When compared to non-obese smokers, obese smokers have a clear reduction in life expectancy (24, 25). Obesity induces several inflammatory markers and cytokines that might contribute to cardiovascular risk. Cigarette smoking, especially in chronic smokers, has also been linked to the induction of several cytokines, such as intracellular adhesion molecule-1 (ICAM-1), tumor necrosis- α (TNF-α), and oxidative stress molecules, while decreasing adiponectin concentrations, inducing insulin resistance, and promoting endothelial dysfunction, which is an early marker of atherosclerosis (26). Furthermore, smoking has also been linked to insulin resistance and low HDL cholesterol levels (27). The figure shows the additional effects of smoking in obese individuals.
In addition to being a risk factor for arteriosclerosis and ischemic stroke, smoking also increases intra-abdominal (visceral) adipose tissue such that smokers have more of this harmful type of fat compared to non-smokers, even after adjusting for markers of total adiposity (28, 29). These results strongly suggest that body fat distribution can be modified by behavioural factors such as cigarette smoking, despite a well-documented genetic susceptibility to intra-abdominal adiposity (30). This finding is especially important given that intra-abdominal obesity has been reported to be closely associated with the features of the metabolic syndrome increasing the risk of CVD and type 2 diabetes (31).

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