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Background: The need for prophylactic iron during pregnancy is uncertain. Objective: We tested the hypothesis that administration of a daily iron supplement from enrollment to 28 wk of gestation to initially iron-replete, nonanemic pregnant women would reduce the prevalence of anemia at 28 wk and increase birth weight. Design: Between June 1995 and September 1998, 513 low-income pregnant women in Cleveland were enrolled in the study before 20 wk of gestation. Of these, 275 had a hemoglobin concentration [less than or equal to] 110 g/L and a ferritin concentration [less than or equal to] 20 [micro]g/L and were randomly assigned to receive a monthly supply of capsules containing either 30 mg Fe as ferrous sulfate or placebo until 28 wk of gestation. At 28 and 38 wk of gestation, women with a ferritin concentration of 12 to Results: Compared with placebo, iron supplementation from enrollment to 28 wk of gestation did not significantly affect the overall prevalence of anemia or the incidence of preterm births but led to a significantly higher mean ([+ or -] SD) birth weight (206 [+ or -] 565 g; P = 0.010), a significantly lower incidence of low-birth-weight infants (4% compared with 17%; P = 0.003), and a significantly lower incidence of preterm low-birth-weight infants (3% compared with 10%; P = 0.017). Conclusion: Prenatal prophylactic iron supplementation deserves further examination as a measure to improve birth weight and potentially reduce health care costs. KEY WORDS Iron deficiency, anemia, iron supplementation, pregnancy, low birth weight, small-for-gestational age infants, preterm delivery

Objective: To better characterize childhood growth and further assess potential limitations of the current National Center for Health Statistics and World Health Organization international growth reference. Design: The LMS method was used for curve fitting to summarize the changes in height and weight distributions by 3 curves representing the skewness (L), median (M), and coefficient of variation (S). A series of polynomial regression procedures was applied to smooth the L, M, and S curves. Setting: Subset data from 18 states contributing clinic data to the Centers for Disease Control and Prevention Pediatric Nutrition Surveillance System were used for this research reference. Methods: We chose only those clinics in which the height and weight distributions of children closely matched with those of the first and second National Health and Nutrition Examination Surveys. Results: Unlike the current international growth reference, the new reference has no disjunction at 24 months of age because it is based on a single data source for children aged 0 to 59 months. The reference also better characterizes the growth for infants than the current international reference, a fact we demonstrated with data from the National Health and Nutrition Examination Surveys, Pediatric Nutrition Surveillance System 1995, and the Davis Area Research on Lactation, Infant Nutrition, and Growth studies. Conclusions: The current National Center for Health Statistics and World Health Organization international growth reference needs to be updated. The methods used in this study will be useful to evaluate other data sets and to evaluate future modifications of growth references. Arch Pediatr Adolesc Med. 1998;152:471-479, The reference standard used by the the World Health Organization and the National Center for Health Statistics needs to be updated for accuracy and relevance. In reviewing data from the Centers for Disease Control and Prevention Pediatric Nutrition Surveillance System, it was found that height and weight distributions have changed, especially at age 24 months, where the old standards are disjoined. The new reference data also is an improvement regarding growth for infants.

The 1990 pregnancy weight gain recommendations of the Institute of Medicine hold valid, and a recommendation for maximal weight gain among very overweight women should be added. Data were analyzed on 53,541 mother-infant pairs on the relationships among prepregnancy weight, pregnancy weight gain, and low or high infant birth weight. Optimal weight gain ranges were ranges that minimized the incidence of both low and high birth weight since both associate with increased complications. The population consisted of low-income women giving birth in 1990 and 1991 in eight states. The population provided enough data on very overweight women to calculate a maximal pregnancy weight-gain in this group, which the data used by the Institute of Medicine did not. Data analysis concluded that very overweight women should not gain more than 25 pounds. It was confirmed that average weight women should ideally gain 25 to 35 pounds, and overweight women should gain 15 to 25 pounds.

