Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For many decades there has been adequate information for the elimination of acute dietary deficiency diseases. Scurvy, beri-beri, and pellagra, once serious scourges, are now seen only rarely. The severe forms of protein-energy malnutrition, kwashiorkor and marasmus, have also decreased greatly. Nonetheless, mild to moderate forms of protein-energy deficiency, exacerbated by infection, continue to impair growth and development in a majority of the low-income pre-school age populations of most developing countries. Deficiencies of iron, iodine, and vitamin A are still widespread in developing countries. Fortunately, the success of the WHO/UNICEF "Child Survival and Development Revolution" in persuading most developing countries to introduce expanded programs of immunization, growth monitoring, and appropriate feeding of young children, control of diarrheal disease, and specific campaigns against avitaminosis A, iodine deficiency disorders, and the functional consequences of iron deficiency, will accelerate the decline of acute deficiency diseases in the developing world. Diets are changing among the more affluent in these countries, however, and it is time for them to stress dietary goals for the health of rich and poor alike. For the first time there is enough information regarding dietary risk factors for chronic disease to provide an opportunity in the 1990s to accelerate the dietary changes that have already brought significant health benefits to some populations in North America and Europe. The changes, which include a lower dietary intake of fat, particularly saturated fat, less salt, and more green and yellow vegetable and whole grain cereals, can be expected to influence favorably morbidity from cardiovascular diseases and some kinds of cancer. For maximum benefit, these measures need to be combined with the avoidance of obesity, reasonable physical activity, abstention from, or moderate use of, alcohol, and avoidance of tobacco in any form. Since there is already considerable momentum toward these changes in North America and some European countries, the 1990s are likely to see substantial further progress in the reduction of chronic diseases known to be influenced by diet.
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PMID:Nutrition: prospects for the 1990s. 219 71

The regulation of expression of hepatic iron-related proteins was examined during iron deficiency caused by scurvy in guinea pigs. Previous studies showed that some effects of scurvy, such as suppression of collagen gene expression, result from events associated with weight loss. During the initial phase of scurvy when vitamin C is depleted but animals grow normally, serum iron levels decreased to 50% of normal. During the second phase of scurvy when animals lose weight, there was a further decrease in iron levels to 10-15% of normal. Serum transferrin levels increased during scurvy, but this increase was related neither to the rate of weight loss nor to hepatic transferrin mRNA expression, which decreased. Serum ferritin levels of diminished early in scurvy with a preferential loss of the L subunit. In liver, however, both ferritin animals gaining weight. Ferritin gene expression during vitamin C deficiency was correlated with serum ferritin levels in that the level of mRNA for the H subunit remained relatively constant while that of the L subunit decreased early. Transferrin receptor mRNA expression in liver was induced as soon as iron levels decreased early in scurvy, which is similar to results reported for iron-depleted cultured cells. In contrast to results in cell culture, expression of iron regulatory protein 1 mRNA was decreased to approximately 50% of normal early in scurvy with a concomitant decrease in hepatic cytosolic aconitase activity. Our data indicate that iron deficiency occurs early during vitamin C deficiency and leads to changes in expression of iron-related proteins that differ in some aspects from regulation by iron in cell culture. Other events associated with weight loss in late scurvy may play a further role in this regulation.
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PMID:Gene expression of iron-related proteins during iron deficiency caused by scurvy in guinea pigs. 856 10

The early years of the 20th century were notable for improvements in general sanitation, dairying practices and milk handling. Most infants were breast-fed, often with some formula feeding as well. Availability of the home icebox permitted safe storage of milk and infant formula, and by the 1920s, feeding of orange juice and cod liver oil greatly decreased the incidence of scurvy and rickets. Use of evaporated milk for formula preparation decreased bacterial contamination and curd tension of infant formulas. From 1930 through the 1960s, breast-feeding declined and cow's milk and beikost were introduced into the diet at earlier and earlier ages. Although commercially prepared formulas, including iron-fortified formulas replaced home-prepared formulas, few infants were breast-fed or formula fed after 4-6 mo of age. Iron deficiency was prevalent. From 1970 through 1999, a resurgence of breast-feeding was associated with a prolongation of formula feeding and an increase in usage of iron-fortified formulas. By the end of the century, formula feeding of older infants had largely replaced feeding of fresh cow's milk and the prevalence of iron deficiency had greatly decreased.
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PMID:Infant feeding in the 20th century: formula and beikost. 1116 May 71

