Effect of obesity on short- and long-term mortality postcoronary revascularization: a meta-analysis

Objective: Overweight and obesity are often assumed to be risk factors for postprocedural mortality in patients with coronary artery disease (CAD). However, recent studies have described an “obesity paradox”—a neutral or beneficial association between obesity and mortality postcoronary revascularization. We reviewed the effect of overweight and obesity systematically on short‐ and long‐term all‐cause mortality post‐coronary artery bypass grafting (CABG) and post‐percutaneous coronary intervention (PCI). Methods: We searched the Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, Scopus, and Web of Science to identify cohort, case control, and randomized controlled studies evaluating the effect of obesity on in‐hospital/short‐term (within 30 days) and long‐term (up to 5 years) mortality. Full‐text, published articles reporting all‐cause mortality between individuals with and without elevated BMI were included. Two reviewers independently assessed studies for inclusion and performed data extraction. Results: Twenty‐two cohort publications were identified, reporting results in ten post‐PCI and twelve post‐CABG populations. Compared to individuals with non‐elevated BMI levels, obese patients undergoing PCI had lower short‐ (odds ratio (OR) 0.63; 95% confidence interval (CI) 0.54–0.73) and long‐term mortality (OR 0.65; 95% CI 0.51–0.83). Post‐CABG, obese patients had lower short‐term (OR 0.63; 95% CI 0.56–0.71) and similar long‐term (OR 0.88; 95% CI 0.60–1.29) mortality risk compared to normal weight individuals. Results were similar in overweight patients for both procedures. Conclusions: Compared to non‐obese individuals, overweight and obese patients have similar or lower short‐ and long‐term mortality rates postcoronary revascularization. Further research is needed to confirm the validity of these findings and delineate potential underlying mechanisms.     

Impact of physician BMI on obesity care and beliefs

Using a national cross-sectional survey of 500 primary care physicians conducted between 9 February and 1 March 2011, the objective of this study was to assess the impact of physician BMI on obesity care, physician self-efficacy, perceptions of role-modeling weight-related health behaviors, and perceptions of patient trust in weight loss advice. We found that physicians with normal BMI were more likely to engage their obese patients in weight loss discussions as compared to overweight/obese physicians (30% vs. 18%, P = 0.010). Physicians with normal BMI had greater confidence in their ability to provide diet (53% vs. 37%, P = 0.002) and exercise counseling (56% vs. 38%, P = 0.001) to their obese patients. A higher percentage of normal BMI physicians believed that overweight/obese patients would be less likely to trust weight loss advice from overweight/obese doctors (80% vs. 69%, P = 0.02). Physicians in the normal BMI category were more likely to believe that physicians should model healthy weight-related behaviors-maintaining a healthy weight (72% vs. 56%, P = 0.002) and exercising regularly (73% vs. 57%, P = 0.001). The probability of a physician recording an obesity diagnosis (93% vs. 7%, P < 0.001) or initiating a weight loss conversation (89% vs. 11%, P ≤ 0.001) with their obese patients was higher when the physicians' perception of the patients' body weight met or exceeded their own personal body weight. These results suggest that more normal weight physicians provided recommended obesity care to their patients and felt confident doing so.     

Skeletal muscle lipid metabolism with obesity

The objectives of this study were to 1). examine skeletal muscle fatty acid oxidation in individuals with varying degrees of adiposity and 2). determine the relationship between skeletal muscle fatty acid oxidation and the accumulation of long-chain fatty acyl-CoAs. Muscle was obtained from normal-weight [n = 8; body mass index (BMI) 23.8 +/- 0.58 kg/m(2)], overweight/obese (n = 8; BMI 30.2 +/- 0.81 kg/m(2)), and extremely obese (n = 8; BMI 53.8 +/- 3.5 kg/m(2)) females undergoing abdominal surgery. Skeletal muscle fatty acid oxidation was assessed in intact muscle strips. Long-chain fatty acyl-CoA concentrations were measured in a separate portion of the same muscle tissue in which fatty acid oxidation was determined. Palmitate oxidation was 58 and 83% lower in skeletal muscle from extremely obese (44.9 +/- 5.2 nmol x g(-1) x h(-1)) patients compared with normal-weight (71.0 +/- 5.0 nmol x g(-1) x h(-1)) and overweight/obese (82.2 +/- 8.7 nmol x g(-1) x h(-1)) patients, respectively. Palmitate oxidation was negatively (R = -0.44, P = 0.003) associated with BMI. Long-chain fatty acyl-CoA content was higher in both the overweight/obese and extremely obese patients compared with normal-weight patients, despite significantly lower fatty acid oxidation only in the extremely obese. No associations were observed between long-chain fatty acyl-CoA content and palmitate oxidation. These data suggest that there is a defect in skeletal muscle fatty acid oxidation with extreme obesity but not overweight/obesity and that the accumulation of intramyocellular long-chain fatty acyl-CoAs is not solely a result of reduced fatty acid oxidation.     