To determine the appropriateness of race-specific criteria for anemia, we used the sample of women of childbering age from the Second National Health and Examination Survey to examine the relationship between hemoglobin and iron status for blacks and whites. After adjustment for major factors known to cause hemoglobin variation, including iron nutrition status, black women overall had a significantly lower mean hemoglobin value (126 [+ or -] 12 g/L) than white women (134 [+ or -] 11 g/L). Comparison of the probability plots of black and white hemoglobin distributions found the difference across the distributions to not be uniform, likely because a subset of black women had lower hemoglobin values rather than because of a generalized lowering. This finding suggests that it may not be appropriate to have a separate criteria for all blacks to accommodate the subset with lower hemoglobin. However, evaluation of the screening performance of hemoglobin found that race-specific anemia criteria (10 g/L difference) yielded a comparable sensitivity and specificity in detecting iron deficiency for both races. In contrast, a fixed anemia criterion did not yield comparable screening performances for the two races. This functional evaluation supports considering race-specific anemia criteria for screening iron deficiency.

* Objective: To determine the incidence of acute mountain sickness in a general population of visitors to moderate elevations, the characteristics associated with it, and its effect on physical activity. * Design: A cross-sectional study. * Setting: Resort communities located at 6300 to 9700 feet elevation in the Rocky Mountains of Colorado. * Participants: Convenience sample of 3158 adult travelers, 16 to 87 years old (mean age [[+ or -] SD], 43.8 [+ or -] 11.8 years). * Results: Twenty-five percent of the travelers to moderate elevations developed acute mountain sickness, which occurred in 65% of travelers within the first 12 hours of arrival. Fifty-six percent of those with symptoms reduced their physical activity. The odds favoring acute mountain sickness were 3.5 times as large for visitors whose permanent residence was below 3000 feet elevation as for those whose residence was above 3000 feet; 2.8 times as large for visitors with previous symptoms of acute mountain sickness; and twice as large in travelers younger than 60 years. Women, obese persons, those in poor or average physical condition, and those with underlying lung disease also had a higher occurrence of acute mountain sickness (P < 0.05). * Conclusions: Acute mountain sickness occurs in 25% of visitors to moderate altitudes and affects activity in most symptomatic visitors. Persons who are younger, less physically fit, live at sea level, have a history of acute mountain sickness, or have underlying lung problems more often develop these symptoms., Acute mountain sickness may affect about a quarter of people traveling to moderate altitudes. Acute mountain sickness, which occurs following rapid ascent from low to high elevations, is characterized by headache, fatigue, shortness of breath and sleeplessness. Of 3,140 travelers to the Colorado Rocky Mountains to altitudes between 6,300 and 9,700 feet, 25% developed three or more symptoms of acute mountain sickness. Almost 75% reported at least one symptom. Headache was the most common symptom and vomiting was the least. Travelers who permanently resided at elevations below 3,000 feet were more likely to get sick as were people with a previous history of altitude sickness. People under age 60, those in poor or average physical condition and those with lung disease were also more likely to develop acute mountain sickness.

Iron deficiency in children may be prevented by breast feeding, the use of iron-fortified formula, and delay in use of cow's milk until late in infancy. Whether all children should be tested for anemia, a decrease in the number of red blood cells, remains unclear. Although anemia rarely occurs in the United States, children who are fed cow's milk early in infancy or formula not fortified with iron are at risk of iron deficiency. The need for extra dietary sources of iron or iron supplements also remains uncertain. Although breast-fed infants have an adequate supply of iron in the first six months of life, they may require iron supplements thereafter. The iron status was determined in 854 nine-month-old infants, who were fed either cow's milk without added iron, iron-supplemented cow's milk, or human milk, or else were injected with iron dextran. Iron deficiency was indicated if at least two of three biochemical tests for iron levels in the body were abnormal. Iron deficiency anemia was defined as a level of hemoglobin, the oxygen-carrying pigment of red blood cells, of less than 110 grams per liter. Iron deficiency was detected in 37.5 percent of infants fed cow's milk without iron; 26.5 percent of infants fed human milk; 8.0 percent of infants fed an iron-supplemented formula; and 1.3 percent of infants injected with iron dextran. Iron deficiency anemia developed in 20.2 percent of infants fed cow's milk without iron; 14.7 percent of breast-fed infants; 6.0 percent of infants fed iron-supplemented cow's milk; and no infants injected with iron dextran. These findings show that iron supplements are beneficial in infants fed cow's milk without added iron, screening for anemia may be unnecessary in infants fed iron-fortified formula, and breast-fed infants may require iron supplements after six months of age. (Consumer Summary produced by Reliance Medical Information, Inc.)