A child responds to a deficiency of an essential nutrient either by continuing to grow and consuming body stores with eventual reduction in the bodily functions (Type I) or by reducing growth and avidly conserving the nutrient to maintain the concentration of the nutrient in the tissues (Type II). Examples of Type I nutrient deficiency are anemia (iron deficiency), beri-beri (thiamin deficiency), pellagra (niacin or nicotinic acid deficiency), scurvy (vitamin C or ascorbic acid deficiency), xerophthalmia (vitamin A or retinol deficiency) and iodine deficiency disorders. Diagnosis is relatively simple via clinical symptoms and measurement of the concentration of the nutrient itself. There are no characteristic symptoms to distinguish which Type II nutrient deficiency an individual has; all deficiencies result in the poor growth, stunting, and wasting generally ascribed to protein-energy malnutrition. In Type II, growth stops, the body starts to conserve the nutrient, and its excretion falls to very low levels. In severe deficiency the body may start to break down its own tissues and the reduction of appetite accompanies this condition. An animal can die from zinc deficiency even though it is has a normal concentration of zinc in its tissues, but it can respond rapidly to small amount of dietary zinc. The mechanisms by which the body stops growing in response to nutritional lack are similar to the hormonal picture seen in endocrine disease (reduction of the production of the hormonal mediators of growth, down-regulation of receptors, and reduction of protein synthesis). Growth failure is the clinical sign characteristic of a diet deficient in protein, zinc, magnesium, phosphorus, and potassium. Wasting may be also ascribed to toxins, infection, worms, or persistent diarrhea. Anorexia is another common response in nutrient deficiency. Only a supplementation diet with a balance of nutrients will promote rapid recovery.
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PMID:Specific deficiencies versus growth failure: type I and type II nutrients. 1234 13

We describe the case of a 40-year-old female patient who developed severe pulmonary hypertension and life-threatening right-sided heart failure in association with dietary scurvy and iron deficiency. Supplementation with oral vitamin C and iron very likely contributed to her complete cure. Scurvy-associated pulmonary arterial hypertension could result from impaired availability of endothelial nitric oxide, but inappropriate activation of the hypoxia-inducible family (HIF) of transcription factors could play an even more important role. HIF coordinates the body's responses to hypoxia, and its activity is regulated by oxygen-dependent prolyl hydroxylases, which need vitamin C and iron as cofactors. Deficiency of these cofactors could lead to uncontrolled HIF activity and pulmonary vasoconstriction responsive to vitamin C and iron administration.
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PMID:Reversible pulmonary hypertension associated with vitamin C deficiency. 2279 43

Pulmonary arterial hypertension (PAH) is characterized by sustained vasoconstriction, vascular remodeling, inflammation, and in situ thrombosis. Although there have been important advances in the knowledge of the pathophysiology of PAH, it remains a debilitating, limiting, and rapidly progressive disease. Vitamin D and iron deficiency are worldwide health problems of pandemic proportions. Notably, these nutritional alterations are largely more prevalent in PAH patients than in the general population and there are several pieces of evidence suggesting that they may trigger or aggravate disease progression. There are also several case reports associating scurvy, due to severe vitamin C deficiency, with PAH. Flavonoids such as quercetin, isoflavonoids such as genistein, and other dietary polyphenols including resveratrol slow the progression of the disease in animal models of PAH. Finally, the role of the gut microbiota and its interplay with the diet, host immune system, and energy metabolism is emerging in multiple cardiovascular diseases. The alteration of the gut microbiota has also been reported in animal models of PAH. It is thus possible that in the near future interventions targeting the nutritional status and the gut dysbiosis will improve the outcome of these patients.
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PMID:Impact of Nutrition on Pulmonary Arterial Hypertension. 3193 13