Associations between parental and child overweight and obesity

Results of the analysis showed that parents and children overweight/obesity were significantly correlated. The sample includes 318 pairs of mothers and children, and 336 pairs of fathers and children at the age 11.3 +/- 0.4 years in Trogir, Croatia. Child overweight and obesity were defined according to body mass index (BMI) 25 and 30 equivalents (kg/m2). The prevalence of total overweight in girls was 25.6% and among boys was 20.5%. Mother's weight (p = 0.003) and BMI (p = 0.006) were greater in obese than in other groups of children. Overweight/obese children were more often found among overweight/obese mothers (p = 0.009) and fathers (p = 0.039). Correlation between overweight/obese children and their father (odds ratio 3.2, 95% CI 1.5-6.8) was stronger than between overweight/obese children and their mothers (odds ratio 2.2, 95% CI 1.2-3.9). Associations with mothers' and daughters' overweight/obesity were stronger (p = 0.017) than mothers' and sons'(p = 0.12). Correlations between children's BMI and fathers' BMI (r = 0.265, p < 0.0001) and between children's BMI and mothers' BMI (r = 0.173, p = 0.002) were significant. Children whose parents are overweight/obese look for greater attention in future preventive programme.     

Lp(a) and risk of recurrent cardiac events in obese postinfarction patients

Studies of recurrent coronary events in obese postinfarction patients show mixed results despite potential importance of obesity-related pathophysiologic processes and associated markers in establishing and predicting risk. The study aim was to determine specific markers of recurrent risk in obese postinfarction patients. Nondiabetic patients of the Thrombogenic Factors and Recurrent Coronary Events (THROMBO) postinfarction study were classified according to BMI as normal weight (<25 kg/m(2)), overweight (25.0-29.9 kg/m(2)), and obese (> or = 30 kg/m(2)). Cox multivariable regression with adjustment for significant clinical covariates was performed in each group monitoring outcome (cardiac death, myocardial infarction (MI), or unstable angina with 26 months follow-up) as a function of 17 thrombogenic, inflammatory, and metabolic blood markers and 17 cardiovascular disease-associated genetic polymorphisms. Results revealed no statistically significant genetic or blood marker variables in normal or overweight patients. For obese postinfarction patients, elevated lipoprotein(a) (Lp(a))was found to be a highly significant risk marker with hazard ratio and 95% confidence interval of 3.94 (2.11-7.35), P = 0.000017 (upper tertile vs. lower two tertiles). Additionally, elevated Lp(a) was found to interact with the -75G>A polymorphism of the apolipoprotein A-I gene and the -250G>A polymorphism of the hepatic lipase gene in establishing risk. We conclude that interactions of elevated Lp(a) with polymorphisms of the apolipoprotein A-I and hepatic lipase genes, primarily reflective of altered lipoprotein metabolism, play an important role in the establishment of recurrent coronary event risk in obese, nondiabetic postinfarction patients. These findings suggest close monitoring and consideration of weight reduction for obese postinfarction patients with elevated Lp(a) levels.     