Objective: To examine whether the prevalence of childhood anemia in white low-income children has continued to decline into the 1990s. Design: An examination of 14 years of hematocrit data from the Centers for Disease Control and Prevention's Pediatric Nutrition Surveillance System in Vermont from 1981 through 1994. Setting: Public health clinics for the Special Supplemental Nutrition Program for Women, Infants, and Children in Vermont. The same screening method and criteria for identifying and defining anemia and the same quality-assurance procedures were used during the 14 years. The program eligibility criteria were also consistent except for part of 1991 and 1992. Main Outcome Measure: The annual prevalence of anemia. Results: Between 1981 and 1994, the prevalence of anemia halved (from 7.9% to 3.6%, P [is less than] .001). For children aged 6 to 24 months, this decline was from 7.8% to 4.6% (P [is less than] .001); for children aged 2 to 5 years, the decline was from 7.9% to 3.1% (P [is less than] .001). Conclusion: The decline in the prevalence of anemia among low-income children observed by the Centers for Disease Control and Prevention's Pediatric Nutrition Surveillance System up to the mid-1980s has continued into the 1990s in Vermont. This finding indicates that iron nutrition in infancy and early childhood is still improving. Arch Pediatr Adolesc Med. 1997; 151:928-930, The rate of anemia among children in low-income families, which had been declining as a result of the work of public pediatric nutrition programs, has continued to decline. As shown in 14 years of records from 1991 to 1994 in Vermont, the rate of anemia has been reduced by half, from 7.9% to 3.6%. This improvement in iron nutrition has been supported and monitored by the Special Supplemental Nutrition Progam for Women, Infants, and Children in Vermont. They were chosen for this study because they have used the same screening method since the 1970's, while many other agencies changed theirs in the late 1980's, making comparisons difficult.

An association between moderate anemia and poor perinatal outcomes has been found through epidemiologic studies, although available evidence cannot establish this relation as causal. Anemia may not be a direct cause of poor pregnancy outcomes, except in the case of maternal mortality resulting directly from severe anemia due to hypoxia and heart failure. Preventing or treating anemia, whether moderate or severe, is desirable. Because iron deficiency is a common cause of maternal anemia, iron supplementation is a common practice to reduce the incidence of maternal anemia. Nevertheless, the effectiveness of large-scale supplementation programs needs to be improved operationally and, where multiple micronutrient deficiencies are common, supplementation beyond iron and folate can be considered. High hemoglobin concentrations are often mistaken as adequate iron status; however, high hemoglobin is independent of iron status and is often associated with poor health outcomes. Very high hemoglobin concentrations cause high blood viscosity, which results in both compromised oxygen delivery to tissues and cerebrovascular complications. Epidemiologic studies have also found an association between high maternal hemoglobin concentrations and an increased risk of poor pregnancy outcomes. Evidence does not suggest that this association is causal; it could be better attributed to hypertensive disorders of pregnancy and to preeclampsia. The pathophysiologic mechanism of these conditions during pregnancy can produce higher hemoglobin concentrations because of reduced normal plasma expansion and cause fetal stress because of reduced placental-fetal perfusion. Accordingly, higher than normal hemoglobin concentrations should be regarded as an indicator of possible pregnancy complications, not necessarily as a sign of adequate iron nutrition, because iron supplementation does not increase hemoglobin higher than the optimal concentration needed for oxygen delivery. Am J Clin Nutr 2000;72(suppl):272S-9S. KEY WORDS Hemoglobin, anemia, polycythemia, iron deficiency, birth outcomes, preeclampsia, iron supplementation, pregnancy

