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Adeel S.,Metabolism and Lipids | Vydareny K.H.,Emory University | Kumari M.,Metabolism and Lipids | Shah E.,Metabolism and Lipids | And 4 more authors.
Journal of Investigative Medicine | Year: 2013

Postmenopausal osteoporosis is associated with estrogen deficiency and rapid bone loss. The mechanism by which estrogen deficiency results in bone loss has not been fully explained. Studies in mice rendered acutely estrogen deficient by ovariectomy have suggested that estrogen deficiency results in an activated T-lymphocyte phenotype and increased production of pro-osteoclastic cytokines. The aim of this study was to translate these findings from mouse models that suggest that the T lymphocyte plays an important role in the etiology of postmenopausal osteoporosis. We recruited premenopausal women who underwent ovariectomy for benign gynecologic conditions or for prophylaxis against ovarian cancer and a group of matched control women without ovariectomy (OVX). Subjects provided blood samples to characterize T-lymphocyte phenotype by flow cytometry and for T-lymphocyte culture and collection of conditioned media. Bone mineral density at the lumbar spine and left femoral neck was performed annually for 2 years, and volumetric measurements by computed tomography (CT) of the thymus were obtained during the first 6 months. We enrolled 6 patients who underwent OVX and 13 control women. The OVX subjects had a significant loss of bone mineral density at the lumbar spine and left femoral neck. The volumetric thymus measurements suggested an increase in thymus size in the OVX subjects but did not reach statistical significance owing to the small sample size. The T-lymphocyte phenotype in the OVX subjects demonstrated increased T-lymphocyte activation by flow cytometry compared to the control subjects. Our findings support the hypothesis that estrogen deficiency leads to an activated T-lymphocyte phenotype, which may contribute to the bone loss seen in estrogen deficiency. Larger clinical studies are necessary to confirm these findings. Copyright © 2013 by The American Federation for Medical Research. Source

Feldman J.,University of Minnesota | Brown G.R.,East Tennessee State University | Deutsch M.B.,University of California at San Francisco | Hembree W.,Columbia University | And 5 more authors.
Current Opinion in Endocrinology, Diabetes and Obesity | Year: 2016

Purpose of review Transgender individuals experience unique health disparities but are the subject of little focused health research. This manuscript reviews current literature on transgender medical and mental health outcomes and proposes research priorities to address knowledge gaps. Recent findings Published research in transgender healthcare consists primarily of case reports, retrospective and crosssectional studies, involving largely European settings. Challenges to US-based transgender health research include a diverse population where no single center has sufficient patient base to conduct clinical research with statistical rigor. Treatment regimens are heterogeneous and warrant study for best practices. Current research suggests increased mortality and depression in transgender individuals not receiving optimal care, and possibly a modest increase in cardiovascular risk related to hormone therapy. Current evidence does not support concerns for hormone-related malignancy risk. Summary The priorities for transgender medical outcomes research should be to determine health disparities and comorbid health conditions over the life span, along with the effects of mental health, medical, and surgical interventions on morbidity and mortality. Specific outcomes of interest based on frequency in the literature, potential severity of outcome, and patient-centered interest, include affective disorders, cardiovascular disease, malignancies, fertility, and time dose-related responses of specific interventions. © 2016 Wolters Kluwer Health, Inc. All rights reserved. Source

Ganji V.,Georgia State University | Zhang X.,Georgia State University | Tangpricha V.,Metabolism and Lipids | Tangpricha V.,Atlanta Medical Center
Journal of Nutrition | Year: 2012

Prevalence of hypovitaminosis D from previous NHANES reports did not account for assay changes and drifts over time. Thus, published NHANES reports on vitamin D status for the U.S. population were likely either over- or underestimated. We investigated changes in vitamin D status in the U.S. using assay-adjusted serum 25-hydroxyvitamin D [25(OH)D] data from NHANES, 1988-1994 (n = 18,641) and three cycles of NHANES, 2001-2006 (n = 23,424). Changes in geometric mean serum 25(OH)D and prevalence estimates for various serum 25(OH)D cut points (<25, <30, <40, <50, and <75 nmol/L) were determined. From 1988-1994 to 2001-2006, geometric mean serum 25(OH)D significantly decreased by 9% in all participants, 12% in men, 14% in blacks, 16% in 12- to 15-y-old adolescents, 16% in 20- to 30-y-old adults, 13% in nonsupplement users, and 12% in persons with BMI >80th percentile (P < 0.001). From 1988-1994 to 2001-2006, prevalence of serum 25(OH)D<30 nmol/L increased from 5 to 10% in all participants, from 3 to 8% in men, from 22 to 38% in blacks, from 3 to 8% in 12- to 15-y-old adolescents, from 5 to 12% in 20- to 30-y-old adults, from 6 to 14% in nonsupplement users, and from 8 to 17% in persons with BMI >80th percentile (P < 0.001). Previous NHANES reports overestimated the increase in prevalence of hypovitaminosis D. The recent decline in vitamin D status in the U.S. is more likely due to increased prevalence of obesity and other lifestyle changes but not to changes in milk consumption. Source

