Jeanine B Albu

St. Luke's Hospital, CID, Iowa, United States

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Publications (89)391.26 Total impact

  • Russell Rising · Kathryn Whyte · Jeanine Albu · Xavier Pi-Sunyer ·
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    ABSTRACT: Background: The most common methods for obtaining human resting metabolic rate (RMR) use either a ventilated hood connected to a metabolic cart (VH_MC) or calculation by many prediction equations utilizing the person's height and weight. These methods may be inherently inaccurate. The objective of this study is to compare the accuracy for the measurement of RMR by three methods: a new whole room indirect calorimeter specific for this purpose (RMR_WRIC), VH_MC and calculation by the Mifflin equation (ME). First, the VH_MC (Vmax Encore 2900, Carefusion Inc, San Diego, CA) and RMR_WRIC (Promethion GA-6/FG-1, Sable Systems Intl, Las Vegas, NV) were subjected to 10, one-hour ethanol (99.8 % purity) and propane (99.5 % purity) combustion tests, respectively, for simulated metabolic measurements. Thereafter, 40 healthy adults (22 M/18 F, 78.0 ± 24.5 kg, BMI = 25.6 ± 4.8, age 36.6 ± 13.4 years) had one-hour RMR (kcal), ventilation (liters) rates of oxygen (VO2), carbon dioxide (VCO2) and RQ (VCO2/VO2) measured after a 12-h fast with both the VH_ MC and the RMR_WRIC in a randomized fashion. The resting state was documented by heart rate. The RMR was also calculated using the ME, which was compared to both the RMR_WRIC and the VH_MC. All simulated and human metabolic data were extrapolated to 24-h and analyzed (SPSS, Ver. 22). Results: Comparing stoichiometry to actual combustion, the VH_MC underestimated simulated RMR (p < 0.05), VO2 (p < 0.05), VCO2 (p < 0.05) and the RQ. Similarly the RMR_WRIC underestimated simulated RMR (p < 0.05) and VO2 while overestimating VCO2 and the RQ. There was much greater variability in the simulated metabolic data between combustion and the VH_MC as compared to that of the RMR_WRIC. With regards to the volunteers, the RMR, RQ, VO2 and VCO2 determined by the VH_MC tended to be lower in comparison to these measurements determined by the RMR_WRIC. Finally, RMR calculated utilizing the ME was significantly (p < 0.05) less than the RMR_WRIC but similar to that obtained by the VH_MC. Conclusion: The RMR_WRIC was more accurate and precise than either the VH_MC or ME, which has implications for determining energy requirements for individuals participating in weight loss or nutrition rehabilitation programs.
    Nutrition & Metabolism 12/2015; 12(1). DOI:10.1186/s12986-015-0043-0 · 3.26 Impact Factor
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    ABSTRACT: To determine whether a weight-maintaining, moderate (50%) high-fat diet is deleterious to insulin sensitivity in healthy premenopausal women. 23 African-American and non-Hispanic white, healthy, overweight, and obese premenopausal women recruited in New York City, USA, fed either a eucaloric, 1-week long high-fat (50% of total Kcal from fat) diet or a eucaloric, 1-week long low-fat (30% of total Kcal from fat) diet, assigned in a randomized crossover design. Peripheral insulin sensitivity and metabolic flexibility during a euglycemic hyperinsulinemic (80 mU/m(2)/min) clamp measured during the follicular phase of the menstrual cycle, at the end of each diet period. Peripheral insulin sensitivity (mg kg/fat-free mass/min (µU/mL)×10(-1)) was not decreased after the high-fat diet vs the low-fat diet (0.09±0.01 vs 0.08±0.01, p=0.09, respectively) in the combined group of African-American and white women, with no significant diet by race interaction (p=0.6). Metabolic flexibility (change in substrate utilization, ΔNPRQ, in response to insulin during the clamp) was similarly unaltered by the diet (0.12±0.01 vs 0.11, p=0.48, for the high-fat diet vs the low-fat diet, respectively) in the combined group of women, with no significant diet by race interaction (p=0.9). African-American women had a lower insulin clearance compared with the white women, regardless of the diet (p<0.05). We conclude that a short term (1 week), moderate (50%), eucaloric high-fat diet does not lower peripheral insulin sensitivity in healthy, overweight and obese premenopausal women.
