BACKGROUND: Not all obese individuals show cardiometabolic abnormalities. We examined metabolically healthy obesity (MHO) and its associates in 2530 Mongolian Chinese adults. METHODS: MHO was defined by waist circumference, low-density lipoprotein (LDL-C) cholesterol, high-density lipoprotein cholesterol (HDL-C), triglycerides (TGs), systolic blood pressure (SBP), diastolic blood pressure (DBP), and glucose. RESULTS: Only 3.0% of the participants had MHO, with 0.8% of men and 4.5% of women having this condition (P < 0.001 for sex difference). Despite striking differences in obesity measures, MHO individuals had a comparable cardiometabolic profile to that for metabolically healthy, nonobese individuals (MHNO) and an improved cardiometabolic profile, i.e., lower levels of blood pressure, glucose, insulin, LDL-C, TGs, and higher levels of HDL-C compared to metabolically abnormal individuals (all P < 0.01, except for insulin). MHO individuals had lower levels of high-sensitivity C-reactive protein and soluble intercellular adhesion molecule-1, compared to metabolically abnormal individuals, and had comparable levels of these markers to those in MHNO individuals. Furthermore, only 5.3% of MHO individuals had a family history of hypertension, comparable to 5.0% in MHNO individuals, and much lower than 15.9% in metabolically abnormal, nonobese individuals and 12.8% in metabolically abnormal, obese individuals (overall P < 0.001). CONCLUSIONS: We conclude that MHO is associated with a low inflammation state, and family history of hypertension may play a role in the MHO phenotype.
BACKGROUND: Not all obese individuals show cardiometabolic abnormalities. We examined metabolically healthy obesity (MHO) and its associates in 2530 Mongolian Chinese adults. METHODS: MHO was defined by waist circumference, low-density lipoprotein (LDL-C) cholesterol, high-density lipoprotein cholesterol (HDL-C), triglycerides (TGs), systolic blood pressure (SBP), diastolic blood pressure (DBP), and glucose. RESULTS: Only 3.0% of the participants had MHO, with 0.8% of men and 4.5% of women having this condition (P < 0.001 for sex difference). Despite striking differences in obesity measures, MHO individuals had a comparable cardiometabolic profile to that for metabolically healthy, nonobese individuals (MHNO) and an improved cardiometabolic profile, i.e., lower levels of blood pressure, glucose, insulin, LDL-C, TGs, and higher levels of HDL-C compared to metabolically abnormal individuals (all P < 0.01, except for insulin). MHO individuals had lower levels of high-sensitivity C-reactive protein and soluble intercellular adhesion molecule-1, compared to metabolically abnormal individuals, and had comparable levels of these markers to those in MHNO individuals. Furthermore, only 5.3% of MHO individuals had a family history of hypertension, comparable to 5.0% in MHNO individuals, and much lower than 15.9% in metabolically abnormal, nonobese individuals and 12.8% in metabolically abnormal, obese individuals (overall P < 0.001). CONCLUSIONS: We conclude that MHO is associated with a low inflammation state, and family history of hypertension may play a role in the MHO phenotype.
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