Eric Brown

Personal update: The Brown Lab is up and running at Virginia Commonwealth University where I've joined as a faculty member in the Microbiology and Immunology Department.

I will be launching a research program focused on understanding the molecular mechanisms that prevent chronic inflammation and promote its resolution. This will include work on sphingolipid-immune interactions, extracellular vesicle biology and HLA-associated mechanisms in diseases such as IBD and spondyloarthritis.

The Brown Lab will be recruiting talented scientists to fill multiple positions. Feel free to reach out directly if this research area interests you.

New article out on something I've been thinking about for awhile studying arthritis and lipids. Is the lipid paradox really a paradox?

Across every chronic inflammatory condition studied, namely rheumatoid arthritis, sepsis, cancer, and chronic infection patients with the lowest LDL have the highest mortality. This is called the “lipid paradox.” The standard explanation centers around reverse causality. Illness or inflammation itself suppresses cholesterol synthesis, so low LDL marks severe disease rather than causing harm.

To me, that explanation is incomplete. It assumes LDL has purely a metabolic function and each particle has equally inert cargo, neutral until proven harmful. The assumption is wrong. What is missed is context and immune function of LDL itself. Circulating LDL has critical roles in innate immunity, detoxification and tissue repair. The LDL cargo and context mean more than the concentration. And the key role of LDL in immunity and tissue repair is often overlooked.

ericmichaelbrown.substack.com/p/is-the-lipid…

Most mouse studies claiming a “high-fat diet” (HFD) effect in rodent studies are not actually testing saturated fat. They’re testing a processed rodent chow loaded with oxidized omega-6 lipids from poor quality lard and soybean oil. Nearly every obesity, metabolic syndrome, inflammation, or chronic disease study using the standard HFD model relies on a diet with a distorted fatty acid profile; high omega-6 PUFA, low omega-3 PUFA, and high in lipid peroxidation products. This article breaks down what the rodent HFD really contains and why labeling it as “high in saturated fat” misleads nutrition science.

Starting to write more. Mostly for myself- there are too many ideas stuck in my head and in drafts. I'll be sharing what I’m learning about nutrition, lipids, immunity, and other biology topics. Can follow along here: ericmichaelbrown.substack.com

Our most recent work on sphingolipids is now published in @cellhostmicrobe! t.co/LeWWjVM07O
Here we discovered a mechanism by which bacterial sphingolipids in outer membrane vesicles promote anti-inflammatory responses in immune cells, through activation of the mevalonate pathway and cholesterol biosynthesis, which was essential for IL-10 secretion. This discovery was the product of many years of teamwork with @emilytemple_, and others in the @TheXavierLab and Clary Clish's metabolomics group at the @broadinstitute. Here’s a thread on what we found, how we found it and and why it matters 🧵👇