Today we saw a patient with progressive multiple sclerosis (MS) for more than 30 years. Unfortunately, she is now severely disabled and confined to a wheelchair. Everything started about six weeks after a severe episode of food poisoning.
Her current food allergy profile (grade 3-4 reactions to virtually every food tested) indicates an extremely active leaky gut. Neither Tobias nor I have ever seen such a dramatic IgE antigen profile. There is virtually no food that does not trigger an inflammatory reaction.
None of the intensive and professionally performed neuromodulation treatments she previously received (at another SOZO Center) produced any improvement whatsoever. This is highly unusual. In our own practice we have never encountered a patient in whom we could not achieve at least some degree of improvement.
This case immediately reminded me of a remarkable study that I came across a few months ago. In my opinion, it provides some of the strongest evidence so far that an intestinal bacterial infection may act as a trigger for multiple sclerosis.
How could that possibly work? Can gut bacteria really trigger MS?
The venous blood vessels of the intestinal tract are largely valveless, and the same is true for much of the lymphatic drainage. It is therefore easy to imagine that under conditions of increased intra-abdominal pressure—such as coughing, bending over, or straining—retrograde venous flow from the intestinal circulation toward the spinal venous system may occur. In this way, bacterial exotoxins, lipopolysaccharides (LPS) from bacterial cell walls, or perhaps even entire bacteria could potentially reach the spinal cord and trigger local neuroinflammation.
Twin Study – A Major Milestone
A few months ago I came across a remarkable study on Twitter.
The investigators examined 81 pairs of identical twins in which only one twin had developed multiple sclerosis. This elegant design allowed the researchers to control for genetic background as well as many environmental factors.
The Study
Yoon H, Gerdes LA, Beigel F, et al.
Multiple sclerosis and gut microbiota: Lachnospiraceae from the ileum of MS twins trigger MS-like disease in germfree transgenic mice—An unbiased functional study.
- Proceedings of the National Academy of Sciences (PNAS), April 2025. DOI: 10.1073/pnas.2423000122
- The study title links to a summary published by the Max Planck Institute. A link to the original full-text PDF is here.
What did the researchers do?
- Studied 81 pairs of identical twins, with MS affecting only one twin in each pair.
- Performed comprehensive analyses of the gut microbiome.
- In four twin pairs they additionally obtained terminal ileum biopsies, because this is one of the key sites where intestinal immune activation occurs.
- The intestinal microbiota was then transferred into germ-free transgenic mice genetically predisposed to develop experimental autoimmune encephalomyelitis (EAE), the standard animal model of MS.
The most important finding
Among more than fifty bacterial taxa, two members of the Lachnospiraceae family clearly stood out:
- Lachnoclostridium (formerly classified within the Clostridia group)
- Eisenbergiella tayi
These bacteria were significantly more abundant in the twins with MS. More importantly, they were also detected in the recipient mice, which subsequently developed an MS-like autoimmune disease.
Why is this so important?
Previous microbiome studies had mainly shown one thing:
“Patients with multiple sclerosis have a different gut microbiome.”
This study went one decisive step further.
- Genetically almost identical human subjects
- Functional proof in an animal model
- Identification of specific bacterial candidates
This represents one of the strongest pieces of evidence available so far that certain intestinal bacteria may actively contribute to the development of multiple sclerosis. While this still does not prove causality in humans, it goes far beyond a simple association.
The Clostridia Connection
Interestingly, the bacteria identified were not Clostridium perfringens or one of the classic pathogenic Clostridia. Instead, the researchers identified Lachnoclostridium, a member of the Lachnospiraceae family that evolved taxonomically from the former Clostridia group. They also identified Eisenbergiella tayi.
The experimental design was particularly impressive:
- 81 pairs of identical twins, with MS present in only one twin.
- Bacterial communities from the terminal ileum were analyzed.
- The identified bacterial populations were transferred into germ-free transgenic mice genetically predisposed to develop EAE.
- The recipient mice developed experimental autoimmune encephalomyelitis (EAE) significantly more often when they received bacteria derived from the MS twins.
The most exciting part came next.
The investigators isolated individual bacterial candidates and ultimately identified two organisms as the principal disease drivers:
- Lachnoclostridium species
- Eisenbergiella tayi
These two bacteria alone were sufficient to reproduce susceptibility to disease in the mice. The animals developed:
- markedly increased Th17 cells
- stronger autoimmune responses directed against myelin
- a substantially higher incidence of clinical EAE.
This is important because, for the first time, several of the Bradford Hill criteria for causality are at least partially fulfilled:
- Association in humans
- Genetic control through identical twins
- A biologically plausible mechanism
- Functional reproducibility in an animal model
Altogether, this provides substantially stronger evidence than most previous microbiome association studies.
Lachnoclostridium belongs to the anaerobic Firmicutes (formerly classified within the Clostridia group). It therefore seems highly worthwhile to investigate whether these bacteria can be selectively targeted—for example by bacteriophages, highly specific antibiotics, competitive probiotics, or fecal microbiota transplantation (FMT). The present study, however, did not address therapeutic interventions. Its major contribution is demonstrating that specific intestinal bacteria may be more than innocent bystanders: in genetically susceptible hosts they may actively initiate autoimmune disease.
Progressive MS appears to be a fundamentally different disease from relapsing-remitting MS
At least that is what we experience in daily clinical practice.
Progressive MS responds only minimally to the Coimbra Protocol, which often works remarkably well in patients with relapsing-remitting MS. Likewise, conventional brain-directed neuromodulation has generally produced disappointing results in these patients.
This observation also fits remarkably well with MRI findings. In patients with chronic progressive MS, follow-up brain MRI scans frequently reveal very few new lesions, even though the patients continue to deteriorate clinically.
From a practical point of view, this has gradually changed my own understanding of the disease.
Today I increasingly regard chronic progressive MS as primarily a disease of the spinal cord.
Only after we started directing neuromodulation toward the spinal cord itself did we begin to see meaningful clinical improvements.
These improvements are rarely dramatic and often do not last as long as we would like. It frequently seems as though our regenerative interventions are gradually overtaken by the underlying progressive disease process.
Nevertheless, the concept that specific pathogenic intestinal bacteria may continuously drive disease activity opens an entirely new therapeutic avenue that deserves serious investigation.
A practical challenge for clinicians
From my perspective, one obvious goal is to develop an effective therapeutic strategy directed against pathogenic intestinal Clostridia and related bacterial communities.
Tobias Eisenkolb, the naturopath working in my practice, has achieved remarkably encouraging results in many patients suffering from chronic fatigue syndromes and other long-standing, unexplained illnesses. These are often individuals who have spent years consulting physician after physician, while conventional investigations repeatedly reported “normal findings” and no treatment produced lasting improvement.
His diagnostic approach combines a specialized urinary metabolite analysis with targeted microbiome testing. Based on these findings, he frequently applies relatively simple antimicrobial strategies—for example lemon balm tincture in selected patients with suspected chronic viral activation or oregano oil in patients with microbiome patterns suggesting overgrowth of Clostridia—combined with intensive detoxification protocols intended to reduce Herxheimer reactions.
In our own practice, these approaches have produced sufficiently convincing clinical results that I now routinely refer this entire group of patients directly to Tobias instead of managing them myself.
Fortunately, Tobias will soon also be joining our Brain Center in Vienna.
Our goal over the coming months is to develop a structured and clinically effective treatment program specifically targeting the intestinal microbiome.
Unfortunately, Tobias is already fully booked in our Vöcklabruck practice for the remainder of this year.
However, appointments may still be available at our Brain Center in Vienna.
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