Our data indicates that type 2 diabetes patients who smoke have significantly higher central adiposity, according to VFT and WC values, than non-smokers. Heavy smokers particularly have higher central adiposity than light smokers. When further adjustment was made for diabetes medication and HbA1c levels, this association between smoking status and abdominal obesity, although slightly attenuated, remained significant. Heavy smokers had higher abdominal obesity OR values than light smokers, even after adjusting for BMI. Among current smokers, heavy smokers showed significantly higher VFT values. For instance, participants who smoked more than 20 cigarettes per day showed higher VFT values than those who smoked less than 10 cigarettes per day. However, no dose-response relationship between the number of cigarettes smoked and abdominal obesity was observed.
Our study's consistent results demonstrate that current smokers have higher abdominal obesity than never- and ex-smokers. Shimokata et al. [14
] previously reported positive association between smoking and abdominal obesity, regardless of whether BMI values were low. The WHR actually increased in patients who started smoking, despite their weight loss. However, according to data from the Scottish Health Survey, a decrease was observed in weight and BMI values of smokers compared to non-smokers [15
]. Additionally, a recent study conducted in Turkey states that smoking inhibits visceral fat accumulation in women [16
]. The study found that current smokers showed 26% less fat mass and 30% less visceral adipose tissue than non-smokers, although the differences were statistically insignificant for the men's data. Simon et al. [17
] reported higher WHR for current smokers than subjects who quit smoking. Other studies claim that there is no significant association between smoking and fat distribution. Seidell et al. [10
] state that smoking does not cause BMI increase, but that heavy smoking leads to higher WC. Moreover, one study claims that cigarette smoking is not related to a specific distribution pattern of body fat. Thus, studies report inconsistent conclusions regarding the relationship between obesity and smoking.
Some studies that claim an association between smoking and abdominal obesity have shown higher abdominal obesity levels in smokers compared to non-smokers; however, the mechanisms responsible for those results have not been proven conclusively. Previous studies have also shown an association between smoking and hormonal changes. Smokers of 2.4 mg Federal Trade Commission nicotine cigarettes have increased plasma beta-endorphin and cortisol levels, compared to non-smokers [18
]. Significantly, increased cortisol levels lead to increased insulin resistance, which is associated with abdominal fat and diabetes [19
]. Many epidemiological studies have demonstrated increased levels of testosterone, free testosterone, and androgen in men smokers [20
]. In one such study, smokers had higher mean plasma estradiol levels compared to non-smokers [23
]. Exposure to androgens is linked to abdominal fat in premenopausal women [25
]. However, a negative correlation links testosterone and abdominal fat distribution in men [26
]. Therefore, the relationship between smoking, body fat distribution, and sex hormones remains unclear and may be further complicated by confounding factors such as alcohol consumption and stress levels.
Nicotine consumption was previously shown to temporarily enhance metabolism during resting as well as during light physical activity. However, there has been no evidence that nicotine enhances human body energy expenditure in the long term. Moreover, some studies have demonstrated that smokers and non-smokers have similar basal metabolic rates. On the other hand, it has also been reported that smokers tend to weigh less than non-smokers and that smokers gain weight after quitting. Several studies have demonstrated that body weight seems to be highest in ex-smokers, lowest in current smokers, and intermediate in never-smokers [27
]. Nevertheless, these results are controversial (not all results follow this pattern), and the biological mechanism involved has not been established. Additionally, most studies have investigated the association between smoking and obesity in healthy subjects. This association mechanism may be different in diabetes patients. Therefore, carefully designed follow-up studies of diabetic patients are required to consolidate the correlations documented in the present study.
Nevertheless, this study has some limitations. First, we only used baseline measurements obtained during each individual's first visit, for characterization. We did not account for possible changes in smoking status or other lifestyle behaviors during follow-up; there is the possibility that diabetic patients' WC, VFT, and glycemic control-related living habits had already changed by the time of the follow-up. Second, due to the cross-sectional design, this study could not elucidate mechanisms or determine the direction of causality. Third, although we adjusted for several known potential confounders, we cannot completely rule out the possibility of residual confounding such as stress and secondhand smoke. Stress-dependent cortisol values, in particular, have been strongly associated with abdominal obesity [30
]. Finally, the contribution of fat mass distribution may vary among different populations. Accordingly, our results may differ from those of studies using data obtained from women or other ethnic group participants. Therefore, further investigation, using a longitudinal study design, is needed to determine whether smoking causes abdominal obesity in general.
This study also has several strengths. This study was performed using a relatively large cohort of type 2 diabetes performed in one institute. Additionally, both WC and VFT were measured using ultrasonography and were used as indices of abdominal obesity. Moreover, all data, including anthropometric indices, were obtained by a single trained study staff member. VFT is a simple noninvasive alternative to computed tomography and a reliable index for visceral fat measurement and identification of diabetic patients [13
]. Furthermore, we assessed the association of abdominal obesity with not only smoking status but also smoking amount. Previous studies have lacked such detailed and accurate measurements of smoking amount. This study is important because it confirms a positive relationship between high smoking amount and abdominal obesity, where both are common risk factors in patients with type 2 diabetes.
In conclusion, our study found that smoking status was closely related to abdominal obesity. Further research is needed to elucidate the association of smoking status and/or smoking patterns and abdominal obesity. The findings of this study should be cross-validated to different populations; hence, further large-scale prospective studies are needed in type 2 diabetic patients. Re-evaluation of our conclusions should be continued since smoking may influence abdominal obesity, leading to other unfavorable health outcomes.