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ALS and the gut microbiome, part two: What can we actually do with this science?


In the first part of this 2-part series, we explored why amyotrophic lateral sclerosis, ALS, may not be only a disease of motor neurons. We looked at early digestive symptoms, changes in the gut barrier, disturbed microbial communities, immune activation, and the small molecules that can travel from the bowel into the blood.


The natural question is this: if the gut is involved, can we do anything about it?


Can diet help? Can prebiotics, probiotics, postbiotics, faecal microbiota transplantation, or microbial metabolites change the course of the disease? Could therapies that influence gut-related pathways become part of future ALS care?


The honest answer is both hopeful and humbling.


The gut is now one of the most interesting areas in ALS research. But interest is not the same as proof. The field has produced promising animal studies, some encouraging human signals, a few high-profile disappointments, and many unanswered questions. The gut may be part of the ALS story, but it is not yet a proven therapeutic doorway.


A therapy can be biologically interesting without yet being clinically useful. In ALS, this gap between mechanism and medicine is especially important because people do not have time to waste on overpromised interventions. A mouse study can show us where to look. A biomarker study can show us what might be changing. But only well-designed human trials can tell us whether an intervention meaningfully slows decline, improves symptoms, or helps someone live better for longer.


A useful way to think about ALS research is as a map being redrawn. For decades, the main roads were labelled motor neurones, muscles, brain, and spinal cord. Gut research has added new roads: microbiome, inflammation, intestinal barrier, immune regulation, bile acids, short-chain fatty acids, and cellular energy metabolism. But not every road on a map is safe to travel yet. Some are still under construction.


This article walks through what we know, what we do not know, and what this emerging field may realistically mean for people living with ALS today.



Food is fuel for the person and information for the microbiome


Diet is one of the strongest modifiable influences on the gut microbiome. Fibre, resistant starches, polyphenols, fats, protein and fermented foods can influence microbial composition and metabolite production, although responses vary between individuals (Vinelli et al., 2022; Valentino et al., 2024).


In ALS, however, food has to be viewed through a wider lens. Nutrition is not only about feeding the microbiome. It is also about protecting the person living with a physically demanding, progressive disease.


Unintended weight loss and lower body mass index are associated with poorer outcomes in ALS, so any gut-focused approach has to begin with preserving energy intake, protein intake, swallowing safety and body weight (Dardiotis et al., 2018; Goutman et al., 2023). Many people with ALS are already managing fatigue, swallowing changes, reduced appetite, constipation, reflux, slower gut motility or the emotional strain of eating when the body is changing. In that setting, a strict “gut-healing” plan can quickly become counterproductive if it reduces calories, protein, pleasure or food choice.


In ALS, microbiome nutrition has to start close to the ground. Before asking whether a meal contains the ideal fibres, fermented foods or polyphenols, we have to ask whether it can actually be eaten, swallowed safely, enjoyed, digested comfortably, and repeated tomorrow. A diet that looks perfect on paper but leads to weight loss, anxiety around food or fewer calories is not supportive. It is another stressor.


Once that foundation is protected, diet quality still has a role.


Fibre-containing foods such as oats, legumes, fruit, vegetables, ground seeds and cooked-and-cooled starchy foods can provide material for microbial fermentation. Gut bacteria can turn some of these fibres into short-chain fatty acids, including acetate, propionate and butyrate, which are involved in gut-barrier function, immune regulation and bowel health (Vinelli et al., 2022).


Human ALS microbiome research has reported altered gut microbial composition, microbial diversity and metabolite pathways, although the field is still developing and causality is not established (Di Gioia et al., 2020; Kaul et al., 2024; Chakraborty et al., 2026).


That does not mean simply adding more fibre will change the course of ALS. It means bowel function, microbial fermentation and tolerance to fibre deserve attention, especially where constipation, bloating or reduced motility are already part of the picture.