Endothelial t-PA release is impaired in overweight and obese adults but can be improved with regular aerobic exercise

Endothelial release of tissue-type plasminogen activator (t-PA) regulates fibrinolysis and is considered to be a primary endogenous defense mechanism against thrombosis. Adiposity is associated with an increased risk of atherothrombotic events. We determined the influence of overweight and obesity on the capacity of the vascular endothelium to release t-PA and the effects of regular aerobic exercise on endothelial t-PA release in previously sedentary overweight and obese adults. First, we studied 66 sedentary adults: 28 normal-weight (BMI < 25 kg/m2); 22 overweight (BMI > or = 25 and < 30 kg/m2); and 16 obese (BMI > or = 30 kg/m2). Net endothelial t-PA release was determined in vivo in response to intrabrachial infusions of bradykinin (BK) and sodium nitroprusside. Second, we studied 17 overweight and obese adults who completed a 3-mo aerobic exercise intervention. Net release of t-PA in response to BK was approximately 45% lower (P < 0.01) in overweight (from 0.1 +/- 0.4 to 41.7 +/- 4.9 ng x 100 ml tissue(-1) x min(-1)) and obese (-0.1 +/- 0.6 to 47.7 +/- 5.2 ng x 100 ml tissue(-1) x min(-1)) compared with normal-weight (0.1 +/- 0.8 to 77.5 +/- 6.7 ng x 100 ml tissue(-1) x min(-1)) adults. There was no difference in t-PA release between the overweight and obese groups. Exercise training significantly increased t-PA release capacity in overweight and obese adults (from -0.3 +/- 0.5 to 37.1 +/- 4.9 ng x 100 ml tissue(-1) x min(-1) before training vs. 1.0 +/- 0.9 to 65.4 +/- 6.3 ng x 100 ml tissue(-1) x min(-1) after training) to levels comparable with those of their normal-weight peers. These results indicate that overweight and obesity are associated with profound endothelial fibrinolytic dysfunction. Importantly, however, regular aerobic exercise can increase the capacity of the endothelium to release t-PA in this at-risk population.     

Primary antiphospholipid antibody syndrome—one further aspect of thrombophilia in overweight and obese patients with venous thromboembolism

Objective: Overweight and obesity are established risk factors for venous thromboembolism (VTE). We examined the difference in the frequency of primary antiphospholipid antibody syndrome (PAPS) in VTE patients according to their BMI. Design and Methods: We included 998 VTE patients treated at our institution between 2009 and 2011 in a retrospective data analysis. Thrombophilia screening including evaluation for APS (lupus anticoagulant, anti‐cardiolipin, and anti‐B2‐glycoprotein‐I IgG and IgM antibodies) was performed in all patients. Results: PAPS was diagnosed in 6.8% (24/355) of normal weight (BMI < 24 kg/m²) VTE patients, in 11.1% (50/452) of overweight (BMI 25–30 kg/m²) VTE patients, and in 15.7% (30/191) of obese (BMI > 31 kg/m²) VTE patients. The difference of PAPS occurrence between these groups was statistically significant (P = 0.001). PAPS patients demonstrated higher fibrinogen levels as compared to non‐PAPS patients (median 416.0 md/dl vs. 352.0 mg/dl, P = 0.001). Furthermore, fibrinogen levels increased significantly according to the body weight of patients (median normal weight patients 330.0 mg/dl vs. overweight patients 359.0 mg/dl vs. obese patients 415.0 mg/dl, P = 0.001). Conclusion: PAPS seems to be more frequent in overweight and obese patients. As PAPS patients showed significantly higher fibrinogen levels and as fibrinogen levels increased significantly according to the body weight of patients, an elevated inflammatory state in overweight and obese patients as a reason for the increased PAPS occurrence can be assumed.     

Body adiposity and type 2 diabetes: increased risk with a high body fat percentage even having a normal BMI

