ME/CFS for 18 years, recently diagnosed with D-Lactic acidosis as cause of symptoms and illness.


Senior Member
Hi 'Husband of',
sorry not to get back sooner; you need to go back to the beginning of my post; Ketosis is not exactly the aim and would be dangerous, but a Ketogenic or Palao diet, best explained on Dr. Sarah Myhills web page

The aim is to find alternative food sources to avoid, what to all intents and purposes, is a hidden Gut 'infection' due to the abnormal increase of naturally occurring Bacterial in Overgrowth causing fermentation of Simple Carbohydrates; that will not allow you to process many of the 'normal' foods to energy that we have been using since we started Farming and using grains around 40,000 years ago; the very low Carbohydrate diet is a return to a more primitive diet that would have been used pre-farming; but FODMAPS diets utilize starches (complex Carbohydrates) that your body takes longer to break down and will not ferment easily, especially in the small intestine (very simple explanation). You could start with Dr. Myhills Stoneage or Palao diet to see if your symptoms improve. Many ME/CFS have related gastrointestinal symptoms.

This is about reducing abnormal levels of D-Lactic producing Bacteria and reducing abnormal fermentation of D-Lactic producing Bacteria, or other Organic acids produced by other Bacterial Overgrowth; by reducing Simple Sugars and using Low Fermenting Carbohydrates so that the Bacteria cannot produce high levels of D-Lactate (it is now believed that we can process a small ammount of D-Lactate unless that ability is missing, which is another possible cause of D-Lactic acidosis). The FODMAP diet is similar to diets used for IBS, Diabetes and other forms of SIBO with low Fruit Sugars; I now use a FODMAP diet, but used a very Low Carbohydrate diet for a year or so after diagnosis in 2017.

ME/CFS has been related to altered and less diverse microbiome with decreases of Firmicutes and increase of Bacteroidetes (Gram positive bacteria). Firmicutes are more effective in extracting energy from foods.

Low fermenting diets will also assist with other forms of Bacterial Overgrowths or SIBO, causing the production of Organic acids with similar neurotoxicity that may be associated with ME/CFS.

In D-Lactic acidosis diet needs to reduce any abnormal fermentation of certain Carbohydratres to D-Lactate instead of L-lactate (which is our normal source of energy when converted to Glucose and Energy in the Pyruvate/Glucose Chain). ''l-lactate formation occurs via the reduction of pyruvate catalyzed by lactate dehydrogenase. l-lactate removal takes place via its oxidation into pyruvate, which may be oxidized or converted into glucose. ... Enzymes of the gluconeogenesis pathway sequentially convert pyruvate into glucose.'' ''By digesting food, you break it down into smaller and smaller parts. Carbohydrates turn into glucose. Protein becomes amino acids. Fat breaks down to triglycerides and fatty acids. All these smaller parts of food can be used for energy. '' So we can also get energy from proteins and fats as we did pre farming.

You have to cut out all simple sugars and alcohol such as Lager and Beers which are high in Carbohydrates; The worst Carbohydrates for me are Bread, Pasta or wheat based products that ferment easily eg. Pizza.

I used a very low close to non-Carbohydrate Diet at first; mainly Meats, Fish, Eggs, Hard Cheese, some Veg and low sugar fruits such as Blueberries and Cranberries; This diet was the best for me, but I found it very hard to stick to permanently and it takes great imagination to create meals (Dr. Myhill has produced a Palao Ketogenic Cook Book); but would be a good place to start (after checking with your health professionals first). But I was later offered a FODMAP diet that allows low fermenting Carbohydrates and use this coupled with antibiotics that only temporarily stop the symptoms by reducing the Overgrowth, but I have found that symptoms still come back gradually even though reduced, there must still be some fermentation, enough to cause me symptoms.

Antibiotics can also make things worse but give me temporary reprieve; and long term use has already caused resistance in several antibiotics, and antibiotics have been implicated in causing other heath ptoblems due to the effect on other microbiome species, including low or lack of significant species; but there may be some light at the end of the tunnel, because Phage Therapy for Superbugs is already being tested in Belgium and it may eventually become an acceptble treatment for these forms of Microbiome disorders;

The only other alternatives for me is Probiotics or Faecal Transplant; FMT although successful in some patients (and has been used for C.diff infections, MS, ME etc.) may not work for all and may also need more than one treatment.

I have found specific Non-D-Lactic producing Probiotics in combinations that will stop my symptoms, but they are expensive and hit and miss in terms of quality and quantity needed (the NHS will no longer fund Probiotics because they state that they are deemed to have low efficacy) ; but there is interest in Micobiome replacement therapy at the Dove Clinic; GFRT - Gut Flora Replacement Therapy - The Dove Clinic
although D-Lactic producing Bacteria would need to be avoided for a Subset of patients who have D-Lactic producing Overgrowths.

