Fusarium, the Microbiome, and the Many Possible Pathways of PATM

After years of collecting patient histories, correspondence, and laboratory reports, one impression has become increasingly difficult to ignore: there may not be one single underlying cause of PATM or MEBO. Instead, different people may arrive at a similar set of symptoms through different biological pathways.

We do have a growing list of possible culprits and triggers, and we are beginning to see that some patients can be matched by particular findings. But it remains a list—with many different candidates rather than one universal explanation. 

Last week, for example, we received a letter from a young woman in the United States who had experienced MEBO for approximately a decade. She was only recently diagnosed with biliary dyskinesia, a disorder affecting the movement of bile from the gallbladder.

This is not the first story of this type that we have encountered. In the past, we heard from a young man in China who had experienced PATM for approximately eight years and from a 37-year-old man in the United States who reported having PATM since he was 14. Both suspected problems with their gallbladder as a culprit.

These stories align with our observation that disturbances in different parts of the gastrointestinal system may sometimes contribute to a similar downstream phenomenon.

And then today, we received another intriguing history, this time from a man in Finland.

He believes that his PATM began following exposure to a water-damaged building and that Fusarium, a genus of fungi, may be involved. He subsequently had testing that detected mycotoxins associated with Fusarium, and he has developed a detailed hypothesis connecting fungal metabolism, intestinal processes, volatile organic compounds (VOCs), and the reactions experienced by people around him. This aligns with several other stories linked to mycotoxins, although those patients did not test specifically for fungi in their systems.

His interpretation is still a hypothesis. Nevertheless, Fusarium is another candidate that deserves to be investigated. 

Fungi and yeasts are still relatively understudied compared with bacteria, particularly when it comes to the human microbiome and gastrointestinal ecosystem.

At the same time, laboratory technology continues to evolve. Testing methods are becoming more sophisticated, and laboratories are expanding the range of microorganisms and metabolites they can detect.

That matters because what we are able to find depends, to some extent, on what we know how to look for.

The Finnish patient's testing was performed by Great Plains Laboratory, the same laboratory used by several other people in the PATM/MEBO community—along with Metametrix, Genova Diagnostics, Viome, and Biohm. We have not yet found one microorganism that is consistently present across all of these cases.

Interestingly, however, there are already some preliminary overlaps.

For example, among the people whose histories and laboratory results we have examined, Citrobacter freundii and E. coli have appeared in more than one case. These findings are far too limited to establish causation - both organisms can be found in the human gastrointestinal tract of individuals not reporting MEBO/PATM issues - but repeated observations are worth documenting and investigating.

Our microbiome study provides another piece of the puzzle. Using 16S rRNA sequencing, we found several microorganisms that appeared in common among participants. Some of these may represent opportunistic organisms or secondary changes resulting from another underlying disturbance, meaning that we may have been observing consequences rather than the original cause. I will be sharing more data from this study separately, but one important finding was the remarkably high heterogeneity among participants. Even with approximately 100 participants, the sample was not large enough to overcome that heterogeneity and identify a single consistent microbial signature.

This is another reason why I am increasingly hesitant to look for one universal culprit. The microorganisms we detect may sometimes be part of the downstream effects of whatever initially disrupted the individual's gastrointestinal ecosystem.

And Fusarium gives us yet another direction to explore.

 

PATM appears not to be a single disease with a single pathogen, but rather an umbrella for several conditions, just as similar symptoms in other medical conditions can arise from very different underlying problems.

One person might have a disorder affecting bile flow. Another might have bacterial dysbiosis. Another might have fungal involvement. Another might have a different gastrointestinal, metabolic, or systemic problem that we have not yet identified.

The common denominator may therefore not be the original cause, but rather what happens downstream.

Different disturbances could potentially alter the intestinal environment, microbiome, metabolism, or the volatile compounds released by the body. If those downstream changes are capable of producing similar external effects, they could potentially lead to what patients experience as PATM or MEBO.