Colourful plant foods add another layer. Berries, pomegranate, cocoa, green tea, herbs, spices, colourful vegetables and extra-virgin olive oil contain polyphenols and other plant compounds that are partly transformed by gut microbes into smaller metabolites. In the COSMOS study, people with ALS who reported higher intakes of antioxidant- and carotenoid-rich foods, especially vegetables and fruit, had better functional and respiratory scores at baseline (Nieves et al., 2016). Because COSMOS was observational and cross-sectional at baseline, it cannot prove that these foods slowed ALS, and it cannot tell us whether the microbiome was responsible. Still, it sits comfortably with the broader idea that nutrient-dense, plant-rich foods may support a healthier internal environment.


Fats also connect the plate to the gut. Omega-3-rich foods such as oily fish may influence inflammatory lipid mediators, while the type and amount of fat eaten can affect bile-acid release and bile-acid signalling. Bile acids are made by the liver, released into the gut, modified by gut bacteria and recycled through the body, placing them at the crossroads of digestion, microbes, metabolism and inflammation.


This is one reason bile-acid biology is being discussed within broader gut-microbiome-metabolism research in ALS, alongside short-chain fatty acids, trimethylamine-N-oxide and other microbial metabolites (Kaul et al., 2024; Chakraborty et al., 2026).


Fermented foods such as live yoghurt, kefir, sauerkraut and kimchi may suit some people, because they can contain live microbes, fermentation products and microbial metabolites that interact with the gut ecosystem (Valentino et al., 2024). They are not automatically suitable for everyone. Swallowing safety, reflux, bloating, histamine sensitivity, high salt intake, medication interactions and immune status all matter. In ALS, fermented foods are best thought of as optional foods to consider when tolerated, not as a treatment strategy.


The aim is not to turn eating into another medical project. It is to nourish the person and the gut ecosystem at the same time.


For one person, that might mean oily fish, olive oil, soft cooked vegetables, stewed fruit, soups, smoothies, ground seeds, yoghurt or kefir if tolerated, and fortified porridge. For another, it might mean texture-modified meals, oral nutrition supplements or gastrostomy feeding with careful bowel support. The “right” diet is the one that fits the person’s stage of disease, protects weight and swallowing safety, supports bowel regularity, and keeps food as enjoyable and manageable as possible.


One group of nutrients shows why the food-microbiome-ALS story needs careful interpretation: omega-3 fats. They are biologically plausible, commonly discussed, and supported by some interesting observational signals, but food-based patterns and high-dose supplementation should not be treated as the same thing.



Omega-3 fats: promising, but not simple


Omega-3 fatty acids have attracted particular attention in ALS. These include alpha-linolenic acid, ALA, found in flaxseed, chia seeds, walnuts, and some leafy greens, and the longer-chain omega-3s eicosapentaenoic acid, EPA, and docosahexaenoic acid, DHA, found mainly in oily fish.


A pooled analysis of five large prospective cohorts found that higher dietary omega-3 intake was associated with lower ALS risk, with alpha-linolenic acid contributing to the inverse association (Fitzgerald et al., 2014). In a separate post hoc analysis of 449 participants from the EMPOWER trial, higher plasma ALA was associated with longer survival and slower functional decline in ALS (Bjornevik et al., 2023).


This sounds encouraging, but it needs careful handling.


These studies do not prove that omega-3 supplementation slows ALS. One is about risk before disease, and the other is an observational analysis within a clinical trial dataset rather than a randomised omega-3 intervention. Plasma ALA may reflect diet, metabolism, overall nutritional status, or other health-related factors.


Animal data are also mixed, and ALS biology is not simple. The effect of a nutrient may depend on dose, form, timing, sex, disease stage, oxidative environment, and the wider diet.


For now, omega-3-rich foods can reasonably sit within a balanced nutritional strategy, especially where oily fish, walnuts, chia, or flax are tolerated. But high-dose supplementation should be treated differently from food. It should be discussed with a clinician, particularly where there are swallowing issues, anticoagulant medications, bleeding risk, weight loss, planned surgery, or gastrointestinal intolerance.



Feeding the friendly: prebiotics and the case for fibre


Prebiotics are food components that humans cannot fully digest, but gut bacteria can ferment. In practical terms, they are ingredients that feed parts of the microbiome.


When gut bacteria ferment certain fibres, they produce short-chain fatty acids, including butyrate. Butyrate helps nourish colon cells, supports the intestinal barrier, and can influence immune regulation (Vinelli et al., 2022).


