Obesity in women of childbearing age: risks, prevention, and treatment.

This article reviews the health burden of obesity, its treatment and prevention, and potential barriers to care with special emphasis on adult women of childbearing age. From 1988 to 1994, 22% of nonpregnant women 18-49 years old in the United States were overweight (body mass index [BMI] >/= 25-29.9), and 22% were obese (BMI >/= 30). Both conditions increase the risk of chronic disease and mortality, and among women of childbearing age, overweight and obesity also increase the risk of infertility and adverse pregnancy outcomes.The three main strategies for preventing obesity are weight maintenance, weight loss for overweight and obese persons, and physical activity for all. More than 44% of nonpregnant women of childbearing age are trying to lose weight, and more than 33% are trying to maintain weight, but less than 21% of women of childbearing age use the recommended combination of physical activity and caloric restriction to try to lose or maintain weight. Pregnant women should try to gain no more than the recommended weight gain range for their prepregnancy BMI, yet about one third gain more weight.Although research has shown that advice from physicians can have an impact on their patients' eating habits and physical activity, many health professionals either provide no such advice or give inappropriate advice to women of childbearing age. Barriers may include inadequate reimbursement, time constraints, and lack of professional training. Frequent contact with women of childbearing age provides obstetricians and gynecologists and nurse specialists an opportunity to prevent and treat obesity successfully.

Validity of self-reported pregnancy delivery weight: an analysis of the 1988 National Maternal and Infant Health Survey. NMIHS Collaborative Working Group.

This study examined the validity of self-reported delivery weight among 3,518 respondents to the 1988 National Maternal and Infant Health Survey. Self-reported delivery weight was ascertained from a mail survey administered during the postpartum period. Measured delivery weight was obtained by abstraction of medical records from the hospital of delivery. On average, a woman's reported delivery weight was 2.82 pounds (1 pound = 0.45 kg) less than her measured delivery weight (p < 0.001). The level of underreporting increased significantly with increases in prepregnancy body mass index, current body mass index, pregnancy weight gain, and weight change from delivery to recall. Reporting error also increased among women who were non-White, less educated, and unmarried; whose pregnancy was unintended; and who initiated prenatal care late, responded late to the survey questionnaire, became pregnant again before responding, and reported a delivery weight ending in zero. When reported delivery weight was used to calculate weight gain and was categorized into typical weight gain categories, 30-40% of women were classified incorrectly. An empirical evaluation of how this misclassification might impact epidemiologic analyses indicated that associations between weight gain and birth weight were attenuated when weight gain was based on reported delivery weight rather than on measured delivery weight.

The validity of self-reports of past body weights by U.S. adults.

Past weight or patterns of weight change may be more important to chronic disease risk than current weight. Self-reports, however, are often the only source of information about past body weight. To date, very few studies have examined factors affecting the validity of self-reported past body weight. We examined the validity of self-reported past body weights of 1,931 U.S. adults who were participants in the First National Health and Nutrition Examination Survey (1971-1975) and were interviewed again in the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study (1982-1984). We compared the body weight measured during the initial examination (1971-1975) with the recalled 1971-1975 body weight reported during the follow-up interview (1982-1984). Recalled past weight was strongly correlated with previously measured weight (r = 0.73 for men, and r = 0.74 for women). Men overestimated their past body weight, whereas women underestimated their past weight. Although 39% of men and 41% of women estimated their past weight within 5 pounds, approximately 17% of women and 10% of men underestimated their past weight more than 15 pounds. Accuracy of reporting was influenced by sex, race, current body mass index, and the amount of weight gained over the 10 years following the initial examination. These factors should be considered when using recalled weight in epidemiologic studies.

Iron nutrition does not account for the hemoglobin differences between blacks and whites.

Many researchers have reported lower hemoglobin concentrations in blacks than in whites, but the reason for this difference is unknown. Data for 2515 persons (in 3-12 y and 18-45 y age groups) from the Second National Health and Nutrition Examination Survey (NHANES II) were evaluated to investigate the roles of iron intake and biochemical iron status indicators in explaining black and white differences in hemoglobin concentration. Dietary iron intake was estimated from one 24-h food recall, and hemoglobin, serum ferritin, transferrin saturation and erythrocyte protoporphyrin were measured by standard laboratory methods. Hemoglobin levels were substantially lower in black children (120.3 g/L) than in white children (126.8 g/L). Hemoglobin concentrations were also lower in black women (128.4 g/L) than in white women (133.9 g/L), and in black men (144.8 g/L) than in white men (153.2 g/L). Blacks had lower hemoglobin concentration than whites at most levels of dietary iron intake, serum ferritin, transferrin saturation and erythrocyte protoporphyrin. Despite their lower hemoglobin levels, blacks had higher serum ferritin levels than whites. These results suggest that the difference in hemoglobin concentrations between blacks and whites in the United States is the result of factors other than iron intake and iron status. More specific investigations of both the genetic and environmental determinants of iron utilization in blacks are needed.

