Obesity has reached epidemic proportions in the United States: more than 20% of adults are clinically obese as defined by a body mass index of 30 kg/m2 or higher, and an additional 30% are ...overweight. Environmental, behavioral, and genetic factors have been shown to contribute to the development of obesity. Elevated body mass index, particularly caused by abdominal or upper‐body obesity, has been associated with a number of diseases and metabolic abnormalities, many of which have high morbidity and mortality. These include hyperinsulinemia, insulin resistance, type 2 diabetes, hypertension, dyslipidemia, coronary heart disease, gallbladder disease, and certain malignancies. This underscores the importance of identifying people at risk for obesity and its related disease states.
...in June 2013 the NHLBI initiated collaboration with the ACC and AHA to work with other organizations to complete and publish the guidelines noted above and make them available to the widest ...possible constituency. ...the format of the recommendations differs from other ACC/AHA guidelines. Each recommendation has been mapped from the NHLBI grading format to the ACC/ AHA Classification of Recommendation/Level of Evidence (COR/ LOE) construct (Table 1) and is expressed in both formats. Because of the inherent differences in grading systems and the clinical questions driving the recommendations, alignment between the NHLBI and ACC/AHA formats is in some cases imperfect. According to the 1998 "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults- The Evidence Report" (5), overweight is defined as a body mass index (BMI) of 25 kg/m2 to 29.9 kg/m2 and obesity as a BMI of >30 kg/m2.
OBJECTIVE: To assess the risk factors for the presence and severity of obstructive sleep apnea (OSA) among obese patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: Unattended polysomnography ...was performed in 306 participants. RESULTS: Over 86% of participants had OSA with an apnea-hypopnea index (AHI) greater-than-or-equal5 events/h. The mean AHI was 20.5 ± 16.8 events/h. A total of 30.5% of the participants had moderate OSA (15 less-than or equal to AHI <30), and 22.6% had severe OSA (AHI greater-than-or-equal30). Waist circumference (odds ratio 1.1; 95% CI 1.0-1.1; P = 0.03) was significantly related to the presence of OSA. Severe OSA was most likely in individuals with a higher BMI (odds ratio 1.1; 95% CI 1.0-1.2; P = 0.03). CONCLUSIONS: Physicians should be particularly cognizant of the likelihood of OSA in obese patients with type 2 diabetes, especially among individuals with higher waist circumference and BMI.
Weight loss is recommended to treat obstructive sleep apnea (OSA).
To determine whether the initial benefit of intensive lifestyle intervention (ILI) for weight loss on OSA severity is maintained at ...10 years.
Ten-year follow-up polysomnograms of 134 of 264 adults in Sleep AHEAD (Action for Health in Diabetes) with overweight/obesity, type 2 diabetes mellitus, and OSA were randomized to ILI for weight loss or diabetes support and education (DSE).
Change in apnea-hypopnea index (AHI) was measured. Mean ± SE weight losses of ILI participants of 10.7 ± 0.7, 7.4 ± 0.7, 5.1 ± 0.7, and 7.1 ± 0.8 kg at 1, 2, 4, and 10 years, respectively, were significantly greater than the 1-kg weight loss at 1, 2, and 4 years and 3.5 ± 0.8 kg weight loss at 10 years for the DSE group (
values ≤ 0.0001). AHI was lower with ILI than DSE by 9.7, 8.0, and 7.9 events/h at 1, 2, and 4 years, respectively (
values ≤ 0.0004), and 4.0 events/h at 10 years (
= 0.109). Change in AHI over time was related to amount of weight loss, baseline AHI, visit year (
values < 0.0001), and intervention independent of weight change (
= 0.01). OSA remission at 10 years was more common with ILI (34.4%) than DSE (22.2%).
Participants with OSA and type 2 diabetes mellitus receiving ILI for weight loss had reduced OSA severity at 10 years. No difference in OSA severity was present between ILI and DSE groups at 10 years. Improvement in OSA severity over the 10-year period with ILI was related to change in body weight, baseline AHI, and intervention independent of weight change.
The frequency of remission of type 2 diabetes achievable with lifestyle intervention is unclear.
To examine the association of a long-term intensive weight-loss intervention with the frequency of ...remission from type 2 diabetes to prediabetes or normoglycemia.
Ancillary observational analysis of a 4-year randomized controlled trial (baseline visit, August 2001-April 2004; last follow-up, April 2008) comparing an intensive lifestyle intervention (ILI) with a diabetes support and education control condition (DSE) among 4503 US adults with body mass index of 25 or higher and type 2 diabetes.
Participants were randomly assigned to receive the ILI, which included weekly group and individual counseling in the first 6 months followed by 3 sessions per month for the second 6 months and twice-monthly contact and regular refresher group series and campaigns in years 2 to 4 (n=2241) or the DSE, which was an offer of 3 group sessions per year on diet, physical activity, and social support (n=2262).
