The Missing Link in Parkinson’s Gut Research: Why SIBO Remains Undetected in Fecal Microbiome Studies

In the last decade, Parkinson’s research has increasingly turned toward the gut—particularly the microbiome—as a potential early warning system for disease onset and progression. But despite the flood of microbiome studies, most still rely on fecal sampling, which largely represents the bacterial population of the large intestine, not the small intestine, where critical dysfunction may begin.

This presents a fundamental blind spot.

Small Intestinal Bacterial Overgrowth (SIBO) and its often-overlooked symptoms, drivers, and metabolic byproducts may be crucial to understanding the gut-brain connection in Parkinson’s. Clinical observations, cutting-edge research, and insights from experts like Dr. William Davis (Super Gut), Dr. Daniel Paredes, and new findings on microbes like Desulfovibrio and Methanobrevibacter smithii all suggest a more upstream origin to this disease process. In addition, Helicobacter pylori (H. pylori), long known for its role in ulcers, may be playing a quiet but critical role in altering gut terrain and disrupting dopamine therapy.

Most microbiome research, especially in Parkinson’s, analyzes stool samples, but this approach overlooks microbial activity in the small intestine—the first major interface for nutrients, immune surveillance, and microbial regulation.

In a healthy gut, the small intestine is relatively low in microbial density compared to the colon. But when colonic bacteria migrate into the small bowel and overgrow, a condition known as SIBO arises. This overgrowth disrupts digestion, motility, nutrient absorption, and immune tolerance—all issues implicated in Parkinson’s disease.

Fecal sampling can't capture these changes. It’s like looking at a river delta and assuming you understand what’s happening at its source.

A compromised small intestine sets the stage for bacterial infiltration and fermentation. This terrain can be altered by low stomach acid (common in aging and Parkinson’s), poor motility (due to vagal nerve dysfunction), pancreatic insufficiency, or medications such as antibiotics and proton pump inhibitors. As this terrain degrades, colonic species migrate and flourish in the small intestine, leading to fermentation of carbohydrates and proteins—producing gas, toxic byproducts, and inflammation.

One major and often-overlooked contributor to this altered digestive terrain is Helicobacter pylori (H. pylori). Known for its ability to survive in the acidic environment of the stomach, H. pylori produces urease, which breaks down urea into ammonia and carbon dioxide, effectively raising stomach pH.

This shift has several downstream consequences: impaired protein digestion due to reduced acid, decreased defense against pathogens entering from food or the mouth, and promotion of small intestinal overgrowth, as bacteria that would normally be killed by acid now survive and migrate.

But H. pylori’s impact goes even further for those with Parkinson’s.

A research group from Harvard University demonstrated that H. pylori can bind to and metabolize L-Dopa, the primary medication used to manage Parkinson’s symptoms. This “eating” of L-Dopa leads to reduced availability of the drug for absorption, unpredictable “on-off” periods where motor control fluctuates, and gastrointestinal symptoms, including the “concrete-like” stools observed in our BioCollective samples from patients with H. pylori overgrowth and poor motility.

In this light, H. pylori isn’t just a stomach bacterium—it’s a critical upstream disruptor of both digestion and dopamine therapy in Parkinson’s.

In Super Gut, Dr. William Davis emphasizes that healing must begin in the upper GI tract, not just by supplementing with probiotics but by addressing SIBO directly. Davis uses targeted bacterial strains to “weed out” overgrowth and reseed the gut. He describes improvements not just in digestion but in mental clarity, mood, and neurological symptoms—key concerns for people with Parkinson’s. His work shows that addressing SIBO can have profound systemic effects—long before the colonic microbiome ever shifts.

When undigested proteins reach the small intestine due to poor digestion or enzyme function, they are fermented by bacteria, producing ammonia, putrescine, cadaverine, and polyamines like spermidine.

Dr. Daniel Paredes has highlighted polyamine metabolism as a key signaling axis between the gut and brain. While some polyamines are essential in small amounts, excess production in SIBO conditions can contribute to neuroinflammation, oxidative stress, and blood-brain barrier disruption. This may help explain why some people with Parkinson’s have altered ammonia detoxification and signs of encephalopathy-like symptoms, including brain fog, fatigue, and irritability.

New research out of Finland has identified Desulfovibrio (link to my blog on this topic), a hydrogen sulfide–producing genus, as significantly elevated in people with Parkinson’s.

Hydrogen sulfide (H2S) is a paradox: at low levels, it's a beneficial signaling molecule; at high levels, it's neurotoxic and mitochondrially disruptive. Elevated H2S can slow gut motility, damage the gut lining, create systemic toxicity, and impair cellular respiration in neurons. This may explain diarrhea or alternating bowel patterns in some Parkinson’s patients and could link directly to mitochondrial dysfunction observed in the disease.

Standard SIBO breath tests often miss hydrogen sulfide, unless using a test like TrioSmart, which captures H2, CH4, and H2S. This adds another blind spot in conventional research and diagnosis.

Another overlooked player is Methanobrevibacter smithii, a dominant methane-producing archaeon linked to constipation-type SIBO. It consumes hydrogen to produce methane, slowing motility and creating a cycle of stasis and overgrowth. Recent studies have found elevated levels of M. smithii in people with Parkinson’s. But the issue doesn’t stop at methane.