    07/2015; 3(1):e000100. DOI:10.1136/bmjdrc-2015-000100
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    ABSTRACT: The purpose of this randomized controlled clinical trial was to determine the effect of a 14-week high-intensity interval-training (HIIT) intervention with weight stability on metabolic flexibility, insulin sensitivity and cardiorespiratory fitness in sedentary, premenopausal, non-diabetic, overweight/obese African-American women. Twenty-eight subjects were allocated to one of two groups: HIIT, which performed three sessions/week of four high-intensity cycling intervals; or CON, which maintained their normal level of physical activity. Diet was controlled for all subjects to ensure weight stability. Pre and post intervention, subjects completed an incremental cycling test to limit of tolerance and, following a 10-day high-fat controlled feeding period, a euglycemic-hyperinsulinemic clamp to determine insulin sensitivity and substrate oxidation. Nine members of HIIT (age, 29 ± 4 yr; body mass, 90.1 ± 13.8 kg) and 11 members of CON (age, 30 ± 7 yr; body mass, 85.5 ± 10.7 kg) completed the study. HIIT experienced increased limit of tolerance (post, 1124 ± 202 s; pre, 987 ± 146 s; P<0.05), gas exchange threshold (post, 1.29 ± 0.34 L∙min(-1); pre, 0.97 ± 0.23 L∙min(-1); P<0.05) and fat oxidation at the same absolute submaximal work rate compared to CON (P<0.05 for group-by-time interaction in all cases). However, changes in Vo2peak, insulin sensitivity, free-fatty-acid suppression during insulin stimulation and metabolic flexibility were not different in HIIT compared to CON. High-intensity interval training with weight stability increased exercise fat oxidation and tolerance in subjects at risk for diabetic progression, but did not improve insulin sensitivity or fat oxidation in the post-absorptive or insulin-stimulated state. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 06/2015; 119(4):jap.00306.2015. DOI:10.1152/japplphysiol.00306.2015 · 3.06 Impact Factor
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    ABSTRACT: Dietary components have potential to arrest or modify chronic disease processes including obesity, cancer, and comorbidities. However, clinical research to translate mechanistic nutrition data into clinical interventions is needed. We have developed a one-year transitional postdoctoral curriculum to prepare nutrition scientists in the language and practice of medicine and in clinical research methodology before undertaking independent research. Candidates with an earned doctorate in nutrition science receive intensive, didactic training at the interface of nutrition and medicine, participate in supervised medical observerships, and join ongoing clinical research. To date, we have trained four postdoctoral fellows. Formative evaluation revealed several learning barriers to this training, including deficits in prior medical science knowledge and diverse perceptions of the role of the translational nutrition scientist. Several innovative techniques to address these barriers are discussed. We propose the fact that this “train the trainer” approach has potential to create a new translational nutrition researcher competent to identify clinical problems, collaborate with clinicians and researchers, and incorporate nutrition science across disciplines from “bench to bedside.” We also expect the translational nutrition scientist to serve as an expert resource to the medical team in use of nutrition as adjuvant therapy for the prevention and management of chronic disease.
    01/2015; 2015(11):1-6. DOI:10.1155/2015/954808
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    ABSTRACT: Hepatic fat is related to insulin resistance (IR) and visceral adipose tissue (VAT) in HIV+ and uninfected individuals. Growth hormone (GH) reduces VAT but increases IR. We evaluated the effects of recombinant human GH (rhGH) and rosiglitazone (Rosi) on hepatic fat in a substudy of a randomized controlled trial. HIV+ subjects with abdominal obesity and IR (QUICKI < 0.33) were randomized to rhGH 3 mg daily, Rosi 4 mg twice daily, the combination, or double placebo. Hepatic fat was measured by magnetic resonance spectroscopy (MRS), visceral fat by MRI, and IR by frequently sampled IV glucose tolerance tests at baseline and week 12. 31 subjects were studied at both time points. Significant correlations between hepatic fat and VAT (r = 0.41, p=0.02) and QUICKI (r = 0.39, p<0.05) were seen at baseline. Insulin resistance rose with rhGH but not Rosi. When rhGH treatment groups were combined, hepatic fat expressed as percent change decreased significantly (p<0.05) but did not change in Rosi (p=0.71). There were no correlations between changes in hepatic fat and VAT (p=0.4) or QUICKI (p=0.6). In a substudy of 21 subjects, a trend was noticed between changes in hepatic fat and serum IGF-1 (p=0.09). Hepatic fat correlates significantly with both VAT and IR, but changes in hepatic fat do not correlate with changes in VAT and glucose metabolism. Hepatic fat content is reduced by rhGH but Rosi has no effect. These results suggest an independent effect of growth hormone or IGF-1 on hepatic fat. The study was registered at (NCT00130286).
