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PubMed1983

Nutritional disturbances in Crohn's disease.

A wide range of nutritional disturbances may be found in patients with Crohn's disease. As more sophisticated tests become available to measure vitamin and trace element deficiencies, so these are being recognized as complications of Crohn's disease. It is important to recognize nutritional deficiencies at an early stage and initiate appropriate treatment. Otherwise many patients, experiencing what can be a chronic and debilitating illness, may suffer unnecessarily from the consequences of deprivation of vital nutrients.

Anemia↗
PubMed2004

Homocysteine and cardiovascular disease: interactions between nutrition, genetics and lifestyle.

Homocysteine is a sulfur-containing amino acid that arises during methionine metabolism. Although its concentration in plasma is only about 10 micromolar, even moderate hyperhomocysteinemia is associated with increased incidence of cardiovascular disease and Alzheimer's disease. Elevations in plasma homocysteine are commonly found as a result of vitamin deficiencies, polymorphisms of enzymes of methionine metabolism, and renal disease. Pyridoxal, folic acid, riboflavin, and Vitamin B(12) are all required for methionine metabolism, and deficiency of each of these vitamins result in elevated plasma homocysteine. A polymorphism of methylenetetrahydrofolate reductase (C677T), which is quite common in most populations with a homozygosity rate of 10-15 %, is associated with moderate hyperhomocysteinemia, especially in the context of marginal folate intake. Plasma homocysteine is inversely related to plasma creatinine in patients with renal disease. This is due to an impairment in homocysteine removal in renal disease. The role of these factors, and of modifiable lifestyle factors, in affecting methionone metabolism and in determining plasma homocysteine levels is discussed.

Avitaminosis↗
PubMed1995

Current status of nutritional deficiencies in Canadian aboriginal people.

Since the Nutrition Canada Survey (1973) there has been clear evidence that Aboriginal people have low intakes of many nutrients such as iron, vitamin D, calcium, folate, vitamin A, and fluoride. Recent surveys suggest that the situation has not changed. Children are most likely to be affected clinically. More than half of Aboriginal children in some subpopulations in Manitoba suffer a period of iron deficiency, which may affect development. Nutritional rickets is still a common problem in Manitoba. We have seen cases of megaloblastic anemia due to folate deficiency. The relationship of the well-described low folate intake in pregnancy and birth defects has received no attention for the Aboriginal population. In a recent survey of Inuit children, dental caries of the primary teeth were present in over 70% of children, with a mean DMF (decayed, missing, and filled) index of 1.8 teeth in children under 2 and 9.5 in children 6 to 8 years. Although clinical vitamin A deficiency is not seen, there is now good evidence that subclinical deficiency increases susceptibility to infections. Although not all Aboriginal populations suffer all of these deficiencies, the problems are sufficiently widespread to suggest this is an urgent problem. It will not be solved simply by education. There must be a political will and a coordinated effort to make a balanced diet available to all at an affordable cost.

Avitaminosis↗
PubMed1982

Liver disease and protein needs.

Protein deficiency is often associated with liver disease. The principal cause of protein deficiency is decreased dietary intake. Deficiencies in digestion and absorption that are common in alcoholics contribute to protein deficiency in alcoholic liver disease. The protein requirements in most patients with compensated chronic liver disease are not different from normal, but increase during episodes of hepatocellular deterioration. An increased demand for protein after liver injury drains nitrogen from other organs such as muscle. Aromatic amino acids released from muscle in increased amounts accumulate in the circulation of patients with chronic liver disease because of their decreased hepatic metabolism. By contrast branched chain amino acids decrease in the circulation because of their preferential uptake by extrahepatic tissues. Decreases in urea synthesis in liver disease result in the accumulation of ammonia. The causes of the decrease in urea synthesis include decreases in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. The resulting increase in ammonia in association with an increased accumulation and entry of aromatic amino acids into the brain are important factors in the pathogenesis of hepatic encephalopathy. Circulating proteins synthetized by the liver, such as albumin and clotting factors, are frequently decreased in chronic liver disease. Vitamin deficiencies that are common in liver disease contribute to abnormalities of protein metabolism. Hepatic regeneration following hepatic resection or injury is adversely affected by protein and vitamin deficiencies and by alcohol ingestion.

Amino Acids↗