# Dietary Vitamin C Intake Affects Lung Function Through White Blood Cell

**Authors:** Biao Hu, Lu Yuan, Yueyang Zhang, Weiling Deng, Haoyu Zhong, Chengyu Miao, Chudong Wang, Jiaxin Cai

PMC · DOI: 10.1002/fsn3.70299 · Food Science & Nutrition · 2025-05-14

## TL;DR

This study shows that dietary vitamin C may improve lung function by reducing white blood cell count, suggesting a potential anti-inflammatory mechanism.

## Contribution

The study identifies a novel mediating role of white blood cells in the relationship between dietary vitamin C intake and lung function.

## Key findings

- Dietary vitamin C intake was negatively associated with white blood cell (WBC) count.
- WBC count was negatively associated with lung function.
- Vitamin C intake showed a positive association with lung function through a significant mediation effect via WBC.

## Abstract

As an antioxidant, vitamin C has been increasingly used in the treatment of various pulmonary diseases in recent years. However, the mechanism by which vitamin C affects lung function remains unclear to this day. Given its low cost and low risk, vitamin C is highly suitable for widespread use as a conventional treatment, making research into its mechanisms of influencing lung function necessary. Considering the potential association between vitamin C and white blood cells (WBCs), it may influence lung function by affecting white blood count (WBC). The potential impacts of WBCs on the lungs may include damage to the lung parenchyma through proteases released by these cells, as well as the effects of inflammatory factors on alveolar epithelial cells, among other mechanisms. This study aims to explore the potential relationship between dietary vitamin C intake, WBC, and lung function through a cross‐sectional study. This cross‐sectional study included data from 15,738 participants in the National Health and Nutrition Examination Survey (NHANES) from three time periods: 2007–2008, 2009–2010, and 2011–2012. Parallel mediation analysis was conducted using a multivariable logistic regression model to assess the relationships between dietary vitamin C intake, WBC, and lung function. Following the cross‐sectional study, we further incorporated Mendelian randomization (MR) analysis to strengthen the validity of the findings. The results of this cross‐sectional study showed that dietary vitamin C intake was negatively associated with WBC (p < 0.05, β < 0), while WBC was also negatively associated with lung function. In contrast, dietary vitamin C intake was positively associated with lung function, with a significant positive mediation effect (p < 0.05, β > 0). These findings suggest that vitamin C may influence lung function by modulating WBC levels. The study may reveal part of the mechanism through which vitamin C affects lung function, specifically through the mediation of WBC. The roles of inflammation and proteases could be potential underlying mechanisms. However, further research is required to clarify the biochemical mechanisms. This study provides a reference for the clinical use of vitamin C in the treatment of related pulmonary diseases and promotes further research into its broader effects.

This study found that dietary vitamin C intake is positively associated with lung function and negatively associated with WBC count, which in turn negatively impacts lung function. Mediation analysis and Mendelian randomization suggest that vitamin C may enhance lung function partially through reducing WBC. These findings highlight a potential anti‐inflammatory mechanism by which vitamin C benefits pulmonary health.

## Linked entities

- **Chemicals:** vitamin C (PubChem CID 54670067)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, TUBA1B (tubulin alpha 1b) [NCBI Gene 10376] {aka K-ALPHA-1}, EPX (eosinophil peroxidase) [NCBI Gene 8288] {aka EPO, EPP, EPX-PEN, EPXD}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, CTSB (cathepsin B) [NCBI Gene 1508] {aka APPS, CPSB, KWE, RECEUP}
- **Diseases:** DM (MESH:D003920), sepsis (MESH:D018805), pulmonary diseases (MESH:D008171), impaired pulmonary health (OMIM:603663), Hypertension (MESH:D006973), ARDS (MESH:D012128), inflammation (MESH:D007249), lung inflammation (MESH:D011014), CGD (MESH:D006105), infection (MESH:D007239), Smoking (MESH:D015208), type 1 diabetes (MESH:D003922), obese (MESH:D009765), COPD (MESH:D029424), pulmonary fibrosis (MESH:D011658), overweight (MESH:D050177), bronchitis (MESH:D001991)
- **Chemicals:** glucose (MESH:D005947), Alcohol (MESH:D000438), ROS (MESH:D017382), Vitamin C (MESH:D001205)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

47 references — full list in the complete paper: https://tomesphere.com/paper/PMC12076004/full.md

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Source: https://tomesphere.com/paper/PMC12076004