    Antiviral therapy 12/2014; DOI:10.3851/IMP2927 · 3.02 Impact Factor
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    Ari Shechter · Russell Rising · Scott Wolfe · Jeanine B. Albu · M-P St-Onge ·
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    ABSTRACT: Background/Objectives The extent to which alterations in energy expenditure (EE) in response to sleep restriction contribute to the short sleep-obesity relationship is not clearly defined. Short sleep may induce changes in resting metabolic rate (RMR), thermic effect of food (TEF), and postprandial substrate oxidation. Subjects/Methods Ten females (age and BMI: 22-43 y and 23.4-28 kg/m2) completed a randomized, crossover study assessing the effects of short (4 h/night) and habitual (8 h/night) sleep duration on fasting and postprandial RMR and respiratory quotient (RQ). Measurements were taken after 3 nights using whole-room indirect calorimetry. The TEF was assessed over a 6-h period following consumption of a high-fat liquid meal. Results Short vs. habitual sleep did not affect RMR (1.01 ± 0.05 and 0.97 ± 0.04 kcal/min; p=0.23). Fasting RQ was significantly lower after short vs. habitual sleep (0.84 ± 0.01 and 0.88 ± 0.01; p=0.028). Postprandial EE (short: 1.13 ± 0.04 and habitual: 1.10 ± 0.04, p=0.09) and RQ (short: 0.88 ± 0.01 and habitual: 0.88 ± 0.01, p=0.50) after the high-fat meal were not different between conditions. TEF was similar between conditions (0.24 ± 0.02 kcal/min in both; p=0.98), as was the ~6-h incremental area under the curve (1.16 ± 0.10 and 1.17 ± 0.09 kcal/min x 356 min after short and habitual sleep, respectively; p=0.92). Conclusions Current findings observed in non-obese healthy premenopausal women do not support the hypothesis that alterations in TEF and postprandial substrate oxidation are major contributors to the higher rate of obesity observed in short sleepers. In exploring a role of sleep duration on EE, research should focus on potential alterations in physical activity to explain the increased obesity risk in short sleepers.
    International journal of obesity (2005) 12/2013; 38(9). DOI:10.1038/ijo.2013.239 · 5.00 Impact Factor
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    ABSTRACT: Objective: The overexpression of the adipose gene (adp/WDTC1) in mice inhibits lipid accumulation and improves the metabolic profile. Subcutaneous fat adp expression in humans and its relation to metabolic parameters was evaluated. Design and methods: Abdominal subcutaneous fat adp expression, insulin sensitivity (clamp), and respiratory quotient (RQ; indirect calorimetry) were assessed in: 36 obese and 56 BMI-, race-, and sex-matched type 2 diabetic volunteers (Look AHEAD Adipose Ancillary Study); 37 nondiabetic Pima Indians including obese (n = 18) and nonobese (n = 19) subjects and; 62 nonobese nondiabetic subjects at the Pennington Center in the ADAPT study. Results: In the Look AHEAD Study, adp expression normalized for cyclophilin B was higher in males versus females (1.27 ± 0.06 vs. 1.11 ± 0.04; P < 0.01) but not after controlling for body fat. Adp expression was not influenced by the presence of diabetes but was related to body fat (r = -0.23; P = 0.03), insulin sensitivity (r = 0.23; P = 0.03) and fasting/insulin-stimulated RQ (r = 0.31 and 0.33; P < 0.01). In Pima Indians, adp expression was also higher in males versus females (1.00 ± 0.05 vs. 0.77 ± 0.05; P = 0.02) and higher in nonobese versus obese (1.02 ± 0.05 vs. 0.80 ± 0.06; P = 0.03). In the ADAPT study, there was no difference in adp expression between males and females. Conclusion: Consistent with animal studies, our results suggest that high adp expression in human adipose tissue is associated with lower adiposity and enhanced glucose utilization.
