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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medical nutrition therapy is the only accepted treatment for celiac disease. This paper summarizes a review of scientific studies using the gluten-free diet, nutritional risk factors, controversial elements of the diet, and its implementation in treating celiac disease. Treatment for celiac disease requires elimination of the storage proteins found in wheat, rye, and barley. The inclusion of oats and wheat starch is controversial. Research supports that oats may be acceptable for patients with celiac disease and can improve the nutritional quality of the diet. However, use of oats is not widely recommended in the United States because of concerns of potential contamination of commercial oats. Studies assessing the contamination of commercial oats are limited. Research indicates no differences in patients choosing a strict wheat starch-containing, gluten-free diet vs. a naturally gluten-free diet. Factors other than trace gluten may be the cause of continued villous atrophy in some patients. The impact of nutrient malabsorption caused from untreated celiac disease is well documented. The diet and gluten-free products are often low in B vitamins, calcium, vitamin D, iron, zinc, magnesium, and fiber. Few gluten-free products are enriched or fortified, adding to the risk of nutrient deficiencies. Patients newly diagnosed or inadequately treated have low bone mineral density, imbalanced macronutrients, low fiber intake, and micronutrient deficiencies. Also troubling is the increased incidence of obesity seen in persons with celiac disease following a gluten-free diet. Because of the nutritional risks associated with celiac disease, a registered dietitian must be part of the health care team that monitors the patient's nutritional status and compliance on a regular basis.
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PMID:Dietary guidelines and implementation for celiac disease. 1582 19

The article identifies 2 national healthcare problems that are occurring in the United States. The first national healthcare problem is obesity and the second is osteoporosis. What do these 2 healthcare problems have in common? They go hand in hand in teenagers and adults who have undergone weight reduction surgeries. These surgical procedures place a person at risk for osteoporosis because of the surgical procedure causing malabsorption that comes from the bypassing of the duodenum, which is the primary location for the absorption of calcium. This new high-risk population needs to become educated regarding osteoporosis and the treatment measures that can be instituted to prevent this disease. Osteoporosis is a disease where the bones of the body become very fragile and can easily break. Any bone can be affected by osteoporosis and fracture. There is no cure for osteoporosis but this disease can be controlled and prevented. This article discusses various treatment and prevention measures, ranging from dietary changes to the addition of medications.
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PMID:The effects of weight loss on calcium and bone. 1604 Dec 27

Surgery is not a cure for obesity but is an effective tool for limiting food consumption. If severely obese patients do not respond to a treatment plan that includes nutritional, exercise, and behavioral interventions plus antiobesity drugs, bariatric surgery may be appropriate. Proper diet selection after bariatric surgery involves more than the energy value and macronutrient composition. Adequate vitamin and mineral composition of the diet is essential to ensure that surgery improves nutritional status. Malabsorption is present to some extent with most surgeries. Therefore, diet after surgery should be monitored closely for adequacy by a nutritionist.
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PMID:Dietary and medical therapy of obesity. 1606 Oct 81

Antiobesity surgery largely is "behavioral surgery"--the results rely on behavioral factors more than on the technical performance of the procedure. Therefore, patient selection and pre- and postoperative patient education are critical for outcome. The operations rely on mechanical and biochemical mechanisms, such as: (1)limiting food consumption through restriction by activating satiety or nimiety; (2) increasing or decreasing appetitive gastrointestinal peptides; and (3) reducing substrate stores by way of malabsorption or increased thermogenesis to ensure weight loss. The balance between physiologic mechanisms that promote weight loss and motivational factors that cause maladaptive eating is the greatest challenge to effective surgical treatment of obesity.
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PMID:Patient selection and the physiology of gastrointestinal antiobesity operations. 1606 Oct 82

The United States Preventive Services Task Force has provided an evidence-based guideline indicating that bone mineral density (BMD) testing is appropriate for all women aged 65 or older. This does not preclude BMD testing in younger postmenopausal women but places the onus on the treating physician to justify the procedure to the patient and often the patient's insurance carrier. There are very few circumstances in which BMD testing is appropriate for healthy premenopausal women, but BMD testing in younger postmenopausal women is often appropriate: when there is a family history of osteoporosis with fracture, a personal history of fracture as an adult, and a medical, surgical or therapeutic history that might be associated with accelerated bone loss or increased risk of fracture. Medical conditions include intestinal diseases associated with malabsorption, such as non-tropical sprue, or primary hyperparathyroidism. Women who have neurologic conditions that increase the risk of falling should also be tested. There are data to suggest that patients with hemoglobinopathy are at increased risk for osteoporosis. Surgical conditions include the increasingly performed surgery for obesity and other surgery resulting in bowel resection (e.g., for inflammatory bowel disease). The major medication-related concern is corticosteroid therapy, but chronic or over-treatment with thyroxine, and chronic heparin therapy, should also be considered risk factors for osteoporosis. When performing a BMD test for the first time, it is essential to remember that 50% of women at menopause will have a negative T-score, but this does not imply that the patient has indeed lost any bone from her peak bone mass.
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PMID:Is BMD testing appropriate for all menopausal women? 1633 12

