Metabolic syndrome (MetS) is a growing global health concern due to its association with an increased risk of cardiovascular diseases (CVD), diabetes mellitus (DM), and all-cause mortality.¹ MetS is characterized by a cluster of conditions, including central obesity, hypertension, dyslipidemia, and insulin resistance, which collectively contribute to systemic inflammation and oxidative stress.² Recent studies suggest that MetS also adversely affects pulmonary function, potentially through mechanisms such as chronic low-grade inflammation, endothelial dysfunction, and mechanical restriction due to visceral adiposity.³⁻⁵ However, the extent of pulmonary

impairment and the underlying pathophysiological mechanisms remain unclear.

Pulmonary function tests (PFTs) are essential tools for assessing respiratory health, with key parameters such as forced vital capacity (FVC), forced expiratory volume in 1 second (FEV₁), and the FEV₁/FVC ratio providing insights into obstructive and restrictive lung patterns.⁶ Emerging evidence indicates that individuals with MetS exhibit reduced lung function, even in the absence of overt respiratory disease.⁷ The present study explores the impact of MetS on pulmonary function by analyzing PFT parameters in affected individuals compared to healthy controls, aiming to clarify the relationship between metabolic dysfunction and respiratory impairment.

Study Design & Participants

This cross-sectional study enrolled 150 participants, comprising 75 individuals with metabolic syndrome (MetS) and 75 age- and sex-matched healthy controls. Participants were recruited from outpatient clinics and community health screenings between Jan 2024 to June 2024. 

Inclusion criteria: patients between 30-60 years of age.

Exclusion criteria included a history of chronic respiratory diseases (e.g., asthma, COPD), active smoking, recent respiratory infections, or other conditions affecting pulmonary function.

Metabolic Syndrome Diagnosis

MetS was diagnosed using the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria, requiring the presence of ≥3 of the following:⁸

• Abdominal obesity (waist circumference ≥102 cm in men, ≥88 cm in women)
• Elevated triglycerides (≥150 mg/dL or on medication)
• Reduced HDL cholesterol (<40 mg/dL in men, <50 mg/dL in women or on medication)
• Hypertension (blood pressure ≥130/85 mmHg or antihypertensive use)
• Fasting glucose ≥100 mg/dL (or diabetes diagnosis)

Pulmonary Function Tests (PFTs)

Spirometry was performed using a [insert spirometer model] following the American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines.⁹

• Key parameters measured included:
• Forced Vital Capacity (FVC)
• Forced Expiratory Volume in 1 second (FEV₁)
• FEV₁/FVC ratio
• Peak Expiratory Flow Rate (PEFR)

Each participant underwent at least three reproducible maneuvers, with the highest value used for analysis.

Statistical Analysis

Data were analyzed using SPSS version 26 (IBM Corp., USA). Continuous variables were expressed as mean ± standard deviation (SD), and categorical variables as frequencies (%). Group comparisons were made using:

Independent Student’s t-test (for normally distributed data)

Chi-square test (for categorical variables)

Multivariate linear regression (to adjust for confounders like age, sex, and BMI)

A p-value <0.05 was considered statistically significant.

Table 1: Baseline Characteristics of Study Participants

MetS participants had significantly higher BMI, blood pressure, fasting glucose, and triglycerides, along with lower HDL-C (p < 0.001 for all). No significant differences in age or sex distribution (p > 0.05), confirming successful matching.

Table 2: Pulmonary Function Parameters

MetS patients exhibited significantly reduced FVC, FEV₁, and PEFR (p < 0.001), suggesting restrictive lung impairment. The lower FEV₁/FVC ratio (p = 0.002) indicated mild airway obstruction, though the primary pattern was restrictive. Differences remained significant after adjusting for confounders (BMI, age, sex).

Table 3: Predictors of Reduced FVC in MetS Patients

A multivariate linear regression (Table 3) revealed that waist circumference (β = −0.32, p = 0.001) and fasting glucose (β = −0.25, p = 0.008) were independent predictors of reduced FVC in MetS patients.

The present study demonstrates a significant association between metabolic syndrome (MetS) and impaired pulmonary function, characterized by restrictive lung patterns and mild airway obstruction.

Restrictive Lung Impairment in MetS

The observed reduction in FVC (% predicted) and FEV₁ (% predicted) in MetS patients supports a restrictive ventilatory defect, consistent with prior studies.¹⁰ this pattern may stem from:

• Mechanical restrictiondue to visceral adiposity limiting diaphragmatic excursion and chest wall compliance.¹¹
• Systemic inflammation, as elevated pro-inflammatory cytokines (e.g., IL-6, TNF-α) in MetS may promote lung tissue fibrosis.¹²

Our regression analysis further highlights waist circumference as an independent predictor of reduced FVC (β = −0.32, p = 0.001), underscoring the role of central obesity. This aligns with Leone et al., who reported that abdominal obesity accounted for 20% of lung function variability in MetS.¹⁰

Mild Airway Obstruction

The lower FEV₁/FVC ratio in MetS patients (p = 0.002) suggests concurrent mild airway obstruction, possibly due to:

• Endothelial dysfunctionimpairing pulmonary vascular compliance.¹³
• Hyperglycemia-induced oxidative stress, which may damage airway smooth muscle.¹⁴ Park et al. similarly noted a trend toward obstructive changes in MetS, though restrictive deficits dominated.¹⁰

Metabolic Drivers of Pulmonary Decline

The strong association between fasting glucose and reduced FVC (β = −0.25, p = 0.008) echoes findings by Yeh et al., who proposed that insulin resistance accelerates lung aging via advanced glycation end-products (AGEs).¹³ Notably, triglycerides and hypertension showed weaker correlations, contradicting some earlier studies.^{15, 16} This discrepancy may reflect our cohort’s exclusion of smokers and pre-existing lung disease, isolating MetS-specific effects.^17,18

Limitations

Cross-sectional design precludes causal inferences. Lack of imaging data (e.g., CT scans) to quantify visceral fat or lung fibrosis. Single-center recruitment, limiting generalizability.

This study adds to the growing body of evidence that MetS is associated with clinically significant pulmonary dysfunction. The findings emphasize the need for a more integrated approach to managing MetS that considers its multisystem effects, including those on respiratory health. Future research should focus on elucidating the precise mechanisms linking metabolic and pulmonary dysfunction and evaluating whether targeted interventions can improve both metabolic and respiratory outcomes in this high-risk population.

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