    Obesity 11/2013; 21(11). DOI:10.1002/oby.20371 · 3.73 Impact Factor
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    Ari Shechter · Russell Rising · Jeanine B Albu · Marie-Pierre St-Onge ·
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    ABSTRACT: Epidemiologic evidence has shown a link between short sleep and obesity. Clinical studies suggest a role of increased energy intake in this relation, whereas the contributions of energy expenditure (EE) and substrate utilization are less clearly defined. Our aim was to investigate the effects of sleep curtailment on 24-h EE and respiratory quotient (RQ) by using whole-room indirect calorimetry under fixed-meal conditions. Ten females aged 22-43 y with a BMI (in kg/m(2)) of 23.4-27.5 completed a randomized, crossover study. Participants were studied under short- (4 h/night) and habitual- (8 h/night) sleep conditions for 3 d, with a 4-wk washout period between visits. Standardized weight-maintenance meals were served at 0800, 1200, and 1900 with a snack at 1600. Measures included EE and RQ during the sleep episode on day 2 and continuously over 23 h on day 3. Short compared with habitual sleep resulted in significantly higher (±SEM) 24-h EE (1914.0 ± 62.4 kcal compared with 1822.1 ± 43.8 kcal; P = 0.012). EE during the scheduled sleep episode (0100-0500 and 2300-0700 in short- and habitual-sleep conditions, respectively) and across the waking episode (0800-2300) were unaffected by sleep restriction. RQ was unaffected by sleep restriction. Short compared with habitual sleep is associated with an increased 24-h EE of ∼92 kcal (∼5%)-lower than the increased energy intake observed in prior sleep-curtailment studies. This finding supports the hypothesis that short sleep may predispose to weight gain as a result of an increase in energy intake that is beyond the modest energy costs associated with prolonged nocturnal wakefulness. This trial was registered at as NCT01751581.
    American Journal of Clinical Nutrition 10/2013; 98(6). DOI:10.3945/ajcn.113.069427 · 6.77 Impact Factor
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    ABSTRACT: Recombinant human growth hormone (rhGH) reduces visceral adipose tissue (VAT) volume in HIV-infected patients but can worsen glucose homeostasis and lipoatrophy. We aimed to determine if adding rosiglitazone to rhGH would abrogate the adverse effects of rhGH on insulin sensitivity (SI) and subcutaneous adipose tissue (SAT) volume. Randomized, double-blind, placebo-controlled, multicenter trial using a 2×2 factorial design in which HIV-infected subjects with abdominal obesity and insulin resistance were randomized to rhGH 3 mg daily, rosiglitazone 4 mg twice daily, combination rhGH + rosiglitazone, or double placebo (control) for 12 weeks. The primary endpoint was change in SI by frequently sampled intravenous glucose tolerance test from entry to week 12. Body composition was assessed by whole body magnetic resonance imaging (MRI) and dual Xray absorptiometry (DEXA). Seventy-seven subjects were randomized of whom 72 initiated study drugs. Change in SI from entry to week 12 differed across the 4 arms by 1-way ANCOVA (P = 0.02); by pair-wise comparisons, only rhGH (decreasing SI; P = 0.03) differed significantly from control. Changes from entry to week 12 in fasting glucose and glucose area under the curve on 2-hour oral glucose tolerance test differed across arms (1-way ANCOVA P = 0.004), increasing in the rhGH arm relative to control. VAT decreased significantly in the rhGH arms (-17.5% in rhGH/rosiglitazone and -22.7% in rhGH) but not in the rosiglitazone alone (-2.5%) or control arms (-1.9%). SAT did not change significantly in any arm. DEXA results were consistent with the MRI data. There was no significant rhGH x rosiglitazone interaction for any body composition parameter. The addition of rosiglitazone abrogated the adverse effects of rhGH on insulin sensitivity and glucose tolerance while not significantly modifying the lowering effect of rhGH on VAT. NCT00130286.
