Abstract
Background: In 1980, Reuben Andresen observed that in certain individuals, obesity did not increase mortality, introducing an atypical phenotype called "healthy obese". Other studies reported that 10-15 % of lean individuals presented insulin resistance, hyperglycemia and dyslipidemia. The objective of this study was to evaluate biochemical and clinical characteristics of metabolic phenotypes in Maracaibo city. Methods: A descriptive, cross-sectional sub-analysis of The Maracaibo City Metabolic Syndrome Prevalence Study, with a randomized multistage sampling was performed including 1226 non diabetic individuals from both sexes. For phenotype definition, the subjects were first classified according to their BMI into Normal-Weight, Overweight and Obese; then divided in metabolically healthy and unhealthy using a two-step analysis cluster being predictive variables: HOMA2-IR, HOMA2-βcell, triglycerides. To evaluate the relationship with coronary risk, a multiple logistic regression model was performed. Results: In the studied population, 43.9% (n=538) were healthy normal weight, 5.2% (n=64) unhealthy normal weight, 17.4% (n=217) healthy obese and 33.5% (n=411) unhealthy obese subjects. Atypical phenotypes, Metabolically Unhealthy Normal-Weight (MUNW) was more frequent in males (56.3%), whereas Metabolically Unhealthy Obese (MUO) was more frequent in females (51.3%). This phenotypes had a higher coronary event risk, especially for obese individuals (MHO: OR=1.85 CI95%: 1.11-3.09; p=0.02 and MUO: OR=2.09 CI95%: 1.34-3.28; p<0.01). Conclusion: Individuals with atypical metabolic phenotypes are common in Maracaibo city. Related factors may include insulin resistance, basal glucose, and triglycerides levels. Lastly, obese subjects show a higher coronary event risk even those with normal metabolic status.
Highlights
The phrase: “For this reason, the actual clinical practice catalogues an obese patient as an “unhealthy” patient and a lean patient is considered “healthy”, should be modified to make its medical meaning clearer, because it is evident for everybody that many lean people are unhealthy.the paper will gain interest if the authors comment what is the importance of researching the “atypical phenotypes”in general
Metabolic phenotypes and sociodemographic characteristics In the evaluation of the epidemiologic behavior of the metabolic phenotypes according to sex, we found that healthy normal-weight (HNW) and Metabolically Unhealthy Obese (MUO) individuals were predominately females (62.5%, n=336; 51.3%, n=211 respectively), while the atypical phenotypes were predominately males (MUNW: 56.3%, n=36; metabolically healthy obese (MHO): 52.6%, n=112. χ2=22.53, p
A statistically significant association was found between age groups and metabolic phenotypes (χ2= 211.91, p
Summary
The phrase: “For this reason, the actual clinical practice catalogues an obese patient as an “unhealthy” patient and a lean patient is considered “healthy”, should be modified to make its medical meaning clearer, because it is evident for everybody that many lean people are unhealthy.the paper will gain interest if the authors comment what is the importance of researching the “atypical phenotypes”in general. It is important that the authors comment the extent to what Maracaibo city population is representative of other Latin American populations. In 1980, Reuben Andresen observed that in certain individuals, obesity did not increase mortality, introducing an atypical phenotype called “healthy obese”. The objective of this study was to evaluate biochemical and clinical characteristics of metabolic phenotypes in Maracaibo city. Methods: A descriptive, cross-sectional sub-analysis of The Maracaibo City Metabolic Syndrome Prevalence Study, with a randomized multistage sampling was performed including 1226 non diabetic individuals from both sexes. The subjects were first classified according to their BMI into Normal-Weight, Overweight and Obese; divided in metabolically healthy and unhealthy using a two-step analysis cluster being predictive variables: HOMA2-IR, HOMA2-βcell, triglycerides.
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