Park Y.,Emory University | Le N.-A.,Metabolism and Lipids | Yu T.,Emory University | Strobel F.,Emory University | And 6 more authors.
Journal of Nutrition | Year: 2011

The content of sulfur amino acid (SAA) in a meal affects postprandial plasma cysteine concentrations and the redox potential of cysteine/cystine. Because such changes can affect enzyme, transporter, and receptor activities, meal content of SAA could have unrecognized effects on metabolism during the postprandial period. This pilot study used proton NMR ( 1H-NMR) spectroscopy of human plasma to test the hypothesis that dietary SAA content changes macronutrient metabolism. Healthy participants (18-36 y, 5 males and 3 females) were equilibrated for 3 d to adequate SAA, fed chemically defined meals without SAA for 5 d (depletion), and then fed isoenergetic, isonitrogenous meals containing 56 mg·kg -1·d -1 SAA for 4.5 d (repletion). On the first and last day of consuming the chemically defined meals, a morning meal containing 60% of the daily food intake was given and plasma samples were collected over an 8-h postprandial time course for characterization of metabolic changes by 1H-NMR spectroscopy. SAA-free food increased peak intensity in the plasma 1H-NMR spectra in the postprandial period. Orthogonal signal correction/partial least squares-discriminant analysis showed changes in signals associated with lipids, some amino acids, and lactate, with notable increases in plasma lipid signals (TG, unsaturated lipid, cholesterol). Conventional lipid analyses confirmed higher plasma TG and showed an increase in plasma concentration of the lipoprotein lipase inhibitor, apoC-III. The results show that plasma 1H-NMR spectra can provide useful macronutrient profiling following a meal challenge protocol and that a single meal with imbalanced SAA content alters postprandial lipid metabolism. © 2011 American Society for Nutrition. Source

Middleton J.P.,Emory University | Bhagavathula A.P.,Emory University | Gaye B.,Emory University | Alvarez J.A.,Metabolism and Lipids | And 13 more authors.
Journal of Pediatric Gastroenterology and Nutrition | Year: 2013

BACKGROUND:: Vitamin D deficiency and low bone mineral density (BMD) are complications of inflammatory bowel disease. Vitamin D deficiency is more prevalent among African Americans compared with whites. There are little data comparing differences in serum 25-hydroxyvitamin D (25OHD) concentrations and BMD between African American and white children with Crohn disease (CD). METHODS:: We compared serum 25OHD concentrations of African American children with CD (n=52) to white children with CD (n=64) and healthy African American controls (n=40). We also analyzed BMD using dual-energy x-ray absorptiometry results from our pediatric CD population. RESULTS:: African American children with CD had lower serum 25OHD concentrations (16.1 [95% confidence interval, CI 14.5-17.9] ng/mL) than whites with CD (22.3 [95% CI 20.2-24.6] ng/mL; P<0.001). African Americans with CD and controls exhibited similar serum 25OHD concentration (16.1 [95% CI 14.5-17.9] vs 16.3 [95% CI 14.4-18.4] ng/mL; NS). African Americans with CD exhibited no difference in serum 25OHD concentration when controlling for seasonality, disease severity, and surgical history, although serum 25OHD concentration was significantly decreased in overweight children (body mass index ≥85%, P=0.003). Multiple regression analysis demonstrated that obese African American girls with CD had the lowest serum 25OHD concentrations (9.6 [95% CI 6.8-13.5] ng/mL). BMD was comparable between African American and white children with CD (z score -0.4±0.9 vs -0.7±1.2; NS). CONCLUSIONS:: African American children with CD are more likely to have vitamin D deficiency compared with white children with CD, but have similar BMD. CD disease severity and history of surgery do not affect serum 25OHD concentrations among African American children with CD. African American children have low serum 25OHD concentrations, independent of CD, compared with white children. Future research should focus on how race affects vitamin D status and BMD in children with CD. Copyright 2013 by ESPGHAN and NASPGHAN. Source

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