Hydrogen sulfide production

Hydrogen sulfide is the gas behind the rotten-egg smell. Its effects in your gut depend on how much reaches the lining and how quickly your cells process it. Experiments in cells and animals show both protective effects and injury. Human studies have linked sulfur-processing microbes with several bowel diseases, but those findings don't establish what an individual stool production score predicts.

This stool marker uses microbial DNA to estimate your gut microbes' capacity to produce hydrogen sulfide. The estimate reflects sulfur-related functions in the microbial community, rather than measuring the gas itself. It's a research-stage marker. Its value for diagnosing disease, choosing treatment, or predicting future illness hasn't been established.

Where the Gas Comes From

Many gut bacteria can release sulfide from cysteine. Cysteine is one of the building blocks of protein. The material available to these bacteria comes from food and from substances your body releases into the intestine, including mucus and shed cells.

Other bacteria use sulfate. Sulfate is a sulfur-containing compound found in food, water, and intestinal secretions. Desulfovibrio includes species that turn it into sulfide. Bilophila wadsworthia uses a different route: it obtains sulfite from compounds such as taurine and converts that into sulfide. Taurine is present in some foods and is also attached to some of the bile acids your body uses in digestion.

The capacity to make sulfide is widespread. One analysis found bacteria with predicted cysteine-degrading genes in all 6,623 healthy participants examined. Another survey of about 17,000 bacterial genomes identified sulfide-related genes across 142 bacterial genera. These findings broaden the list of possible producers well beyond sulfate-reducing bacteria. They don't establish which route produces the most gas in your intestine.

Why the Amount at the Gut Lining Matters

Your own cells also produce hydrogen sulfide. Colon cells can break it down through reactions in their mitochondria. Mitochondria are structures inside cells that produce usable energy. Experiments in human colon cell lines show that processing small amounts of sulfide can support energy production, while higher exposure can inhibit it.

At sufficiently high concentrations in laboratory experiments, sulfide interferes with the machinery cells use to consume oxygen and can impair their use of butyrate. Butyrate is a fatty acid made by gut bacteria from dietary fiber and is an important fuel for the colon lining. Mouse and laboratory studies also suggest that sulfide can weaken chemical bonds in protective mucus. Other animal experiments have found that supplying sulfide can promote mucus production and reduce inflammation.

Those effects depend on the experimental conditions, the source of sulfide, and the tissue's ability to process it. A microbial DNA estimate doesn't measure the concentration reaching your colon cells or their capacity to clear it. There is no established score that separates beneficial from harmful exposure.

Ulcerative Colitis and Crohn's Disease

Ulcerative colitis and Crohn's disease are forms of inflammatory bowel disease. Studies have reported differences in sulfide-producing microbes and sulfur metabolism in people with these conditions. Findings vary by the bacteria examined, treatment, and whether researchers study stool or intestinal tissue, so the relationship is more complicated than having more sulfate-reducing bacteria.

In one Crohn's disease study, stool cultures produced detectable sulfide in about 56% of samples from people with the disease, compared with about 17% of samples from healthy controls. Researchers deliberately grew these cultures in the presence of oxygen to investigate a particular bacterial sulfate-processing route. This was a laboratory culture experiment, not a measurement of gas exposure inside the intestine or a validation of this stool score.

Human biopsy studies have also found lower amounts or activity of some enzymes involved in sulfide handling in inflammatory bowel disease. These tissue findings suggest that the lining's response may matter alongside microbial production. They don't establish whether altered sulfide handling causes inflammation or develops because of it.

If you have colitis or Crohn's, this result can describe an aspect of your microbiome being studied in the disease. It hasn't been shown to identify active inflammation, predict a flare, or improve treatment decisions beyond established monitoring.

Colon and Rectal Cancer

Laboratory experiments have found that sulfide can damage DNA under particular conditions, including experiments in a human colon cell line with DNA repair inhibited. Human stool studies provide a separate kind of evidence. In an analysis involving 667 participants, several sulfur-related genes were more abundant in people with colorectal cancer. Cancer itself can change the intestinal environment, so this comparison cannot establish which changes came first.

A prospective study followed 48,246 men for 26 years. Researchers first used stool and dietary information from 307 men to develop a diet score associated with sulfur-metabolizing bacteria. Men in the highest quarter of that dietary score had about 43% higher risk of cancer in the lower colon and rectum than those in the lowest quarter, after adjustment for other risk factors. There was no clear association with cancer in the upper colon.

That finding concerns a dietary pattern associated with a microbial community. It doesn't translate into a cancer risk estimate for your stool result, and it doesn't prove sulfide caused the association. This marker hasn't been validated for detecting cancer or precancerous polyps.

Mortality and Cardiovascular Disease

A study of 74,037 adults in the southern United States examined a similar dietary score over an average of 13.9 years. Most participants had low incomes, and about two thirds were Black. The score was developed using stool microbiome data from 514 Black participants.

Among Black participants, those in the highest quarter of the score had about 21% higher risk of death from any cause than those in the lowest quarter. Cardiovascular mortality was about 18% higher. Similar associations were reported among White participants. These were adjusted observational findings based on diet, not measurements of stool sulfide or this production score. They don't show that lowering the score prolongs life.

Diarrhea and Irritable Bowel Syndrome

In one study comparing irritable bowel syndrome subtypes, people with diarrhea-predominant IBS had higher breath hydrogen sulfide and greater representation of sulfide-producing bacteria, including Desulfovibrio and Fusobacterium. Methane-producing microbes were more closely associated with constipation. The study combined breath measurements with stool microbial profiling; it didn't establish a diagnostic role for this stool production score.

A 2026 study found differences in small-intestinal gene activity among people grouped by breath sulfide, breath methane, and bacterial cultures from the small intestine. The sulfide-defined group had more extensive differences in gene activity, and experiments in rats provided some supporting findings. The human comparison was observational and used breath and small-intestinal samples. It doesn't establish that a stool score explains your diarrhea.

Parkinson's Disease, an Open Question

Small human studies have reported more Desulfovibrio in stool from people with Parkinson's disease. One proposed explanation involves bacterial sulfide contributing to cellular injury and abnormal protein accumulation, but that mechanism remains a hypothesis supported mainly by experimental work. Measuring these bacteria is also different from measuring sulfide production. No validated evidence shows that this stool score predicts Parkinson's disease.

When Results Can Be Misleading

• Genetic capacity and active production differ: finding a microbial gene doesn't show how actively it is being used. Available nutrients, interactions among microbes, and conditions inside the intestine influence actual gas production.
• Stool represents only part of the gut: microbes in stool can differ from those attached to the lining or living in the small intestine. This result cannot locate an area of overgrowth.
• Recent changes can affect the sample: changes in diet, antibiotics, laxatives, bowel preparation, and intestinal transit can alter the microbial community represented in stool.
• Collection and analysis matter: preservation, DNA extraction, sequencing, and the reference databases used to identify microbial functions can affect an estimate. Different laboratories' scores are not interchangeable.
• The score doesn't measure tissue exposure: it doesn't account for how much sulfide is bound to other compounds, consumed by other microbes, or cleared by your intestinal cells.

Tracking Your Trend

Repeated measurements can describe changes in the estimated microbial capacity, but a change can reflect biological variation or differences in sampling and analysis. No validated amount of change has been shown to represent improved gut health. A falling score doesn't by itself demonstrate that inflammation has improved or disease risk has fallen.