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Metabolic syndrome and the lung

05-09-2019
The definition of metabolic syndrome (MetS) has evolved over time; currently MetS is defined by a group of clinical features such as abdominal obesity, hyperglycemia, hypertriglyceridemia, hypertension and low-density lipoprotein cholesterol. Although data from the national health and nutrition survey from 1999 to 2010 show that age-adjusted prevalence fell from 25.5% in 1999 to 2000 to 22.9% in 2009 to 2010 in the United States, MetS is still strikingly common. This affects around 60% of obese people and more than one fifth of the population.

In various other countries around the world there are high or even higher percentages among their population. MetS has been shown in previous studies to be associated with disease development. This includes cardiovascular diseases (CVD), diabetes mellitus (DM), hepatic steatosis and cancer. The evidence from the study indicates that MetS may also be associated with pulmonary function disorders. The relationship remains unclear.
In various cross-sectional and longitudinal studies, a link between metabolic syndrome (MetS) and lung diseases has been observed. This syndrome has been identified as an independent risk factor for aggravation of respiratory complaints, greater pulmonary function disorders, pulmonary hypertension and asthma. In this review various possible mechanisms are discussed to explain these associations such as nutritional factors and the effect of adiposity and fat-induced inflammation on the lungs, and the role of other comorbidities that often accompany MetS, such as OSA and obesity.

The recognition that MetS affects the lung is, in contrast to the known association between asthma and obesity, relatively new. The individual components, despite scary controversy as to whether MetS is a unique disease law, are independently associated with changes in lung function or lung disease.

There is uncertainty about the relative contribution that each metabolic factor has to adversely affect the airways; it is also unclear how many of the MetS-related lung effects occur independently of obesity. Despite these epidemiological limitations, the proposed mechanistic routes strongly suggest that this association is probably causal. Given the widespread prevalence of MetS in the general population, it is imperative that we continue to understand how this metabolic disorder affects the lungs and how it can prevent complications.

Several major studies published in the last 10 years show a connection between MetS and lung function disorders in adults and children. One of the largest cross-sectional studies in a French population of 121,965 adult subjects showed that MetS was associated with greater pulmonary function disorder (defined as FEV1 or FVC MetS has also been evaluated as a risk factor for other chronic lung diseases, such as COPD and restrictive lung disease. Hyperglycaemia can also be associated with poorer results after an exacerbation. A variety of mechanisms may play a role between components of MetS and pulmonary function disorders and probably include the interaction between adiposity-induced changes at multiple levels and airways in the lung.

There is ample evidence to suggest that OSA can induce or aggravate most if not all metS components. Some of these effects can be improved through the use of CPAP; however, inconsistent and modest benefits suggest that other factors besides intermittent hypoxia or the extent of AHI play a role.

Every MetS component contributes to lung disease. Whether treatment with MetS will reduce the effects on the respiratory tract is still unclear. Despite minimizing the risk of respiratory comorbidity, despite this uncertainty, it is wise to treat every part of MetS optimally.

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