Today’s Solutions: December 09, 2025

BY THE OPTIMIST DAILY EDITORIAL TEAM

It’s long been the butt of jokes, but the science is catching up: fart gas might actually be good for you.

Researchers at Johns Hopkins Medicine say that hydrogen sulfide, the chemical behind that telltale rotten-egg smell, might help protect the aging brain from cognitive decline, including Alzheimer’s disease. While the idea of your body benefiting from its own flatulence may sound absurd, the study, published in Proceedings of the National Academies of Science, takes it quite seriously.

“Our new data firmly link aging, neurodegeneration and cell signaling using hydrogen sulfide and other gaseous molecules within the cell,” said Dr. Bindu Paul, the study’s lead scientist.

What hydrogen sulfide actually does (besides stink)

Hydrogen sulfide is toxic in large amounts, but your body naturally produces tiny, controlled doses to regulate everything from blood flow to inflammation. According to Dr. Solomon Snyder, one of the study’s co-authors, the gas plays a role in cell signaling by modifying proteins in a process called sulfhydration.

But here’s the kicker: sulfhydration levels decline with age, and even more dramatically in people with Alzheimer’s.

“Using the same method, we now confirm a decrease in sulfhydration in the AD brain,” said collaborator Dr. Milos Filipovic, referring to Alzheimer’s disease. In other words, the body’s natural production of hydrogen sulfide may decline just when the brain needs it most.

Fart power: tested on mice, with surprising results

To explore this link, researchers used genetically modified mice that mimic human Alzheimer’s disease. The mice were injected with NaGYY, a compound that slowly releases hydrogen sulfide into the body.

After 12 weeks, the treated mice showed some seriously promising improvements.

Behavioral tests revealed that cognitive and motor function improved by 50 percent compared to untreated mice. The ones who received the hydrogen sulfide treatment were more physically active and could better recall the locations of platform edits. This is kind of like remembering where you left your keys.

“The results showed that the behavioral outcomes of Alzheimer’s disease could be reversed by introducing hydrogen sulfide,” the research team wrote.

The science behind the stink

But what exactly was happening in the brain? The study pointed to a common enzyme called GSK3β (glycogen synthase beta), which normally helps regulate cellular processes.

When hydrogen sulfide levels are healthy, GSK3β works as a signaling molecule. But in its absence, it starts to stick too closely to another protein called Tau.

When Tau and GSK3β bind too often, Tau forms clumps in neurons. Those clumps block communication between nerve cells and eventually cause them to die, a defining feature of Alzheimer’s progression.

“This leads to the deterioration and eventual loss of cognition, memory and motor function,” the research team explained.

“Understanding the cascade of events is important to designing therapies that can block this interaction like hydrogen sulfide is able to do,” said Daniel Giovinazzo, PhD student and first author of the study.

A big whiff of hope

Until recently, scientists didn’t have a good way to simulate the body’s precise, low-dose hydrogen sulfide production in lab settings. That changed with the compound NaGYY, which can mimic the body’s natural gas-making abilities.

“This compound does just that and shows by correcting brain levels of hydrogen sulfide, we could successfully reverse some aspects of Alzheimer’s disease,” said Dr. Matt Whiteman, one of the study’s co-authors.

The team is continuing to explore how adjusting the body’s hydrogen sulfide levels could open new doors for treating neurodegenerative diseases. And while sniffing your own farts probably isn’t the answer, the science behind this sulfurous gas is now being taken seriously by some of the world’s leading medical researchers.

Source study: Proceedings of the National Academies of Science—Hydrogen sulfide is neuroprotective in Alzheimer’s disease by sulfhydrating GSK3β and inhibiting Tau hyperphosphorylation

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