You can also have a Microbiome test performed at Atlas The Atlas Microbiome Test shows how gut bacteria impact your health (

You may have missed this report at the beginning of my posts; Increased D-Lactic Acid Intestinal Bacteria in Patients with Chronic Fatigue Syndrome;

D-Lactate is an unwanted abnormal fermentation to the Organic acid; D-Lactate, which is a Neurotoxin and Poison; directly related to lack of energy, because D-Lactate causes fluctuating acidosis and greatly affects Mitochondrial Function and Neurological symptoms are caused when the Neurotoxin enters the Blood Stream and Spinal Fluid to cause abnormal fatigue, encephalopathy and multiple symptoms including pain (as in Myalgic Encephalitis).

It is possible to have more than one form of Bacterial Overgrowth once the microbiome becomes compromised; In D-Lactic acidosis there are often at least two different competing species and possibly other Overgrowths. It is what is driving these changes that is important; you could also try drinking water that is not Chlorinated or contain Fluoride; because these chemicals also affect the microbiome. We have most probably caused these problems that allow other competing elements such as Virus in Covid-19 to make changes to our microbiome similar to ME/CFS

We are all different and it may take some experimentatioin!
Concerning GFRT,
I had not fully realised that GFRT is a Colonic treatment from the Dove Clinic and would not be affecing the small bowel; ''It is the process of implanting the beneficial intestinal bacteria and yeasts, from specific varied probiotic supplements, in significant quantities, not affecting the small intestine. I will have to try it if I can get funding. It has reportedly had a beneficial effect on the microbiome for ''Allergies, Asthma, Obesity, Cancer, Chronic. Fatigue Syndrome, Parkinson's Disease, Irritable Bowel Syndrome and Ulcerative Colitis.''


Senior Member
Sub Clinical Effects of D-Lactate;

Hi kangaSue,
have not been too good so have only just been able to look at your most interesting reports.

I had been off antibiotics for some months to have a D-Lactic assay performed to have FMT. I has been very hard, but I believed that it would be worth the effort to have a possible permanent cure from a tested donor;

I was tested for D-Lactate on the 7th May while unwell and with encephalopathy, but the D-Lactate test was taken long after the worst symptoms had stopped (D-Lactate is known to be transient, much like ME/CFS symptoms can change through the day). I fell ill around 10.00 and was tested at 2.30; It took over an hour waiting for an Ambulance and 3/4 hour just to wait for Covid tests and have the blood test performed on a ward; but I still had a subclinical result of 0.8mmol/litre that shows production of D-Lactate (I now need to have the symptoms properly induced in hospital because I have to achieve the full 3mmol/litre for FMT for licensing reasons).

I was also using the FODMAP diet because I was not sure that I could cope using the worst fermenting foods if symptoms spiralled too far out of controll (wheat products, bread and pasta etc.) Symptoms are reduced using the FODMAP diet, but can still be bad enough.

But even after the worst symptoms had stopped, I still felt achy, weak and unwell at the point my blood was taken; which made me wonder if others would have similar effects at a subclinical level. In fact the more I read, the more that I realise that there is no absolute surety of the plasma concentration ranges because so few D-Lactic assays have been performed; and they do not take into account individual reaction to the neurotoxin or allergy and there may be other Organic Acids compounding the problem which may go undetected;

''The pathophysiological mechanism is not fully known,7 but plasma D-lactate levels do not correlate to symptom severity, so that other organic acids may act as false neurotransmitters.4 ''

Can you or anyone corroborate what the normal production of D-Lactate Blood Plasma is; I have found at least 2 different possible answers? I have 11 to 70 nmol/L normal and Sub-Clinical 50micromol to 2.0mmol/litre. 3mmol/litre or over as acidosis.

There is now some interest in Sub-Clinical D-Lactate; with reports that D-Lactate is a cause of Sleep Apnoea and intermittent Hypoxia which would cause abnormal fatigue, even after a nights sleep (I was also diagnosed with sleep apnoea when my symptoms first began. I did eventually find a cure for my Sleep Apnoeas; Nightly Oxygen recommended by Dr. Myhill, used for over a year has stopped the symptoms for good, but I also had some control over the D-Lactic symptoms at that point).

Serum D-lactate concentration in healthy adults ranges from 11 to 70 nmol/L (5,7–9). Urine excretion is ∼0.1 μmol/h (10).