    PLoS ONE 04/2013; 8(4):e61160. DOI:10.1371/journal.pone.0061160 · 3.23 Impact Factor

  • Journal of the American Academy of Nutrition and Dietetics 09/2012; 112(9):A73. DOI:10.1016/j.jand.2012.06.257 · 3.47 Impact Factor
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    ABSTRACT: Recent research has shown an inverse relationship between bone marrow adipose tissue (BMAT) and bone mineral density (BMD). There is a lack of evidence at the macro-imaging level to establish whether increased BMAT is a cause or effect of bone loss. This cross-sectional study compared the BMAT and BMD relationship between a younger adult group at or approaching peak bone mass (PBM; age 18.0-39.9 years) and an older group with potential bone loss (PoBL; age 40.0-88.0 years). Pelvic BMAT was evaluated in 560 healthy men and women with T1-weighted whole-body magnetic resonance imaging. BMD was measured using whole-body dual-energy X-ray absorptiometry. An inverse correlation was observed between pelvic BMAT and pelvic, total and spine BMD in the younger PBM group (r=-0.419 to -0.461, P<0.001) and in the older PoBL group (r=-0.405 to -0.500, P<0.001). After adjusting for age, sex, ethnicity, menopausal status, total body fat, skeletal muscle, subcutaneous and visceral adipose tissue, neither subject group (younger PBM vs older PoBL) nor its interaction with pelvic BMAT significantly contributed to the regression models with BMD as dependent variable and pelvic BMAT as independent variable (P=0.434-0.928). Our findings indicate that an inverse relationship between pelvic BMAT and BMD is present both in younger subjects who have not yet experienced bone loss and also in older subjects. These results provide support at the macro-imaging level for the hypothesis that low BMD may be a result of preferential differentiation of mesenchymal stem cells from osteoblasts to adipocytes.
    European journal of clinical nutrition 04/2012; 66(9):983-8. DOI:10.1038/ejcn.2012.35 · 2.71 Impact Factor
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    ABSTRACT: The relationship between bone marrow adipose tissue and bone mineral density is different between African Americans and Caucasians as well as between men and women. This suggests that the mechanisms that regulate the differentiation and proliferation of bone marrow stromal cells may differ in these populations. It has long been established that there are ethnic and sex differences in bone mineral density (BMD) and fracture risk. Recent studies suggest that bone marrow adipose tissue (BMAT) may play a role in the pathogenesis of osteoporosis. It is unknown whether ethnic and sex differences exist in the relationship between BMAT and BMD. Pelvic BMAT was evaluated in 455 healthy African American and Caucasian men and women (age 18-88 years) using whole-body T1-weighted magnetic resonance imaging. BMD was measured using whole-body dual-energy X-ray absorptiometry. A negative correlation was observed between pelvic BMAT and total body BMD or pelvic BMD (r = -0.533, -0.576, respectively; P < 0.001). In multiple regression analyses with BMD as the dependent variable, ethnicity significantly entered the regression models as either an individual term or an interaction with BMAT. Menopausal status significantly entered the regression model with total body BMD as the dependent variable. African Americans had higher total body BMD than Caucasians for the same amount of BMAT, and the ethnic difference for pelvic BMD was greater in those participants with a higher BMAT. Men and premenopausal women had higher total body BMD levels than postmenopausal women for the same amount of BMAT. An inverse relationship exists between BMAT and BMD in African American and Caucasian men and women. The observed ethnic and sex differences between BMAT and BMD in the present study suggest the possibility that the mechanisms regulating the differentiation and proliferation of bone marrow stromal cells may differ in these populations.
    Osteoporosis International 12/2011; 23(9):2293-301. DOI:10.1007/s00198-011-1873-x · 4.17 Impact Factor
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    ABSTRACT: To describe the potential long-term risk of malnutrition after Roux-en-Y gastric bypass (GBP) through an uncommon occurrence of inflammatory bowel disease (IBD) postoperatively, which posed a serious threat to the nutritional status and the life of the patient. We present a case report of a 44-year-old woman in whom Crohn disease developed 4 years after she had undergone GBP. The double insult of IBD and GBP resulted in severe malnutrition, with a serum albumin concentration of 0.9 g/dL (reference range, 3.5 to 5.0), weight loss, and watery diarrhea necessitating 6 hospital admissions during a period of 7 months. Ultimately, the administration of total parenteral nutrition with aggressive macronutrient, vitamin, and mineral repletion resulted in substantial improvement in the patient's strength, function, and quality of life, in parallel with diminished symptoms of IBD. Rarely, IBD develops after GBP, but the relationship between the 2 conditions remains unclear. Regardless, in addition to the altered anatomy after bariatric surgery, the further insult of IBD poses a severe threat to the nutritional status of affected patients. Malnutrition needs to be recognized and aggressively treated. Nutritional markers should be followed closely in this population of bariatric patients in an effort to avert the onset of severe malnutrition.
