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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Vitamin C is unevenly distributed throughout all body cells and fluids. A total-body pool of 900 mg (5.11 mmol) in an adult male meets the following criteria of a satisfactory vitamin C status: it is threefold higher than one that prevents scurvy, no known health advantages accrue at higher pool sizes, absorption efficiency is high and urinary loss low at appropriate intakes, and a 1-mo reserve allows for periods of low intake or stress. To maintain a suitable body pool in healthy 76-kg men and 62-kg women requires daily intakes (RDI) of 40 mg (227 mumol) and 30 mg (170 mumol), respectively. Reasons for not increasing RDI values to enhance iron absorption and to prevent nitrosamine formation are given. The specific association of normal intakes of dietary vitamin C with cancer is very weak and not quantifiable. Advisable intakes for children, pregnant and lactating women, and the elderly are considered. The present recommendations are in better accord with current information than are the 1980 RDA values.
Serum vitamin C levels were compared in smokers and nonsmokers in relation to dietary and supplemental intake of vitamin C, using data from the Second National Health and Nutrition Examination Survey. Smokers reported a lower mean daily intake (53 mg) of vitamin C than nonsmokers (65 mg) and a higher percentage (41% compared to 31%) consuming less than 70% RDA. Smoking status of respondents was judged by carboxyhemoglobin levels or by questionnaire. With both methods, percent of nonsupplemented smokers with serum vitamin C 0.3 mg/dl or less was two or more times as high as nonsupplemented nonsmokers at similar dietary intake levels. When smokers and nonsmokers with similar dietary vitamin C intake were ranked by serum C level, median and mean serum C for smokers was consistently lower than nonsmokers by approximately 0.2 mg/dl. By using the parallel bioassay methods, it was estimated that smokers would need an additional 59 mg/day dietary vitamin C (95% confidence interval of 52-68 mg/day) based on median values or 65 mg/day (53-79 mg/day) based on mean values to attain serum C levels comparable to nonsmokers.
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)
Anemia associated with vitamin A deficiency and increased liver iron has implicated vitamin A in the regulation of iron release from the liver. To study this relationship further, groups of weanling rats were fed diets as follows: low iron/low vitamin A, low iron/high vitamin A, normal iron/normal vitamin A, high iron/low vitamin A and high iron/high vitamin A. After 6 weeks the animals were killed, and blood and liver samples were taken for analyses of hemoglobin, hematocrit, red blood cell count, serum and liver vitamin A, serum and liver iron and total iron-binding capacity. Low dietary iron, but not low vitamin A intake, affected hemoglobin, hematocrit and red blood cell counts but not serum vitamin A levels. Mean serum vitamin A levels were not significantly lower in groups fed high dietary iron. High dietary iron was also associated with lower mean liver vitamin A levels; these differences were statistically significant only for the low vitamin A diet group. A high vitamin A intake was associated with a significantly lower mean hepatic iron level for the high dietary iron intake group. These data support the hypothesis that vitamin A is involved in the regulation of iron release from the liver.
This is a report of the effects of sugars on salt metabolism and on blood pressure. Twenty young men, none of whom had a personal or family history of hypertension, were orally hydrated after an overnight fast and required to lie recumbent for 6 h except for urinary voiding and blood pressure measurements which were performed at 1/2 h intervals. Venous blood samples were drawn at hourly intervals. The volunteers were kept constantly hydrated by giving them water to drink equivalent to the volumes of urine voided. Two hours from the start of the experiment each subject was given one of the following sugars: glucose, fructose, sucrose, galactose, lactose, or water alone. After oral hydration the subjects appeared to develop natriuresis and kaliuresis. This was quickly abolished by ingestion of either glucose, fructose, sucrose, or lactose, but not by galactose or water alone. Fructose was the most potent antinatriuretic agent. Both glucose and sucrose significantly elevated systolic blood pressure. This lasted for 2 h after glucose ingestion and 1 h after sucrose ingestion.
High blood pressure is recognized as a major risk factor for both coronary heart disease and stroke. The role of diet in the genesis of hypertension has been hotly disputed. Recently, sucrose was reported to augment the hypertensive effects of salt in experimental animals. A review of many reports suggests that not only carbohydrates but also proteins and fats can alter blood pressure. Whether salt retention is a cause of elevated blood pressure remains to be ascertained. We have shown recently that sucrose and glucose elevate blood pressure transiently, and sucrose and fructose cause different degrees of salt retention in humans who have been fasting.
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Plasma amino acids were determined in humans after surgical trauma. The plasma amino acids were combined into several groups to determine if specific groups were responsible for alterations. The total concentration of plasma amino acids decreased after the operation and returned to preoperative levels and were elevated by postoperative day 10. The glucogenic amino acids, particularly aspartate and glutamate, were responsible for the decrease. The ketogenic and aromatic amino acids increased after operation. These results are confirmed by those reported in the rat and in humans with other types of operations. Plasma amino acids are not reliable indexes of the type of diet or of malnutrition and, based upon our previous data, are not likely to be reliable indexes of the degree or severity of trauma. The alterations observed after trauma do suggest that basic metabolic pathways are altered after trauma. As has been suggested previously, the alterations in plasma amino acids may relate to their use and possible need as gluconeogenic precursors. Prompt restoration of the plasma pools of those amino acids which appear to be depleted with surgical trauma may influence the course of convalescence.
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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