Patient histories are not clinical trials, and an association between two findings does not establish causation. We also have to be careful with laboratory tests: detecting an organism, metabolite, or mycotoxin does not automatically tell us where it came from or whether it is responsible for someone's symptoms.

Nevertheless, patterns are worth recording.

If the same organism appears repeatedly in unrelated patients, that deserves investigation. If several people improve after treatment of a particular gastrointestinal disorder, that deserves investigation. If a fungal organism repeatedly appears in patients with similar symptoms, that deserves investigation too.

And if entirely different medical conditions appear to precede the same phenomenon, that may be an important clue in itself.

For now, our list remains a list.

But we might eventually map it to the different pathways that can lead to the PATM/MEBO phenomenon and to what those pathways have in common.

 

REFERENCES

Gabashvili IS  Cutaneous Bacteria in the Gut Microbiome as Biomarkers of Systemic Malodor and People Are Allergic to Me (PATM) Conditions: Insights From a Virtually Conducted Clinical Trial JMIR Dermatol 2020;3(1):e10508
URL: https://derma.jmir.org/2020/1/e10508
DOI: 10.2196/10508

MEBO and PATM--associated multispecies microbiomes mostly from stool, but also skin, oral, nasal, and genital sites   https://www.ncbi.nlm.nih.gov/sra?linkname=bioproject_sra_all&from_uid=1413303

Ledoux, M.-P., Dicop, E., Sabou, M., Letscher-Bru, V., Castelain, V., Danion, F., & Herbrecht, R. (2024). Fusarium, Scedosporium and Other Rare Mold Invasive Infections: Over Twenty-Five-Year Experience of a European Tertiary-Care Center. Journal of Fungi, 10(4), 289. https://doi.org/10.3390/jof10040289 

 

Can Gallbladder Problems Cause Body Odor?

People living with persistent body odor or unexplained bad breath often search for answers beyond the skin and mouth. One organ that occasionally comes up in these discussions is the gallbladder. While gallbladder disease is not considered a common cause of chronic body odor, disorders affecting bile production and bile flow can contribute to digestive disturbances, changes in the gut microbiome, and, in some cases, unpleasant odors. As a matter of fact, one of such cases was described in medical literature in 1904. 

Understanding the connection begins with understanding what the gallbladder does.

The Gallbladder's Role

The gallbladder is a small organ located beneath the liver. It stores and concentrates bile, a digestive fluid produced by the liver that helps break down dietary fats and assists in the absorption of fat-soluble vitamins (A, D, E, and K). When you eat a meal containing fat, the gallbladder contracts and releases bile into the small intestine.

When this process is disrupted, digestion may suffer. Poor fat digestion can lead to gastrointestinal symptoms, changes in the intestinal microbiome, and altered metabolism—all of which may influence the production of odor-causing compounds.

Gallstones (Cholelithiasis)

Cholelithiasis refers to the formation of gallstones inside the gallbladder. Gallstones are usually composed of cholesterol, bilirubin pigments, or a mixture of both. They develop when bile contains too much cholesterol or bilirubin, too few bile salts, or when the gallbladder does not empty efficiently.

Many people with gallstones have no symptoms. Others experience:

• Pain in the upper right abdomen, especially after fatty meals

• Nausea and vomiting

• Fever (if infection develops)

• Jaundice

• Bloating or indigestion

Some patients report unpleasant breath or body odor during symptomatic episodes. Although this is not a classic medical sign of gallstones, digestive stagnation, bacterial overgrowth, and impaired bile flow may increase the production of sulfur-containing compounds that smell like rotten eggs.

Stones in the Common Bile Duct (Choledocholithiasis)

Sometimes gallstones leave the gallbladder and become lodged in the common bile duct, blocking the flow of bile from the liver into the intestine.

Symptoms often include:

• Severe abdominal pain

• Nausea and vomiting

• Fever

• Jaundice

• Dark urine and pale stools

This condition requires prompt medical evaluation because obstruction can damage the liver and pancreas or lead to infection.

Cholangitis

Cholangitis is an infection and inflammation of the bile ducts, usually caused by obstruction from a gallstone, although tumors or strictures can also be responsible.