A simple way to picture prebiotics is as compost for the gut garden. You are not planting one single species. You are improving the soil so that a healthier ecosystem has a better chance of growing.


In ALS animal models, gut-directed prebiotic and fibre-related approaches have shown biologically interesting effects, including effects on microbial balance, intestinal barrier function and inflammatory signalling. But this evidence is still mainly preclinical, and there is not yet a controlled human trial showing that a specific prebiotic slows ALS progression. Reviews of gut-modulating approaches in ALS distinguish mechanistic promise from clinical proof (Eddin et al., 2024; Chakraborty et al., 2026).


In practice, fibre has to be personalised in ALS. Some people do well with cooked vegetables, oats, ground flaxseed, chia, legumes, fruit purées, or fibre supplements. Others experience bloating, discomfort, constipation, diarrhoea, or swallowing difficulties. More fibre is not always better if fluid intake is low or gut motility is poor.


The practical principle is not “push fibre at all costs”. It is to support microbial fermentation where possible, while protecting comfort, hydration, bowel regularity, and calorie intake.



Bottling the bacteria: probiotics under closer scrutiny


Probiotics are live microorganisms that may offer a health benefit when taken in adequate amounts. In ALS, they are an obvious area of interest because the gut microbiome appears altered in at least some patients.


The key human study is sobering.


Di Gioia and colleagues carried out a 6-month probiotic intervention using a multi-strain product in people with ALS. The probiotic appeared to influence aspects of gut microbial diversity, but it did not shift the microbiome towards a healthy control profile, and it did not produce a measurable clinical benefit on ALS progression as assessed by ALSFRS-R, the standard functional rating scale used in ALS trials (Di Gioia et al., 2020).


That finding tells us that adding live bacteria to the gut of someone with established ALS does not automatically translate into disease modification. The microbiome is not like an empty car park where we can simply add the “right” vehicles. It is more like a crowded city, with existing residents, traffic patterns, food supplies, immune surveillance, medications, inflammation, and disease-related changes all shaping who can settle and what they can do.


The animal literature remains interesting, but the lesson is not “take any probiotic”. It is almost the opposite.


Probiotic effects are strain-specific. The species name on a supplement label tells you very little. “Lactobacillus” or “Bifidobacterium” is not enough. It is like saying “dog” when what matters is whether you are dealing with a guide dog, a sheepdog, or a guard dog. Same broad category, very different function.


For people with ALS, the careful conclusion is this: there is currently no good human evidence that any probiotic regimen slows ALS progression. Some strains may support constipation, bowel regularity, bloating or gut comfort in selected people, but that is symptom support, not proven disease modification.



The rise and fall of AMX0035: an important lesson in hope and caution


Before moving from gut biology into possible interventions, it is worth pausing on AMX0035, marketed as Relyvrio in the United States and Albrioza in Canada.


AMX0035 was not a probiotic, microbiome treatment, supplement, or diet therapy. It was an ALS drug made from two compounds: sodium phenylbutyrate and taurursodiol. Its relevance here is that taurursodiol is a bile-acid-related compound, and bile acids sit at an important crossroads between the gut, liver, microbes, metabolism, inflammation, and cellular stress.


Bile acids are often thought of as digestive chemicals that help us absorb fats. But they also act as signalling molecules. They are produced by the liver, released into the gut, modified by gut bacteria, and then recycled back through the body. In that sense, bile-acid biology is one of the clearest examples of how the gut microbiome can influence wider metabolic and immune signalling.


That is why AMX0035 matters in a microbiome-and-ALS discussion. It did not test the microbiome directly, but one part of the drug targeted a gut-linked metabolic pathway. Sodium phenylbutyrate was included to help cells manage stress in the endoplasmic reticulum, the cell’s protein-folding and quality-control centre. Taurursodiol was included to influence mitochondrial stress, involving the tiny structures that produce cellular energy.


In simple terms, AMX0035 tried to help vulnerable motor neurones cope better by targeting two stressed systems in ALS: protein handling and energy production. One of those tools, taurursodiol, came from a bile-acid-related pathway that overlaps with gut-liver-microbe biology.