Obesity is the major risk factor for the development of prediabetes and type 2 diabetes. BMI is widely used as a surrogate measure of obesity, but underestimates the prevalence of obesity, defined as an excess of body fat. We assessed the presence of impaired glucose tolerance or impaired fasting glucose (both considered together as prediabetes) or type 2 diabetes in relation to the criteria used for the diagnosis of obesity using BMI as compared to body fat percentage (BF%). We performed a cross-sectional study including 4,828 (587 lean, 1,320 overweight, and 2,921 obese classified according to BMI) white subjects (66% females), aged 18-80 years. BMI, BF% determined by air-displacement plethysmography (ADP) and conventional blood markers of glucose metabolism and lipid profile were measured. We found a higher than expected number of subjects with prediabetes or type 2 diabetes in the obese category according to BF% when the sample was globally analyzed (P < 0.0001) and in the lean BMI-classified subjects (P < 0.0001), but not in the overweight or obese-classified individuals. Importantly, BF% was significantly higher in lean (by BMI) women with prediabetes or type 2 diabetes as compared to those with normoglycemia (NG) (35.5 ± 7.0 vs. 30.3 ± 7.7%, P < 0.0001), whereas no differences were observed for BMI. Similarly, increased BF% was found in lean BMI-classified men with prediabetes or type 2 diabetes (25.2 ± 9.0 vs. 19.9 ± 8.0%, P = 0.008), exhibiting no differences in BMI or waist circumference. In conclusion, assessing BF% may help to diagnose disturbed glucose tolerance beyond information provided by BMI and waist circumference in particular in male subjects with BMI <25 kg/m(2) and over the age of 40.     

Obesity paradox in amputation risk among nonelderly diabetic men

The association between BMI and amputation risk is not currently well known. We used data for a cohort of diabetic patients treated in the US Department of Veterans Affairs Healthcare System in 2003. Men aged <65 years at the end of follow-up were examined for their amputation risk and amputation-free survival during the next 5 years (2004-2008). Compared to overweight individuals (BMI 25-29.9 kg/m(2)), the risks of amputation and treatment failure (amputation or death) were higher for patients with BMI <25 kg/m(2) and were lower for those with BMI ≥30 kg/m(2). Individuals with BMI ≥40 kg/m(2) were only half as likely to experience any (hazard ratios (HR) = 0.49; 95% confidence interval (CI), 0.30-0.80) and major amputations (HR = 0.53; 95% CI, 0.39-0.73) during follow-up as overweight individuals. While the amputation risk continued to decrease for higher BMI, amputation-free survival showed a slight upturn at BMI >40 kg/m(2). The association between obesity and amputation risk in our data shows a pattern consistent with "obesity paradox" observed in many health conditions. More research is needed to better understand pathophysiological mechanisms that may explain the paradoxical association between obesity and lower-extremity amputation (LEA) risk.     

ST 段抬高心肌梗死靶血管长病变急诊介入治疗的安全性及疗效分析

目的:探讨ST段抬高急性心肌梗死(ST-elevation myocardial infarction,STEMI)患者靶血管长病变(病变>25 mm)急诊经皮冠状动脉介入(percutaneous coronary intervention,PCI)治疗的临床疗效及安全性。方法:回顾性收集2009年1月-2010年6月因STEMI就诊于沈阳军区总医院并急诊行PCI处理的患者442例,以靶病变长度分为两组,即≤25 mm为短病变组(n=235)和>25mm为长病变组(n=207),均急诊行PCI治疗,分析和比较两组患者术前的基线资料、术中资料及并发症的发生情况、辅助措施(临时起搏、IABP、血栓抽吸装置)应用情况,术后30天、2年电话或临床随访,记录主要不良心血管事件(major adverse cardiac events,MACE)的发生情况。结果:与短病变组比较,长病变组吸烟者更多(81.6%vs 62.6%,P=0.000);以三支病变偏多(34.8%vs 24.7%,P=0.037);多枚支架使用率更高(1.47±0.63 vs 1.04±0.28,P=0.000),平均支架总长度显著增加(29.80±7.02 mm vs 22.95±5.58mm,P=0.000),手术成功率、术中并发症及辅助措施应用情况比较差异无统计学意义(P>0.05),30天及2年随访MACE的发生率比较差异无统计学意义(P>0.05)。结论:与急诊PCI治疗的STEMI短病变患者对比,长病变患者虽然病变复杂,多枚支架使用率高,平均支架总长度增加,但术中并发症、30天、2年内MACE与短病变患者相当,提示在以药物洗脱支架为主的介入治疗时代,急诊PCI处理STEMI靶血管长病变具有良好的疗效及安全性。     