    Endocrine Practice 12/2011; 18(2):e21-5. DOI:10.4158/EP11200.CR · 2.81 Impact Factor
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    ABSTRACT: AngII (angiotensin II) may contribute to cardiovascular risk in obesity via adverse effects on insulin sensitivity and endothelial function. In the present study, we examined the effects of ARB (angiotensin receptor blocker) therapy (losartan, 100 mg/day) on insulin sensitivity and endothelial function in 53 subjects with stage I hypertension, abdominal obesity and impaired fasting glucose. The study design was a randomized double-blinded parallel design placebo-controlled multi-centre trial of 8 weeks duration. We used the hyperinsulinaemic-euglycaemic clamp technique to measure insulin sensitivity (expressed as the 'M/I' value) and RH-PAT (reactive hyperaemia-peripheral arterial tonometry) to measure endothelial function. Additional measures included HOMA (homoeostasis model assessment)-B, an index of pancreatic β-cell function, and markers of inflammation [e.g. CRP (C-reactive protein)] and oxidative stress (e.g. F2-isoprostanes). ARB therapy did not alter insulin sensitivity [5.2 (2.7) pre-treatment and 4.6 (1.6) post-treatment] compared with placebo therapy [6.1 (2.9) pre-treatment and 5.3 (2.7) post-treatment; P value not significant], but did improve the HOMA-B compared with placebo therapy (P=0.05). ARB therapy also did not change endothelial function [RH-PAT, 2.15 (0.7) pre-treatment and 2.11 (0.7) post-treatment] compared with placebo therapy [RH-PAT, 1.81 (0.5) pre-treatment and 1.76 (0.7) post-treatment; P value not significant]. Markers of inflammation and oxidative stress were not significantly changed by ARB therapy. In conclusion, ARB therapy did not alter peripheral insulin sensitivity or endothelial function in this cohort of patients with essential hypertension, abdominal obesity and impaired fasting glucose, but did improve pancreatic β-cell function.
    Clinical Science 08/2011; 122(4):193-202. DOI:10.1042/CS20110284 · 5.60 Impact Factor
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    ABSTRACT: Background: Obesity is known to be associated with an increased risk of death, but current definitions of obesity are based on data from white populations. We examined the association between body mass index (BMI) and the risk of death in a large population of adult Chinese people. Methods: We examined the association between body mass index (BMI) and all-cause mortality prospectively among 58,738 men and 65,718 women aged 20 years and older enrolled in 1998-1999 from four national health screening centres in Taiwan. We used Cox proportional hazards regression analyses to estimate the relative risks of all-cause mortality for different BMI categories during a maximum follow-up of 10 years. Results: A total of 3947 participants died during the follow-up period. The lowest risk of death was observed among men and women who had a BMI of 24.0-25.9 (mean 24.9). After adjustment for age, smoking status, alcohol intake, betel-nut chewing, level of physical activity, income level and education level, we observed a U-shaped association between BMI and all-cause mortality. Similar U-shaped associations were observed when we analyzed data by age (20-64 or ≥ 65 years), smoking (never, < 10 pack-years or ≥ 10 pack-years) and presence of a pre-existing chronic disease, and after we excluded deaths that occurred in the first three years of follow-up. Interpretation: BMI and all-cause mortality had a U-shaped association among adult Chinese people in our study. The lowest risk of death was among adults who had a BMI of 24.0-25.9 (mean 24.9). Our findings do not support the use of a lower cutoff value for overweight and obesity in the adult Chinese population.
    Canadian Medical Association Journal 03/2011; 183(6). DOI:10.1503/cmaj.100303 · 5.96 Impact Factor
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    ABSTRACT: Left ventricular assist devices (LVADs) are increasingly used as therapeutic options for patients with advanced congestive heart failure (CHF), many of whom suffer from diabetes mellitus (DM). The aim of this study was to evaluate the effect of restoration of normal cardiac output using LVAD support on diabetes control in patients with advanced CHF. A retrospective chart review of all clinic patients supported with long-term LVADs between July 2008 and July 2009 at Columbia University Medical Center was performed. Patients with DM diagnosed prior to device implantation were included in this analysis. Clinical and laboratory data within 1 month preceding and 6 months following LVAD implantation were collected. Of 43 LVAD patients followed in our clinic during the study period, 15 had a diagnosis of DM. Thirteen of the 15 patients were male, mean age was 63 ± 11 years, and the pre-LVAD left ventricular ejection fraction (LVEF) was 16.5 ± 5.7%. Fasting glucose levels, HbA1c, and daily insulin requirement within 1 month before and an average of 4.0 ± 2.3 months after LVAD placement were 157.7 ± 50.6 vs. 104.1 ± 21.4 mg/dL, 7.7 ± 0.9 vs. 6.0 ± 0.8.%, and 53.3 ± 51.7 vs. 24.2 ± 27.2 IU, respectively (P < 0.05 for all comparisons). Six of the 15 patients were completely free of antidiabetic medications and had blood glucose < 126 mg/dL as well as HbA1c < 6% after LVAD. Body mass index (BMI) was slightly increased after LVAD (28.7 ± 5.3 vs. 30.2 ± 4.1 kg/m², P NS). Restoration of normal cardiac output after LVAD implantation improves diabetic control in patients with advanced CHF. Additional studies are warranted to determine the mechanisms that worsen or possibly induce DM in patients with advanced CHF.