The phase 2 CENTAUR trial reported a modest slowing of functional decline and a later survival signal. This contributed to regulatory approval in the United States in 2022. However, the larger phase 3 PHOENIX trial did not confirm benefit on ALSFRS-R or key secondary outcomes. Amylyx announced plans to remove Relyvrio/Albrioza from the United States and Canadian markets in April 2024 after PHOENIX, and FDA withdrawal of approval followed in 2025 (Amylyx Pharmaceuticals, 2024; U.S. Food and Drug Administration, 2025).


This is painful, but scientifically important.


AMX0035 shows why ALS research must hold hope and rigour together. Gut-linked pathways such as bile-acid signalling may be biologically relevant, but relevance is not the same as proven treatment benefit. A plausible mechanism, a positive phase 2 trial, and urgent patient need are not enough if a larger, more definitive trial fails.


Early trials can look like a lighthouse seen through fog. They may show a light in the distance, but phase 3 trials tell us whether it is really land, or only a reflection on the water.


So AMX0035 should not be presented as proof that bile acids, the microbiome, or gut-derived metabolites can treat ALS. It shows something more cautious: gut-linked metabolic pathways are scientifically interesting enough to reach ALS drug development, but they still need robust human trials before they can be translated into clinical claims.



The molecules microbes make: butyrate and the wider postbiotic field


Postbiotics are bioactive products made by microbes, or derived from microbial fermentation, rather than live bacteria themselves. They may include short-chain fatty acids, bacterial cell components, peptides, enzymes, or other metabolites.


In theory, postbiotics have advantages over probiotics. They are easier to standardise, may be more stable, and do not rely on live organisms surviving the stomach, settling in the gut, and behaving as expected.


Butyrate is the best-known postbiotic in this field.


In ALS mouse models, butyrate has been reported to improve microbial balance, gut integrity and lifespan, but this remains preclinical evidence and does not establish human ALS efficacy (Zhang et al., 2017).


Translating butyrate into human ALS therapy is not straightforward. Oral butyrate can be difficult to tolerate because of smell, taste, dosing, and rapid absorption. It is also not clear whether giving butyrate directly reproduces the broader biological effects of having a healthy butyrate-producing microbiome.


Think of it like receiving a food delivery versus rebuilding a kitchen. A butyrate supplement may deliver one finished product. A healthier microbial ecosystem may produce that product in the right place, alongside many other useful signals. Those are not necessarily equivalent.


At present, butyrate remains mechanistically promising but clinically unproven in ALS.



Akkermansia and NAD+: a promising story, not a therapy yet


In part one, we discussed Akkermansia muciniphila, a mucus-associated gut bacterium that showed protective effects in SOD1 transgenic ALS mice in the landmark study by Blacher and colleagues (Blacher et al., 2019).


The protective effect appeared partly related to nicotinamide, a form of vitamin B3 and precursor for NAD+, a molecule involved in mitochondrial energy production and cellular stress resilience (Blacher et al., 2019).


This is exciting because motor neurones are extremely energy-demanding cells. They are like long-distance power cables: large, metabolically active, and vulnerable when energy systems falter. If microbial metabolites influence NAD+ biology, they could theoretically affect the resilience of motor neurones.


But there is a major gap.


Akkermansia has not yet been tested as an ALS therapy in a properly powered human randomised controlled trial. NAD+ precursors such as nicotinamide riboside and nicotinamide mononucleotide are being studied in ageing and neurodegeneration more broadly, but their evidence in ALS remains limited.


So this is a pathway to watch, not a clinical recommendation.



Methylcobalamin: an old vitamin returns with new evidence



One of the most significant recent ALS developments is the Japanese approval of high-dose methylcobalamin, also called mecobalamin, under the brand name Rozebalamin.


Methylcobalamin is a form of vitamin B12. At ordinary nutritional doses, B12 supports red blood cell production, nerve function, and one-carbon metabolism. At ultra-high pharmacological doses, it has been studied as a possible ALS therapy.


