Growth, sexual maturation, and dietary fiber in pubertal girls.
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Biomedical subjects
Publications and source records attributed to H H Sandstead.
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Zinc deficiency occurs in individuals and populations whose diets are low in sources of readily bioavailable zinc such as red meat, and high in unrefined cereals that are rich in phytate and dietary fibers. Dietary zinc deficiency was described nearly three decades ago among the poor of the Middle East. It is now known to occur in children and adolescents from widely diverse areas including Egypt, Iran, Turkey, China, Yugoslavia, Canada, and the United States; and among pregnant women from Iran, Turkey, the United Kingdom, Australia, and the United States. Major manifestations include retarded growth and development and an increased incidence of pregnancy complications. Other manifestations may include suppressed immunity, poor healing, dermatitis, and impairments in neuropsychological functions. Precise information as to the numbers of people affected by dietary zinc deficiency is not available. Even so the nature of diets associated with zinc deficiency suggests that mild deficiency is common in some populations.
In a previous report of a zinc supplementation trial in pregnant adolescents zinc effect varied according to maternal weight (wt) status--normal (90-110% of expected wt), light or heavy, prompting this analysis of effects of wt status and gestational wt gain on fetal heaviness relative to length and gestational age (GA) and other pregnancy outcomes. One-third of adolescents shifted in or out of normal wt by delivery, creating seven outcome groups--light-light, light to normal, normal to light, normal-normal, normal to heavy, heavy to normal, and heavy-heavy. These wt class change groups varied significantly as to intrauterine growth (SGA, low AGA, high AGA, and LGA); by weekly grams gain per cm height (ht), birth wt, infant wt/length ratio, and occurrence of low birth wt (LBW). Infants with above average intrauterine growth had an advantage in: absolute size, length of hospital stay, rates of LBW, fetal demise, rates of low Apgar score, and "other" complications. This association between intrauterine growth and maternal wt class change suggests that promotion of wt gain might lower rates of LBW. Birthwt varied by quartiles of weekly wt change (gm) per cm ht in women grouped by their percent of expected wt: in the lowest quartile (Q1) only one group in seven reached average Bwt (3025 grams); with Q4 gain all groups did. Thus, the parameter wt gain/wk/cm ht deserves study as a tool for monitoring wt status and gain to identify those pregnant adolescents in greatest need for nutritional counseling and to set wt gain goals.
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The hypothesis that dietary fiber lowers serum cholesterol was tested in 10 healthy men, 19 to 54 years old, who ate a mixed diet similar to the diets of many American adult males, that contained 16% of calories as protein (70% from animal), 40% as fat (P/S = 0.3), 44% as carbohydrate (9% of calories as sucrose) and 3 g of crude fiber. The energy intake ranged from 2700 to 3500 kcal adjusted to their height and weight. Weight and fitness were held constant. After 30 days of equilibration on the basal diet, they ate 26 g of either soft white wheat bran, corn bran (CB), soybean hulls (SH), textured vegetable protein, or hard red spring wheat bran (HRS) for periods of 28 to 30 days each in no particular sequence. Each fiber was fed to four to six subjects. The dietary fiber contents of soft white wheat bran, CB, SH, and HRS were: 44, 92, 87, and 51%, respectively. Mean daily fecal weight increased (P less than or equal to 0.01) from 72.4 to 144, 68 to 128, and 81 to 151 g when CB, SH, and HRS were fed respectively. No effects were noted with soft white wheat bran or textured vegetable protein. Total plasma cholesterol decreased 12% with HRS (P less than or equal to 0.05) and 14.0% with SH (P less than or equal to 0.05). Low density lipoprotein cholesterol decreased 21% with HRS (P less than or equal to 0.05). High density lipoprotein cholesterol did not change with any of the dietary fiber sources nor did the ratio of high density lipoprotein cholesterol to total cholesterol. Some triglyceride lowering effect was seen with all sources of dietary fiber (P less than or equal to 0.01). There was a significant direct correlation between the area under the oral glucose tolerance curves and the levels of total cholesterol (r = 0.57, P less than or equal to 0.0001) and low density lipoprotein cholesterol (r = 0.49, P less than or equal to 0.0007), and between fasting plasma glucose and triglycerides (r = 0.32, P less than or equal to 0.03). Results were replicated when subjects were fed the same fiber source on two occasions at 2 to 4 month intervals.