    European Journal of Heart Failure 02/2011; 13(2):195-9. DOI:10.1093/eurjhf/hfq204 · 6.53 Impact Factor
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    ABSTRACT: Nutritional status is assessed by measuring BMI or percent body fat (%fat). BMI can misclassify persons who carry more weight as fat-free mass and %fat can be misleading in cases of malnutrition or in disease states characterized by wasting of lean tissue. The fat-free mass index (FFMI) is proposed to assess body composition in individuals who have a similar body composition but differ in height allowing identification of those suffering from malnutrition, wasting or those that possess a relatively high muscle mass. The purpose was to determine whether the FFMI differs in a group of racially/ethnically diverse adults. Cross-sectional. Subjects were a multi-ethnic sample (Caucasian, CA; African American, AA; Hispanic, HIS and Asian, AS) of 1339 healthy males (n = 480) and females (n = 859) ranging in age from 18-110 years. Total body fat, total fat-free mass and bone mineral density were estimated using dual energy X-ray absorptiometry. FFMI differed among the four ethnic groups (P ≤ 0.05) for both genders. A curvilinear relationship was found between age and FFMI for both genders although the coefficients in the quadratic model differed between genders (P ≤ 0.001) indicating the rate of change in FFMI differed between genders. The estimated turning point where FFMI started to decline was in the mid 20s for male and mid 40s for female participants. An age × gender interaction was found such that the rate of decline was greater in male than female participants (P ≤ 0.001). For both genders, FFMI was greatest in AA and the least in AS (P ≤ 0.001). There was no significant interaction between race and age or age(2) (P = 0.06). However, male participants consistently had a greater FFMI than female participants (P ≤ 0.001). These findings have clinical implications for identifying individuals who may not be recognized as being malnourished based on their BMI or %fat but whose fat-free mass corrected for height is relatively low.
    International journal of obesity (2005) 01/2011; 35(1):121-7. DOI:10.1038/ijo.2010.111 · 5.00 Impact Factor
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    ABSTRACT: To investigate the association between body mass index (BMI) and waist circumference (WC) and all-cause mortality of Chinese residents in long-term care facilities in Taiwan. Prospective cohort study. Eight long-term care facilities in Taiwan. Three hundred fifty-four residents aged 60 and older (median 78.4, range 60-101; 156 men, 198 women) were recruited during the study period. Anthropometrics and metabolic parameters were measured at baseline. Mean BMI was 21.7 ± 4.2 kg/m(2) (range 11.6-35.3 kg/m(2) , and mean WC was 82.4 ± 10.9 cm (range 55.0-124.0 cm). Mortality data were from the Department of Health in Taiwan. There were 219 deaths during the 5 years of follow-up. After adjusting for age, sex, albumin, Karnofsky performance status scale, hypertension, and diabetes mellitus, subjects in the highest quartile of BMI (27.3 ± 2.8 kg/m(2) ) and WC (96.7 ± 7.4 cm) had a significantly lower mortality rate than did subjects in the lowest quartile (BMI, 16.7 ± 1.7 kg/m(2) ; WC, 69.6 ± 4.2 cm). After further stratification according to central obesity status, the subjects in the two highest BMI quartiles had a lower mortality rate than those in the lowest BMI quartile but only in the central obesity group (≥ 90 cm in men or ≥ 80 cm in women). The adjusted relative risk for all-cause mortality in the highest versus lowest BMI quartile was 0.17 (95% confidence interval = 0.05-0.57). BMI and WC were negative predictors for all-cause mortality in older Chinese adults living in long-term care facilities. Participants with higher WC and BMI had lower all-cause mortality.
