Nutritional deficiency

Deficiency Diseases. Not only did cereals make an important contribution to improving the general status of humankind, but they also were important dietary components of some groups of people who showed certain nutritional deficiencies. This observation led to the discovery of some of the vitamins. These deficiency diseases have been most prominently associated with use of rice, com, and wheat. 

Ingestion of chloroform is followed immediately by a severe burning in the mouth and throat, pain in the chest and abdomen, and vomiting. Loss of consciousness and Hver injury may foUow depending on the amount swallowed. The tendency of chloroform to produce Hver injury is significantly augmented in alcohoHcs and persons with nutritional deficiencies. 

The ACGIH recommended maximum time-weighted average concentration in the workplace atmosphere for eight-hour daily exposure is 10 ppm. OSHA has set the permissible exposure level at 2 ppm. It maybe desirable to exclude alcohoHcs, persons with chronic disorders of the Hver, kidneys, and central nervous system, and those with nutritional deficiencies from working with chloroform. 

Goldberger and Lillie in 1926 found that rats fed certain nutritionally deficient diets developed dermatitis acrodynia, a skin disorder characterized by edema and lesions of the ears, paws, nose, and tail. Szent-Gyorgyi later found that a factor he had isolated prevented these skin lesions in the rat. He proposed the name vitamin Bg for his factor. Pyridoxine, a form of this vitamin found in plants (and the form of Bg sold commercially), was isolated in 1938 by three research groups working independendy. Pyridoxal and pyridoxamine, the forms that predominate in animals, were... 

Nutritional deficiency of vitamin B12—Eat a balanced diet diat includes seafood, eggs, meals, and dairy products. 

A knowledge of normal metabohsm is essential for an understanding of abnormalities underlying disease. Normal metabolism includes adaptation to periods of starvation, exercise, pregnancy, and lactation. Abnormal metabolism may result from nutritional deficiency, enzyme deficiency, abnormal secretion of hormones, or the actions of drugs and toxins. An important example of a metabolic disease is diabetes mellitus. 

The reported risk factors for HIV-associated sensory neuropathy are varied and may have changed since the availability of HAART. In the pre-HAART era, age, nutritional deficiencies, alcohol exposure, higher HIV viral load, and low CD4 counts (Moyle and Sadler 1998 Childs et al. 1999), as well as mood, other neurologic disorders and functional abnormalities (Schifitto et al. 2002) were neuropathy risk factors. In the HAART era, the use of NRTI (Cherry et al. 2006 Pettersen et al. 2006) and exposure to protease inhibitor (PI) medication (Pettersen et al. 2006 Smyth et al. 2007) are considered additional risk factors. Although hepatitis C mono-infection has been associated with peripheral nerve disease, and there is... 

Root exudation of extraordinary high amounts of specific carboxy lutes (e.g ci-u-ate, malate. oxalate, pbytosiderophores) in response to nutritional deficiency stress or Al toxicity in some plant species cannot simply be attributed to diffusion processes. The controlled release of these compounds, involved in mobilization of mineral nutrients and in detoxification of Al. may be mediated by more specific mechanisms. Inhibitory effects by exogenous application of various anion chan-... 

Formation of strictures, abscesses, fistulae, and obstructions in patients with CD is possible. Patients with CD may develop significant weight loss or nutritional deficiencies secondary to malabsorption of nutrients in the small intestine, or as a consequence of multiple small- or large-bowel resections. Common nutritional deficiencies encountered in IBD include vitamin B12, fat-soluble vitamins, zinc, folate, and iron. Malabsorption in children with CD may contribute to significant reductions in growth and development. 

Nutritional deficiencies Altered defense mechanisms, impaired mucosal integrity, or enhanced pathogenic potential of fungus... 

However, results obtained by Koo et al. (1991) indicate that low to moderate lead exposure (average lifetime PbB level range of 4.9-23.6 pg/dL, geometric mean of 9.8 pg/dL, n=105) in young children with adequate nutritional status, particularly with respect to calcium, phosphorus, and vitamin D, has no effect on vitamin D metabolism, calcium and phosphorus homeostasis, or bone mineral content. The authors attribute the difference in results from those other studies to the fact that the children in their study had lower PbB levels (only 5 children had PbB levels >60 pg/dL and all 105 children had average lifetime PbB levels <45 pg/dL at the time of assessment) and had adequate dietary intakes of calcium, phosphorus, and vitamin D. They concluded that the effects of lead on vitamin D metabolism observed in previous studies may, therefore, only be apparent in children with chronic nutritional deficiency and chronically elevated PbB levels. Similar conclusions were reached by IPCS (1995) after review of the epidemiological data. 

The toxicokinetic and toxicological behavior of lead can be affected by interactions with essential elements and nutrients (for a review see Mushak and Crocetti 1996). In humans, the interactive behavior of lead and various nutritional factors is particularly significant for children, since this age group is not only sensitive to the effects of lead, but also experiences the greatest changes in relative nutrient status. Nutritional deficiencies are especially pronounced in children of lower socioeconomic status however, children of all socioeconomic strata can be affected. 