Partial or complete remission of diabetes, defined as transition from meeting diabetes criteria to a prediabetes or nondiabetic level of glycemia (fasting plasma glucose <126 mg/dL and hemoglobin A1c <6.5% with no antihyperglycemic medication). RESULTS Intensive lifestyle intervention participants lost significantly more weight than DSE participants at year 1 (net difference, -7.9%; 95% CI, -8.3% to -7.6%) and at year 4 (-3.9%; 95% CI, -4.4% to -3.5%) and had greater fitness increases at year 1 (net difference, 15.4%; 95% CI, 13.7%-17.0%) and at year 4 (6.4%; 95% CI, 4.7%-8.1%) (P < .001 for each). The ILI group was significantly more likely to experience any remission (partial or complete), with prevalences of 11.5% (95% CI, 10.1%-12.8%) during the first year and 7.3% (95% CI, 6.2%-8.4%) at year 4, compared with 2.0% for the DSE group at both time points (95% CIs, 1.4%-2.6% at year 1 and 1.5%-2.7% at year 4) (P < .001 for each). Among ILI participants, 9.2% (95% CI, 7.9%-10.4%), 6.4% (95% CI, 5.3%-7.4%), and 3.5% (95% CI, 2.7%-4.3%) had continuous, sustained remission for at least 2, at least 3, and 4 years, respectively, compared with less than 2% of DSE participants (1.7% 95% CI, 1.2%-2.3% for at least 2 years; 1.3% 95% CI, 0.8%-1.7% for at least 3 years; and 0.5% 95% CI, 0.2%-0.8% for 4 years).
In these exploratory analyses of overweight adults, an intensive lifestyle intervention was associated with a greater likelihood of partial remission of type 2 diabetes compared with diabetes support and education. However, the absolute remission rates were modest. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00017953.
This 56‐week, randomized, placebo‐controlled trial examined the efficacy and safety of naltrexone plus bupropion as an adjunct to intensive behavior modification (BMOD). A total of 793 participants ...(BMI = 36.5 ± 4.2 kg/m2) was randomly assigned in a 1:3 ratio to: (i) placebo + BMOD (N = 202); or (ii) naltrexone sustained‐release (SR, 32 mg/day), combined with bupropion SR (360 mg/day) plus BMOD (i.e., NB32 + BMOD; N = 591). Both groups were prescribed an energy‐reduced diet and 28 group BMOD sessions. Co‐primary end points were percentage change in weight and the proportion of participants who lost ≥5% weight at week 56. Efficacy analyses were performed on a modified intent‐to‐treat population (ITT; i.e., participants with ≥1 postbaseline weight while taking study drug (placebo + BMOD, N = 193; NB32 + BMOD, N = 482)). Missing data were replaced with the last observation obtained on study drug. At week 56, weight loss was 5.1 ± 0.6% with placebo + BMOD vs. 9.3 ± 0.4% with NB32 + BMOD (P < 0.001). A completers analysis revealed weight losses of 7.3 ± 0.9% (N = 106) vs. 11.5 ± 0.6% (N = 301), respectively (P < 0.001). A third analysis, which included all randomized participants, yielded losses of 4.9 ± 0.6 vs. 7.8 ± 0.4%, respectively (P < 0.001). Significantly more NB32 + BMOD‐ vs. placebo + BMOD‐treated participants lost ≥5 and ≥10% of initial weight, and the former had significantly greater improvements in markers of cardiometabolic disease risk. NB32 + BMOD was generally well tolerated, although associated with more reports of nausea than placebo + BMOD. The present findings support the efficacy of combined naltrexone/bupropion therapy as an adjunct to intensive BMOD for obesity.
BACKGROUND: The extent to which adipose tissue (AT) distribution is different between persons with type 2 diabetes (T2DM) and nondiabetic control subjects remains unclear. OBJECTIVE: The aim of this ...study was to establish whether total body adiposity and its distribution, quantified by using state-of-the-art whole-body magnetic resonance imaging, differs between these 2 groups. DESIGN: This cross-sectional evaluation included 93 participants (n = 56 women and 37 men) in the Look AHEAD (Action for HEAlth in Diabetes) Trial with T2DM who had a mean (±SD) age of 58.3 ± 6.6 y and body mass index (in kg/m²) of 31.6 ± 3.1 and 93 healthy non-T2DM control subjects (n = 64 women and 29 men) who had a mean (±SD) age of 60.6 ± 17.1 y and body mass index of 29.6 ± 3.0. All participants self-reported being of African American or white ancestry. Magnetic resonance imaging-derived in vivo measures of total-body AT (TAT) and its distribution, subcutaneous AT (SAT), visceral AT (VAT), and intermuscular AT (IMAT) were acquired. Linear regression models were developed for each AT compartment to adjust for important covariates of race, sex, age, height, and weight and to examine potential interactions of covariates. RESULTS: These models showed significantly less SAT (African American: -1.2 kg; white: -2.4 kg; both P = 0.001), including less femoral-gluteal SAT, more VAT (African American: 0.7 kg, P < 0.001; white: 1.8 kg, P = 0.007), and more IMAT (0.5 kg, P = 0.001) in the T2DM group. CONCLUSION: We concluded that AT distribution is significantly altered in T2DM, ie, more VAT and IMAT--2 depots known to exacerbate insulin resistance--and less SAT in persons with T2DM than in healthy control subjects, a novel finding that we posit may compound the risk of insulin resistance.
