Active clinical trials for "Lactose Intolerance"

The goal of this study was to examine the effects of self-perceived lactose intolerance (SPLI) as it relates to calcium intake and specific health problems that have been attributed to reduced intake of calcium and foods from the dairy group in a nationally representative multi-ethnic sample of adults.

Most people are born with the ability to digest lactose, a dissacharide consisting of β-D-glucose and β-D-galactose, because of the presence of lactase at the brush border of the small intestine. In about 75% of the world population the activity of this enzyme decreases after weaning (primary hypolactasia or lactase-nonpersistence), resulting in incomplete digestion of lactose and lactose malabsorption in adulthood (1). Secondary forms of lactose malabsorption may be due to inflammation or functional loss of the intestinal mucosa such as celiac disease, infectious enteritis or Crohn's disease. Very rarely, lactase deficiency is congenital due to an autosomal recessive genetic disorder, preventing lactase expression from birth (2). Whereas some people with lactose malabsorption are asymptomatic, most lactose-nonpersisters experience symptoms like abdominal pain, bloating, excess flatulence or diarrhea. Lactose intolerance refers to the syndrome of having one or more symptoms after consumption of lactose-containing food (3). At present, the origin of the symptoms of lactose-intolerance is not well understood. Several studies have indicated a poor correlation between lactose maldigestion and symptoms of lactose intolerance (4). In a study by Vonk et al. (2003), lactose intolerant subjects with severe symptoms (diarrhea) and intolerant subjects with only mild symptoms (without diarrhea) did not differ in degree of lactose digestion in the small intestine indicating a similar lactase activity and leading them to the hypothesis of a "colon resistence factor" (5). It was suggested that the colonic processing of maldigested lactose may play a role in the symptoms experienced by lactose intolerant patients. When lactose is malabsorbed and enters the colon, it is rapidly fermented by the resident microbiota into a variety of metabolites including lactate, formate, succinate and short chain fatty acids (SCFA, acetate, propionate, butyrate) as well as gases (H2, CO2 and CH4). When incubating fecal samples from lactose-tolerant and intolerant subjects with lactose, the samples from the lactose-intolerant subjects showed faster production rates of D- and L-lactate, acetate, propionate and butyrate, as compared to tolerant subjects (6). Although the colon is thought to possess a high capacity to absorb SCFA, it was hypothesized that a temporary accumulation of these metabolites due to rapid fermentation of maldigested lactose could be responsible for abdominal pain, excess flatulence and bloating (7;8). Possible mechanisms proposed to explain how SCFA might induce symptoms included an increase in the osmotic load that draws fluid to the colonic lumen, changes in colonic motility and an increased colonic sensitivity (9-11). However, the calculated amount of fluid drawn in the colon is unlikely to cause symptoms considering the high water absorbing capacity of the colon and the effect of SCFA on colonic motility and colonic sensitivity have only been observed in rats and not in humans. More recently, Campbell et al. introduced the bacterial metabolic toxin hypothesis, stating that also other bacterial metabolites, such as alcohols, aldehydes, acids and ketones, resulting from carbohydrate fermentation play a role in the pathogenesis of lactose-intolerance. These metabolites might inhibit bacterial growth and affect eukaryotic cells (12). In our own previous studies in which we related colonic fermentation patterns to parameters of cytotoxicity, we identified compounds like propionic acid, medium chain fatty acids, 1-octanol and heptanal as more prevalent in the most cytotoxic samples (13), supporting the hypothesis of Campbell et al. Therefore, it seems necessary to include not only SCFA, but also other metabolites, in the investigation of the pathogenesis of lactose intolerance. Differences in fermentation patterns might be associated with differences in the composition and/or activity of the intestinal microbiota. Evidence on the potential role of the colonic microbiota in lactose intolerance is very limited. Total bacterial numbers were not significantly different between 16 intolerant and 11 tolerant lactose maldigesters although a negative correlation between total bacteria and symptom score was found (14). Similarly, the composition of fecal microbiota was not different between 5 intolerant and 7 tolerant subjects (6).

The purpose of this study is to assess that two β-galactosidase Producing Probiotic Strains help improve lactose digestion in subjects with lactose maldigestion.

The purpose of this study is to determine if twice or three times daily supplementation of Lactobacillus acidophilus MPH734 (Lacto-FreedomTM, or LF), for one week, affects acute (immediate), subacute (7 days), and post-treatment discontinuation (30-, 60-, and 90- day) lactose metabolism, gastrointestinal symptoms, and clinical markers of inflammation and safety compared to a placebo.

It is currently assumed that all patients are lactose intolerant post bone marrow transplantation. This pilot study is to assess what the incidence of lactose intolerance is after bone marrow transplantation in children. This will be done using a lactose breath test.

