Context-Obesity is associated with hypoferremia, but it is unclear if this condition is caused by insufficient iron stores or diminished iron availability related to inflammation-induced iron sequestration.Objective-To examine the relationships between obesity, serum iron, measures of iron intake, iron stores and inflammation. We hypothesized that both inflammation-induced sequestration of iron and true iron deficiency were involved in the hypoferremia of obesity.Design-Cross-sectional analysis of factors anticipated to affect serum iron. Setting-Outpatient clinic visits.Patients-Convenience sample of 234 obese and 172 non-obese adults.Main outcome measures-Relationships between serum iron, adiposity, and serum transferrin receptor, C-reactive protein, ferritin, and iron intake analyzed by analysis of covariance and multiple linear regression.Results-Serum iron was lower (75.8 ± 35.2 vs 86.5 ± 34.2 g/dl, P=0.002), whereas transferrin receptor (22.6 ± 7.1 vs 21.0 ± 7.2 nmol/l, P=0.026), C-reactive protein (0.75 ± 0.67 vs 0.34±0.67 mg/dl, P<0.0001) and ferritin (81.1 ± 88.8 vs 57.6 ± 88.7 mg/l, P=0.009) were higher in obese than non-obese subjects. Obese subjects had a higher prevalence of iron deficiency defined by serum iron (24.3%, confidence intervals (CI) 19.3-30.2 vs 15.7%, CI 11.0-21.9%, P=0.03) and transferrin receptor (26.9%, CI 21.6-33.0 vs 15.7%, CI 11.0-21.9%, P=0.0078) but not by ferritin (9.8%, CI 6.6-14.4 vs 9.3%, CI 5.7-14.7%, P=0.99). Transferrin receptor, ferritin and C-reactive protein contributed independently as predictors of serum iron.Conclusions-The hypoferremia of obesity appears to be explained both by true iron deficiency and by inflammatory-mediated functional iron deficiency.

ABSTRACT. Objective. Relatively little is known about how excess body mass affects adolescents' capacity to perform sustained exercise. We hypothesized that most of the difficulty that severely overweight adolescents have with sustained exercise occurs because the metabolic costs of moving excess mass result in use of a high proportion of their total oxygen reserve.Methods. We compared results from a maximal cycle ergometry fitness test in 129 severely overweight adolescents who had BMIs of 41.5 ؎ 9.7 kg/m 2 and ages of 14.5 ؎ 1.8 years (range: 12.1-17.8 years) and 34 nonoverweight adolescents who had BMIs of 20.1 ؎ 2.9 kg/m 2 and ages of 14.5 ؎ 1.5 years (range: 12.0 -18.1 years). Oxygen uptake (V O 2 ) was compared at 3 times: during a 4-minute period of unloaded cycling (ULV O 2 ), at the lactate threshold estimated by gas exchange (LTV O 2 ), and at maximal exertion (V O 2 max). Heart rate was obtained at rest and at V O 2 max. Participants also completed a 12-minute walk/ run performance test to obtain distance traveled (D12) and heart rate. Results. Absolute LTV O 2 and V O 2 max and LTV O 2 as a percentage of V O 2 max were not different in overweight and nonoverweight adolescents during the cycle test.However, absolute ULV O 2 was significantly greater in overweight adolescents: ULV O 2 accounted for 35 ؎ 8% of V O 2 max (and 63 ؎ 15% of LTV O 2 ) in overweight adolescents but only 20 ؎ 5% of V O 2 max (and 39 ؎ 12% of LTV O 2 ) in nonoverweight adolescents. Resting heart rate before initiating the cycle test was significantly greater in overweight than nonoverweight adolescents (94 ؎ 14 vs 82 ؎ 15 beats per minute). However, maximal heart rate during the cycle test was significantly lower in overweight adolescents (186 ؎ 13 vs 196 ؎ 11 beats per minute). During the walk/run test, mean D12 was significantly shorter for overweight than for nonoverweight adolescents (1983 ؎ 323 vs 1159 ؎ 194 m). D12 was negatively related to BMI SDS (r ‫؍‬ ؊0.81) and to ULV O 2 (r ‫؍‬ ؊0.98).Discussion. Overweight and nonoverweight adolescents had similar absolute V O 2 at the lactate threshold and at maximal exertion, suggesting that overweight adolescents are more limited by the increased cardiorespiratory effort required to move their larger body mass through space than by cardiorespiratory deconditioning. ABBREVIATIONS. V o 2 max, maximum oxygen uptake; SDS, SD score; ULV o 2 , unloaded oxygen uptake; LTV o 2 , oxygen uptake at the lactate threshold; V o 2 max, oxygen uptake at maximal exertion; HRR, heart rate reserve; RPE, rating of perceived exertion; bpm, beats per minute; D12, distance achieved at 12 minutes during walk/run test; ANCOVA, analysis of covariance. O verweight during childhood has been identified as a major health problem in the United States. 1-4 Pediatric overweight commonly presages adult obesity 5 and is associated with the development of weight-related comorbid conditions and increased morbidity. [6][7][8] Decreased physical activity and a more sedentary lifestyle have been implicated as importan...