Oxidant Stress in Healthy Normal‐weight,Overweight, and Obese Individuals

This study was undertaken to investigate the association among BMI and lipid hydroperoxide (LH), total antioxidant status (TAS), superoxide dismutase (SOD), and reduced glutathione (GSH). Ninety (n = 90) healthy males and females (n = 23/67) (29 normal weight (BMI: 22.74 ± 0.25 kg/m²), 36 overweight (BMI: 27.18 ± 0.23 kg/m²), and 25 obese (33.78 ± 0.48 kg/m²)) participated in the study. Data collected included anthropometric measures, fasting blood glucose, lipid profile, LH, TAS, and enzymatic antioxidants (SOD, and reduced GSH). The results of the study showed that obese individuals had significantly increased LH levels compared to normal‐weight individuals (obese vs. normal weight (0.88 ± 0.05 vs. 0.67 ± 0.03 µmol/l, P < 0.01)) but the increased levels were not significantly different when compared to the overweight group (obese vs. overweight (0.88 ± 0.05 vs. 0.79 ± 0.05 µmol/l)). No other consistent significant differences in TAS, SOD, and GSH were identified between groups. This study concluded that only obesity and not moderate overweight elevates LH levels. Furthermore, the levels of TAS, SOD, and GSH in obesity do not explain the increased LH levels observed in obesity.     

Impact of Body Mass Index on In-Hospital Complications in Patients Undergoing Percutaneous Coronary Intervention in a Japanese Real-World Multicenter Registry

Background

Obesity is associated with advanced cardiovascular disease. However, some studies have reported the “obesity paradox” after percutaneous coronary intervention (PCI). The relationship between body mass index (BMI) and clinical outcomes after PCI has not been thoroughly investigated, especially in Asian populations.

Methods

We studied 10,142 patients who underwent PCI at 15 Japanese hospitals participating in the JCD-KICS registry from September 2008 to April 2013. Patients were divided into four groups according to BMI: underweight, BMI <18.5 (n=462); normal, BMI ≥18.5 and <25.0 (n=5,945); overweight, BMI ≥25.0 and <30.0 (n=3,100); and obese, BMI ≥30.0 (n=635).

Results

Patients with a high BMI were significantly younger (p<0.001) and had a higher incidence of coronary risk factors such as hypertension (p<0.001), hyperlipidemia (p<0.001), diabetes mellitus (p<0.001), and current smoking (p<0.001), than those with a low BMI. Importantly, patients in the underweight group had the worst in-hospital outcomes, including overall complications (underweight, normal, overweight, and obese groups: 20.4%, 11.5%, 8.4%, and 10.2%, p<0.001), in-hospital mortality (5.8%, 2.1%, 1.2%, and 2.7%, p<0.001), cardiogenic shock (3.5%, 2.0%, 1.5%, and 1.6%, p=0.018), bleeding complications (10.0%, 4.5%, 2.6%, and 2.8%, p<0.001), and receiving blood transfusion (7.6%, 2.7%, 1.6%, and 1.7%, p<0.001). BMI was inversely associated with bleeding complications after adjustment by multivariate logistic regression analysis (odds ratio, 0.95; 95% confidence interval, 0.92–0.98; p=0.002). In subgroup multivariate analysis of patients without cardiogenic shock, BMI was inversely associated with overall complications (OR, 0.98; 95% CI, 0.95–0.99; p=0.033) and bleeding complications (OR, 0.95; 95% CI, 0.91–0.98; p=0.006). Furthermore, there was a trend that BMI was moderately associated with in-hospital mortality (OR, 0.94; 95% CI, 0.88–1.01; p=0.091).

Conclusions

Lean patients, rather than obese patients are at greater risk for in-hospital complications during and after PCI, particularly for bleeding complications.     