Typical symptoms include:

• Fever and chills

• Right upper abdominal pain

• Jaundice

Because bile is no longer flowing normally, digestion becomes impaired, and bacterial metabolism may change dramatically. Cholangitis is a medical emergency requiring immediate treatment with antibiotics and often procedures to relieve the obstruction.

Cholecystitis

Cholecystitis is inflammation of the gallbladder, most commonly caused by a gallstone blocking the cystic duct. Trapped bile causes irritation, swelling, and sometimes infection.

Symptoms include:

• Persistent pain in the upper right abdomen

• Fever

• Nausea and vomiting

• Tenderness over the gallbladder

Some people also report digestive symptoms such as constipation, bloating, bad taste in the mouth, bad breath, or increased body odor. Pale, greasy, or foul-smelling stools may occur when bile is not reaching the intestine normally.

Why Might Gallbladder Disease Affect Odor?

Several mechanisms have been proposed:

Changes in the gut microbiome. Reduced bile flow alters the intestinal environment. Bile normally helps regulate bacterial populations, so impaired bile secretion may allow certain bacteria to flourish. Even in the 1904 article about Cholelithiasis and Cholecystitis, a microbe Eberth's bacillus, was mentioned. It is the historical name for Salmonella typhi, the rod-shaped bacterium that causes typhoid fever. (that causes body odor to resemble freshly baked brown bread or warm, musty baked bread). But, of course, in most odor cases the responsible microbes are much more benign. 

Small intestinal bacterial overgrowth (SIBO). Poor bile flow can contribute to bacterial overgrowth in susceptible individuals. Some bacteria produce volatile sulfur compounds and other odor-causing metabolites.

Fat malabsorption. Inadequate bile impairs fat digestion, leading to fermentation of undigested nutrients and changes in stool odor.

Volatile metabolites. Researchers are increasingly studying volatile organic compounds (VOCs) produced by human metabolism and gut microbes. Alterations in bile acid metabolism may change the profile of VOCs released through breath, skin, urine, and stool, although much remains to be learned.

Does Gallbladder Removal Eliminate Body Odor?

Not necessarily.

Many people undergo cholecystectomy (gallbladder removal) and recover without digestive problems. Others continue to experience gastrointestinal symptoms because the underlying issue was not the gallbladder itself but rather changes in bile acid metabolism, the gut microbiome, liver function, or intestinal motility.

If body odor began before surgery and persists afterward, it may be worthwhile to investigate other contributing factors such as:

• Small intestinal bacterial overgrowth (SIBO)

• Bile acid malabsorption

• Gut dysbiosis

• Liver disease

• Metabolic disorders

• Trimethylaminuria or other rare metabolic conditions

When to Seek Medical Care

Seek prompt medical attention if gallbladder symptoms are accompanied by:

• Fever or chills

• Jaundice

• Severe abdominal pain lasting several hours

• Persistent vomiting

• Confusion or low blood pressure

These symptoms may indicate an obstructed bile duct or cholangitis, both of which require urgent treatment.

The Bottom Line

Gallbladder disease is not a common cause of chronic body odor, but it can contribute indirectly through impaired bile flow, altered digestion, and changes in the gut microbiome. For some individuals, treating gallbladder disease improves digestive symptoms and associated odors. For others, persistent odor signals that additional metabolic or gastrointestinal factors remain to be investigated.

As research into metabolomics, the microbiome, bile acids, and volatile organic compounds continues to advance, we are gaining a better understanding of the complex relationship between digestion and body odor. Rather than viewing odor as an isolated symptom, it may be more helpful to consider it as one clue within a larger network of metabolic and gastrointestinal health.

 

 

REFERENCES

Chen Y, Weng Z, Liu Q, Shao W, Guo W, Chen C, Jiao L, Wang Q, Lu Q, Sun H, Gu A. FMO3 and its metabolite TMAO contribute to the formation of gallstones. Biochimica et biophysica acta (BBA)-Molecular basis of disease. 2019 Oct 1;1865(10):2576-85.

