Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
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A total of 2484 newly detected metabolic bone diseases during the past 17 years comprised 79.67% cases of osteoporoses and 20.33% of osteomalacia. The group of osteoporoses included 325 patients (16.43%) with the primary form of the disease, in 1654 patients (83.57%) a cause of decalcification of bones (secondary form) was found. With advancing time the number of secondary osteoporoses rises steadily, while the number of primary cases remains at the same level. In the aetiology of demineralization a major part was played by lactose intolerance, maldigestion and malabsorption, idiopathic, hypercalciuria, diabetes and steroids. The female: male ratio in primary osteoporoses was 4.71:1 and in secondary osteoporoses 2.35:1. Primary osteomalacia was recorded in 113 patients (22.38%) and secondary in 392 (77.62%). Here too with advancing time the number of secondary forms is increasing. The largest groups are hepatic and renal affections, smaller ones malabsorption and antiepileptic drugs. The female: male ratio in primary osteomalacia is 2.13:1 and in secondary osteomalacia 2.26:1. With the development of knowledge on the aetiopathogenesis of bone demineralizations we expect in future a further increase of secondary forms of the disease at the expanse of primary ones.
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PMID:[Secondary osteopenia]. 228 20

Since the establishment of a new social order in 1949, China's attempts to feed and nurture its large population has been a topic of serious study in many disciplines. This review focuses on dietary sources of Chinese population and incidence, increase and decline of important diet related health disorders in China during the last four decades. Literature published since 1949 on goiter, rickets, riboflavin deficiency, beri beri, vision impairment, favism, cancer, atherosclerosis and coronary heart disease, hypertension, dental and smoking related diseases, diabetes mellitus, pancreatitis, lactose intolerance, mineral deficiency, Kashin-Beck disease, parasitic diseases and genetic disorders are reviewed. Also presented selectively are reports related to ethnodietetics, health care, maternal health and pediatric care as well as longevity. In the 1980s, total caloric intake of Chinese population showed a 19% increase on a daily basis from that of late 1940s. In overall terms, plant derived foods supplied 93% of energy, 87% of protein and 55% of fat to the Chinese. Among the animal foods, pork remains the most common and least expensive form of meat, contributing more than 90% of China's total meat production excluding poultry and fish. In 1949, the life expectancy in China was only 36 years. In early 1980s, it has increased to 68 years. This increase in life expectancy is attributed mostly to improved nutrition and lowering of mortality due to decrease in infectious diseases. Though population, disease and mortality statistics of modern China are spotty and sometimes questionable, common consensus among the researchers is that since 1949 the public health situation in China has improved tremendously.
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PMID:Nutrition and health in China, 1949 to 1989. 229 45

90 patients with chronic diarrhoea underwent this prospective study. They were seen in a private hospital of Lima during 1990 and 1991. According to a methodologic plan for determining sources and the diseases that originate chronic diarrhoea. In all patients hematologic, bioquimic, coprocultures, coproparasitologic exams were done, chest and intestinal transit X-rays. All underwent duodenal content culture. Colon X-ray in 25 cases; proctosigmoidoscopy in 14 and upper digestive endoscopy in 19 patients. Abdominal echography in 12 and TAC in 2 cases. The final results showed as determinant diseases for chronic diarrhoea, according to their frequency: enteroparasitosis (23.3%), functional digestive disorders (20.0%), intestinal bacterial overpopulation (15.5%) of unknown origin (8.8%), colon diverticulus (7.7%) proven and probably (5.5%), lactose intolerance (3.3%), diabetes mellitus (2.2%), and in one case (1.1%) the following: intestinal linfoma, pancreas malignancy, AIDS, colonic and deformation and megaloblastic anemia. The causes of chronic diarrhoea are several and multifactorals and in this study we prove the preeminence of the intestinal parasitosis, functional disorders and intestinal bacterial overpopulation and with less frequency other pathologies.
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PMID:[Clinical and etiologic study of 90 cases of chronic diarrhea]. 821 99

Celiac disease is a permanent intolerance to ingested gluten that results in immunologically mediated inflammatory damage to the small-intestinal mucosa. Celiac disease is associated with both human leukocyte antigen (HLA) and non-HLA genes and with other immune disorders, notably juvenile diabetes and thyroid disease. The classic sprue syndrome of steatorrhea and malnutrition coupled with multiple deficiency states may be less common than more subtle and often monosymptomatic presentations of the disease. Diverse problems such as dental anomalies, short stature, osteopenic bone disease, lactose intolerance, infertility, and nonspecific abdominal pain among many others may be the only manifestations of celiac disease. The rate at which celiac disease is diagnosed depends on the level of suspicion for the disease. Although diagnosis relies on intestinal biopsy findings, serologic tests are useful as screening tools and as an adjunct to diagnosis. The treatment of celiac disease is lifelong avoidance of dietary gluten. Gluten-free diets are now readily achievable with appropriate professional instruction and community support. Both benign and malignant complications of celiac disease occur but these can often be avoided by early diagnosis and compliance with a gluten-free diet.
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PMID:The widening spectrum of celiac disease. 1007 17