In September 2024, Rozebalamin was approved in Japan for slowing progression of functional impairment in ALS. The approval followed JETALS, a multicentre, placebo-controlled, double-blind phase 3 trial in early-stage ALS. Participants received 50 mg mecobalamin intramuscularly twice weekly or placebo, and the trial reported slower ALSFRS-R decline over 16 weeks in the treatment group (Oki et al., 2022; Eisai Co., Ltd., 2024).


This is important, but the details matter.


The trial focused on people within one year of symptom onset, with relatively early-stage disease and specific eligibility criteria. That means the result cannot automatically be generalised to all people with ALS, especially those with later-stage disease, very slow progression, very rapid progression, or different clinical profiles.


It is also important not to blur the line between nutritional B12 and pharmacological methylcobalamin. Rozebalamin is not the same as taking an over-the-counter B12 tablet. It uses a very high dose, delivered by injection, under medical supervision.


The gut connection is indirect but relevant. B12 and folate are involved in one-carbon metabolism, and the gut microbiome may influence B-vitamin availability and related metabolic pathways. However, the approved methylcobalamin therapy itself is not a microbiome treatment.


For people outside Japan, this is a topic to raise with your MD, not something to source through unregulated channels.



The bold experiment: faecal microbiota transplantation


Faecal microbiota transplantation, FMT, is one of the most dramatic microbiome interventions. Rather than adding a few bacterial strains, it transfers a complex stool-derived microbial community from a screened donor into the recipient.


FMT is established for recurrent Clostridioides difficile infection, but in ALS it remains experimental.


A randomised, double-blind, placebo-controlled trial of FMT in sporadic ALS was published in 2024. The study included 27 people and did not find a significant difference between FMT and placebo in ALSFRS-R decline, although the FMT group showed improvements in constipation, depression and anxiety symptoms (Feng et al., 2024).


That result is both disappointing and useful.


It does not support FMT as a proven disease-modifying ALS therapy. But it suggests the procedure may be feasible and may improve some symptoms that matter deeply to daily life.


The safety caveat is essential. FMT can transmit pathogens or antimicrobial resistance genes if donor screening and manufacturing standards are inadequate. It should not be attempted outside regulated medical or research settings.


If the microbiome is a rainforest, FMT is not planting a few trees. It is importing a whole ecosystem. That may one day be powerful, but it also means the intervention needs rigorous control.



Where the field may go: precision microbiome medicine


The next stage of ALS microbiome research is unlikely to rely on broad interventions alone.


The field is moving towards precision microbiome medicine: matching the right intervention to the right patient subgroup, based on microbial composition, microbial function, immune state, genetics, diet, feeding method, medication history, and disease stage.


Two people with ALS may have very different gut environments. One may have constipation, low fibre tolerance, and gastrostomy feeding. Another may still eat orally, have diarrhoea, use antibiotics frequently, and carry a C9ORF72 expansion. A third may have relatively stable digestion but marked weight loss.


A single microbiome treatment is unlikely to fit all three.


The 2026 McCourt study points towards a more precise research direction for microbiome therapy. Its important lesson is not simply that gut bacteria may be altered in ALS, but that specific microbial products, such as inflammatory bacterial glycogen, may interact with specific genetic and immune vulnerabilities, including C9ORF72-related immune dysfunction. The study reported inflammatory forms of glycogen in faecal samples from people with ALS more often than in healthy controls, while experimental work suggested bacterial glycogen could influence gut and brain immune responses (McCourt et al., 2026).


Future gut-targeted therapies may therefore need to move beyond generic probiotics and towards identifying, reducing, or neutralising the microbial signals most relevant to each person.


Future research may use multi-omics approaches, combining metagenomics, metabolomics, transcriptomics, inflammatory markers, and clinical data. In plain English, this means looking not just at “which bacteria are there”, but also at what they are doing, which molecules they are making, how the immune system is responding, and how that connects with disease activity.


The future question will probably not be, “Does the microbiome matter in ALS?”


It will be more precise: “Which microbiome features matter, in which patients, at which stage, and can we safely change them?”



What is ready now, and what is not?


At this stage, the gut-microbiome science in ALS falls into three broad categories.


Ready for supportive care: protecting weight, maintaining protein and energy intake, managing constipation, supporting hydration, reviewing medications that affect the bowel, adapting texture for swallowing safety, and including tolerated fibre-rich and nutrient-dense foods where possible.