Lactase is high in the newborn intestine, allowing him to digest the high amounts of lactose present in breastmilk. From weaning, lactase is genetically programmed to decrease, reaching residual levels in the adult. This situation occurs in 75% of the world population and is known as "adult primary hypolactasia" while the remaining 25% is "lactase persistent" i.e. maintains in adulthood lactase values similar to these of newborns. In subjects with hypolactasia, the intake of milk products can produce digestive symptoms, making that the affected individuals spontaneously reduce the consumption of these products and, therefore, their intake of calcium and proteins. In addition to lactose-free milk and exogenous lactase, a strategy for the intolerant subjects to continue consuming dairy products is, for example, to consume yogurt, due to the fact that the lactase of the yogurt bacteria continues to function in the intestine of the consumer, hydrolyzing lactose and decreasing the development of digestive symptoms. Similarly, many probiotic strains, such as L. acidophilus NCFM, L. casei CRL431, B. longum 401 and B. bifidum Orla Jensen 1424, express β-galactosidases that hydrolyze lactose, preventing its fermentation and the production of gases. The acute administration of these strains improves lactose tolerance. In addition, a recent study reported that dietary supplementation of intolerant subjects for 4 weeks with L. casei Shirota and B. breve Yakult reduced digestive symptoms and breath hydrogen excretion not only at the end of the period of administration of the probiotics but also 3 months after having discontinued the use of probiotics. Based on this background, the aim of this study is to determine whether the regular consumption of an ice cream with the strain B. bifidum 900791 improves lactose intolerance in hypolactasic subjects, even after the suspension of the consumption of the product. To determine if this effect is due to the adaptation of the microbiota, the investigators will also evaluate changes in the composition of the microbiota and the generation of volatile fatty acids.

Lactose is a carbohydrate found in milk,and Lactase Deficiency (LD) is a condition in which the small intestine cannot digest this carbohydrate due to absent or insufficient amounts of lactase.Individuals with LD may be intolerant of lactose in the diet and experience abdominal cramps, bloating and diarrhea; however the response is variable.Some tolerate moderate amounts of lactose without adverse effect,whereas others experience severe symptoms in response to even small doses. These problems may be representative of wider issues regarding individual tolerance to diet containing ubiquitous poorly absorbed, fermentable carbohydrates (such as: fructose, fructans)and be relevant to symptom generated in patients with diarrhea predominant irritable bowel syndrome (D-IBS). This project will investigate the effects of diet,lifestyle stress and psychiatric dietary on the development of functional gastrointestinal symptoms. Lactose will be used to assess tolerance to dietary challenge, a test that is particularly relevant in a Chinese population with a high prevalence of lactase deficiency.

The hypothesis underlying this study is that failure to recognise the role of lactose intolerance among patients with ulcerative colitis has led to inappropriate dietary advice and treatment with drugs that contain lactose as a filler. These failures exacerbate symptoms and lead to the unnecessary use of immune suppressant drugs. There is disagreement amongst researchers regarding the amount of lactose needed to cause symptoms in those who are lactose intolerance. The general consensus is that the amount of lactose in a glass of milk (12 grams) is enough to cause mild symptoms in most patients who are lactose intolerant (1). However, there have been a number of studies and case studies that argue that much lower amounts can cause symptoms (2, 3, 4, 5). This could be as little as 0.02 grams (6). Ulcerative colitis is a chronic relapsing inflammatory disease of the colon and rectum, characterised by recurrent episodes of abdominal pain and profuse diarrhoea. The prevalence of lactose intolerance in patients with ulcerative colitis is not greater than in the general population, but there is no evidence as to whether these patients are more sensitive to lactose. This study will identify the threshold at which symptoms of lactose intolerance develop in those who have both lactose intolerance and ulcerative colitis, to provide appropriate advice and treatment in the management of patients with these conditions.

Bloating, gas, pain and diarrhea are common complaints. Routine investigations are negative; these patients are labeled as IBS. In these patients, whether testing for carbohydrate malabsorption or small intestinal bacterial overgrowth (SIBO) is useful is unclear. Investigators aim to assess the prevalence of SIBO, fructose and lactose intolerance, the usefulness of breath tests, and predictive value of pre-test symptoms.

The hypothesis underlying this study is that failure to recognise the role of lactose intolerance among patients has led to inappropriate dietary advice and treatment with drugs that contain lactose as a filler. These failures exacerbate symptoms and lead to the unnecessary use of immune suppressant drugs. This study will identify the threshold at which symptoms of lactose intolerance develop, to provide appropriate advice and treatment in the management of patients.