If you are squeamish, maybe turn away now. We are going to be talking about poop.
Not just any poop, the kind that might help heal a broken body. Because when you look closely enough, what comes out of us might hold clues to how we can get better.
This is a story about what is inside us, what connects our bodies and our minds, and how something as simple as the gut might change the way we think about diseases like ALS.
Why the gut matters
For years before my ALS diagnosis, my gut was simply not right.
Loose stools. Constant urgency. Practically diarrhea, almost like it became normal.
I ignored it. I rationalised it. I told myself it was stress, diet swings, maybe just bad luck.
Then, shortly after I was diagnosed, I started reading about the gut and brain and how they speak to each other. That was when I began to wonder how long this had been part of my story. About six months ago, I changed my approach. A cleaner way of eating, what I call dirty keto. I cut the junk, focused on whole foods, and kept it realistic. My gut changed. It calmed down. Regular. Predictable.
I wish I had done a microbiome test at diagnosis. A baseline would have mattered. Now my microbiome looks healthy on paper. Good diversity. Few obvious red flags. Maybe that is part of why my progression seems slower than average. Maybe it is coincidence. I will never know for sure.
Here is the truth. The gut matters. For people living with ALS, the gut may matter more than we have realised.
What the microbiome is and why it matters
Imagine your gut as a dense rainforest.
Instead of trees, it is filled with trillions of living microbes. Bacteria, fungi, and viruses. All interacting in an ecosystem more complex than a coral reef. This is your microbiome, and its genes outnumber your human genes by a factor of hundreds.
These microbes help digest food, produce vitamins, regulate your immune system, and create molecules that affect the brain. When this community is balanced, the system works quietly in the background. When the balance is lost, inflammation rises, nutrients are not processed correctly, and the gut barrier becomes leaky, which lets toxins circulate more freely.
Unlike your DNA, your microbiome can change quickly. Food, sleep, stress, infections, and medications all reshape the terrain. That is both the challenge and the opportunity. A system that can be damaged quickly can also recover with care and consistency.
Probiotic supplements can help, but they are limited. The common names you see on most labels, Lactobacillus, Bifidobacterium, and Streptococcus, cover a small slice of what lives in a healthy adult gut. Most of the important species are not in capsules yet. That is why the foundation remains simple but powerful. Eat real food rich in fibre and colour. Sleep well. Move daily. Limit processed foods that disrupt the gut’s natural balance. These are not miracle fixes. They are where stability begins.
The gut and the brain
The gut and the brain are in constant conversation. This is not mystical thinking. It is physiology. Signals move along the vagus nerve in both directions. The immune system carries messages when the gut is inflamed. Microbes produce small molecules that enter the blood and influence brain chemistry and energy.
Publications mentioning the gut and brain have surged over the last decade. The same pattern appears even when you include older terms like neurogastroenterology, enteric nervous system, or psychoneuroimmunology. Different words, same story. A field that is new, growing fast, and becoming more relevant to diseases like ALS.
The explosion in research comes from a simple but powerful realisation. The gut is not just a digestive organ. It is a sensory and signaling system that influences mood, immunity, and inflammation. Advances in sequencing technology made it possible to map the trillions of bacteria that live inside us and to see how those communities shift in disease. Suddenly, researchers could measure what was once invisible.
At the same time, scientists studying neurological and psychiatric disorders began noticing the same pattern across very different diseases. Whether it was Parkinson’s, Alzheimer’s, or depression, the gut microbiome looked altered. What began as a curiosity has turned into one of the most active frontiers in medicine. The question is no longer whether the gut and brain communicate. It is how much that communication shapes the course of illness, and how we might use it to change the outcome.
What we know from other diseases
Parkinson’s disease
In Parkinson’s, research has shown that gut changes can appear before brain symptoms. In one human and animal study, researchers found that shifting gut bacteria could influence how the disease progressed. The idea that Parkinson’s may begin in the gut, with abnormal proteins moving up the vagus nerve, is now taken seriously by many clinicians.
Alzheimer’s disease
In mouse models, changing the gut microbiome can change how amyloid plaques form in the brain. Removing or altering certain microbes reduced inflammation and improved memory in those models (early review). Human data also show that people with Alzheimer’s often have less microbial diversity and more species that promote inflammation.
Bipolar disorder and mood
The gut’s influence on the brain is not limited to movement or memory. It reaches into mood and motivation. A 2022 Deakin University study reported early signs that fecal microbiota transplants might help people with treatment resistant depression and bipolar disorder. The science caught public attention again in 2025, when Australian Story profiled Jane Dudley, a woman whose debilitating bipolar symptoms disappeared after a series of home prepared microbiota transplants. Her psychiatrist described the change as bordering on miraculous, and Professor Gordon Parker of UNSW called it one of the most exciting developments of his career. It is a single story, not a clinical trial, but it helped motivate planned trials at Deakin’s Food and Mood Centre.
What this could mean for ALS
The same connection is beginning to appear in ALS research. It does not mean the gut causes ALS. It suggests the gut can shape the terrain. It can tilt inflammation, change energy balance, and alter how nerve cells handle stress.