Vitamin D3 is synthesized in the skin during summer under the influence of ultraviolet light of the sun, or it is obtained from food, especially fatty fish. After hydroxylation in the liver into 25-hydroxyvitamin D (25(OH)D) and kidney into 1,25-dihydroxyvitamin D (1,25(OH)2D), the active metabolite can enter the cell, bind to the vitamin D-receptor and subsequently to a responsive gene such as that of calcium binding protein. After transcription and translation the protein is formed, e.g. osteocalcin or calcium binding protein. The calcium binding protein mediates calcium absorption from the gut. The production of 1,25(OH)2D is stimulated by parathyroid hormone (PTH) and decreased by calcium. Risk factors for vitamin D deficiency are premature birth, skin pigmentation, low sunshine exposure, obesity, malabsorption and advanced age. Risk groups are immigrants and the elderly. Vitamin D status is dependent upon sunshine exposure but within Europe, serum 25(OH)D levels are higher in Northern than in Southern European countries. Severe vitamin D deficiency causes rickets or osteomalacia, where the new bone, the osteoid, is not mineralized. Less severe vitamin D deficiency causes an increase of serum PTH leading to bone resorption, osteoporosis and fractures. A negative relationship exists between serum 25(OH)D and serum PTH. The threshold of serum 25(OH)D, where serum PTH starts to rise is about 75nmol/l according to most surveys. Vitamin D supplementation to vitamin D-deficient elderly suppresses serum PTH, increases bone mineral density and may decrease fracture incidence especially in nursing home residents. The effects of 1,25(OH)2D and the vitamin D receptor have been investigated in patients with genetic defects of vitamin D metabolism and in knock-out mouse models. These experiments have demonstrated that for active calcium absorption, longitudinal bone growth and the activity of osteoblasts and osteoclasts both 1,25(OH)2D and the vitamin D receptor are essential. On the other side, bone mineralization can occur by high ambient calcium concentration, so by high doses of oral calcium or calcium infusion. The active metabolite 1,25(OH)2D has its effects through the vitamin D receptor leading to gene expression, e.g. the calcium binding protein or osteocalcin or through a plasma membrane receptor and second messengers such as cyclic AMP. The latter responses are very rapid and include the effects on the pancreas, vascular smooth muscle and monocytes. Muscle cells contain vitamin D receptor and several studies have demonstrated that serum 25(OH)D is related to physical performance. The active metabolite 1,25(OH)2D has an antiproliferative effect and downregulates inflammatory markers. Extrarenal synthesis of 1,25(OH)2D occurs under the influence of cytokines and is important for the paracrine regulation of cell differentiation and function. This may explain that vitamin D deficiency can play a role in the pathogenesis of auto-immune diseases such as multiple sclerosis and diabetes type 1, and cancer. In conclusion, the active metabolite 1,25(OH)2D has pleiotropic effects through the vitamin D receptor and vitamin D responsive elements of many genes and on the other side rapid non-genomic effects through a membrane receptor and second messengers. Active calcium absorption from the gut depends on adequate formation of 1,25(OH)2D and an intact vitamin D receptor. Bone mineralization mainly depends on ambient calcium concentration. Vitamin D metabolites may play a role in the prevention of auto-immune disease and cancer.
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PMID:Vitamin D physiology. 1656 71

Bariatric surgery is an effective treatment for patients with clinically severe obesity. In addition to significant weight loss, it is also associated with improvements in comorbidities. Unfortunately, bariatric surgery also has the potential to cause a variety of nutritional and metabolic complications. These complications are mostly due to the extensive surgically induced anatomical changes incurred by the patient's gastrointestinal tract, particularly with roux-en-Y gastric bypass and biliopancreatic diversion. Complications associated with vertical banded gastroplasty are mostly due to decreased intake amounts of specific nutrients. Macronutrient deficiencies can include severe protein-calorie malnutrition and fat malabsorption. The most common micronutrient deficiencies are of vitamin B12, iron, calcium, and vitamin D. Other micronutrient deficiencies that can lead to serious complications include thiamine, folate, and the fat-soluble vitamins. Counseling, monitoring, and nutrient and mineral supplementation are essential for the treatment and prevention of nutritional and metabolic complications after bariatric surgery.
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PMID:Nutritional and metabolic complications of bariatric surgery. 1661 38