    Journal of the American Geriatrics Society 11/2010; 58(11):2092-8. DOI:10.1111/j.1532-5415.2010.03148.x · 4.57 Impact Factor
  • Niyati Parekh · Yong Lin · Richard B Hayes · Jeanine B Albu · Grace L Lu-Yao ·
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    ABSTRACT: Insulin and glucose may influence cancer mortality via their proliferative and anti-apoptotic properties. Using longitudinal data from the nationally representative Third National Health and Nutrition Examination Survey (NHANES III; 1988-1994), with an average follow-up of 8.5 years to death, we evaluated markers of glucose and insulin metabolism, with cancer mortality, ascertained using death certificates or the National Death Index. Plasma glucose, insulin, C-peptide, and lipid concentrations were measured. Anthropometrics, lifestyle, medical, and demographic information was obtained during in-person interviews. After adjusting for age, race, sex, smoking status, physical activity, and body mass index, for every 50 mg/dl increase in plasma glucose, there was a 22% increased risk of overall cancer mortality. Insulin resistance was associated with a 41% (95% confidence interval (CI) (1.07-1.87; p = 0.01) increased risk of overall cancer mortality. These associations were stronger after excluding lung cancer deaths for insulin-resistant individuals (HR: 1.67; 95% CI: 1.15-2.42; p = 0.01), specifically among those with lower levels of physical activity (HR: 2.06; 95% CI: 1.4-3.0; p = 0.0001). Similar associations were observed for other blood markers of glucose and insulin, albeit not statistically significant. In conclusion, hyperglycemia and insulin resistance may be 'high-risk' conditions for cancer mortality. Managing these conditions may be effective cancer control tools.
    Cancer Causes and Control 04/2010; 21(4):631-42. DOI:10.1007/s10552-009-9492-y · 2.74 Impact Factor
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    ABSTRACT: Epidemiologic studies suggest that insulin-like growth factor-1 (IGF-1) is associated with obesity and, more recently, cancer. This study investigates multiple lifestyle, physiologic, and anthropometric determinants of circulating IGF-1 concentrations. Nationally representative data were used from the cross-sectional Third National Health and Nutrition Examination (NHANES III, 1988-1994) survey, which measured IGF-1 concentrations in blood, from a subsample of participants who were examined in the morning. After exclusion of persons with missing data, 6,058 men and women 20 years of age or older were included in the study. The mean IGF-1 concentrations were 260 ng/mL in the entire population and were higher among men as compared with women (278.8 vs. 241.3 ng/mL; p<0.0001). IGF-1 decreased with increasing age (p<0.0001), body mass index (p<0.0001), and waist circumference (p<0.0001). Individuals with metabolic syndrome had lower IGF-1 concentrations after adjustment for covariates (p=0.0008). IGF-1 was inversely associated with increasing number of metabolic syndrome abnormalities (p=0.0008). All associations were stronger among women compared with men except across concentrations of glucose. IGF-1 concentrations did not vary by any other lifestyle or physiologic factors. Age, adiposity, hyperglycemia, and metabolic syndrome influenced circulating IGF-1 concentrations. Diet and physical activity had no impact on IGF-1 in this nationally representative population.
    Annals of epidemiology 03/2010; 20(3):182-93. DOI:10.1016/j.annepidem.2009.11.008 · 2.00 Impact Factor

Publication Stats

3k Citations
391.26 Total Impact Points


  • 1997-2015
    • St. Luke's Hospital
      CID, Iowa, United States
  • 1992-2013
    • Saint Luke's Hospital (NY, USA)
      New York City, New York, United States
  • 2001-2012
    • Columbia University
      • • Institute of Human Nutrition
      • • College of Physicians and Surgeons
      • • Department of Medicine
      • • Division of Endocrinology
      New York, New York, United States
  • 2010
    • Asia University
      • College of Health Science
      臺中市, Taiwan, Taiwan
  • 2006-2009
    • Aurora St. Luke's Medical Center
      Milwaukee, Wisconsin, United States
    • University of Alabama at Birmingham
      Birmingham, Alabama, United States
  • 2008
    • Pennington Biomedical Research Center
      Baton Rouge, Louisiana, United States
  • 1998-2007
    • CUNY Graduate Center
      New York, New York, United States
  • 1987-1992
    • Icahn School of Medicine at Mount Sinai
      • Department of Pediatrics
      Borough of Manhattan, New York, United States