A staggering 4000 million people cannot digest lactose, the sugar in milk, properly. All mammals, apart from white Northern Europeans and few tribes in Africa and Asia, lose most of their lactase, the enzyme that cleaves lactose into galactose and glucose, after weaning. Lactose intolerance causes gut and a range of systemic symptoms, though the threshold to lactose varies considerably between ethnic groups and individuals within a group. The molecular basis of inherited hypolactasia has yet to be identified, though two polymorphisms in the introns of a helicase upstream from the lactase gene correlate closely with hypolactasia, and thus lactose intolerance. The symptoms of lactose intolerance are caused by gases and toxins produced by anaerobic bacteria in the large intestine. Bacterial toxins may play a key role in several other diseases, such as diabetes, rheumatoid arthritis, multiple sclerosis and some cancers. The problem of lactose intolerance has been exacerbated because of the addition of products containing lactose to various foods and drinks without being on the label. Lactose intolerance fits exactly the illness that Charles Darwin suffered from for over 40 years, and yet was never diagnosed. Darwin missed something else--the key to our own evolution--the Rubicon some 300 million years ago that produced lactose and lactase in sufficient amounts to be susceptible to natural selection.
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PMID:The molecular basis of lactose intolerance. 1680 12

Current nutrition recommendations, directed towards populations, are based on estimated average nutrient requirements for a target population and intend to meet the needs of most individuals within that population. They also aim at preventing common diseases such as obesity, diabetes and cardiovascular disease. For infants with specific genetic polymorphisms, e.g. some inborn errors of metabolism, adherence to current recommendations will cause disease symptoms and they need personalized nutrition recommendations. Some other monogenic polymorphisms, e.g. adult hypolactasia, are common but with varying prevalence between ethnic groups and within populations. Ages at onset as well as the degree of the resulting lactose intolerance also vary, making population-based as well as personalized recommendations difficult. The tolerable intake is best set by each individual based on symptoms. For polygenetic diseases such as celiac disease, type-1 diabetes and allergic disease, current knowledge is insufficient to suggest personalized recommendations aiming at primary prevention for all high-risk infants, although it may be justified to provide such recommendations on an individual level should the parents ask for them. New technologies such as nutrigenetics and nutrigenomics are promising tools with which current nutrition recommendations can possibly be refined and the potential of individualized nutrition be explored. It seems likely that in the future it will be possible to offer more subgroups within a population personalized recommendations.
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PMID:Do we need personalized recommendations for infants at risk of developing disease? 1862 4

Probiotics are live organisms that are primarily used to improve gastrointestinal disorders such as diarrhea, irritable bowel syndrome, constipation, lactose intolerance, and to inhibit the excessive proliferation of pathogenic intestinal bacteria. However, recent studies have suggested that probiotics could have beneficial effects beyond gastrointestinal health, as they were found to improve certain metabolic disorders such as hypertension. Hypertension is caused by various factors and the predominant causes include an increase in cholesterol levels, incidence of diabetes, inconsistent modulation of renin and imbalanced sexual hormones. This review discusses the antihypertensive roles of probiotics via the improvement and/or treatment of lipid profiles, modulation of insulin resistance and sensitivity, the modulation of renin levels and also the conversion of bioactive phytoestrogens as an alternative replacement of sexual hormones such as estrogen and progesterone.
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PMID:The improvement of hypertension by probiotics: effects on cholesterol, diabetes, renin, and phytoestrogens. 1986 17

A staggering 4000 million people cannot digest lactose, the sugar in milk, properly. All mammals, apart from white Northern Europeans and few tribes in Africa and Asia, lose most of their lactase, the enzyme that cleaves lactose into galactose and glucose, after weaning. Lactose intolerance causes gut and a range of systemic symptoms, though the threshold to lactose varies considerably between ethnic groups and individuals within a group. The molecular basis of inherited hypolactasia has yet to be identified, though two polymorphisms in the introns of a helicase upstream from the lactase gene correlate closely with hypolactasia, and thus lactose intolerance. The symptoms of lactose intolerance are caused by gases and toxins produced by anaerobic bacteria in the large intestine. Bacterial toxins may play a key role in several other diseases, such as diabetes, rheumatoid arthritis, multiple sclerosis and some cancers. The problem of lactose intolerance has been exacerbated because of the addition of products containing lactose to various foods and drinks without being on the label. Lactose intolerance fits exactly the illness that Charles Darwin suffered from for over 40 years, and yet was never diagnosed. Darwin missed something else--the key to our own evolution--the Rubicon some 300 million years ago that produced lactose and lactase in sufficient amounts to be susceptible to natural selection.
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PMID:The molecular basis of lactose intolerance. 1996 Aug 66