Effect of weight loss in adults on estimation of risk due to adiposity in a cohort study

The effect of overweight and obesity on the risk of fatal disease tends to attenuate with age. To evaluate whether this effect is partly attributable to disease-related weight loss, we examined the prebaseline history of weight loss and diseases associated with weight loss among adults enrolled in a cohort study. We conducted an analysis of 7,855 adult cohort members of the Adventist Health Study (AHS) I who had provided anthropometric data on surveys at baseline and 17 years prior to baseline. Among adults in the recommended range of BMI (19-25 kg/m(2)) at baseline we found that: (i) the prevalence of prebaseline weight loss of 5 kg/m(2) from an overweight or obese state was 20.4% and increased with age (12.6% for <65 years; 27.7% for 65-84 years; 36.7% for >85 years) and (ii) prebaseline weight loss of 5 kg/m(2) from an overweight or obese state was associated with diabetes (odds ratio (OR) = 2.91 95% confidence interval (CI) = (2.16, 3.93)), coronary heart disease (OR = 1.84 95% CI = (1.42, 2.40)), and high blood pressure (OR = 1.51 95% CI = (1.26, s1.82)). During 12 years of follow-up, we found evidence that hazard ratios for adiposity can be confounded by disease-related weight loss. Our findings raise the possibility that prebaseline weight loss can confound the estimation of risk due to adiposity at baseline in a cohort study.     

Fueling the Obesity Epidemic? Artificially Sweetened Beverage Use and Long‐term Weight Gain

We have examined the relationship between artificially sweetened beverage (ASB) consumption and long-term weight gain in the San Antonio Heart Study. From 1979 to 1988, height, weight, and ASB consumption were measured among 5,158 adult residents of San Antonio, Texas. Seven to eight years later, 3,682 participants (74% of survivors) were re-examined. Outcome measures were incidence of overweight/obesity (OW/OB(inc)) and obesity (OB(inc)) (BMI > or = 25 and > or = 30 kg/m(2), respectively), and BMI change by follow-up (DeltaBMI, kg/m(2)). A significant positive dose-response relationship emerged between baseline ASB consumption and all outcome measures, adjusted for baseline BMI and demographic/behavioral characteristics. Consuming >21 ASBs/week (vs. none) was associated with almost-doubled risk of OW/OB (odds ratio (OR) = 1.93, P = 0.007) among 1,250 baseline normal-weight (NW) individuals, and doubled risk of obesity (OR = 2.03, P = 0.0005) among 2,571 individuals with baseline BMIs <30 kg/m(2). Compared with nonusers (+1.01 kg/m(2)), DeltaBMIs were significantly higher for ASB quartiles 2-4: +1.46 (P = 0.003), +1.50 (P = 0.002), and +1.78 kg/m(2) (P < 0.0001), respectively. Overall, adjusted DeltaBMIs were 47% greater among artificial sweetener (AS) users than nonusers (+1.48 kg/m(2) vs. +1.01 kg/m(2), respectively, P < 0.0001). In separate analyses--stratified by gender; ethnicity; baseline weight category, dieting, or diabetes status; or exercise-change category--DeltaBMIs were consistently greater among AS users. These differences, though not significant among exercise increasers, or those with baseline diabetes or BMI >30 kg/m(2) (P = 0.069), were significant in all 13 remaining strata. These findings raise the question whether AS use might be fueling--rather than fighting--our escalating obesity epidemic.     

The muscle strength and size response to upper arm, unilateral resistance training among adults who are overweight and obese

Overweight and obesity result in musculoskeletal impairments that limit exercise capacity. We examined if the muscle strength and size response to resistance training (RT) differed among 687 young (mean +/- SEM, 24.2 +/- 0.2 years) overweight and obese (OW) compared to normal weight (NW) adults as denoted by the body mass index (BMI). Subjects were 449 NW (22.0 +/- 0.1 kg.m(-2), 23.4 +/- 0.3 years) and 238 OW (29.2 +/- 0.2 kg.m(-2), 25.6 +/- 0.4 years) men (n = 285) and women (n = 402) who underwent 12 weeks (2 d.wk(-1)) of RT of the nondominant arm. Maximum voluntary contraction (MVC) and 1 repetition maximum (1RM) assessed peak elbow flexor strength. Magnetic resonance imaging measured the biceps muscle cross sectional area (CSA). Multiple dependent variable analysis of covariance tested if muscle strength and size differed among BMI groups pre-, post-, and pre-to-post-RT. Overweight and obese had greater MVC, 1RM, and CSA than NW pre- and post-RT (p < 0.001). Maximum voluntary contraction and 1RM gains were not different between BMI groups pre- to post-RT (p >or= 0.05). When adjusted for baseline values, NW had greater relative MVC (21.2 +/- 1.0 vs. 17.4 +/- 1.4%) and 1RM (54.3 +/- 1.5 vs. 49.0 +/- 2.0%) increases than OW (p < 0.05). Normal weight also had greater allometric MVC (0.48 +/- 0.02 kg.kg(-0.67) vs. 0.40 +/- 0.03 kg.kg(-0.67)) and 1RM (0.25 +/- 0.00 vs. 0.22 +/- 0.01 kg.kg(-0.67)) gains than OW (p < 0.05). CSA gains were greater among OW than NW (3.6 +/- 0.2 vs. 3.2 +/- 0.1 cm(2)) (p < 0.001); however, relative CSA increases were not different between BMI groups (19.4 +/- 0.5 vs. 18.4 +/- 0.7%) (p >or= 0.05). Despite similar relative muscle size increases, relative and allometic strength gains were less among OW than NW. These findings indicate the short-term relative and allometric muscle strength response to RT may be attenuated among adults who are overweight and obese.     

