# Association between dietary fatty acid intake and preserved ratio impaired spirometry in U.S. adults: a population-based cross-sectional study

**Authors:** Xiang Liu, Wei Zeng, Wangyan Zhou, Dayang Zheng, Xu Yang, Weijun Liao

PMC · DOI: 10.3389/fnut.2025.1622795 · Frontiers in Nutrition · 2025-07-30

## TL;DR

Higher intake of saturated and polyunsaturated fatty acids is linked to a lower risk of a lung condition called PRISm in U.S. adults.

## Contribution

First population-based study to show that dietary saturated and polyunsaturated fatty acids are inversely associated with PRISm.

## Key findings

- Each standard deviation increase in saturated fatty acid intake was linked to a 14% lower odds of PRISm.
- Polyunsaturated fatty acid intake was associated with a 12% lower odds of PRISm.
- Monounsaturated fatty acid intake showed no significant association with PRISm.

## Abstract

Preserved ratio impaired spirometry (PRISm) is increasingly recognized as a clinically relevant but underdiagnosed lung function abnormality. This pulmonary phenotype is clinically significant yet remains insufficiently studied. Although dietary fatty acids are known to have anti-inflammatory and immune-regulating properties, their relationship with PRISm has not been previously explored. This study aimed to evaluate the associations between intake of saturated (SFA), monounsaturated (MUFA), and polyunsaturated fatty acids (PUFA) and the prevalence of PRISm in U.S. adults.

We conducted a cross-sectional analysis using data from 9,103 adults in the 2007–2012 National Health and Nutrition Examination Survey (NHANES). Dietary intake of SFA, MUFA, and PUFA was assessed from two 24-h dietary recalls. Fatty acid variables were log-transformed and standardized. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between fatty acid intake and PRISm, adjusting for sociodemographic, behavioral, and clinical covariates. Nonlinear relationships were examined using restricted cubic splines. A two-sided p-value <0.05 was considered statistically significant.

Among the study population (mean age 45.6 ± 15.8 years; 47.7% male), 1,362 participants (15.0%) exhibited the PRISm phenotype. In models controlling for demographic, lifestyle, and clinical variables, each standard deviation increase in SFA [0.86 (0.75–0.99)] and PUFA [0.88 (0.79–0.99)] intake was associated with a statistically significant reduction in the odds of PRISm. MUFA intake was not significantly related to PRISm. Restricted cubic spline analysis indicated no evidence of non-linearity in these associations. The inverse relationships for SFA and PUFA were also consistent across demographic and clinical subgroups.

Greater consumption of saturated and polyunsaturated fatty acids was associated with a lower prevalence of PRISm in a nationally representative adult population. These associations were consistent across key demographic and clinical subgroups. If confirmed in prospective studies, our findings may inform early dietary strategies to support pulmonary health.

Created with BioRender.com.

Associations of dietary fatty acid subtypes with PRISm (preserved ratio impaired spirometry) are illustrated. Saturated fat, monounsaturated fat, and polyunsaturated fat rich foods are shown with a diagram of lungs labeled “Healthy” and “PRISm”. Results indicate a significant association between higher saturated and polyunsaturated fat intake with lower odds of PRISm among adults without COPD, while monounsaturated fat shows no significant association. Three graphs display the log odds ratio of PRISm against standardized intakes of each fat type, with confidence intervals and p-values noted.

## Full-text entities

- **Genes:** PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468] {aka CIMT1, FPLD3, GLM1, NR1C3, PPARG1, PPARG2}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, APOB (apolipoprotein B) [NCBI Gene 338] {aka FCHL2, FLDB, LDLCQ4, apoB-100, apoB-48}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** asthma (MESH:D001249), lung dysfunction (MESH:D008171), chronic diseases (MESH:D002908), frailty (MESH:D000073496), impaired spirometry (MESH:D060825), non-obstructive pulmonary impairment (MESH:D008173), airway inflammation (MESH:D007249), atherogenic (MESH:D050197), malnutrition (MESH:D044342), nutritional deficit (MESH:D009748), lung function impairment (MESH:D003072), dyspnea (MESH:D004417), obese (MESH:D009765), COPD (MESH:D029424), diabetes (MESH:D003920), cancer (MESH:D009369), emphysema (MESH:D004646), impaired pulmonary function (OMIM:608852), hypertension (MESH:D006973), PRISm (MESH:C537758), pulmonary inflammation (MESH:D011014), lung function decline (MESH:D055370)
- **Chemicals:** alcohol (MESH:D000438), calcium (MESH:D002118), vitamin D (MESH:D014807), MUFA (MESH:D005229), omega-3 (MESH:D010743), Fatty acid (MESH:D005227), leukotrienes (MESH:D015289), dietary fatty acid (-), triglyceride (MESH:D014280), leukotriene B4 (MESH:D007975), prostaglandins (MESH:D011453), fish oil (MESH:D005395), cholesterol (MESH:D002784), lipid (MESH:D008055), fat (MESH:D005223), eicosanoids (MESH:D015777), prostaglandin E2 (MESH:D015232), PUFA (MESH:D005231), carbohydrate (MESH:D002241)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12343235/full.md

## References

65 references — full list in the complete paper: https://tomesphere.com/paper/PMC12343235/full.md

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Source: https://tomesphere.com/paper/PMC12343235