Sagar NM, Cree IA, Covington JA, Arasaradnam RP. The interplay of the gut microbiome, bile acids, and volatile organic compounds. Gastroenterology research and practice. 2015;2015(1):398585.

McDonald CM, Reid EK, Pohl JF, Yuzyuk TK, Padula LM, Vavrina K, Altman K. Cystic fibrosis and fat malabsorption: Pathophysiology of the cystic fibrosis gastrointestinal tract and the impact of highly effective CFTR modulator therapy. Nutrition in Clinical Practice. 2024 Apr;39:S57-77.

Stockton CG. Diagnosis of Cholelithiasis and Cholecystitis, with Remarks on Medical Treatment. Buffalo Medical Journal. 1904 Apr;43(9):573.

Stavropoulos G, van Munster K, Ferrandino G, Sauca M, Ponsioen C, van Schooten FJ, Smolinska A. Liver impairment—the potential application of volatile organic compounds in hepatology. Metabolites. 2021 Sep 11;11(9):618. 

http://www.bodyodor777.com 

What Is BM109?

Many people living with TMAU know how hard daily life can be.
The smell caused by the condition can affect friendships, work, school, relationships, and mental health. Some people feel isolated or hopeless because there are very few treatments available.

Now, there may finally be some hopeful news.

A biotechnology company called BioMe Inc. in Seoul, South Korea, has received approval from the U.S. Food and Drug Administration (FDA) to begin testing a new treatment called BM109 in real TMAU patients.

This is important because it means the treatment has moved beyond laboratory testing and is now entering human clinical trials.

BM109 is a new kind of treatment called a live biotherapeutic product (LBP).

That means it uses living helpful bacteria to improve health.

The bacteria used in BM109 is a naturally discovered bacteria called:

Paracoccus aminovorans

BioMe says these bacteria can:

• Break down TMA

• Break down TMAO

• Help remove odor-causing chemicals from the body

The goal is simple:

Reduce the chemicals that cause the smell before they build up.

This is different from many current treatments that only try to manage symptoms.

The FDA has now allowed BM109 to move into Phase 1/2a clinical trials.

That means researchers will now test:

• Safety

• Side effects

• Whether it actually helps TMAU patients

The studies will involve real people with TMAU, not healthy volunteers.

The trials will be led by researchers connected to:

• Yale University

• Mayo Clinic

These are respected medical institutions in the United States.

It is important to stay realistic.

BM109 is NOT approved yet.

The treatment is still being tested.

That means:

• Nobody knows yet how well it will work

• Nobody knows if it will work for everyone

• It could still fail during trials

But this is still a very meaningful step because TMAU has received very little research attention for many years.

For many patients, simply seeing a treatment move into human trials brings hope.

BioMe says TMAO may also be connected to:

• Heart disease

• Stroke

• Kidney disease

Because of this, the company hopes BM109 may someday help with those conditions too.

But right now, the main focus is TMAU.

BioMe is also working on another bacteria-based product called BM107A.

This product is being studied for:

• IBS (irritable bowel syndrome)

• Colon health

• Constipation

• Inflammation

• Brain and cognitive health

It works differently from BM109 and focuses on producing a healthy substance called butyrate in the gut.

People with TMAU often feel ignored by the medical system.

Many have spent years searching for answers, support, and understanding.

While BM109 is still experimental, this news shows that researchers are finally taking TMAU more seriously.

For now, the best thing patients can do is stay informed, stay connected with support communities, and watch for future updates from clinical trials.

Hope may still be early - but it is real.

REFERENCES

You JS, Yoon CE, Kim JB, Alrahman MA, Jung HY, Yoon MY, Kim YB, Lee SG, Nam HS, Yoon SS. Microbiome-Targeted Reduction of Circulating Trimethylamine N-Oxide Mitigates Ischemic Stroke Risk. bioRxiv. 2026:2026-04.

