Does drinking alcohol raise my hs-CRP?

Yes, dose-dependently. Alcohol raises hs-CRP through two primary mechanisms: hepatic inflammation from alcohol metabolism (acetaldehyde is directly toxic to liver cells and activates the NF-kB pathway) and gut permeability effects (chronic alcohol use increases intestinal permeability, allowing bacterial lipopolysaccharides to translocate from the gut into the portal circulation, driving systemic IL-6 production and hs-CRP elevation). The effect is proportional to dose and is not offset by the putative cardioprotective effects of moderate drinking, which Mendelian randomization studies have found to be a statistical artifact of observational research.

A man drinking two glasses of wine per night, 35 units per week, who presents with persistent hs-CRP elevation has an identifiable driver that no dietary supplement and no anti-inflammatory protocol will fully address while the alcohol intake continues. The alcohol-hs-CRP relationship is clinically relevant and underappreciated in conversations about anti-inflammatory lifestyle design. (GBD 2016 Alcohol Collaborators, Lancet, 201831310-2/fulltext))

Cardiologist's calibrated position, Solid (1) for the alcohol-hs-CRP dose-response relationship at higher intake levels. Promising (2) for mild elevations from moderate consumption.

What to do: If your hs-CRP is elevated and your alcohol intake exceeds 14 units per week, reduce intake for 60 days before attributing persistent elevation to other causes.

For the full picture, read Inflammation's Invoice.

## Category 19: Alcohol
Deep Dive: The Bourbon Collector's Honest Reckoning