Rimonabant, a selective cannabinoid-1 receptor blocker, may reduce body weight and improve cardiometabolic risk factors in patients who are overweight or obese.
To compare the efficacy and safety of ...rimonabant with placebo each in conjunction with diet and exercise for sustained changes in weight and cardiometabolic risk factors over 2 years.
Randomized, double-blind, placebo-controlled trial of 3045 obese (body mass index > or =30) or overweight (body mass index >27 and treated or untreated hypertension or dyslipidemia) adult patients at 64 US and 8 Canadian clinical research centers from August 2001 to April 2004.
After a 4-week single-blind placebo plus diet (600 kcal/d deficit) run-in period, patients were randomized to receive placebo, 5 mg/d of rimonabant, or 20 mg/d of rimonabant for 1 year. Rimonabant-treated patients were rerandomized to receive placebo or continued to receive the same rimonabant dose while the placebo group continued to receive placebo during year 2.
Body weight change over year 1 and prevention of weight regain during year 2. Additional efficacy measures included changes in waist circumference, plasma lipid levels, and other cardiometabolic risk factors.
At year 1, the completion rate was 309 (51%) patients in the placebo group, 620 (51%) patients in the 5 mg of rimonabant group, and 673 (55%) patients in the 20 mg of rimonabant group. Compared with the placebo group, the 20 mg of rimonabant group produced greater mean (SEM) reductions in weight (-6.3 0.2 kg vs -1.6 0.2 kg; P<.001), waist circumference (-6.1 0.2 cm vs -2.5 0.3 cm; P<.001), and level of triglycerides (percentage change, -5.3 1.2 vs 7.9 2.0; P<.001) and a greater increase in level of high-density lipoprotein cholesterol (percentage change, 12.6 0.5 vs 5.4 0.7; P<.001). Patients who were switched from the 20 mg of rimonabant group to the placebo group during year 2 experienced weight regain while those who continued to receive 20 mg of rimonabant maintained their weight loss and favorable changes in cardiometabolic risk factors. Use of different imputation methods to account for the high rate of dropouts in all 3 groups yielded similar results. Rimonabant was generally well tolerated; the most common drug-related adverse event was nausea (11.2% for the 20 mg of rimonabant group vs 5.8% for the placebo group).
In this multicenter trial, treatment with 20 mg/d of rimonabant plus diet for 2 years promoted modest but sustained reductions in weight and waist circumference and favorable changes in cardiometabolic risk factors. However, the trial was limited by a high drop-out rate and longer-term effects of the drug require further study. Clinical Trials Registration ClinicalTrials.gov Identifier: NCT00029861.
Obesity is becoming a global epidemic in both children and adults. It is associated with numerous comorbidities such as cardiovascular diseases (CVD), type 2 diabetes, hypertension, certain cancers, ...and sleep apnea/sleep-disordered breathing. In fact, obesity is an independent risk factor for CVD, and CVD risks have also been documented in obese children. Obesity is associated with an increased risk of morbidity and mortality as well as reduced life expectancy. Health service use and medical costs associated with obesity and related diseases have risen dramatically and are expected to continue to rise. Besides an altered metabolic profile, a variety of adaptations/alterations in cardiac structure and function occur in the individual as adipose tissue accumulates in excess amounts, even in the absence of comorbidities. Hence, obesity may affect the heart through its influence on known risk factors such as dyslipidemia, hypertension, glucose intolerance, inflammatory markers, obstructive sleep apnea/hypoventilation, and the prothrombotic state, in addition to as-yet-unrecognized mechanisms. On the whole, overweight and obesity predispose to or are associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden death because of their impact on the cardiovascular system. The pathophysiology of these entities that are linked to obesity will be discussed. However, the cardiovascular clinical evaluation of obese patients may be limited because of the morphology of the individual. In this statement, we review the available evidence of the impact of obesity on CVD with emphasis on the evaluation of cardiac structure and function in obese patients and the effect of weight loss on the cardiovascular system.
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