Influence of ascorbic acid on the thermic effect of feeding in overweight and obese adult humans

The thermic effect of feeding (TEF: increase in energy expenditure following acute energy intake) is an important physiological determinant of total daily energy expenditure and thus energy balance. Approximately 40% of TEF is believed to be mediated by sympathoadrenal activation and consequent beta-adrenergic receptor stimulation of metabolism. In sedentary adults, acute administration of ascorbic acid, a potent antioxidant, augments the thermogenic response to beta-adrenergic stimulation. We hypothesized that acute ascorbic acid administration augments TEF in sedentary overweight and obese adults. Energy expenditure was determined (ventilated hood technique) before and 4 h after consumption of a liquid-mixed meal (caloric equivalent 40% of resting energy expenditure (REE)) in 11 sedentary, overweight/obese adults (5 men, 6 women; age: 24 +/- 2 years; BMI: 28.5 +/- 1.0 kg/m(2) (mean +/- s.e.)) on two separate, randomly ordered occasions: during continuous intravenous administration of saline (placebo control) and/or ascorbic acid (0.05 g/kg fat-free mass). Acute ascorbic acid administration prevented the increase in plasma concentration of oxidized low-density lipoprotein in the postprandial state (P = 0.04), but did not influence REE (1,668 +/- 107 kcal/day vs.1,684 +/- 84 kcal/day; P = 0.91) or the area under the TEF response curve (33.4 +/- 2.4 kcal vs. 30.5 +/- 3.6 kcal; P = 0.52) (control vs. ascorbic acid, respectively). Furthermore, acute ascorbic acid administration had no effect on respiratory exchange ratio, heart rate, or arterial blood pressure in the pre- and postabsorptive states (all P > 0.64). These data imply that the attenuated TEF commonly observed with sedentary lifestyle and obesity is not modulated by ascorbic acid-sensitive oxidative stress.     

Clinical Profile and Management of Patients With Hypertension and Chronic Ischemic Heart Disease According to BMI

Obesity is associated with numerous risk factors and comorbidities such as hypertension, metabolic syndrome, type 2 diabetes, and cardiovascular diseases. However, numerous studies have reported an obesity paradox; the overweight and obese patients with established cardiovascular disease have better prognosis than those with a BMI <25 kg/m². This study was designed to assess potential differences in the clinical profile and management of hypertensive outpatients with chronic ischemic heart disease in obese and lean patients that could explain these two apparently contradictory points. Overweight and obesity were defined as a BMI 25–29.9 kg/m² and ≥30 kg/m², respectively. Cardiovascular risk factors goals were considered according to European Society of Hypertension‐European Society of Cardiology 2003, National Cholesterol Education Program Adult Treatment Panel III and American Diabetes Association 2005 guidelines. A sample of 2,024 patients (66.8 ± 10.1 years; 31.7% women) was included. Of these, 0.1% had a BMI <20 kg/m²; 17.1% BMI 20–24.9 kg/m²; 53.7% BMI 25–29.9 kg/m²; 23.7% BMI 30–34.9 kg/m²; 4.3% BMI 35–39.9 kg/m²; and 1.1% BMI ≥40 kg/m². The subgroup of patients with BMI ≥30 kg/m² had a higher proportion of women, diastolic dysfunction, diabetes, dyslipidemia, left ventricular hypertrophy, and heart failure. There was an inverse relationship between risk factors control rates and BMI (all comparisons BMI 20–24.9 kg/m² vs. 25–29.9 kg/m² vs. ≥30 kg/m²): blood pressure (BP) control (51.7% vs. 42.4% vs. 29.2%, P < 0.001); low‐density lipoprotein cholesterol (LDL‐C) control (35.2% vs. 30.5% vs. 27.9%, P = 0.03) and diabetes control (38.6% vs. 27.6% vs. 22.2%, P = 0.023). In conclusion, in patients with hypertension and chronic ischemic heart disease, as BMI increases, the clinical profile worsens as well as risk factors control rates.     

