Energy intake, not energy output, is a determinant of body size in infants

BACKGROUND: It has been proposed that the primary determinants of body weight at 1 y of age are genetic background, as represented by parental obesity, and low total energy expenditure. OBJECTIVE: The objective was to determine the relative contributions of genetic background and energy intake and expenditure as determinants of body weight at 1 y of age. DESIGN: Forty infants of obese and 38 infants of lean mothers, half boys and half girls, were assessed at 3 mo of age for 10 risk factors for obesity: sex, risk group (obese or nonobese mothers), maternal and paternal body mass index, body weight, feeding mode (breast, bottle, or both), 3-d energy intake, nutritive sucking behavior during a test meal, total energy expenditure, sleeping energy expenditure, and interactions among them. RESULTS: The only difference between risk groups at baseline was that the high-risk group sucked more vigorously during the test meal. Four measures accounted for 62% of the variability in weight at 12 mo: 3-mo weight (41%, P = 0.0001), nutritive sucking behavior (9%, P = 0.0002), 3-d food intake (8%, P = 0.0002), and male sex (3%, P = 0.05). Food intake and sucking behavior at 3 mo accounted for similar amounts of variability in weight-for-length, body fat, fat-free mass, and skinfold thickness at 12 mo. Contrary to expectations, neither total nor sleeping energy expenditure at 3 mo nor maternal obesity contributed to measures of body size at 12 mo. CONCLUSIONS: Energy intake contributes significantly to measures of body weight and composition at 1 y of age; parental obesity and energy expenditure do not.     

Left ventricular pseudoaneurysm after mitral valve replacement

Development of left ventricular pseudoaneurysm is a rare complication of mitral valve surgery and requires urgent surgical intervention. We describe a case of pseudoaneurysm of membranous septum following repeat mitral valve replacement with the use of multimodality imaging.     

Carboxybiotin translocation mechanisms suggested by diffraction studies of biotin and its vitamers.

Biotin is a coenzyme that fixes CO2 for transfer in a family of carboxylase, decarboxylase, and transcarboxylase enzymes. Their enzyme reactions involve two basic steps during which a carboxybiotinyl intermediate forms at one site and translocates to a second (distinct) site for CO2 transfer. Our diffraction studies of biotin and its vitamers suggest that translocation involves rotation about one, or at most two, bonds in biotin's valeryl chain. The rotations are energetically economical gauche in equilibrium trans rotations about the two valeryl bonds nearest the biotin bicyclic ring. They move a carbon atom of a CO2 moiety bound at N-1' approximately 7 A, a distance in accord with spectroscopic measurements of one of the biotin enzymes. From our studies we infer that sulfur in biotin imparts to the valeryl chain a conformational variability necessary for bond rotation and, hence, translocation between catalytic sites.     

Association of Roadway Proximity with Fasting Plasma Glucose and Metabolic Risk Factors for Cardiovascular Disease in a Cross-Sectional Study of Cardiac Catheterization Patients

Background

The relationship between traffic-related air pollution (TRAP) and risk factors for cardiovascular disease needs to be better understood in order to address the adverse impact of air pollution on human health.

Objective

We examined associations between roadway proximity and traffic exposure zones, as markers of TRAP exposure, and metabolic biomarkers for cardiovascular disease risk in a cohort of patients undergoing cardiac catheterization.

Methods

We performed a cross-sectional study of 2,124 individuals residing in North Carolina (USA). Roadway proximity was assessed via distance to primary and secondary roadways, and we used residence in traffic exposure zones (TEZs) as a proxy for TRAP. Two categories of metabolic outcomes were studied: measures associated with glucose control, and measures associated with lipid metabolism. Statistical models were adjusted for race, sex, smoking, body mass index, and socioeconomic status (SES).

Results

An interquartile-range (990 m) decrease in distance to roadways was associated with higher fasting plasma glucose (β = 2.17 mg/dL; 95% CI: –0.24, 4.59), and the association appeared to be limited to women (β = 5.16 mg/dL; 95% CI: 1.48, 8.84 compared with β = 0.14 mg/dL; 95% CI: –3.04, 3.33 in men). Residence in TEZ 5 (high-speed traffic) and TEZ 6 (stop-and-go traffic), the two traffic zones assumed to have the highest levels of TRAP, was positively associated with high-density lipoprotein cholesterol (HDL-C; β = 8.36; 95% CI: –0.15, 16.9 and β = 5.98; 95% CI: –3.96, 15.9, for TEZ 5 and 6, respectively).