Certain subgroups of the population may be more susceptible to the toxic effects of lead exposure. These include crawling and house-bound children (<6 years old), pregnant women (and the fetus), the elderly, smokers, alcoholics, and people with genetic diseases affecting heme synthesis, nutritional deficiencies, and neurological or kidney dysfunction. This is not an exhaustive list and reflects only current data available, further research may identify additional susceptible subgroups. 

Animal studies indicate that nutritional deficiencies in a number of essential elements (e.g., calcium, iron, zinc, copper, phosphorus) may impact the toxicokinetic and toxicological behavior of lead (ATSDR 1993 Chaney et al. 1989). In infants and children, lead retention has been shown to be inversely correlated with calcium intake (Johnson and Tenuta 1979 Sorrell et al. 1977 Ziegler et al. 1978). Zinc has been shown to have a protective effect against lead toxicity in a number of animal species (Goyer 1986 Haeger-Aronsen et al. 1976 Brewer et al. 1985 Cerklewski and Forbes 1976). 

If patients are on PPI and nutritional deficiencies occur, the indication and further prescription should be reconsidered, in particular in the elderly... 

Among functional alterations in patients with infectious diarrhea are increased secretion, failure of barrier function and reduction of absorptive function causing dehydration and nutritional deficiency. An understanding of the molecular pathogenesis with regard to each enteric pathogen will likely lead to a quicker diagnosis, more effective treatment and prevention of enteric infections. 

The effect of diet on vulnerability to lead makes interpretation of published information on experimental lead poisoning in waterfowl extremely difficult (Chasko et al. 1984). For example, many mallards on a diet of com die within 10 to 14 days after ingesting a single lead shot, whereas similar birds on a balanced commercial duck ration appear outwardly normal after ingesting as many as 32 pellets of the same size (Wobeser 1981). Also, multiple nutritional deficiencies may have additional effects in potentiating the toxicity of lead in mallards (Carlson and Nielsen 1985). Under conditions of reduced dietary calcium availability, such as can occur in acid-impacted environments, birds risk increased uptake of lead (and other metals) and may accumulate toxic concentrations more rapidly (Scheuhammer 1996). Enhanced accumulation of lead was accompanied by an increased synthesis of metallothioneins and a greater inhibition of ALAD activity (Scheuhammer 1996). 

Levander, O.A. 1979. Lead toxicity and nutritional deficiencies. Environ. Health Perspec. 29 115-125. 

Nutritional deficiencies are common with Crohn s disease. 

Age-related reductions in bone marrow reserve can render the elderly patient more susceptible to anemia that is caused by multiple minor and often unrecognized diseases (e.g., nutritional deficiencies) that negatively affect erythropoiesis. 

Nutritional deficiency diseases are relatively rare in the temperate zone. The etiology of numerous other clinical conditions involve vitamin deficiencies, due to faults in absorption, transfer, or utilization. Because of the central position of the vitamins as sources of coenzymes, such functional deficiencies are important in malabsorption, where the picture is often complicated by multiple deficiencies, in anemias where the defect is in general highly specific, and in many other diseases where the deficiency is secondary to other pathologic events, but nevertheless of grave consequences. 

The establishment of quantitative methods for the determination of vitamins in body fluids and tissues by microbiological assay techniques should stimulate the search for the significance of vitamins in disease, not only in nutritional deficiency, but in the much wider field of all metabolic disturbances. Functional vitamin deficiencies are produced by malabsorption, by inhibitors of the vitamin function through products of the body, and particularly through drugs and other toxic substances. Vitamin deficiencies may be relative deficiencies whenever an individual s metabolism is deranged so as to require enhanced quantities of a given vitamin to cure or to counteract certain symptoms as, e.g., in Darier s disease (keratosis follicularis) (P2a). 

Numerous physiological and environmental factors such as age, stress, nutritional deficiency, and infections may affect the immune system (Sullivan, 1989). Thus, adverse findings in animal studies may reflect these indirect immunotoxic effects rather than the direct immunotoxic potential of a chemical or drug. Indirect immunotoxic effects may be assessed through histopathologic evaluations of endocrine organs such as the adrenals and pituitary. 

The nervous system is the most sensitive target for cyanide toxicity, partly because of its high metabolic demands. High doses of cyanide can result in death via central nervous system effects, which can cause respiratory arrest. In humans, chronic low-level cyanide exposure through cassava consumption (and possibly through tobacco smoke inhalation) has been associated with tropical neuropathy, tobacco amblyopia, and Leber s hereditary optic atrophy. It has been suggested that defects in the metabolic conversion of cyanide to thiocyanate, as well as nutritional deficiencies of protein and vitamin B12 and other vitamins and minerals may play a role in the development of these disorders (Wilson 1965). 

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