Bariatric surgery for the treatment of morbid obesity or overweight refractory to medical therapy was born at the beginning of second half of the twentieth century, and its first steps were uncertain and with a not jet well definite purpose. In fact the main result to be pursued seemed to be simply the reduction of body weight, and any change of anatomy of the digestive tract able to reduce the absorbtion of nutrients was judged adequate. But very early the adverse consequences of malabsorption so obtained became evident, and other operations possibly free from those complications were devised and clinically tested. So aside the by-pass operations many other surgical procedures found their room, all of them aiming to fight the ever more diffuse obesity of the people. This historical review of the various surgical procedures attempted in these last sixty years for morbid obesity is very interesting for a better understanding of the problem and to have a solid basis for future rational choices.
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PMID:[History and pathophysiologic analysis of the various techniques in bariatric surgery]. 1669 15

Peptide YY (PYY) is secreted as a 36 amino acid, straight chain polypeptide, and is found in greatest concentrations in the terminal ileum, colon and rectum. After secretion, dipeptidyl peptidase IV (DPP-IV) cleaves the N-terminal Tyrosine-Proline residues from PYY(1-36), producing PYY(3-36). PYY(1-36) acts at all four human Y receptors, Y1, Y2, Y4 and Y5, while PYY(336) is a specific Y2 receptor agonist. PYY participates in the regulation of appetite and weight balance through hypothalamic-based mechanisms. PYY(1-36) stimulates appetite and weight gain through Y1 and Y5 receptors. PYY(3-36) suppresses appetite and stimulates weight loss through Y2 receptors. GI diseases that cause malabsorption increase both basal and meal-stimulated PYY levels. In contrast, obesity decreases both basal and meal-stimulated PYY levels. Mutations in the human PYY and Y2 receptor genes may contribute to the development of obesity. Small bowel resection elevates PYY levels in humans. Colon resections increase PYY levels in animal models but not in man. PYY changes following bariatric operations are incompletely studied. Vertical banded gastroplasty, open Roux-en-Y gastric bypass and jejunoileal bypass significantly elevate basal and meal-stimulated PYY levels. In dogs with Pavlov pouches, Roux-en-Y duodenojejunostomy (duodenal switch) increases PYY levels compared to Roux-en-Y gastrojejunostomy. DPP-IV activity is increased in obese individuals and remains increased after biliopancreatic diversion. Thus, diseases or operations which cause malabsorption, elevate basal and meal-stimulated PYY levels. Bariatric operations also increase basal and meal-stimulated PYY levels. This suggests that the combination of increased PYY levels and elevated levels of DPP-IV observed after bariatric operations may generate increased circulating levels of PYY(3-36), leading to hypothalamic-mediated suppression of appetite and promotion of weight loss through Y2 receptor mediated mechanisms.
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PMID:Peptide YY(1-36) and peptide YY(3-36): Part II. Changes after gastrointestinal surgery and bariatric surgery. 1675 46

Despite dramatically increased research efforts to discover cures for the rising health issue of obesity, bariatric (obesity) surgery remains the most effective treatment. Obese people and especially those classified as morbidly obese often suffer from associated co-morbid conditions such as type-II diabetes. In most cases, bariatric surgery results in rapid and sustained decreases in excess body weight. Recent reports have identified significant improvements in glucose homeostasis after surgery that are coincident and often precedent to any measurable weight loss. These studies suggest an inhibition or enhancement of a "factor" within the intestinal tract that improves glycemia independent of body fat stores. These observations have sparked renewed investigation into the mechanisms underlying successful obesity surgeries such as gastric bypass. It is becoming increasingly clear that restriction and malabsorption are not the only two mechanisms important for inducing long-term weight loss or the improvements in diabetes. Investigating the hypothesis that the distal intestine (ileum) holds additional answers into a third mechanism, I used the model of ileal transposition to help identify endocrine changes in the gut following obesity surgery. This review will explore the model of ileal transposition and speculate on its usefulness as a tool to dissect out additional mechanisms underlying effective obesity surgeries. Also discussed will be the ileal-produced hormone glucagon-like peptide and its role in mediating the improvements in diabetes and weight loss after bariatric surgery.
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PMID:Ileal transposition provides insight into the effectiveness of gastric bypass surgery. 1678 38


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