Kim SH, Yoon MY, Yoon SS. TMAO and the gut microbiome: implications for the CVD-CKD-IBD axis. Annals of medicine. 2025 Dec 31;57(1):2522324.

https://biz.chosun.com/en/en-science/2026/05/11/6HY2VNJO55COHMPIAMHS3PSPYU/

Why Clean Clothes Still Smell

 A recent study in BMC Biology explored something many people quietly struggle with: why clothes can smell bad even after washing.

We know, it isn’t just sweat - it’s microbes.

• Washing doesn’t fully remove bacteria—it can actually increase certain types of bacteria on clothes.
• Your clothes pick up microbes not only from your body, but also from the washing machine and water.
• Humid drying (slow drying in damp air) is a major problem—it allows bacteria to grow again and recreate bad smells.
• Synthetic fabrics (like polyester) trap more odor-causing compounds than natural fabrics.

In simple terms:
👉 You wash away odor… but bacteria come back - and if clothes stay damp, they multiply and produce smell again.

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What helps

1. Dry clothes FAST

• Don’t leave clothes sitting wet in the machine
• Avoid indoor damp drying if possible
• Use:
  • sunlight ☀️ (UV kills bacteria)
  • a dryer
  • or strong airflow

👉 The study shows humid drying = more bacteria + worse smell

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2. Use the right washing settings

• Wash at higher temperatures (≥60°C when possible)
• Use oxygen bleach or antibacterial detergents occasionally

👉 Low-temp eco washes often leave bacteria behind

---

3. Choose better fabrics

• Prefer:
  • cotton
  • wool
• Be careful with:
  • polyester / gym wear (holds smell more)

---

4. Clean your washing machine

• Run hot empty cycles regularly
• Clean rubber seals
• Leave the door open after use

👉 Machines themselves are a source of odor bacteria

---

5. Use targeted products (if needed)

• Enzyme detergents (break down sweat compounds)
• Oxygen bleach (kills microbes)
• Laundry sanitizers

👉 Not always necessary—but helpful for persistent “permastink”

---

6. Don’t overload or delay laundry

• Overloading reduces cleaning effectiveness
• Letting clothes sit damp = bacteria growth

Going Deeper: What Actually Causes the Smell?

🦠 “Smelliest” bacteria aren’t just one group

The study shows that odor isn’t caused by a single species—it’s a community effect:

• Skin-associated Gram-positive bacteria
  • e.g. Corynebacterium, Staphylococcus, Micrococcus (as also found in Gabashvili, 2020)
  • Key role: break down sweat into short-chain fatty acids (classic BO smell)
• Environment-associated Gram-negative bacteria (after washing)
  • e.g. Pseudomonas, Acinetobacter, Moraxella
  • Key role: thrive in moist conditions and contribute to “musty” or “wet laundry” odours

👉 Washing often replaces skin bacteria with environmental ones, rather than removing microbes entirely

---

🧪 The real culprits: volatile molecules (not just bacteria)

What we smell are volatile organic compounds (VOCs), especially:

• 2- & 3-methylbutanoic acid → cheesy / sweaty
• n-pentanoic, hexanoic acids → rancid / sour
• aldehydes (like octanal) → fatty / “post-wash” smell

These molecules:

• disappear after washing
• reappear during humid drying due to bacterial metabolism

---

🧠 Why single-method science falls short

❌ Sequencing alone is not enough

Metagenomics tells you:

• who is there

But not:

• what they are actively doing
• which ones are producing odours

👉 The paper shows huge taxonomic shifts (who’s present changes a lot)

---

❌ Metabolites alone are not enough

Chemical analysis (VOCs) tells you:

• what smells are present

But not:

• which microbes produced them
• how environmental conditions shaped them

---

🔗 The key insight: function ≠ identity

One of the most interesting findings:

• Microbial composition changes a lot
• Functional pathways stay relatively stable

👉 Different bacteria can produce the same smelly compounds

This is called functional redundancy.

