We thank for the interest in and comments on our study published,[1] recently where we demonstrated that obese obstructive sleep apnea syndrome (OSAS) patients may have an increased rate of metabolic syndrome and higher levels of serum lipids, fasting glucose, insulin resistance, leptin, fibrinogen, and hsCRP than the obese subjects without sleep apnea.[2] Two questions were addressed to us related to this article. First, it was stated that alcohol consumption and smoking history might have been questioned in a way that numerical and reliable data could have been obtained, and the use of two simple questions for these consumptions were not enough. We agree with this comment. The smoking history must have been provided in more detail. Thus, the smokers had a smoking burden of 28.2±7.1 pack-years in the OSAS group and 12.8±5.6 pack-years in the control group. On the other hand, unfortunately, the data on alcohol consumption was very limited in the hospital records where the characteristics of the patients and anthropometric measurements were evaluated. We were aware of the weakness of these data; so we started to ask more detailed questions since January 2011. Alcohol consumption is now assessed using questions on frequency, type, average number of days per week on which alcohol is drunk, and the weekly units of alcohol consumed are calculated. Excess alcohol consumption is defined as > 21 units weekly for men and > 14 units for women.[34]Second, it was recommended to report the CV of all tests as the measurements of serum concentrations of different parameters could be performed by several enzymatic techniques, and each technique has its specific limitation and interference. We thank for the attention on characteristics of the measurement techniques such as glucose, triglyceride (TG), total and high density lipoprotein (HDL)-cholesterol. We did not report all the biochemical analysis in details as we used well-defined and validated methods. In this study, serum glucose levels were measured by using glucose oxidase methods.[5] In practice, glucose oxidase is the classical methodology. When the method of measurement of circulating glucose differs between institutions, the absolute values and variability of patients′ glucose measurements will differ.[6] Therefore, all biochemical measurements were performed at the same laboratory. Besides, the patients in the OSAS and control groups had similar characteristics in terms of interacting factors. Total cholesterol, HDL-cholesterol, and TG were assessed enzymatically on an automatic analyzer (Techicon Dax 48, Bayer Diagnostics, Tokyo, Japan). For routine patient evaluation and follow-up and for monitoring nonlaboratory-based measurements in situations where ultracentrifugation is impractical, low-density lipoprotein (LDL)-cholesterol should be estimated from direct measurements of total cholesterol, TG, and HDL-cholesterol by using the Friedewald equation.[78] So, LDL-cholesterol was calculated by the Friedewald formula [LDL = Total cholesterol – (TG/5+HDL)] in the present study.