Could a common stomach bug help shield the brain from Parkinson’s? New research links H. pylori infection to reduced disease risk, opening fresh avenues in neurodegenerative science.
Study: Helicobacter pylori infection might be a protective factor against Parkinson’s disease. Image Credit: Liya Graphics / Shutterstock
Around half the world has Helicobacter pylori infections, which are typically linked to ulcers. However, a recent study published in Scientific Reports revealed a surprising twist: people with Parkinson’s disease are significantly less likely to test positive for H. pylori infections. This finding has uncovered an unexpected link between a common gastrointestinal infection and neurodegenerative disease, although causality remains unproven.
The gut and the brain
Growing evidence has shown that the gut does more than digest; it is intricately involved in our immune defenses. Scientists now believe that gut health could influence diseases beyond the digestive system, including neurological disorders like Parkinson’s disease. Parkinson’s disease is the second most common neurodegenerative disease globally, especially among older adults. It causes tremors, stiffness, and slower movements, often preceded by digestive symptoms such as constipation and delayed stomach emptying.
Meanwhile, H. pylori infects about half the world’s population and is usually blamed for ulcers and stomach cancer. Recent studies suggest that this bacterium may play a protective role in certain autoimmune and inflammatory conditions, possibly by shaping immune responses early in life. However, the link between H. pylori and Parkinson’s disease remains unclear.
The current study
In the present study, the researchers conducted a case-control investigation at Sichuan Provincial People’s Hospital in China. It included 315 patients diagnosed with Parkinson’s disease between March 2022 and July 2024 using standardized diagnostic criteria and confirmation by neurologists. The control group comprised 22,383 outpatients who had undergone routine testing for H. pylori infection during the same period. It is important to note that the average age of the Parkinson’s disease group (about 65 years) was substantially higher than that of the outpatient controls (about 45 years); statistical adjustments were made for age and other factors in the analyses.
To detect H. pylori, researchers used the non-invasive 13C-urea breath test. The participants drank a solution containing a special form of urea, and breath samples were collected before and 30 minutes after ingestion. The test measured the change in carbon dioxide levels to determine infection status.
Participants with other neurodegenerative conditions, such as Alzheimer’s disease or multiple system atrophy, and those who had used antacids or antibiotics in the four weeks prior were excluded from the study. Importantly, individuals who had previously undergone H. pylori eradication therapy were not excluded, as the study design could not differentiate between current and past infections. While including these individuals may increase “real-world” relevance, the paper frames this primarily as a methodological limitation rather than an explicit design rationale.
The researchers gathered information on age, sex, medical history (including hypertension, diabetes, coronary disease, ulcers, and digestive cancers), and rural or urban residence using medical records and standardized interviews. They then used a series of statistical analyses to investigate potential correlations between Parkinson’s disease and H. pylori infections, and adjusted for these variables in their models.
Key findings
The study found that people with Parkinson’s disease had significantly lower rates of H. pylori infection compared to the general outpatient population. This inverse relationship remained consistent across multiple analyses. A standard diagnostic threshold for the H. pylori test showed that only 28.6% of Parkinson’s disease patients tested positive, compared to 33.9% of controls. With the stricter threshold, 22.5% of Parkinson’s disease patients were positive, compared to 27.5% of controls.
Even after adjusting for age, sex, medical conditions, and living area, the differences remained significant. In multivariate analysis, Parkinson’s patients had a 26% lower odds (OR 0.74, 95% CI: 0.56–0.97, p = 0.030 for DOB ≥ 8) of H. pylori infection. Furthermore, this trend persisted in rural and urban populations, though the contrast was more striking in rural participants, possibly due to fewer lifestyle-related confounders.
To verify these findings further, the researchers applied propensity score matching, creating a statistically balanced subgroup. Even in this refined comparison, the gap persisted—only 22.5% of matched Parkinson’s disease cases tested positive, while 29.7% of controls reported H. pylori infections (p = 0.009).
These findings challenged earlier research that linked H. pylori to worsening Parkinson’s disease symptoms. Previous studies often focused on how the bacterium interfered with levodopa absorption, a key Parkinson’s disease medication. However, those studies had smaller sample sizes, and many did not control for environmental or regional differences. The present paper does not specifically highlight urban/rural or geographic limitations in prior research as a major focus, emphasizing instead sample size and mechanistic uncertainty. Additionally, previous studies often included younger, more urban cohorts or had different geographic distributions, which could affect the results.
The results from the present study suggested a different possibility — that H. pylori may play a protective role against Parkinson’s disease. The authors proposed immune modulation as a possible mechanism, with H. pylori infection, especially in childhood, increasing regulatory T cell activity, which dampens inflammation. This immune shift might reduce the risk of neurodegeneration later in life. However, the study design cannot determine whether H. pylori infection truly protects against Parkinson’s disease, or whether Parkinson’s disease, its treatments, or related factors might reduce H. pylori colonization.
However, the study’s single-center design and inability to distinguish between past and current infections were major limitations. Also, the study did not measure immune markers directly, which limits conclusions about the mechanisms behind this link. Other possible explanations, such as changes in the gastric environment or medication use among Parkinson’s disease patients affecting H. pylori detection, cannot be excluded; these factors were not directly discussed by the study authors. Nonetheless, the paper emphasizes the need for multicenter and mechanistic studies rather than simply larger sample sizes to further validate and explore these findings.
Conclusions
In summary, the findings reported that H. pylori infections were less common among people with Parkinson’s. This suggested that the bacterium might play a protective role by influencing the body’s immune system. Although more research is needed to explore how and why this occurs, these findings open new possibilities for understanding the gut-brain connection and its impact on neurodegenerative diseases like Parkinson’s. The study authors emphasize that causality cannot be established, and recommend further multicenter and mechanistic studies.