PURPOSE: Hemochromatosis is a genetic disorder of iron absorption that affects 5 per 1,000 persons and is associated with reduced health and quality of life. We sought to determine the type and frequency of symptoms that patients experienced before the diagnosis and the treatments that they received. METHODS: We mailed a questionnaire to 3,562 patients with hemochromatosis who were located using patient advocacy groups, physicians, blood centers, newsletters, and the Internet. RESULTS: Of the 2,851 respondents, 99% were white and 62% were men. Circumstances that led to diagnosis of hemochromatosis included symptoms (35%), an abnormal laboratory test (45%), and diagnosis of a family member with hemochromatosis (20%). The mean ([+ or -] SD) age of symptom onset was 41 [+ or -] 14 years. Symptoms had been present for an average of 10 [+ or -] 10 years before the diagnosis was made. Among the 58% of patients with symptoms, 65% had physician-diagnosed arthritis and 52% had liver disease. The most common and troublesome symptoms were extreme fatigue (46%), arthralgia (44%), and loss of libido (26%). Physician instructions to patients included treatment with phlebotomy (90%), testing family members (75%), and avoiding iron supplements (65%). CONCLUSIONS: The diagnosis of hemochromatosis in most patients was delayed. Physician education is needed to increase the detection of patients with the disease and to improve its management. Am I Med. 1999;106:619-624. [C] 1999 by Excerpta Medica, Inc.

Food-based approaches for controlling vitamin A deficiency and its consequences, such as increased mortality, more severe morbidity, and anemia, have become increasingly important, thus prompting a reassessment of the relation between vitamin A intake and status. A nutrition surveillance system in Central Java, Indonesia, assessed the vitamin A intake and serum retinol concentration of women with a child [is less than or equal to] 24 mo old with a semiquantitative 24-h recall method that categorized vitamin A-containing foods into 3 categories of plant foods and into 2 categories of animal foods and identified portions as small, medium, or large. Median vitamin A intake was 335 retinol equivalents (RE)/d (n = 600) and vitamin A intake from plant foods was 8 times higher than from animal roods. Serum retinol concentration was related to vitamin A intake in a dose-response manner. The multiple logistic regression model for predicting the chance for a serum retinol concentration greater than the observed median ([is greater than or equal to] 1.37 [micro]mol/L) included physiologic factors, vitamin A intake from plant [odds ratio (95% CI) per quartile: 1st, 1.00; 2nd, 1.23 (0.75, 2.02); 3rd, 1.60 (0.97, 2.63); and 4th, 2.06 (1.25, 3.40)] and animal [1st and 2nd, 1.00; 3rd, 1.31 (0.86, 2.02): and 4th, 2.18 (1.40, 3.42)] foods, home gardening [(no, 1.00; yes, 1.71 (1.12, 2.60)], and woman's education level [[is less than or equal to] primary school, 1.00; [is greater than or equal to] secondary school, 1.51 (1.02, 2.22)11. Despite the fact that plant foods contributed 8 times as much vitamin A as did animal foods, serum retinol concentrations did not reflect this large difference. Home gardening and woman's education level seemed to reflect longer-term consumption of vitamin A-rich plant and animal foods, respectively. Am J Clin Nutr 1998:68: 1068-74. KEY WORDS Vitamin A intake, plant foods, animal foods, 24-h recall, vitamin A status, home gardening, socioeconomic status, maternal health, Indonesia. humans, women