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The role of leptin in humans remains controversial. Leptin concentrations are highly correlated with body fat stores. We tested whether or not this relation was consistent across the range of body composition encompassing the lean as well as the obese. Individuals participating in community-based comparative research in Nigeria (n = 363), Jamaica (n = 372), and the United States (Maywood, IL; n = 699) had their plasma leptin concentrations and body compositions (with bioelectrical impedance analysis) measured. All participants identified themselves as being black. Body mass index (in kg/[m.sup.2]) ranged from 14 to 62. Large differences in mean plasma leptin were noted across populations for both men and women in Nigeria, Jamaica, and the United States, respectively (men: 2.8, 3.9, and 6.8 [micro]/L; women: 10.3, 18.6, and 27.7 [micro]g/L). An exponential function fit the relation between percentage body fat or total fat mass and leptin for men and women at each site. For women and men the exponential function with either percentage body fat or total fat mass was of the same shape, but increased by a constant in women, yielding higher leptin concentrations than in men at every level of body fat. On the basis of this broad distribution of body composition, the data suggest an exponential response of leptin to increases in body fat stores, consistent with the development of leptin resistance in individuals developing obesity. These findings likewise confirm that men and women exhibit different set points in terms of leptin production. Am J Clin Nutr 1998;67:391-6.

Leptin concentrations in humans are increased with obesity, and women have higher leptin concentrations than men. This sex difference reflects the greater fat mass of women. However, there is evidence that factors other than the size of the adipose tissue mass contribute to serum leptin concentrations. This study was undertaken to determine whether anthropometric factors influenced leptin concentrations in our population. Leptin concentrations were measured in 375 persons from a population study of hypertension and diabetes for whom body-composition data (bio-electrical impedance analysis and anthropometry) were available. Serum leptin concentrations were more than four times higher in women than in men (18.5 [+ or -] 13.9 compared with 3.8 [+ or -] 3.6 ng/L, P [is less than] 0.0001). In individuals with comparable body mass indexes, these differences persisted after adjustment for either percentage fat (P [is less than] 0.05) or fat mass (P [is less than] 0.0001) by multivariate-regression analysis. After fat mass was adjusted for, the serum leptin concentration in both men and women was independent of waist circumference but in women was associated with hip circumference. Hip circumference is a proxy measure of peripheral fat and these results suggest that the larger hips of women may contribute to the sex difference in serum leptin concentration.

A method is presented to estimate a cutoff for hemoglobin concentration appropriate for estimating the prevalence of iron deficiency anemia in poor Jamaican girls 13-14y of age. Iron deficiency was determined from a three-variable model of iron status (serum ferritin, erythrocyte protoporphyrin, and mean corpuscular volume). The most appropriate hemoglobin cut-off was considered the one that minimized misclassification of iron deficiency: that yielding the maximum kappa coefficient for correctly classifying iron deficiency between 100 and 120 g/L, at 1-g/L intervals. By using this method, a hemoglobin cutoff of 107 g/L was considered most appropriate. This cutoff and the other indicators were used to estimate prevalences of iron deficiency and iron deficiency anemia in the Jamaican girls: 7.6% and 4.3%, respectively. This approach should be appropriate for determining hemoglobin cutoffs for iron deficiency anemia in other populations.

Introduction Hypertension and diabetes mellitus contribute substantially to cardiovascular mortality in the Caribbean. Fetal growth retardation has recently been added to the list of established risk factors for these diseases.[1-8] [...]