Associations of visceral and liver fat with the metabolic syndrome across the spectrum of obesity: the AGES-Reykjavik study

Visceral adipose tissue (VAT) is a key pathogenic fat depot in the metabolic syndrome (MetS), but liver fat (LF) may also play an important role. We evaluated associations of VAT and LF with MetS in normal weight, overweight, and obese men and women (BMI <25, 25-29.9, and ≥30 kg/m2, respectively). This analysis included 2,495 participants from the Age, Gene/Environment Susceptibility (AGES)-Reykjavik study with computed tomography measurements for VAT and LF. MetS was defined by ≥3 of the following: larger abdominal circumference, hypertension, elevated triglyceride (TG), low high-density lipoprotein (HDL), impaired fasting glucose (IFG), and microalbuminuria. We estimated the odds of MetS per 1-s.d. increase in VAT and LF, adjusting for key covariates. VAT was associated with an increased odds of MetS in normal weight, overweight, and obese women (odds ratios (OR) = 2.78, 1.63, and 1.43, respectively; all P < 0.01) that diminished in magnitude with increasing BMI (VAT × BMI class interaction P < 0.001). In men, VAT was related to MetS only among the overweight (OR = 1.69, P < 0.01). LF was associated with MetS in the overweight and obese groups in women (OR = 1.38 and 1.45; both P < 0.001) and in men (OR = 1.38, P = 0.01; and OR = 1.27, P = 0.10), but not in the normal weight groups. These BMI-specific relationships persisted when both fat depots were included in the model. VAT and LF were associated with MetS independently of each other, and these relationships were modified by BMI class such that, VAT was the more important depot at lower levels of obesity and LF at higher levels. Importantly, fatty liver may be a novel metabolic risk factor in overweight and obese individuals.     

Lipid oxidation is reduced in obese human skeletal muscle

The purpose of this study was to discern cellular mechanisms that contribute to the suppression of lipid oxidation in the skeletal muscle of obese individuals. Muscle was obtained from obese [body mass index (BMI), 38.3 +/- 3.1 kg/m(2)] and lean (BMI, 23.8 +/- 0.9 kg/m(2)) women, and fatty acid oxidation was studied by measuring (14)CO(2) production from (14)C-labeled fatty acids. Palmitate oxidation, which is at least partially dependent on carnitine palmitoyltransferase-1 (CPT-1) activity, was depressed (P < 0.05) by approximately 50% with obesity (6.8 +/- 2.2 vs. 13.7 +/- 1.4 nmole CO(2).g(-1).h(-1)). The CPT-1-independent event of palmitoyl carnitine oxidation was also depressed (P < 0.01) by approximately 45%. There were significant negative relationships (P < 0.05) for adiposity with palmitate (r = -0.76) and palmitoyl carnitine (r = -0.82) oxidation. Muscle CPT-1 and citrate synthase activity, an index of mitochondrial content, were also significantly (P < 0.05) reduced ( approximately 35%) with obesity. CPT-1 (r = -0.48) and citrate synthase (r = -0.65) activities were significantly (P < 0.05) related to adiposity. These data suggest that lesions at CPT-1 and post-CPT-1 events, such as mitochondrial content, contribute to the reduced reliance on fat oxidation evident in human skeletal muscle with obesity.