Morning Hypercortisolism: A Marker Of Obesity Rather Than Metabolic Syndrome

Background: The metabolic syndrome (MS) has emerged as a clinical and public health crisis. The incidence of the MS has reached epidemic proportions, with more than 1 in 4 adults affected by this disorder worldwide. Cardiovascular mortality in the MS is increased 2-fold compared to those without MS. Aim: The aim of this work was to study the role of cortisol and its circadian rhythm in the MS, the correlation of cortisol to insulin resistance using HOMA model and the correlation of cortisol to various components of the MS. Patients and methods: 50 Subjects were included in this study, they were divided into 3 groups: Group I: Included 10 apparently healthy subjects as a control group. Group II: Included 20 obese non diabetic normotensive subjects. Group III: included 20 MS patients (obese, hypertensive and type 2 diabetic). All subjects of the study were subjected to through history and physical examination including anthropometric measures, routine investigations and measurement of plasma fasting and evening cortisol, fasting insulin, estimation of insulin resistance by HOMA index, estimation of B cell function and C-reactive protein. Results: There was a significant increase in the fasting glucose, fasting insulin, and HOMA index in MS group compared to control group and obese group: HOMA-IR was 1.36±0.175 in control group, 3.3±0.6 in obese group and 11.4±4.5 in MS group. Obese group also showed significant increase in the fasting insulin, HOMA index compared to control group. The results also showed significant increase in total cholesterol, LDL cholesterol, triglycerides and CRP and significant decrease in HDL cholesterol in both obese group and MS group compared to control group. The results showed significant increase in fasting cortisol in both obese group and MS group compared to control group: fasting cortisol in ng/ml was 128±46.2 in control group, 210±79.1 in obese group and 235.1±76.8 in MS group, while no significant difference was found in the evening cortisol in the different groups: evening cortisol in ng/ml was 54.2±22.4 in control group, 59.2±30.6 in obese group and 83.6±35.7 in MS group. Fasting cortisol level was positively correlated with waist circumference, diastolic blood pressure, fasting glucose, total cholesterol, LDL cholesterol, triglycerides and negatively correlated with HDL cholesterol in MS group. While, in obese group fasting cortisol level was found to be positively correlated with waist circumference, total cholesterol, LDL cholesterol, triglycerides and negatively correlated with HDL cholesterol. Conclusion: Fasting cortisol is increased in central obesity and in MS. Evening cortisol in not increased in central obesity or MS. Fasting cortisol level can be used as a marker for central obesity which is considered the main factor in the MS, but can\'t be used as a marker for MS itself. Fasting cortisol is correlated with many features of the MS denoting its role in the pathophysiology of the MS. Further work is still needed to justify the role of cortisol in MS regarding its role in diagnosis, prognosis and therapy.