Promising but not proven as disease-modifying: omega-3-rich dietary patterns, prebiotics, selected probiotics for bowel symptoms, butyrate-related approaches, Akkermansia-linked NAD+ biology, and broader microbiome-informed support.


Experimental or medical-only: faecal microbiota transplantation, high-dose injectable methylcobalamin, enzyme-based approaches targeting bacterial glycogen, and future precision microbiome therapies.


This distinction is not about being pessimistic. It is about protecting hope from being mis-sold. People with ALS deserve access to emerging science, but they also deserve to know which parts are ready for practice and which parts still belong in trials.



What this means, carefully, for people living with ALS today


The evidence supports several careful conclusions.


First, nutrition matters. Maintaining weight, energy intake, protein intake, and swallowing safety should usually take priority over restrictive dietary experiments. Within that priority, a varied, nutrient-dense diet including tolerated plant foods, omega-3-rich foods, adequate protein and sufficient B vitamins is biologically sensible, but should not be presented as a proven disease-modifying diet.


Second, gut symptoms deserve active support. Constipation, reflux, bloating, poor motility, altered appetite, and feeding changes can affect comfort, nutrition, microbial ecology, and quality of life. These symptoms are not trivial. They are part of care.


Third, fibre and prebiotics may be useful, but only when matched to the person. Fibre without enough fluid or motility can worsen constipation. Fermentable fibres may worsen bloating in some people. Cooked, blended, softened, or supplemental forms may be more realistic than raw plant-heavy diets.


Fourth, probiotics should not be oversold. There is no current human evidence that any probiotic slows ALS progression. Some may help digestive symptoms in selected people, but claims should stay within the evidence.


Fifth, FMT is experimental. It should not be attempted at home or through unregulated providers.


Sixth, methylcobalamin is a genuine therapeutic development, but the evidence relates to ultra-high-dose injectable mecobalamin used in a specific early-stage ALS trial population. It should not be confused with ordinary over-the-counter vitamin B12 supplementation.


Finally, the gut-microbiome field offers real hope, but not a hidden cure. Its value lies in widening the therapeutic imagination while keeping both feet on the evidence.


For people living with ALS and the families who love them, the practical message is this: the gut is part of the picture. It may influence inflammation, metabolism, immune regulation, comfort, nutritional status, and perhaps disease biology in some subgroups. But the safest and most useful approach today is still careful, personalised, medically integrated support.


That means protecting weight. Supporting bowel function. Avoiding unnecessary restriction. Considering diet quality without making food stressful. Reviewing medications and supplements carefully. Managing swallowing risk. And, where possible, taking part in well-designed clinical research.


The gut may not hold the answer to ALS. But it may hold some of the clues.


And in a disease where every clue matters, that is reason enough to keep looking.



Personalised brain and gut support at You Nutrition Clinic


At You Nutrition Clinic, we specialise in evidence-led nutrition and functional medicine support for people living with neurodegenerative and neurological conditions. This includes ALS/MND, Parkinson’s disease, Alzheimer’s disease and dementia, brain injury, stroke, and other complex brain-related conditions.


For people with ALS/MND, the gut is not a hidden cure, but it may be one important part of the wider picture. Where clinically appropriate, specialist testing may help explore digestion, nutrient status, metabolic health, microbiome patterns and related markers. These insights can support personalised strategies for digestion, bowel function, nutritional status, resilience and quality of life.


Our team includes Dr Kirstie Lawton (PhD), whose work brings together nutritional science, functional medicine, and neurodegenerative disease, and Kerry Fuguard, who has a keen interest in the microbiome, genetics, and personalised nutrition in ALS/MND. We also have practitioners with specialist interests across other areas of brain health, so the clinic can support many people living with neurological and neurodegenerative conditions.


We work alongside medical care and focus on personalised, practical strategies that are safe, realistic, and tailored to the individual.


To arrange an initial conversation, contact admin@younutritionclinic.com.


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Disclaimer: This article is for informational and educational purposes only and does not constitute medical advice. Always consult with a qualified, registered medical doctor (MD) for diagnosis and treatment decisions.



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