This study found current smokers to have a lower EPA/AA ratio than non-smokers among elderly patients with T2DM, indicating that smoking can detrimentally affect the EPA/AA balance in such patients. Considering that the EPA/AA ratio is a predictor of CVD events in patients with DM [2, 3] and smoking cessation is an achievable and effective option for preventing CVD [7, 8], the findings in this study strongly support the importance of smoking cessation in the management of CVD among elderly patients with T2DM.
Smoking results in various oxidants that are capable of producing free radicals and lipid peroxidation . Patients with T2DM are especially known to have high levels of these oxidants . Polyunsaturated fatty acids, particularly omega-3 acid ethyl esters, undergo oxidation, leading to a reduction in EPA in the presence of oxidants [14–16]. A previous report has indicated that AA levels in smokers (mean age, 50 years) are decreased , which is inconsistent with the findings of our study; however, another report indicated that AA in smokers are not decreased . Of note, the metabolism of AA is not always parallel to that of EPA [19–21], and compared to EPA, smoking has been shown to delay the conversion rate of AA to eicosanoids . These findings may support an impairment of EPA/AA balance, namely, a decrease in the EPA/AA ratio, observed among smokers in our study. Our results should be further analyzed using additional markers, such as oxidative stress markers, in order to clarify the underlying mechanisms.
Similar to EPA, DHA is also an omega-3 polyunsaturated fatty acid. The pathological mechanism underlying the difference between EPA and DHA is unclear. However, clinical studies have reported that lower levels of EPA, but not DHA, were significantly associated with all-cause mortality , and that there was no clear association between the DHA/AA ratio and cardiovascular risk . The results of our study may be in line with these studies [23, 24].
Some reports have shown that smoking worsens blood pressure , glycemic control , and neuropathic conditions [27, 28]. Similar findings were observed in our study. However, from the results of our adjusted analyses, these variables do not seem to have a major influence on the association between smoking status and EPA/AA ratio.
This study has certain limitations. This was a cross-sectional study; thus, further intervention studies are required. Although we saw a significant difference in the association between smoking status and EPA/AA ratio, the small patient number might present a problem in terms of a lower statistical power; thus, a larger-scale study is required. Additionally, as there is no information regarding dietary fish consumption and the dose and duration of smoking (e.g., the Brinkman index), and type of cigarette were not investigated in detail, these must be included into future work.
In summary, the present study suggests that current smoking status and a low EPA/AA ratio may enhance CVD risk in elderly patients with T2DM. Considering an individual’s smoking status coupled with EPA/AA ratio may be important in the management of T2DM, especially in the elderly. Further studies are expected.