The current analysis indicated a high prevalence of metabolic syndrome, and it was noteworthy that in both men and women, individual composition of abdominal obesity, low HDL-C, and high blood pressure was significantly associated with decreasing FVC and FEV1. In addition, MetS and MetS score 4 were negatively correlated with OLD in women.
When we independently predicted FVC, FEV1 and FEV1/FVC ratio for each metabolic component, we found that after adjusting for age and family income group, WC was one of the MetS components associated with the decrease of FVC and FEV1 in males. This was consistent with some studies [13, 20, 21]. At present, it was believed that central obesity (abdominal obesity) was the source of common metabolic diseases and cardiovascular diseases in adults, such as hyperglycemia, hypertension, dyslipidemia and so on, and was the core component of MetS [22]. Most of the current data support the link between MetS and impaired lung function mainly through abdominal obesity. WC, as one of the indicators of abdominal obesity, was related to the deterioration of lung function [23]. Central obesity may affect the mechanical performance of the ventilator because it limits the expansion of the diaphragm. The gender difference may be related to the respiratory movement and fat distribution of the chest wall and abdominal wall, and have different effects on the lung function of women and men [24]. Furthermore, MetS is characterized by systemic inflammation, and endothelial dysfunction caused by this systemic inflammation leads to impaired organ system function [25, 26]. Notably, our study found that males smoke more than females, and that long-term exposure to cigarette smoke causes systemic inflammation [27]. Thus, in active smokers with Mets, since it comes from two sources, visceral fat and lung exposure to cigarette smoke, it may increase systemic inflammation. This may lead to increased endothelial dysfunction and a rapid decline in lung function.
It was worth noting that an important component in our study was HDL-C, and its increase was significantly correlated with decreased FVC and FEV1 in all participants. Consistent with this observation, a representative US sample study found that low HDL-C were associated with impaired lung function [11]. A small case-control study reported that HDL levels in the COPD group were significantly lower than those in the control group (47.1% vs 58%)[28]. A small population study in Mexico [29] observed that subjects with normal or elevated high-density lipoprotein cholesterol had lower FVC than subjects with low-density lipoprotein cholesterol. The pathophysiological role of this link is unknown. Usually chronic inflammation accelerates atherosclerosis in part by altering HDL and its ability to promote reverse cholesterol transport [30, 31]. Since this lipoprotein has anti-fungal, anti-inflammatory, antioxidant and even anti-apoptotic functions, we hope that its high value will have a beneficial effect on lung function [32–34]. But in recent years, the role of high density lipoprotein cholesterol as an atherosclerotic protective agent is changing.
In fact, it has been recognized that their ability to fight inflammation and mobilize cholesterol is severely affected by the oxidation of HDL-related proteins, and even this dysfunctional HDL may have a pro-inflammatory effect. This new approach to the physiology of high-density lipoprotein cholesterol may partly explain our finding that subjects with high cholesterol have a smaller lung volume [35]. At the same time, a genetic and molecular study reported two polymorphisms in apolipoprotein M (APOM)-related genes associated with decreased lung function in two ethnic groups (African-American and European-American). APOM is a kind of lipoprotein associated with high density lipoprotein cholesterol. The change of its gene expression will change the quality and function of high density lipoprotein cholesterol. In fact, the same study found that high levels of high-density lipoprotein cholesterol were associated with a decrease in the FEV1/FVC ratio [36].
In this study, MetS was associated with decreased prediction ability of OLD in females, and MetS score was negatively correlated with the incidence of OLD. This contradicts previous research [15, 37, 38]. However, after careful observation, we found that HDL-C played a crucial role in our study, and it was significantly negatively correlated with FVC and FEV1 in females, while other MetS components had relatively little effect on OLD. Our results are consistent with a previous study that found that in the Japanese population, patients with stage I airflow obstruction (FEV1/FVC < 70% and FEV1 ≥ 80% predicted values) had a lower risk of MetS than patients with normal lung function in the crude model [16].
There are limitations in this study. First of all, our study showed that MetS and its components were associated with decreased lung function, or even a negative correlation. However, due to the limitations of the study design, the causal relationship between the two has not been determined. Second, we also found that HDL, as an important metabolic component, is negatively correlated with impaired lung function, and the pathophysiological relationship between them is still unclear. Studies have shown that the incidence of lung function impairment itself is not clear. Although HDL-C is negatively correlated with FEV1 and FVC, it is statistically significant, but it does not represent lung involvement [39]. Therefore, it is necessary to further study these links.