The cellular immune response of a 17-year-old decerebrate male with acquired zinc deficiency was studied. He had been fed a commercial formula which contained 7.6 mg zinc per kilogram. His caloric intake had been inadequate as judged by his cachexia. A detailed pretreatment nutritional assessment (five separate observations) which included total serum protein and globulins, albumin, folate, vitamins A, B2, C, ceruloplasmin, and plasma zinc, copper, iron, and total iron binding capacity revealed that the patient was deficient only in zinc and calories. His plasma zinc was 41 +/- 5 microgram/d1 compared with our laboratory norm of 89 +/- 9 microgram/d1 for young adult males. Cellular immunity was assessed by delayed skin reactivity to dinitrochlorobenzene and by in vitro lymphocyte transformation studies. Before zinc therapy the patient rendered a negative skin reaction to dinitrochlorobenzene, and the ability of his lymphocytes to undergo blast transformation in response to mitogen stimulation was significantly depressed with a stimulation index of 4.7 +/- 0.8 as compared with 139.1 +/- 77.3 for controls. Within 3 weeks after zinc therapy (22.7 mg zinc per day) he demonstrated a positive delayed skin reaction to dinitrochlorobenzene and a normal lymphocyte response stimulation index = 205.5 +/- 42.6 versus 199.3 +/- 58.2 for control). In addition, a pretreatment facial seborrhea and a decubitus ulcer rapidly healed.
Because zinc apparently has a role in amino acid utilization, we have studied possible consequences of zinc deficiency on the metabolism of amino acids in the intestinal mucosa by examining proteins transported via the mesenteric lymph in zinc-deficient and zinc-supplemented rats. Mesenteric lymph ducts were cannulated under pentobarbital, and on recovery the animals were fed [14C]leucine as a pulse dose by duodenal infusion. Protein output via intestinal lymph was generally constant over the infusion range studied. Total lymph protein output was not affected by zinc deficiency or supplementation. The electrophoretic pattern of the lymph protein revealed a protein band that migrated with the alpha2-globulins coincidental to zinc deficiency; the band disappeared after zinc supplementation. There was an inverse zinc-copper relationship in mesenteric lymph; duodenal infusion of zinc to deficient rats was followed by a decrease in lymph copper. Deficiency of zinc seems to have little influence on the quantitative aspect of protein carried in mesenteric lymph but seems to be involved with the nature of the protein in this body fluid.
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Five adult male volunteers were fed a diet containing (as percent of calories) 16% protein, 40% fat, and 44% carbohydrate, a diet similar to that consumed by many American males. Twenty-six grams of soft white wheat bran or corn bran were added to the daily bread, and the effects on zinc, iron, and copper balance were assessed during the last 12 days of each 30-day study period. The soft white wheat bran appeared to decrease retention of zinc in four subjects but not significantly so. Iron retention was similar in all three treatments. Copper balance was improved by addition of soft white wheat bran and to a lesser degree by corn bran. An apparent copper requirement of 1.28 mg/day for the volunteers was calculated by regression analysis.
Zinc status and the retinol transport system were examined in 18 retinol supplemented cystic fibrosis (CF) patients and 40 age-matched controls. Plasma vitamin A was significantly lower in the CF group as compared to the controls and correlated positively with plasma retinol-binding protein (RBP) in both the CF and control groups. Plasma zinc of the CF group was not significantly lower than controls whereas hair zinc was. Plasma zinc was positively correlated with plasma RBP, vitamin A, and albumin in the CF group but not in the controls. Plasma concentrations of vitamin A, RBP, albumin, and zinc decreased with age in the CF group but not in the controls. The data support previous suggestions that low plasma vitamin A levels in CF are due to defects in the retinol transport system. The zinc status of the CF groups as a whole was judged to be low-normal however a subgroup of CF patients were in the marginal to deficient category. This subgroup also had lower levels of plasma vitamin A and RBP. The data suggest that zinc may be a contributing factor in the low plasma vitamin A/RBP levels of CF patients with marginal or deficient zinc status.
Zinc deprivation from day 110 to 150 of gestation in rhesus monkeys resulted in rash, alopecia, anorexia, decreased feed efficiency, and low plasma zinc in the mothers. Infants of the dams that had been deprived of zinc during gestation displayed a more rapid postnatal growth rate than infants of the control mothers. Infants of the zinc-deprived dams played and explored less than the control infants. They also associated with their mothers a greater percentage of the time and were less active. This study has shown that third trimester maternal zinc deprivation in nonhuman primates can impair behavioral development of offspring.