A review in BMC Medicine pulled these threads together, noting that dysbiosis, barrier damage, and microbial metabolites all seem to influence how the disease behaves.
More recently, a 2024 case study in Frontiers in Cellular Neuroscience described two people with advanced ALS who received fecal microbiota transplants. Both had severely disrupted gut microbiomes before treatment, dominated by Enterococcus species that made up roughly 40 to 50 percent of their total bacteria, levels that are extremely abnormal. After transplant, the Enterococcus populations fell to near zero. The patients showed temporary but meaningful improvements in function, including the ability to breathe independently and eat without choking. These changes were followed by measurable shifts in gut composition toward a more balanced and diverse community.
These results echo an emerging theory that ties certain gut bacteria to the same kind of cellular stress seen in ALS genetics. In On the Origin of Amyotrophic Lateral Sclerosis, researcher Stephen Skolnick traced a potential connection between Enterococcus overgrowth and the buildup of hydrogen peroxide in the body. Hydrogen peroxide is a reactive compound that can damage cells when it accumulates. In familial ALS, a mutation in the enzyme superoxide dismutase (SOD1) causes this same kind of oxidative stress inside neurons. Skolnick’s hypothesis suggests that in sporadic ALS, the same stress might begin in the gut.
If that turns out to be true, it could mean that the microbes we live with have more influence on neurodegeneration than we thought, and that restoring microbial balance might relieve some of that pressure. It is not proof, but it is a testable path that links microbiology, metabolism, and neurology in a way that deserves attention.
Microbiota transplants and restoring balance
Fecal Microbiota Transplantation, or FMT, is the transfer of screened donor stool into a recipient to reset the gut community. A related approach called Microbiota Transfer Therapy, or MTT, follows the same idea and sometimes uses capsules or staged dosing.
FMT is already approved for recurrent Clostridioides difficile infection and can be life saving. It is now being explored in Parkinson’s, autism, inflammatory bowel disease, and mood disorders. In ALS, the research is still early, but it is gathering pace.
Neurologist Dr Richard Bedlack has been one of the few to take a closer look at this connection. After seeing several patients decline rapidly after long hospital stays and antibiotic use, he began to suspect that the gut microbiome might be playing a larger role in ALS than anyone realised. His team at Duke University compared stool samples from people whose ALS was progressing quickly with those whose disease had slowed or stabilised. The difference was striking. Fast progressors had unstable and diverse microbiomes. Slow progressors tended to have simpler communities dominated by a single species, Parabacteroides vulgatus.
When his group transplanted stool from fast progressors into ALS mouse models, the animals declined faster. When they transplanted stool from slow progressors, the disease slowed down. It was one of the first clear signs that what lives in the gut might influence how ALS behaves.
Those findings have led to a new clinical trial between Duke and the University of Minnesota, using encapsulated stool from a single healthy donor with a simple, stable microbiome. The goal is to test whether changing the gut can alter disease progression. This time the approach aims not only to add microbes but to actually shift the composition of the gut itself, something earlier studies struggled to achieve.
The message is not that transplants are a cure. It is that the gut environment clearly interacts with ALS. Fixing that environment, through food, transplant, or new microbial therapies, may shift the curve.
What actually happens during FMT
- A donor is screened for infections and risk factors.
- Material is prepared in a sterile lab.
- It is delivered by colonoscopy, enema, or capsules.
- The recipient supports the new community with diet and follow up.
Safety matters. There have been infections from unscreened material. It is best not attempted as a do it yourself project. It needs medical oversight wherever possible.
How to support your microbiome
Healing the gut does not always need medical intervention. There are simple, daily choices that can restore balance and resilience.
Eat for your microbes
Focus on whole foods. Colour, variety, and fibre feed a healthy microbiome. Vegetables, legumes, nuts, and seeds supply prebiotics, which microbes turn into short chain fatty acids that calm inflammation. Fermented foods like kefir, sauerkraut, and kimchi can help if you tolerate them.
Sleep, move, and breathe
The microbiome responds to stress and rhythm. Regular sleep, sunlight exposure, and gentle movement all support microbial balance. Even breathing exercises and time outside reduce stress hormones that alter gut function.
Light and energy
Red and near infrared light may support both the mitochondria and the microbiome. Early animal studies show reduced gut inflammation and stronger barriers when light therapy is applied to the abdomen. You can read more about how this might relate to ALS in Red Light Therapy and ALS, Hype, Hope, or Both.
Avoid over-sterilising life
We were built to live with microbes, not against them. Constant sanitising, processed foods, and low-fibre diets shrink microbial diversity. Let yourself touch soil, eat fresh foods, and breathe air that is not filtered flat. These small exposures remind your immune system what normal feels like.
Two Stories, One Lesson: Why Testing Early Matters
I wish I had done a microbiome test when I was diagnosed. You only get one chance to see the before picture. If you plan to fight, that baseline gives you something to act on.
My microbiome test results (September 2025, ALS diagnosed in October 2024)
A friend in the ALS community shared his results with me recently. He eats well. He was fit. On paper he looked healthy. His microbiome told a different story. It was dominated by Enterococcus, the same bacteria we discussed earlier in the ALS section.
