# Impact of E-Cigarette Use on Circadian Proteins and Cardiovascular Risk Markers

## TL;DR

This study shows that vaping disrupts circadian proteins and increases inflammation, similar to patterns seen in cardiovascular disease, suggesting a link to higher heart risk.

## Contribution

The study identifies a novel mechanistic link between e-cigarette use and cardiovascular risk through circadian disruption and inflammation.

## Key findings

- Vaping significantly reduced levels of circadian proteins like Melatonin, PER1, PER2, CRY1, and CRY2.
- Vapers showed elevated inflammatory and oxidative stress markers (IFN-γ, MDA) similar to cardiovascular disease patients.
- The observed molecular changes suggest a potential mechanism linking vaping to increased cardiovascular risk.

## Abstract

The increasing popularity of E-cigarettes among young adults has raised concerns about their health effects, particularly on the circadian system, which regulates critical physiological processes. This study examined how vaping influences circadian proteins and inflammatory markers, comparing these effects to those in cardiovascular disease patients. Blood samples from 254 participants, non-vaping controls (n = 90), regular vapers (n = 86), and cardiovascular patients (n = 78), were analyzed for circadian proteins (Melatonin, BMAL1, PER1, PER2, CRY1, CRY2) and inflammatory/oxidative stress markers (IFN-γ, MDA). Vaping significantly decreased Melatonin, PER1, PER2, CRY1, and CRY2, while BMAL1 remained unchanged. Elevated IFN-γ and MDA levels indicated increased inflammation and oxidative stress in vapers. Vaping induces circadian disruption patterns similar to cardiovascular disease, suggesting a potential mechanism linking e-cigarette use to increased cardiovascular risk.

The figure illustrates a progression from vaping exposure toincreased cardiovascular risk. Vaping introduces nicotine and harmful chemicals (low risk stage), leading todisruption of circadian clock proteins (reduced melatonin, PER1/2, CRY1/2; unchanged BMAL1) and elevatedinfl ammatory and oxidative stress markers (IFN-γ, MDA). These molecular alterations resemble patterns observed incardiovascular disease, suggesting a mechanistic link between e-cigarette use and heightened cardiovascular risk.

The figure illustrates a progression from vaping exposure toincreased cardiovascular risk. Vaping introduces nicotine and harmful chemicals (low risk stage), leading todisruption of circadian clock proteins (reduced melatonin, PER1/2, CRY1/2; unchanged BMAL1) and elevatedinfl ammatory and oxidative stress markers (IFN-γ, MDA). These molecular alterations resemble patterns observed incardiovascular disease, suggesting a mechanistic link between e-cigarette use and heightened cardiovascular risk.