Welston Court Science Center

Pembrokeshire, United Kingdom

Welston Court Science Center

Pembrokeshire, United Kingdom

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Campbell A.K.,University of Cardiff | Matthews S.B.,Welston Court Science Center | Vassel N.,University of Cardiff | Cox C.D.,University of Cardiff | And 5 more authors.
Toxicology | Year: 2010

Lactose and food intolerance cause a wide range of gut and systemic symptoms, including gas, gut pain, diarrhoea or constipation, severe headaches, severe fatigue, loss of cognitive functions such as concentration, memory and reasoning, muscle and joint pain, heart palpitations, and a variety of allergies (Matthews and Campbell, 2000; Matthews et al., 2005; Waud et al., 2008). These can be explained by the production of toxic metabolites from gut bacteria, as a result of anaerobic digestion of carbohydrates and other foods, not absorbed in the small intestine. These metabolites include alcohols, diols such as butan 2,3 diol, ketones, acids, and aldehydes such as methylglyoxal (Campbell et al., 2005, 2009). These 'toxins' induce calcium signals in bacteria and affect their growth, thereby acting to modify the balance of microflora in the gut (Campbell et al., 2004, 2007a,b). These bacterial 'toxins' also affect signalling mechanisms in cells around the body, thereby explaining the wide range of symptoms in people with food intolerance. This new mechanism also explains the most common referral to gastroenterologists, irritable bowel syndrome (IBS), and the illness that afflicted Charles Darwin for 50 years (Campbell and Matthews, 2005a,b). We propose it will lead to a new understanding of the molecular mechanism of type 2 diabetes and some cancers. © 2010 Elsevier Ireland Ltd.


Berrill J.W.,University of Cardiff | Gallacher J.,University of Cardiff | Hood K.,University of Cardiff | Green J.T.,University of Cardiff | And 3 more authors.
Neurogastroenterology and Motility | Year: 2013

Background: Irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) are associated with several risk factors for developing cognitive impairment. These include altered cytokine levels, concurrent mood disorders, and the presence of chronic pain. This observational study aimed to explore the cognitive profile of patients with these conditions. Methods: Participants completed the Cardiff Cognitive Battery, a series of computerized neuropsychological performance tests that examine a range of cognitive function including psychomotor speed, memory, and intelligence. A progressive analysis of covariance model was used with demographic details, anxiety and depression scores entered as covariates. Fecal calprotectin levels were measured in IBD patients to determine disease activity. Key Results: In total 231 participants were recruited (150 IBD patients, 40 IBS patients, and 41 healthy controls). IBD patients had significantly lower scores on fluid (p = 0.01) and crystalline intelligence tests (p = 0.028) compared to healthy volunteers, however, this reflected differences in concurrent mood disorder and level of education. When these factors were added as covariates, there was no significant difference between the groups. Duration and activity of disease did not affect cognitive function in IBD patients. Severity of symptoms had no impact on cognition in patients with IBS. Conclusions & Inferences: The results of this observational study do not support the hypothesis that IBS or IBD have an intrinsic disease process that is associated with cognitive dysfunction. It is possible that concurrent mood disorders, in particular depression, may affect the cognitive performance of patients with IBD in specific tasks. © 2013 John Wiley & Sons Ltd.


Campbell A.K.,University of Cardiff | Campbell A.K.,Welston Court Science Center | Matthews S.B.,University of Cardiff | Matthews S.B.,Welston Court Science Center
Biological Journal of the Linnean Society | Year: 2015

While waiting in lodgings to join H.M.S. Beagle just before Christmas 1831, Charles Darwin suffered chest pain and heart palpitations. On his return to England he began to suffer from a range of gut problems and systemic symptoms around the body, which were to plague him for the rest of his life. At least 40 conditions have been proposed to explain Darwin's illness, which left him disabled, sometimes for weeks on end. Here we show that lactose and food intolerance is the only condition that explains all his symptoms. Furthermore, there is now a molecular basis to account for these, based on metabolic toxins produced by microbes in the intestine. This mechanism has important implications in several other diseases, including diabetes, inflammatory bowel disease, Parkinson's disease and some cancers. Lactose intolerance also has fascinating things to tell us about molecular evolution - the origin of lactose, the unique sugar in milk; why white humans were able to invade the plains of Europe after the last ice thaw, some 10 000 years ago; and one of the most intriguing problems in evolution - the origin of a new enzyme such as lactase, the enzyme responsible for cleaving lactose into its constituents monosaccharides, galactose and glucose. © 2015 The Linnean Society of London.


Eadala P.,Morriston Hospital | Matthews S.B.,Welston Court Science Center | Waud J.P.,University of Wales | Waud J.P.,University of Cardiff | And 3 more authors.
Alimentary Pharmacology and Therapeutics | Year: 2011

Background Sensitivity to lactose has been reported in Crohn's disease, but its true role in inflammatory bowel disease (IBD) is unclear. The genetic marker CC13910, on chromosome2, with measurement of breath hydrogen and methane, and gut and systemic symptoms, are now the most comprehensive tests for evaluating sensitivity to lactose. Aim To investigate, for the first time, the prevalence of lactose sensitivity in IBD, using the most comprehensive tests for diagnosing this condition. Methods Prevalence of CC13910 genotype was investigated using RT-PCR in 165 patients (Crohn's disease = 70, ulcerative colitis = 95), and 30 healthy volunteers. Genotype was correlated with breath hydrogen and methane up to 6 h after 50 g of oral lactose, all symptoms being recorded for up to 48 h. Critically, Crohn's disease and ulcerative colitis patients were selected with no record of lactose sensitivity, in remission at the time of the test. Results Lactose sensitivity occurred in a much higher proportion of patients, (approximately 70%), with IBD than previously thought. Seventeen per cent had raised methane, without raised breath hydrogen; those with ulcerative colitis exhibiting most symptoms. All CC patients were lactose sensitive. There was no correlation between genetic phenotype and IBD. As substantial numbers of IBD patients were CT or TT, and were lactose sensitive, this polymorphism cannot explain full down-regulation of the lactase gene. Conclusions Our results have implications for the clinical management of IBD. The high breath methane raised the possibility of a pathogenic role for methanogenic archaebacteria (Archaea) in IBD. This needs to be investigated. © 2011 Blackwell Publishing Ltd.

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