The American Journal of Clinical Nutrition, Volume 22, 1969: Metabolism of ascorbic-1-14C acid in experimental human scurvy.
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Biomedical subjects
Publications and source records attributed to R E Hodges.
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In this summary, the authors have attempted to examine reports of associations between various dietary habits and practices on one hand, and serum lipids or clinical disease on the other hand. There seems to be little doubt that both hypertension and ischemic heart disease have a nutritional background, but in all likelihood, there are other factors such as hereditary traits, occupational hazards, and perhaps personal habits including cigarette smoking, alcohol abuse and prolonged ingestion of medicinal drugs. One of the strongest correlates seems to be the role of complex carbohydrates in regulating blood lipid concentrations. Carbohydrates not only have an effect on the endocrine system that regulates blood volume, but they also influence absorption of fat soluble substances from the digestive tract and if natural fiber is included, it has an effect on fecal bulk, transit time of the fecal stream, and reabsorption of bile acids and neutral sterols. Epidemiologically, there is some evidence that the changes that occurred in the American diet in the years between 1914-1944 may well have played a permissive role in the genesis of a portion of the coronary heart disease, high blood pressure and stroke that occurred in the United States. It is not too farfetched to suggest that had the American servicemen been given more cereal food products including bread and other baked food items, instead of excessive amounts of meat and fats, the dietary pattern of America might well have been substantially different. Furthermore, this difference could easily have influenced the pattern of atherosclerosis and hypertension. A great deal more work is needed to confirm or refute these suggestions.(ABSTRACT TRUNCATED AT 250 WORDS)
Preoperative evaluation of all patients should include evaluation of nutritional status. Factors of greatest clinical usefulness are nutritional history correlated with the clinical situation, and measures of body height and weight, serum albumin concentration, and muscle mass. Depressed immune function suggested by a lack of skin test reactivity to standard antigens may correlate with the risk of postoperative complications and death, but further studies are required to determine the specific relation of nutrient deficiencies and immune function. Micronutrient deficiencies must be identified and corrected rapidly. Nutritional support in patients with nutritional deficiencies should be started preoperatively either by enteral or intravenous techniques and continued postoperatively.
Total parenteral nutrition (TPN) is a potent form of therapy. It is particularly useful in patients who must undergo surgery or those with conditions that preclude normal feeding. The procedure is not without risk, but better understanding of the basic principles involved, refinements in technique, and experience with its use in different situations have combined to improve the results of therapy over those first obtained. TPN represents an important therapeutic advance and emphasizes the need for an undertanding of nutritional principles by physicians and for a team approach to the management of complicated conditions.
Young rats weighing 150 g (initial weight) were fed diets sufficient or deficient in vitamin A. Postweaning rats were used in order to retard the rapid onset of vitamin A deficiency. The effects of the deficiency were studied with respect to impairment of hematopoietic function and anemia. Values for hemoglobin and hematocrit provided evidence of anemia before the signs of severe vitamin A deficiency became apparent. These included alopecia, ocular lesions, and low levels of retinol in plasma and liver. At the point where liver stores of vitamin A were virtually depleted, however, estimates for serum iron, hematocrit, and hemoglobin were elevated to control levels. The latter phenomenon appeared to result from hemoconcentration. These data suggest that anemia may be a component of vitamin A deficiency, but might be masked by the dehydration that accompanies severe depletion of vitamin A.
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Recent studies of experimental vitamin A deficiency in man led the authors to conclude that anemia may result from lack of vitamin A. A review of numerous nutrition surveys in underdeveloped countries enhanced the suspicion that deficiency of vitamin A does contribute to the prevalence of anemia. Preliminary studies of vitamin A-deficient rats confirmed previous observations that anemia may result from lack of this vitamin. The livers of these animals had very low concentrations of vitamin A but normal or increased concentrations of iron. The finding of anemia is in contrast with other reports that vitamin A deficiency may cause elevated values for hemoglobin and hematocrit. The authors suggest that loss of taste and smell as a result of deficiency may account for refusal of experimental animals to eat and drink enough to prevent inanitation and dehydration. The resulting hemoconcentration may mask the true hematological picture, which is one of anemia.
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In order to investigate the role of vitamin A nutriture in the prevalence of anemia in Central America, a retrospective evaluation of the data of the six Institute of Nutrition of Central Americal and Panama/Office for International Research nutrition surveys of Central America and Panama has been made. Three groups of children; 1 to 4, 5 to 8, and 9 to 12 years old, living between 0 and 2,5000 feet above sea level were studeid. Several biochemical and dietary parameters related to anemia were corrleated with plasma levels of retinol. Children between the ages of 5 and 12 years showed a significant positive correlation between hemoglobin and plasma retinol. Children aged 1 to 4 years did not show a similar correlation. In children of all age groups there were positive correlations between plasma retinol and serum iron. Percent saturation of transferrin was also found to be lower when plasma retinol levels were low. Children with an adequate intake of iron, as classified by both dietary information and socioeconomic level, showed a significant positive correlation between plasma retinol levels and iron in their serum. In contrast, no correlation was found when dietary iron was low. In the light of these findings, a possible relationship between vitamin A deficiency and anemia is suggested.