Crohn's disease (CD) is a well known chronic pathological condition whose aetiology has remained unrecognized for nearly a century. Complex immune mechanisms in a specific genetic background causing an abnormal local inflammatory response are thought to be directly responsible for the clinical picture, but no external factor triggering such host responses has been identified. Humans lose the capability of breaking down milk lactose early in life and, afterwards, ingestion of large amounts of lactose causes a transient digestive illness known as lactose intolerance. Some human populations developed mutations for lactase persistence in adulthood that allowed better exploiting a product, milk, from not food-competitive domesticated species. This adaptation to dairy farming could have had as a collateral effect the exposure of human populations to a ruminant parasite with the ability to cause chronic inflammation in the intestine. Humans with a genetic susceptibility might develop a similar inflammatory disease caused by a defect in a highly conserved innate immunity mechanism. Data from different published sources regarding by country CD and type I diabetes incidence, lactose intolerance, livestock population, food production, Gross National Income and human population were submitted to Pearson and Kendall correlation, multiple regression and principal components analyses. Multiple regressions were also applied to a published 20-year time series for CD incidence in Japan. These analyses showed a strong association between country incidence of CD and frequency of lactase persistence as well as other ruminant production and consumption variables that further supports the meaning of those observations. Association of these variables with higher per capita income suggests that IBD incidence would be a side-effect of an otherwise highly successful adaptation. The evolutionarily plausible framework provided by this association with the species suffering a similar inflammatory bowel disease (IBD), its coincidence with the expanse of a cattle breed that could act as a Trojan horse, in addition to recent microbiological, immunological and therapeutical observations consistent with a slow infection type of pathogenesis, supports a mycobacterial aetiology of human IBD. Further research challenging the hypothesis of a shared aetiology by Mycobacterium avium subsp. paratuberculosis of human and ruminant IBD by increasing research on the pathogenesis of the latter and focusing on effective specific antibiotic or immune aetiological therapies seems to be the obvious next step. Either confirmation or rejection of the hypothesis presented here should create new knowledge that will bring closer the eradication of a cause of human and animal suffering.
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PMID:Crohn's disease and ruminant farming. Got lactase? 2045 31

Cardiovascular diseases are one of the major causes of deaths in adults in the western world. Elevated levels of certain blood lipids have been reported to be the principal cause of cardiovascular disease and other disabilities in developed countries. Several animal and clinical trials have shown a positive association between cholesterol levels and the risks of coronary heart disease. Current dietary strategies for the prevention of cardiovascular disease advocate adherence to low-fat/low-saturated-fat diets. Although there is no doubt that, in experimental conditions, low-fat diets offer an effective means of reducing blood cholesterol concentrations on a population basis, these appear to be less effective, largely due to poor compliance, attributed to low palatability and acceptability of these diets to the consumers. Due to the low consumer compliance, attempts have been made to identify other dietary components that can reduce blood cholesterol levels. Supplementation of diet with fermented dairy products or lactic acid bacteria containing dairy products has shown the potential to reduce serum cholesterol levels. Various approaches have been used to alleviate this issue, including the use of probiotics, especially Bifidobacterium spp. and Lactobacillus spp.. Probiotics, the living microorganisms that confer health benefits on the host when administered in adequate amounts, have received much attention on their proclaimed health benefits which include improvement in lactose intolerance, increase in natural resistance to infectious disease in gastrointestinal tract, suppression of cancer, antidiabetic, reduction in serum cholesterol level, and improved digestion. In addition, there are numerous reports on cholesterol removal ability of probiotics and their hypocholesterolemic effects. Several possible mechanisms for cholesterol removal by probiotics are assimilation of cholesterol by growing cells, binding of cholesterol to cellular surface, incorporation of cholesterol into the cellular membrane, deconjugation of bile via bile salt hydrolase, coprecipitation of cholesterol with deconjugated bile, binding action of bile by fibre, and production of short-chain fatty acids by oligosaccharides. The present paper reviews the mechanisms of action of anti-cholesterolemic potential of probiotic microorganisms and probiotic food products, with the aim of lowering the risks of cardiovascular and coronary heart diseases.
Exp Diabetes Res 2012
PMID:Cholesterol-lowering probiotics as potential biotherapeutics for metabolic diseases. 2261 76


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