Hypoferremia is more prevalent in obese than nonobese adults, but the reason for this phenomenon is unknown. To elucidate the role dietary factors play in obesity-related hypoferremia, the intake of heme and nonheme iron and the intake of other dietary factors known to affect iron absorption were compared cross-sectionally from April 2002 to December 2003 in a convenience sample of 207 obese and 177 nonobese adults. Subjects completed 7-day food records, underwent phlebotomy for serum iron measurement, and had body composition assessed by dual-energy x-ray absorptiometry, during a 21-month period. Data were analyzed by analysis of covariance and multiple linear regression. Serum iron (mean±standard deviation) was significantly lower in obese than nonobese individuals (72.0±61.7 vs 85.3±58.1 µg/dL [12.888±11.0443 vs 15.2687±10.3999 µmol/L]; P<0.001). The obese cohort reported consuming more animal protein (63.6±34.5 vs 55.7±32.5 g/day; P<0.001) and more heme iron (3.6±2.8 vs 2.7±2.6 mg/day; P<0.001). Groups did not differ, however, in total daily iron consumption, including supplements. Obese subjects reported consuming less vitamin C (77.2±94.9 vs 91.8±89.5 mg/day; P=0.01), which may increase absorption of nonheme iron, and less calcium (766.2±665.0 vs 849.0±627.2 mg/day; P=0.038), which may decrease nonheme iron absorption, than nonobese subjects. Groups did not significantly differ in intake of other dietary factors that can impact absorption of iron, including phytic acid, oxalic acid, eggs, coffee, tea, zinc, vegetable protein, or copper. After accounting for demographic covariates and dietary factors expected to affect iron absorption, fat mass (P=0.007) remained a statistically significant negative predictor of serum iron. This cross-sectional, exploratory study suggests that obesity-related hypoferremia is not associated with differences in reported intake of heme and nonheme iron or intake of dietary factors that can affect iron absorption.Several studies in children and adults have shown that obesity is associated with low serum iron concentrations (1-3) and a greater prevalence of iron deficiency (4). However, the pathophysiological mechanisms leading to hypoferremia among obese individuals are unknown. One proposed mechanism is an iron-poor diet (5). However, a difference in iron intake between obese and nonobese subjects has not been shown among US adults.

Obese Black Americans are at particularly high risk for vitamin D deficiency and secondary hyperparathyroidism. Physicians should consider routinely supplementing such patients with vitamin D or screening them for hypovitaminosis D.

OUES differs significantly in overweight and nonoverweight adolescents. The wide interindividual variation and the exercise intensity dependence of OUES preclude its use in clinical practice as a predictor of VO2peak.

Cutoff-point-based definitions for pediatric metabolic syndrome have substantial instability in the short and long term. The value of making a cutoff-point-based diagnosis of metabolic syndrome during childhood or adolescence remains in question.

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Purpose Symptoms of psychological distress have been linked to low insulin sensitivity in adults; however, little is known about this relationship in pediatric samples. We therefore examined symptoms of depression and anxiety in relation to insulin sensitivity in adolescents. Methods Participants were 136 non-treatment seeking, healthy adolescents (53.2% female) of all weight strata (BMI-z = 1.08±1.08) between the ages of 12 and 18 years (M = 15.16, SD = 1.55). Adolescents completed questionnaire measures assessing depression and anxiety symptoms. Fasting blood samples for serum insulin and plasma glucose were obtained to estimate insulin sensitivity with the quantitative insulin sensitivity check index (QUICKI). Fat mass and fat-free mass were measured with air displacement plethysmography or dual-energy x-ray absorptiometry. Results Depressive symptoms were associated with higher fasting insulin and decreased insulin sensitivity even after controlling for fat mass, fat-free mass, height, age, pubertal status, race, and sex (ps < 0.01). Conclusions As has been described for adults, depressive symptoms are associated with low insulin sensitivity among healthy adolescents. Further experimental and prospective studies are required to determine the directionality of this link.