---

🧬 Why multi-omics is essential

To truly understand laundry malodour, you need:

1. Metagenomics

• Identify microbial community
• Track shifts (skin → machine microbes)

2. Metabolomics / GC-MS

• Identify actual odour-causing compounds

3. Quantitative methods (e.g. flow cytometry)

• Measure bacterial load changes

4. Environmental context

• Temperature
• Humidity
• Fabric type

💡 Research implications

• Designing detergents should target functions (metabolism, biofilms), not just species
• Drying conditions may be as important as washing chemistry
• Future work:
  • transcriptomics (gene activity)
  • real-time VOC tracking
  • biofilm disruption strategies

REFERENCES

Díez López, C., Van Herreweghen, F., De Pessemier, B. et al. Unravelling the hidden side of laundry: malodour, microbiome and pathogenome. BMC Biol 23, 40 (2025). https://doi.org/10.1186/s12915-025-02147-5

Gabashvili IS Cutaneous Bacteria in the Gut Microbiome as Biomarkers of Systemic Malodor and People Are Allergic to Me (PATM) Conditions: Insights From a Virtually Conducted Clinical Trial JMIR Dermatol 2020;3(1):e10508  doi: 10.2196/10508

Research Over Despair

I am always glad to receive letters from people who, despite facing real difficulties, are motivated to understand their condition and actively look for solutions. This letter was one of those.

It came from a young person who had lived with PATM (People Allergic to Me) for just over a year. In that short time, the condition had disrupted education, lab work, friendships, and mental health. Like many others with PATM, this individual had been told - explicitly or implicitly - that what they were experiencing might not be real.

What struck me most was not the suffering (which, sadly, is familiar), but the decision that followed: instead of giving up, they chose to learn, to research, and to ask whether science might eventually provide answers - not only for themselves, but for others.

Below is a modified, bulletized and anonymized version of my response to their questions, shared here because many patients ask the same things.

Why is PATM still an undiagnosed condition?

PATM is often described as “undiagnosed,” but a more accurate term would be not formally recognized.

For a condition to become a recognized clinical entity, several things usually need to be in place:

• a consistent case definition

• reproducible, objective measurements

• and a plausible pathophysiological mechanism that can be validated by multiple independent groups

At present, PATM does not yet meet all of these thresholds.

One major challenge is heterogeneity. The presentation varies widely from person to person, and triggers differ depending on environment, exposure, and individual biology. Another major obstacle is that current clinical workflows are poorly suited to capture intermittent, airborne chemical events. Many patients describe symptoms that occur in bursts—so a clinical visit may appear “normal,” even when the lived experience is not.

---

What would it take to achieve a formal medical diagnosis?

Large clinical trials can help, but they are rarely the starting point.

The real bottlenecks are:

• reproducible measurement methods

• defining subtypes rather than assuming a single mechanism

• capturing the episodic (“bursty”) nature of emissions

A well-designed, multicenter observational study—with standardized sampling protocols and careful timing relative to symptoms—may be a more realistic bridge step than jumping directly to intervention trials.

An official diagnosis could be beneficial. It can legitimize patients’ experiences in clinical settings, redirect care away from reflexive psychologization and attract more serious research attention. But such a diagnosis has to be built on solid evidence to endure.

---

Is toluene the main irritation-causing substance?

It is unlikely that there is a single universal compound responsible for PATM.

Research on skin gas emission profiles is important because it demonstrates measurable chemical differences, but the broader picture likely involves multiple emitted mixtures and multiple subtypes. In some individuals, compounds such as toluene or related aromatics may contribute to irritation-like symptoms; in others, different chemical patterns may dominate.

Another key factor may be differences in detoxification or clearance. Some people appear more susceptible to everyday exposures—such as secondhand smoke, solvents, or indoor VOCs—not because exposure is higher, but because metabolism and elimination differ.

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What can patients realistically try on their own?

I generally recommend starting with low-risk, high-information approaches:

Structured symptom and exposure logging

Tracking timing, diet, stress, environment (workplace, vehicles, indoor air), laundry and personal care products, and proximity to smoke or solvents can help identify repeatable patterns.

