# Serum butyraldehyde levels are associated with abdominal aortic calcification: a population-based study

## TL;DR

Higher levels of butyraldehyde in the blood are linked to lower risk of abdominal aortic calcification, a marker for cardiovascular disease.

## Contribution

This study identifies butyraldehyde as a novel serum aldehyde inversely associated with vascular calcification in a population-based sample.

## Key findings

- Each log₂-unit increase in butyraldehyde was linked to a 36.7% lower risk of abdominal aortic calcification.
- Butyraldehyde showed the strongest inverse association with AAC in both single and mixture analyses.
- The protective effect of butyraldehyde was more pronounced in individuals with klotho deficiency.

## Abstract

Abdominal aortic calcification (AAC) is a strong predictor of cardiovascular morbidity but lacks effective interventions. Aldehydes, a diverse class of environmental and endogenous compounds, have been implicated in various chronic diseases, yet their individual and combined effects on vascular calcification remain unclear.

This study investigated associations between six serum aldehydes (benzaldehyde, butyraldehyde, heptanaldehyde, hexanaldehyde, isopentanaldehyde, propanaldehyde) and AAC in a nationally representative sample of US adults from the 2013–2014 NHANES. AAC was measured via lateral lumbar spine DXA, and serum aldehydes were quantified using gas chromatography-mass spectrometry. Analyses using weighted logistic regression and quantile g-computation (qgcomp) models, adjusted for demographic and metabolic confounders, revealed the associations between aldehydes and AAC.

This study included 1208 NHANES participants. Each log₂-unit increase in butyraldehyde concentration was associated with a 36.7% lower AAC risk (adjusted OR = 0.633, 95% CI 0.436–0.930), and individuals in the highest tertile of exposure had a 46% reduced risk compared to those in the lowest tertile. After FDR correction for multiple comparisons, butyraldehyde exhibited the strongest association with AAC among the aldehydes examined (FDR-adjusted p = 0.096). None of the other aldehydes showed significant associations with AAC in fully adjusted models. In the mixture analysis, butyraldehyde also demonstrated the strongest inverse association with AAC (β = −0.442). The inverse association between butyraldehyde and AAC was more pronounced in individuals with klotho deficiency.

These findings indicate that butyraldehyde is inversely associated with AAC, not only highlighting its potential role in vascular calcification but also suggesting the necessity of aldehyde-specific assessments in cardiovascular risk assessment. Besides, butyraldehyde may serve as a promising candidate for therapeutic development in high-risk populations.