He believes his microbiome is part of the reason for his rapid progression. In just six months, he lost 17 points on the ALSFRS-R scale, a drop that would shake anyone. When he saw those results, he decided he could not wait for the system to catch up.
My friend's microbiome test (October 2025, ALS diagnosed in March 2025)
He could not find a gastroenterologist in his region who was willing to perform the FMT, even with referral and encouragement from his neurologist. In Australia, the procedure is only approved for treating recurrent C. difficile infections, and many doctors are reluctant to go off-label or outside existing guidelines. That leaves patients in a bind. Even when there is medical interest, there is often no practical pathway forward.
Despite the risks and all the warnings about medical oversight, I can understand why someone would take a DIY path. When you are told there is nothing more that can be done, you start looking for what else might make a difference. For him, that means rebuilding his gut from the ground up, even if he has to do it on his own.
Stories like his remind me why testing early matters, and why we need better data on what people are trying. His results could help explain part of what makes one person’s progression fast and another’s slow. Without that data, we are left guessing. And guessing is not enough for a disease that moves this quickly.
“I’m very fast progressing. I would think you’d want to study me to find out what’s different between me and a slow progressor. Without the data, they’ll never figure it out.”
What can make things worse for the microbiome
Lyme disease and antibiotics
If you spend time in ALS support groups online, you will see plenty of discussion about Lyme disease. The two conditions can share symptoms and sometimes they overlap in confusing ways. There are people who are told they have ALS when it later turns out to be Lyme. There are others who are treated for Lyme, only to discover that what they are facing behaves more like ALS.
It is possible that in some cases Lyme or similar infections stress the body in ways that speed up or mimic ALS symptoms. The science is not settled, but there is a reason to pay attention, especially when antibiotics enter the story.
Lyme is often treated with long courses of antibiotics, and antibiotics can wipe out parts of the gut microbiome that take years to rebuild. In some reported cases, people who had previously rebuilt their gut through microbial therapy experienced regression after antibiotics. It is a reminder that even well meant treatment can have unintended effects. While we learn and experiment, clinical oversight matters wherever it is possible.
Methylene blue and other supplements
People with ALS are brave and practical. Many of us will try things if there is a chance they help. That spirit matters. So does care. Methylene blue has received a lot of attention. Many people with ALS take it. It may be fine at some doses under clinical guidance. It also has a long history as an antiseptic and a dye with antimicrobial properties. That raises a fair question about how it might affect the gut microbiome, especially at higher doses or when combined with other drugs.
The science here is not settled. This is why it is important to dive into the details before stacking many different ideas at once. Outside a clinical setting, you want to understand how supplements and treatments might connect, how they could help, and how they could hurt. You do not want to grab ten ideas from the internet and start them all on the same day. A good plan, a baseline, and careful tracking make a big difference. I wrote about that mindset in The Plan I Wish I Had When I Was Diagnosed.
The system gap and why this matters
Most doctors are bound by what is approved, proven, and reimbursable. That protects patients in many cases. But it can also slow innovation and leave people with few practical options once the standard treatments are exhausted.
People with ALS do not always have the luxury of waiting. They try things. They adjust diets. Add supplements. Explore light therapy. Attempt microbial therapies. Test combinations. These efforts are not random. They are driven by urgency, curiosity, and the will to live.
The problem is that almost none of it is captured. The data is scattered across notebooks, text threads, and memory. Without a way to track what people are trying and how it affects them, we lose the chance to learn. We miss the patterns that might point toward something that works.
There is a gap between lived experience and formal research. Bridging that gap will take better systems, open thinking, and a willingness to learn from the edges; not just from the clinics, but from the people living the disease.
New models for real-world research
This is part of what makes Dr. Richard Bedlack’s R.O.A.R. program (Replication of ALS Reversals) so important. Rather than waiting years for new drugs to pass through traditional trials, the R.O.A.R. model focuses on therapies linked to people who have improved and tests them in small, transparent studies. The protocols are published in a way that others can follow. That means neurologists, researchers, and even individuals with ALS can track the details and potentially join from home with the help of their own care team.
It is a more open and flexible approach. It values real-world evidence and participation that does not require a hospital stay. Bedlack’s model shows that it is possible to study ideas rigorously without shutting out the people most affected.
Other regions are also starting to explore new paths. In Florida, updated Right to Try laws have enabled some clinics to offer investigational treatments to people with terminal conditions outside of traditional trial channels. That flexibility, if used responsibly, creates room for ethical experimentation and faster learning. In diseases like ALS, time is often the most precious resource.
Progress still requires safeguards. It also requires transparency, courage, and a willingness to learn from those who are already trying.
Final Thoughts
The gut is not the cause of everything. It touches almost everything. In ALS, it may not hold the cure, but it might hold one of the keys.
Sometimes healing begins in places we were not taught to look. The gut might be one of those places. A quiet system with the power to shape how the brain and body cope with disease.
If we can understand it better, and if we can track what people are already doing to improve it, we might learn faster. We might even change the story.