Methanobrevibacter produces methanobactins—copper-scavenging molecules that extract copper from the environment. This could have massive implications for dopamine synthesis (as tyrosinase and dopamine-beta-hydroxylase are copper-dependent), iron metabolism (via ceruloplasmin), and mitochondrial health (via cytochrome c oxidase).

Copper deficiency or sequestration may be a hidden contributor to Parkinson’s pathology, immune dysfunction, and energy failure—especially when driven by microbial shifts. Most practitioners still rely on breath tests that only measure hydrogen and methane, missing hydrogen sulfide and ammonia entirely. And stool tests, even those marketed as “comprehensive microbiome analysis,” are still analyzing waste—not activity in the small bowel where the dysfunction often begins.

Signs of SIBO in Parkinson’s may include bloating after meals, constipation or diarrhea, food intolerances (especially to fiber, sulfur, or histamine), brain fog, fatigue, and poor response to typical Parkinson’s medications due to impaired absorption.

We’re finally recognizing the gut-brain axis not just as a metaphor, but as a mechanistic bridge in diseases like Parkinson’s. But to truly shift outcomes, we must stop looking at the exit of the digestive tract for answers and start studying the entry point—where digestion begins, where microbes ferment and signal, and where overgrowth can quietly disrupt the entire body.

Parkinson’s may not start in the colon or the brain—it may start in the small intestine, when the terrain shifts, the bacteria migrate, and the body loses its upstream defenses.

Tools and Practitioners: Where to Begin to Look Upstream

Dr. William Davis recommends a portable tool called the FoodMarble AIRE 2, a personal digestive breath tester that allows individuals to measure hydrogen and methane gas levels after meals. This simple handheld device pairs with a smartphone and helps track real-time fermentation patterns after eating specific foods. While it doesn’t measure hydrogen sulfide, it’s an excellent way to monitor patterns of SIBO activity and food-triggered responses. For people who feel bloated, foggy, or fatigued after eating—even when their stool tests are “normal”—this device offers a way to observe what’s going on higher in the digestive tract.

Unfortunately, most conventional neurologists and gastroenterologists do not screen for SIBO or investigate small bowel terrain, even when patients present with clear gut-brain symptoms.

For those looking for more personalized, terrain-focused support:

• The SIBO Doctor directory (by Dr. Nirala Jacobi) is another excellent resource focused specifically on small intestinal overgrowth: https://www.thesibodoctor.com

• Read Dr. Davis’s SuperGut and follow his work through is Podcast Defiant Health on any of the popular podcast apps.

• The Institute for Functional Medicine (IFM) maintains a “Find a Practitioner” tool where you can locate clinicians trained in systems biology and digestive health: https://www.ifm.org/find-a-practitioner, ask about the practitioners history working with SIBO as this can be more specialized work and not every practitioner has the experience.  See my recent Podcast interview with Dr. Debbie Potts and FDN focusing on healthy aging and the gut-brain connection.  

• If you’re concerned about minerals, energy production, and copper-related imbalances (especially in cases involving Methanobrevibacter smithii or sulfur-processing issues), the Root Cause Protocol (RCP) practitioner directory may be helpful. RCP practitioners are trained to assess magnesium, bioavailable copper, ceruloplasmin, iron recycling, and other mineral interactions that affect mitochondrial and neurological function. Many RCP consultants also understand how gut function impacts mineral dynamics. You can search their directory here: https://therootcauseprotocol.com/rcp-institute-directory/  I’m a trained practitioner but don’t do the individual coaching, I use my knowledge to educate. 

• Check out the educational videos from BEAM minerals to better understand how important they are to gut health.  

Together, these tools and practitioner directories empower individuals to look beyond conventional testing and explore what’s happening upstream—in the small intestine, in the microbial ecosystem, and in the mineral matrix that fuels the brain and body.

What can you do?

1. Test for H. pylori, especially if stools are hard, motility is slow, or L-Dopa response is inconsistent. This is a breath test that can be done at Lab Corp or Quest Labs and can be ordered by your family medical or internist.  

2. Consider a comprehensive breath test (like TrioSmart) that includes hydrogen, methane, and hydrogen sulfide. I have not tried this at home test but its the first one I found that tests for all three SIBO gases.  

3. Work with practitioners who focus upstream—motility, digestion, and microbial balance in the small bowel.  See my previous post about Coach Debbie Potts.

4. Explore targeted antimicrobials or probiotics like those outlined in Super Gut  or BiotiQuest’s protocols.  Or join Dr. Davis Infinite Health Group to join others interested in the gut health journey in this educational group. 

5. Prioritize balanced mineral and nutrient repletion. Instead of isolated mineral supplements, opt for well-rounded options such as Beam Minerals a full spectrum humic/fulvic mineral complex  and consider adding magnesium from sources like Ancient Lakes natural source of liquid magnesium. Also, be aware of micronutrient depletion—especially B vitamins. A recent microbiome meta-analysis showed a strong association between altered microbial composition and B vitamin deficiency, which is relevant for neurological health and cellular energy and has a strong connection to minerals depletion.  Gut bacteria need minerals to produce your B vitamins. 

6. Don’t let “normal” stool tests dismiss your symptoms—look upstream and rethink the terrain.  Standard stool tests are missing the full picture.