Basic medical rule-outs

Even when PATM is the primary concern, it is important to evaluate common contributors to odor or irritation-related conditions, such as reflux, sinus disease, metabolic or endocrine issues, liver and kidney function, medication effects, and dermatologic conditions.

Environmental controls

VOC-related problems are often exposure-amplified. Fragrance-free products, avoiding solvent-heavy cleaners, improving ventilation, and using HEPA plus activated carbon filtration can reduce background “noise” and make patterns easier to recognize.

I generally advise caution with high-risk or expensive interventions unless there is a clear rationale for a particular subtype.

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What about fecal microbiota transplants (FMT)?

FMT is scientifically interesting but should be approached with caution. It is not a general solution for PATM and carries nontrivial risks. If considered at all, it should be under appropriate medical supervision and based on a specific, individualized hypothesis—not as a last-resort experiment.

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Are microbiome or skin-gas profiling tests useful?

They can be, if used carefully.

• Gut microbiome profiling may provide clues, but interpretation is still limited and should always be paired with symptom timelines, diet, and repeat measurements.

• Skin or exhaled gas profiling is conceptually promising because it targets the suspected output directly. However, episodic emissions make timing critical, and passive sampling methods may miss short-lived events.

The usefulness depends less on the technology itself and more on study design.

---

Would wearable or portable gas sensors help?

In principle, yes. Continuous or frequent measurement could finally correlate chemical signatures with symptoms and environmental context.

In practice, true GC–MS–grade performance in a wearable format remains extremely challenging. Field measurements are complicated by changing ambient air, and episodic emissions require high time resolution and careful baseline correction. The idea is sound; the technology is still catching up.

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Could funding agencies support this kind of work?

Possibly more so now than in the past.

Historically, conditions that primarily affect quality of life rather than mortality have struggled to gain funding. When I first applied for support nearly two decades ago, the problem was explicitly described as “not important enough.”

Today, there is broader recognition of the impact of stigma, mental health, and chronic quality-of-life impairment. Advances in exposomics, microbiome science, and wearable sensing technologies make it easier to frame this work as high-risk, high-reward, particularly if the focus is on measurement platforms, subtyping, and mechanism rather than a single compound.

Much of this may sound like a list of obstacles. But compared with even a decade ago, the path forward is clearer.

If PATM turns out not to be one condition but a family of related ones, that is not a failure of science—it is a more accurate description of biology. Progress will likely come not from searching for a single universal cause, but from building frameworks that can accommodate diversity, intermittency, and complexity.

And sometimes, progress begins with a patient who decides that understanding is better than silence.

Diets That Dial Down TMA (and TMAO): What Latest Studies Suggest

This week's TL;DR: Diets that are high in fiber and lower in animal protein, plus Mediterranean-style eating, are emerging as the most food-first ways to reduce gut production of trimethylamine (TMA) and its oxidized form TMAO. Early evidence also points to targeted botanicals and postbiotics as promising add-ons - especially for people with heart or kidney concerns. If you live with MEBO/TMAU, the same general principles may apply.  

What seems to help most

1) High-fiber, lower-protein patterns (especially for CKD).
A fiber-rich, modest-protein intake can rebalance gut microbes and lower circulating TMAO in chronic kidney disease. Think: loads of vegetables, legumes, whole grains, nuts/seeds—while keeping total protein moderate and favoring plant sources. (Udomkarnjananun et al., 2025)

2) Mediterranean diet (MED).
A short, 4-week MED intervention—vegetables, fruits, legumes, whole grains, olive oil, nuts; limited red/processed meat—significantly reduced blood TMAO, even in healthy adults. Men in the study also saw better lipids and anthropometrics. (Deniz & Baş, 2025)
Since fish contains pre-formed TMAO that can worsen odor in TMAU, adapt a fish-free Mediterranean pattern if you’re sensitive.

