Background The combined effect of transitions of metabolic health and weight on cardiovascular disease (CVD) remains unclear. We aimed to examine the association of concurrent changes of metabolic health and weight on CVD over time. Methods and Results The study population consisted of 205 394 from the Korean National Health Insurance Service. Metabolic health was determined by fasting serum glucose, total cholesterol, and blood pressure levels, while obesity was determined by body mass index. All participants were divided into either metabolically healthy nonobese (MHNO), metabolically healthy obese, metabolically unhealthy nonobese, or metabolically unhealthy obese for each of the first (2002-2003) and second (2004-2005) health screening periods, after which participants were followed-up for CVD from 2006 to 2015. Cox proportional hazards regression was used to determine adjusted hazard ratios (aHRs) and 95% CIs. Among initial MHNO participants, those who became metabolically healthy obese (aHR, 1.25; 95% CI, 1.10-1.41), metabolically unhealthy nonobese (aHR, 1.23; 95% CI, 1.15-1.31), and metabolically unhealthy obese (aHR, 1.34; 95% CI, 1.12-1.61) had elevated risk for CVD compared with those who remained MHNO. Conversely, improving metabolic health and obesity were associated with reduced CVD risk among initially metabolically unhealthy nonobese to secondary MHNO (aHR, 0.79; 95% CI, 0.73-0.84), metabolically unhealthy obese to MHNO (aHR, 0.68; 95% CI, 0.58-0.81), and metabolically unhealthy obese to metabolically healthy obese (aHR, 0.73; 95% CI, 0.66-0.80) participants. Conclusions Changes toward metabolically unhealthy or obese states resulted in increased CVD risk. Improving metabolic health along with reducing weight may lead to decreased risk of CVD.
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http://dx.doi.org/10.1161/JAHA.118.011825 | DOI Listing |
Mol Biol (Mosk)
December 2024
Pirogov All-Russia National Research Medical University, Moscow, 117997 Russia.
Obesity is associated with changes in the gut microbiota, as well as with increased permeability of the intestinal wall. In 130 non-obese volunteers, 57 patients with metabolically healthy obesity (MHO), and 76 patients with metabolically unhealthy obesity (MUHO), bacterial DNA was isolated from stool samples, and the 16S rRNA gene was sequenced. The metabolic profile of the microbiota predicted by PICRUSt2 (https://huttenhower.
View Article and Find Full Text PDFPLoS One
December 2024
Sydney School of Veterinary Science, The University of Sydney, Sydney, New South Wales, Australia.
Chlamydiosis is the major infectious disease responsible for significant morbidity and mortality in free-living koalas. Recently, it was reported that 28.5% of koalas infected with chlamydiosis were presented with no overt clinical signs.
View Article and Find Full Text PDFBMC Public Health
December 2024
Air Force Medical Center of PLA, Air Force Medical University, Beijing, China.
Background: Metabolically unhealthy non-obese (MUNO) individuals are at higher risk of cardiovascular diseases, while not receiving sufficient attention. This study was conducted to explore the association between BMI-adjusted CC and MUNO in non-obese US adults using the NHANES database.
Methods: A total of 9,628 non-obese US adults (48.
Scand J Med Sci Sports
December 2024
JP Cardiology, Kongens Lyngby, Copenhagen, Denmark.
Chronic medical conditions caused by the inadequate adaptation of the body to modern lifestyles, such as physical inactivity and unhealthy diets, are on the rise. This study assessed whether a comprehensive lifestyle intervention, including high volumes of supervised exercise, could improve health outcomes. Eight volunteers with lifestyle-related diseases received a 6-month lifestyle intervention consisting of 8000-10 000 steps/day, 6 moderate-intensity endurance and 3 resistance training sessions per week, a 5-week long hike, and dietary advice.
View Article and Find Full Text PDFCell Metab
December 2024
Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland. Electronic address:
Precision medicine is still not considered as a standard of care in obesity treatment, despite a large heterogeneity in the metabolic phenotype of individuals with obesity. One of the strongest factors influencing the variability in metabolic disease risk is adipose tissue (AT) dysfunction; however, there is little understanding of the link between distinct cell populations, cell-type-specific transcriptional programs, and disease severity. Here, we generated a comprehensive cellular map of subcutaneous and visceral AT of individuals with metabolically healthy and unhealthy obesity.
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