of food intolerance are defects in the digestion and/or transport of short-chain fermentable carbohydrates, fermentable oligo-, di-, monosaccharides and polyols (FODMAPs). A common diagnostic tool for food intolerance is the hydrogen breath test, which monitors the production of H2 gas from the fermentation of ingested FODMAPs by colonic microbiota. However, this method is limited due to its relatively poor correlation with gastrointestinal (GI) symptoms experienced by patients. Diagnosis is complicated as food intolerance is often associated with functional GI disorders, while FODMAPs may exert their effects individually or in combination. Further research on the pathophysiology and the impact of intervention strategies for these conditions is required to improve the diagnosis of food intolerance.Methods and analysesThe Lactobreath pilot study is a randomised, two-arm, double-blinded controlled study. 120 healthy, free-living adults will undergo 6-hour postprandial tests with lactose or glucose (control) to investigate the molecular composition of human exhaled breath (exhalome) as a potential source of biomarkers associated with clinical and metabolic traits of lactose malabsorption (Lactobreath profiles). This serves as a proof-of-concept for the future application of this technology in diagnosing food intolerance. We will use a sensitive, non-invasive, real-time measurement technique based on secondary electrospray ionisation coupled with high-resolution mass spectrometry to analyse the chemical profile of the postprandial exhalome after lactose ingestion. Symptoms of lactose intolerance will be assessed using a standardised questionnaire and mechanistically linked to specific key metabolites of the discriminating breath profile. In parallel, a solid-state sensor will measure postprandial hydrogen gas in breath samples, while GI gases (CH4, H2, O2) and intestinal transit time will be monitored using a novel ingestible gas sensor (Atmo Gas capsule). Metabolites in urine, including lactose-derived metabolites, will be investigated using gas chromatography coupled with mass spectrometry. Postprandial bowel sounds will be recorded by wearable sensors (DigeHealth AG). Baseline assessments will be completed before the dietary challenge to capture usual dietary intake (repeated 24-hour recall), faecal microbiota (shallow shotgun sequencing) and to evaluate genetic polymorphisms using saliva samples (PCR analysis of selected penetrant single-nucleotide polymorphisms).Ethics and disseminationThe Lactobreath study has been approved by the Ethics Committee of the Canton of Zurich, Switzerland (#2023-01639). The project results will be published in open-access journals, presented at national and international conferences and communicated to the public and other relevant stakeholders via the communication channels of all investigators and partners. All results derived from the study will be accessible, in line with the Swiss National Science Foundation open access policy.Trial registration numberNCT06177938.

In humans the ability to digest milk lactose is conferred by a β-galactosidase enzyme called lactase-phlorizin hydrolase (LPH). While in some humans (approximately two-thirds of humankind) the levels of this enzyme decline drastically after the weaning phase (a trait known as lactase non-persistence (LNP)), some other individuals are capable of maintaining high levels of LPH lifelong (lactase persistence (LP)), thus being able to digest milk during adulthood. Both lactase phenotypes in humans present a complex genetic basis and have been widely investigated during the last decades. The distribution of lactase phenotypes and their associated single nucleotide polymorphisms (SNPs) across human populations has also been extensively studied, though not recently reviewed. All available information has always been presented in the form of static world maps or large dimension tables, so that it would benefit from the newly available visualization tools, such as interactive world maps. Taking all this into consideration, the aims of the present review were: (1) to gather and summarize all available information on LNP and LP genetic mechanisms and evolutionary adaptation theories, and (2) to create online interactive world maps, including all LP phenotype and genotype frequency data reported to date. As a result, we have created two online interactive resources, which constitute an upgrade over previously published static world maps, and allow users a personalized data exploration, while at the same time accessing complete reports by population or ethnicity.

BACKGROUND: Lactose intolerance (LI) is a common medical problem with limited treatment options. The primary symptoms are abdominal pain, diarrhea, bloating, flatulence, and cramping. Limiting dairy foods to reduce symptoms contributes to low calcium intake and the risk for chronic disease. Adaptation of the colon bacteria to effectively metabolize lactose is a novel and potentially useful approach to improve lactose digestion and tolerance. RP-G28 is novel galacto-oligosaccharide (GOS) being investigated to improve lactose digestion and the symptoms of lactose intolerance in affected patients. METHODS: A randomized, double-blind, parallel group, placebo-controlled study was conducted at 2 sites in the United States. RP-G28 or placebo was administered to 85 patients with LI for 35 days. Post-treatment, subjects reintroduced dairy into their daily diets and were followed for 30 additional days to evaluate lactose digestion as measured by hydrogen production and symptom improvements via a patient-reported symptom assessment instrument. RESULTS: Lactose digestion and symptoms of LI trended toward improvement on RP-G28 at the end of treatment and 30 days post-treatment. A reduction in abdominal pain was also demonstrated in the study results. Fifty percent of RP-G28 subjects with abdominal pain at baseline reported no abdominal pain at the end of treatment and 30 days post treatment (p = 0.0190). RP-G28 subjects were also six times more likely to claim lactose tolerance post-treatment once dairy foods had been re-introduced into their diets (p = 0.0389). CONCLUSIONS: Efficacy trends and favorable safety/tolerability findings suggest that RP-G28 appears to be a potentially useful approach for improving lactose digestion and LI symptoms. The concurrent reduction in abdominal pain and improved overall tolerance could be a meaningful benefit to lactose intolerant individuals. STUDY REGISTRATION: ClinicalTrials.gov NCT01113619 .

Most adverse reactions to food are patient self-reported and not based on validated tests but nevertheless lead to dietary restrictions, with patients believing that these restrictions will improve their symptoms and quality of life. We aimed to clarify the myths and reality of common food intolerances, giving clinicians a guide on diagnosing and treating these cases. We performed a narrative review of the latest evidence on the widespread food intolerances reported by our patients, giving indications on the clinical presentations, possible tests, and dietary suggestions, and underlining the myths and reality. While lactose intolerance and hereditary fructose intolerance are based on well-defined mechanisms and have validated diagnostic tests, non-coeliac gluten sensitivity and fermentable oligosaccharide, disaccharide, monosaccharide, and polyol (FODMAP) intolerance are mainly based on patients’ reports. Others, like non-hereditary fructose, sorbitol, and histamine intolerance, still need more evidence and often cause unnecessary dietary restrictions. Finally, the main outcome of the present review is that the medical community should work to reduce the spread of unvalidated tests, the leading cause of the problematic management of our patients.