A prospective study of infectious diseases following bone marrow transplantation: emergence of Aspergillus and Cytomegalovirus as the major causes of mortality.

We performed a prospective study of infections following bone marrow transplantation in 50 patients treated for aplastic anemia or hematologic malignancy. Early, continuous prophylaxis with trimethoprim/sulfamethoxazole and oral nystatin, and empiric intravenous antimicrobial therapy during febrile granulocytopenic episodes were standard treatment for all patients. The use of trimethoprim/sulfamethoxazole did not appear to adversely affect donor marrow engraftment. Serious gram-negative bacillary and systemic Candida infections were uncommon. Although gram-positive bacterial infections were frequent, they were rarely associated with mortality. Aspergillosis emerged as the single most important infection, contributing to the death of nine patients. Cytomegalovirus diseases developed in 13 patients, seven of whom died. Patient age and chronic myelogenous leukemia were risk factors for the development of fatal infections. This study demonstrates that although certain serious infections can be controlled, there is a critical need for effective measures to prevent and treat aspergillosis and cytomegalovirus disease in these seriously compromised hosts.

Wiskott-Aldrich syndrome: histopathologic findings in the lymph nodes and spleens of 15 patients.

Seventeen lymph nodes and 13 spleens from 15 patients with the Wiskott-Aldrich syndrome were examined histologically. The material included both biopsy and autopsy specimens. Consistent findings included depletion of small lymphocytes from T cell areas (all cases), prominence of the reticulum cell stroma (all cases), the presence of atypical plasma cells with and without plasmacytosis (16 lymph nodes and 11 spleens), and extramedullary hematopoiesis (13 lymph nodes and 9 spleens). Less frequent features noted were tissue eosinophilia, hemophagocytosis, focal fibrosis, and progressive depletion of germinal centers. One case with a unique abundance of transformed lymphocytes is described.

The Wiskott-Aldrich syndrome in the United States and Canada (1892-1979).

Information was collected on 301 cases of the Wiskott-Aldrich syndrome in the United States and Canada Examination of available medical records, death certificates and published case reports on these patients showed that they came from a wide geographic area and many diverse ethnic and racial groups. No significant difference was found in the incidence of cases born between 1947 and 1976; the overall rate was 4.0 per million live male births in the United States. Median survival has increased with time from eight months for patients born before 1935 to 6.5 years for those born after 1964. Seventy-six of the 301 patients (25%) were still alive at last follow-up and ranged in age from 1 to 36 years with a median of 10 years. Causes of death were primarily limited to infections or bleeding, but malignancy represented a significant problem. Twelve percent of the group (36 of 301) developed malignancy, the predominant types being lymphorecticular tumors (23 of 36) and leukemia (7 of 36). The overall relative risk for malignancy was found to be greater than 100 times that of the general population and was found to increase with increasing age.

Wiskott-Aldrich syndrome: detection of carrier state by metabolic stress of platelets.

A stress test has been designed which shows a consistent abnormality in platelets from carriers of the Wiskott-Aldrich-syndrome (W.A.S.) gene. 2-deoxy-D-glucose (D.D.G.), an inhibitor of glycolysis, completely inhibited second-wave adrenaline (epinephrine)-induced aggregation of platelets from 10 W.A.S. carriers, whereas it had no effect on the response of control platelets. Antimycin A (Ant A), an inhibitor of oxidative phosphorylation, had no effect on adrenaline-induced platelet aggregation of either carriers or controls. Incubation of control platelets with a combination of Ant A and D.D.G. inhibited aggregation in a way comparable to the effect of D.D.G. alone on carrier cells. Thus, W.A.S. carriers have a defect in platelet metabolism similar to that produced in normal platelets with Ant A. The D.D.G. stress test is a simple reproducible assay for detection of W.A.S. carriers.