Sulfur Microbial Diet Linked to Early-Onset Colon Polyps

A diet high in processed meat and low in legumes and vegetables may raise the risk of colorectal polyps before age 50. A large prospective study found that association in women, but it did not measure gut bacteria, hydrogen sulfide, or DNA damage in those women. The result points to a plausible lead in early-onset colorectal cancer research, not a settled cause.

That distinction matters. Early-onset colorectal cancer is rising in several high-income countries, including the United States, Canada, and Australia. Diet likely contributes, but obesity, metabolic disease, antibiotic-related microbiome disruption, ultra-processed foods, biological aging, and other exposures may contribute as well. No study has ranked those explanations by importance.

A dietary pattern tied to sulfur-metabolizing bacteria

In a prospective analysis of 30,818 women in the Nurses' Health Study II, higher adherence to the sulfur microbial diet was significantly associated with a greater risk of colorectal adenomas diagnosed before age 50. The association was not statistically significant among women diagnosed at age 50 or older, according to Nguyen et al.'s 2022 study.

Adenomas are precancerous colorectal polyps. They do not guarantee cancer, but the conventional adenoma-to-carcinoma sequence accounts for much of colorectal cancer, including many early-onset cases. The finding therefore concerns a meaningful precursor, not a vague laboratory marker.

The sulfur microbial diet was not a list of sulfur-rich foods. Researchers built the score by linking food-frequency data to the stool abundance of 43 bacterial taxa with sulfur-metabolizing genes in a separate male cohort, the Health Professionals Follow-up Study. In the women's cohort, processed meats, liquor, and low-calorie drinks pushed the score upward. Legumes, mixed vegetables, and fruit juice pushed it downward.

That construction gives the score a biological rationale, but it also creates its biggest weakness. The women in whom adenoma risk was observed did not provide stool samples. Researchers therefore could not show that a higher score predicted more sulfur-metabolizing bacteria, more Bilophila wadsworthensis, more hydrogen sulfide, or any related metabolite in the actual study population.

The study found a diet-adenoma association. It did not demonstrate a diet-to-bacteria-to-hydrogen-sulfide-to-polyp chain in humans.

Why hydrogen sulfide is an appealing hypothesis

Hydrogen sulfide is a chemically credible suspect. At sufficiently high local concentrations, it could generate reactive oxygen species, interfere with mitochondrial respiration by blocking cytochrome c oxidase, and weaken the intestinal barrier. Those mechanisms could, in principle, make colon cells more vulnerable to injury and mutation.

But "could" carries the weight in that paragraph. The available human study did not quantify hydrogen sulfide in colonic tissue, measure oxidative DNA damage, assess ATP depletion in colon cells, or identify a mutation pattern tied to the diet. A mechanism remains a hypothesis until measurements connect its links.

The low-calorie-drink component makes the interpretation even less tidy. Artificially sweetened beverages contain negligible sulfur, so their place in the score suggests that the index may partly track ultra-processed-food intake or overall diet quality rather than sulfur exposure alone. That would still make the association useful, but it would weaken claims that hydrogen sulfide is the specific driver.

The age signal is interesting, not yet an intervention rule

The under-50 result has attracted attention because adolescent diet may matter. Nguyen and colleagues also assessed high-school diet, covering ages 13 through 18, a period when the gut microbiome and lifelong eating habits develop. It is biologically plausible that earlier exposures shape later colorectal risk.

Biological plausibility is not proof of a teenage "critical window." The apparent age difference could reflect a true vulnerability, but it could also result from different statistical power between age groups or features unique to this cohort of female nurses. The study demonstrated the early-onset association only in women, although the dietary score itself was derived in men. It cannot establish that the same result applies to men.

Still, the dietary direction fits wider evidence. A 2022 systematic review by Carroll et al. found that high processed-meat intake and low vegetable and legume intake repeatedly tracked with higher early-onset colorectal adenoma and cancer risk. In a separate prospective analysis, Zheng et al. found that better scores on several overall diet-quality indices, including the Alternative Healthy Eating Index and Dietary Inflammatory Index, were associated with lower risk of early-onset adenomas.

Together, those studies support a practical conclusion with fewer assumptions: processed meat belongs lower in the diet, while legumes and vegetables belong higher. They do not establish that people should avoid all foods containing sulfur. Sulfur is an ordinary part of many nutritious foods and human biology; the study evaluated a broader dietary pattern.

Colon cancer has more than one microbiome story

The sulfur hypothesis is one possible pathway among several. A population-based Ontario case-control study by Chang et al. linked early-onset colorectal cancer with metabolic syndrome, type 2 diabetes, obesity, and physical inactivity. Those findings make it unlikely that one bacterial pathway explains the entire rise.

Other microbial mechanisms may operate separately. Borowsky et al. examined Fusobacterium nucleatum in colorectal tumors and its relationship to specific T-cell subsets, a potential immune-evasion route rather than hydrogen-sulfide genotoxicity. The ColoCare Study also reported clinicopathologic associations with F. nucleatum. These data neither confirm nor refute the sulfur microbial diet finding. They show why "the microbiome causes colon cancer" is too blunt to be useful.

Accelerated biological aging offers another parallel explanation. A 2025 observational study by Sun et al. associated unhealthy lifestyle exposures and colorectal cancer onset with epigenetic aging markers, including DNA methylation loci in TNF, BICC1, DIP2B, and NCF2. It did not test the sulfur microbial diet in the same population, so it cannot connect that score to epigenetic aging.

What to do with this evidence

If you are under 50 and thinking about colorectal cancer prevention, this study supports ordinary advice more than exotic microbiome tactics. Eat fewer processed meats. Build meals around legumes, vegetables, whole plant foods, and other markers of higher overall diet quality. Maintain a healthy weight and stay physically active. Those choices address several plausible risk pathways at once.

Do not buy a hydrogen-sulfide test, treat one diet score as a diagnosis, or assume low-calorie drinks are a proven cause of colon polyps. The central result is observational, its mechanism was not measured in the affected women, and the estimated association was reported as significant only in the younger stratum.

The useful lesson is narrower and stronger: early-onset colorectal cancer probably develops over years through several interacting exposures. Diet is one modifiable part of that picture. The sulfur microbial diet study gives researchers a testable microbial hypothesis; for everyone else, it reinforces a dietary pattern that already has broader evidence behind it.