3) Botanicals with gut–heart effects (CHF).
In patients with chronic heart failure, the Chinese botanical formula Qili Qiangxin (QLQX) reduced BNP, TNF-α, IL-6, and TMAO, pointing to lower systemic inflammation and improved barrier function. Food pattern still matters, but this suggests a potential adjunct under medical guidance. (Zhu et al., 2025)

Qiliqiangxin consists of extracts from eleven traditional Chinese medicinal herbs including for example: Panax ginseng  (ginseng), Astragalus mongholicus  (Mongolian milkvetch), Salvia miltiorrhiza (red sage), Cinnamomum cassia (cinnamon twig), Aconitum carmichaelii (Chinese aconite root), Descurainia sophia (flixweed), Periploca sepium (Chinese silkvine root bark), Alisma plantago-aquatica subsp. orientale (Oriental waterplantain), Carthamus tinctorius (safflower), Polygonatum odoratum (Angular Solomon's seal), and Citrus reticulata (dried mandarin peel)

4) Postbiotics (preclinical but intriguing).
In a choline-boosted, high-fat mouse model of atherosclerosis, Weizmannia coagulans JA845 postbiotics (based on B. coagulans JA845) lowered TMAO, improved the microbiome profile, dampened JAK/STAT3 inflammation, and protected vessels. Human data are pending, but this supports the microbiome-modulation avenue alongside diet. (Ma et al., 2025)

Unlike probiotics (which are live microorganisms) and prebiotics (which are food/substrates that feed beneficial microbes), postbiotics are non-live microbial cells, microbial cell parts, or microbial metabolites (or a mix) that can have beneficial effects. 

Example components might include dead/inactivated bacterial cells, cell wall fragments, microbial metabolites like short-chain fatty acids (SCFAs: butyrate, acetate, propionate), peptides and enzymes.

REFERENCES 

Udomkarnjananun S, Chuaypen N, Metta K, Dissayabutra T, Sodsai P, Kittiskulnam P, Tangkijvanich P. Dietary composition modulate gut microbiota and related biomarkers in patients with chronic kidney disease. Sci Rep. 2025 Oct 16;15(1):36274. doi: 10.1038/s41598-025-20266-5. PMID: 41102296; PMCID: PMC12533112. 

Zhu F, Hu R, Lv C, Wang J, Du X, Zeng X, Huang Y, Ma Y, Yang C, Guo F. Qili Qiangxin ameliorates chronic heart failure: a randomized clinical trial of biomarkers, inflammation, and cardiac outcomes. Front Pharmacol. 2025 Sep 30;16:1605944. doi: 10.3389/fphar.2025.1605944. PMID: 41098835; PMCID: PMC12518405. 

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AI meets MEBO

After a bit of a break since our first podcast back in March, we’re excited to return with a brand new episode for the MEBO and PATM community.

In this video, we’re exploring a big question: Can patients themselves use AI to help uncover potential causes, connections, and treatments for their symptoms?

The episode was generated by NotebookLM, based on our own research and the outputs of multiple large language models answering real questions from patients and researchers about these conditions. It’s a very good discussion overall - balanced, empathetic, and realistic about the challenges - but there are a few small hiccups.

For example, the video says that the paper "Cutaneous Bacteria in the Gut Microbiome as Biomarkers of Systemic Malodor and People Are Allergic to Me (PATM) Conditions" was published in Frontiers in Psychiatry in 2022. In fact, it appeared in JMIR Dermatology, a peer-reviewed journal, but one that isn’t indexed in PubMed - so it often doesn’t register in medical literature searches. Interestingly, when we asked half a dozen more LLMs about this paper, none knew much about it. Some even called it “groundbreaking” or “a beacon” without actually having the details, and a few hallucinated links that don’t exist.

PATM and MEBO are still often misclassified or linked to Olfactory Reference Syndrome, but there is growing recognition that underlying microbial dysbiosis or metabolic disorders may play a role.

Still, the bigger picture is encouraging: LLMs are improving, and that gives hope for people living with under-researched, heterogeneous, and often misunderstood conditions. While this podcast focuses a bit more on social and emotional support than on treatment options, that’s also an essential part of living with these conditions - and it makes this video worth watching.

Let’s dive in and see what AI can - and can’t - offer us right now.

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