Conclusion

Proxy measures of TRAP exposure were associated with intermediate metabolic traits associated with cardiovascular disease, including fasting plasma glucose and possibly HDL-C.

Citation

Ward-Caviness CK, Kraus WE, Blach C, Haynes CS, Dowdy E, Miranda ML, Devlin RB, Diaz-Sanchez D, Cascio WE, Mukerjee S, Stallings C, Smith LA, Gregory SG, Shah SH, Hauser ER, Neas LM. 2015. Association of roadway proximity with fasting plasma glucose and metabolic risk factors for cardiovascular disease in a cross-sectional study of cardiac catheterization patients. Environ Health Perspect 123:1007–1014; http://dx.doi.org/10.1289/ehp.1306980     

Body composition and metabolic factors in obese children and adolescents

OBJECTIVE: Body composition is associated with metablic factors in adults; however, data are limited regarding obese children. This study was undertaken to assess body composition, regional fat distribution, and metabolic factors in obese 6-18-y-old children and adolescents. DESIGN: Cross-sectional assessment. SUBJECTS: Thirty-six obese children and adolescents, (mean+/-s.e.m.) age 11.8+/-0.5 y, BMI 34.1+/-1.2 kg/m(2). MEASUREMENTS: Body composition was assessed by dual energy X-ray absorptiometry and computerized tomography. Fasting insulin, glucose and leptin levels, and the homeostasis model assessment of insulin sensitivity (HOMA-IR) were assessed. RESULTS: The girls had significantly lower glucose levels than the boys. The ethnic group differences (African American children vs white children) in fat mass, total CT fat, subcutaneous CT fat, insulin level, leptin level, and higher HOMA-IR were not significant after adjusting for age or pubertal stage. These differences in abdominal fat and subcutaneous abdominal fat were also not independent of total body fat or BMI. No ethnic group differences in visceral abdominal fat were noted. Insulin level and HOMA IR were associated with leptin level (independent of fat mass) and fat mass. Leptin level was associated with fat mass, total CT fat, and subcutaneous CT fat; however the associations between the CT fat measures and leptin were not independent of total body fat mass. CONCLUSIONS: Neither visceral abdominal fat, subcutaneous abdominal fat, insulin levels, or insulin resistance differed by ethnic group when adjusted for age or pubertal status. This contrasts with findings in adults and non-obese children which suggest lower levels of visceral fat and higher insulin levels and insulin resistance in African American children and adolescents.     

Fear learning circuitry is biased toward generalization of fear associations in posttraumatic stress disorder

Fear conditioning is an established model for investigating posttraumatic stress disorder (PTSD). However, symptom triggers may vaguely resemble the initial traumatic event, differing on a variety of sensory and affective dimensions. We extended the fear-conditioning model to assess generalization of conditioned fear on fear processing neurocircuitry in PTSD. Military veterans (n=67) consisting of PTSD (n=32) and trauma-exposed comparison (n=35) groups underwent functional magnetic resonance imaging during fear conditioning to a low fear-expressing face while a neutral face was explicitly unreinforced. Stimuli that varied along a neutral-to-fearful continuum were presented before conditioning to assess baseline responses, and after conditioning to assess experience-dependent changes in neural activity. Compared with trauma-exposed controls, PTSD patients exhibited greater post-study memory distortion of the fear-conditioned stimulus toward the stimulus expressing the highest fear intensity. PTSD patients exhibited biased neural activation toward high-intensity stimuli in fusiform gyrus (P<0.02), insula (P<0.001), primary visual cortex (P<0.05), locus coeruleus (P<0.04), thalamus (P<0.01), and at the trend level in inferior frontal gyrus (P=0.07). All regions except fusiform were moderated by childhood trauma. Amygdala–calcarine (P=0.01) and amygdala–thalamus (P=0.06) functional connectivity selectively increased in PTSD patients for high-intensity stimuli after conditioning. In contrast, amygdala–ventromedial prefrontal cortex (P=0.04) connectivity selectively increased in trauma-exposed controls compared with PTSD patients for low-intensity stimuli after conditioning, representing safety learning. In summary, fear generalization in PTSD is biased toward stimuli with higher emotional intensity than the original conditioned-fear stimulus. Functional brain differences provide a putative neurobiological model for fear generalization whereby PTSD symptoms are triggered by threat cues that merely resemble the index trauma.