The sulfation of ascorbic acid by an ascorbic acid sulphotransferase was investigated using rat liver and colon homogenates. When Na2 35 SO4 or 3'-phosphoadenylyl [35S]sulfate (P-Ado-P-35S) and ascorbic acid were used as substrates, chromatographic behavior of the reaction products on thin-layer cellulose suggested that ascorbic acid 2-[35S]sulfate was formed. With Na2 35SO4 as the source of radioactive sulfate in the assay system, ATP was found to be an obligatory cofactor. Incorporation of [35S]sulfate frofrom Na2 35SO4 into ascorbic acid 2-[35S]sulfate was also decreased when ATP sulfurylase inhibitors were added to the system. P-Ado-O35S alone in the assay without ATP was an extemely effective sulfating agent. In addition, liver and colon homogenates from vitamin A deficient and sufficient rats were used in one of the studies. Vitamin A deficiency appeared to have little effect on ascorbic acid 2-sulfate formation.
Weekly determinations of serum copper (Cu) and zinc (Zn) were made in eight adult patients receiving total parenteral nutrition (TPN) for 3 to 13 weeks. Serum Cu decreased in all eight patients. Five of eight patients had hypocupremia lasting at least 2 consecutive weeks and three of the five had Cu levels of 30 mug/dl or lower. Low levels of serum ceruloplasmin provided supportive evidence of Cu deficiency in the three patients with the lowest Cu levels. Two patients who had Cu less than or equal to 20 mug/dl demonstrated declines in hemoglobin which were probably due to Cu deficiency. The mean rate of decline in serum Cu was 10.8 mug/dl/week. After resumption of oral feedings in five patients, the mean rate of increase in Cu was 14 mug/dl/week. The sharpest rise in Cu was seen during the 2nd week after oral feedings were resumed in four of the five patients. Three of eight patients had serum Zn levels less than 70 mug/dl for at least 2 consecutive weeks. Serum Zn decreased at a mean rate of 6.6 mug/dl/week. There was a further decline in serum Zn in three of five patients in whom measurements were made after resumption of oral intake. Concentrations of Zn in TPN solutions varied between 0.63 and 1.0 mg/liter. Cu was undetectable in TPN solutions.
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In seven adult patients receiving fat-free total parenteral nutrition (TPN) for 4 to 8 weeks, weekly determinations of plasma fatty acids and total plasma tocopherols were made. Four patients were deficient in essential fatty acids, as defined by triene: tetraene ratio greater than 0.4, at the end of the second week of TPN. Six patients were deficient by the end of the third week and all seven were deficient by the end of the fifth week of TPN treatment. One patient who was deficient in both essential fatty acids and zinc developed a scaling, eczemoid dermatitis that disappeared within 3 weeks after cessation of TPN and resumption of oral feedings containing both fat and zinc. After resumption of oral feedings by three patients, the triene: tetraene ratio returned to normal within 2 weeks. The mean of total plasma tocopherols fell over a period of 7 weeks and in three individuals, reached levels generally associated with deficiency. There were not any obvious clinical manifestations of vitamin E deficiency.
Weanling rats were fed diets with and without the addition of retinyl palmitate at 6,500 units/kg. The supplemented groups were fed either ad libitum or food was restricted daily to that amount consumed by the group of rats receiving the unsupplemented diet. After a 10 week experimental period, signs of vitamin A deficiency were observed (growth plateau, xerophthalmia) and liver values as retinol were only 1% of control values. Relative to the two control groups, vitamin A deficiency resulted in approximately 30% lower liver, 50% lower blood and 40% lower urinary ascorbic acid. Vitamin A deficiency did not appear to result in significant and direct impairment of GAG sulfate metabolism. Although the total amount of GAG in rat skin was increased, the composition of GAG fractions did not appear to be altered by vitamin A deficiency. Studies regarding the incorporation and disappearance of 35S-sulfate in vivo into GAG fractions obtained from skin indicated no serious impairment in GAG turnover with vitamin A deficiency. Twenty-four hour urine samples were also collected for estimation of 35SO4 excreted in GAG and non-GAG fractions. Likewise, little change was observed with respect to radioactivity associated with sulfate fractions excreted in urine. Although many previous studies have directly linked vitamin A with sulfation of GAG, the results reported here suggest that if there is an alteration in GAG sulfate metabolism, it is probably an indirect consequence of vitamin A status.
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