Examining clinical similarities between myalgic encephalomyelitis/chronic fatigue syndrome and d-lactic acidosis: a systematic review

''We stress that d-lactate theory may be relevant for a select subgroup and if not causative, may be a factor that perpetuates or exacerbates neurological symptoms. To date, there is no research that has measured d-lactate levels in ME/CFS. Improved efciency and availability of d-lactate measurement in urine and blood samples is needed. Measurement of d-lactate will clarify its role of d-lactate in this population and may generate an avenue for alternative treatments. Subclinical levels of d-lactate in diverse populations suggest that this may be Wallis et al. J Transl Med (2017) 15:129 Page 19 of 22 extended to other conditions. The proposed continuum is relevant for general physicians, gastroenterologists, psychiatrists and psychologists alike. Awareness of gastrointestinal origins for neurological presentations may hasten diagnostic accuracy, prevent misdiagnosis and improve treatment outcomes.''

L-lactate and D-lactate - clinical significance of the difference;

The current relative lack of availability of D-lactate assays might change now that there is growing research interest in the clinical significance of subclinical elevation of plasma D-lactate concentration [8], i.e. plasma D-lactate concentration in the approximate range (50 µmol/L - 2.0 mmol/L).

It was once supposed that the relatively very small amount of D-lactate normally present in the blood of humans (concentration 5-20 µmol/L in healthy adults [3] compared to 1000 µmol/L, i.e. 1.0 mmol/L for L-lactate) is solely derived from exogenous sources (diet and the carbohydrate-fermenting bacteria normally present in the gastrointestinal tract).

However, it is now clear that despite the absence of D-LDH, D-lactate is both produced and metabolized within human cells, albeit in tiny amounts compared to that of L-lactate. Metabolic production of D-lactate in human cells is the result of the methylgloxal pathway, a minor off-shoot pathway of glycolysis that results in nanomolar production of methylgloxal, a toxic product that is converted to D-lactate [4,5].

In the absence of D-LDH, human cells can metabolize D-lactate to pyruvate by the action of the mitochondrial enzyme D-2-hydroxyacid-dehydroganse [4,5].

In summary, the small amount of D-lactate normally present in blood is derived from three sources:

  • cellular production by the methylgloxal pathway
  • diet (foods containing D-lactate, e.g. yoghurts, soured cream, cheese)
  • lactate-producing bacterial species normally resident in the large intestine (colon).
Overgrowth of bacteria in the colon is a feature of short-bowel syndrome, the only pathology associated with increase in plasma D-lactate concentration of sufficient severity to cause acidosis (D-lactic acidosis).

D-lactate is possibly not the only Holy Grail;
There are other possible Forms of microbial acidosis caused in SIBO/Bacterial Overgrowth with symptoms similar to D-Lactic acidosis according to the American Journal of Nutrition;
D-lactic acidosis may be only one of a number; I have increasing antibiotic resistance and it has been made impossible for me to be allowed to have a D-lactic Assay for FMT, which I still believe has a high probability of stopping my symptoms but my diagnosis is being challenged by the NHS in an obstructive attempt to suppress any diagnosis or treatment and I am now the focus of intimidation and worse; I expect that research has really moved on since I last came online; Can someone post me with the most up to date theories? But I still believe the Microbiome for me is the source of all of my illness.

Hi kangaSue and all who I was messaging,
I have been too afraid to come online on Phoenix Rising since my last post in early 2022, but I have resolved to document what has been happening; I have been threatened (my life in 2021), intimidated and spied on since I last wrote; I know it sounds crazy but I was threatened by staff at a Hospital 2 days after I had surgery and personal information passed to my neighbours; I believe that this is due to some rogue Staff within the NHS.
The NHS is treated as a Sacred Cow where I live (all of my neighbours are in awe of the NHS since Covid-19) and are not aware of how patients with ME/CFS and Long Covid (which I believe have similar origins in the microbiome) are being treated and left to suffer and told it is all psychological when there is so much evidence to the contrary. I have even been challenged by someone that I do not have a diagnosis!; Life is being made unbearable, and one of my neighbours who became aggressive last year has been flying a drone directly over me while I am in my garden; I don't know whether to intimidate or take pictures; and I do not believe that I will ever be allowed a D-lactic Assay to confirm my diagnosis!

Any diagnosis of D-lactic acidosis for FMT has been made impossible for myself; I was invited in to a Hospital to exacerbate an episode of D-Lactic acidosis for Assay using Carbohydrates; and went into the Hospital deliberately with symptoms at the tail end of an earlier exacerbation 3 days prior; but was not allowed to have a D-lactic Assay that day despite symptoms for the whole day after I arrived with speech difficulty due to muscle weakness (which I videoed on my phone). I was definitely not having an exacerbation when the Assay was performed the following day after I had returned to normal (transient symptoms often fluctuate for days before worsening exacerbations; this was the start of illness that was returning some weeks after taking antibiotics to suppress an earlier exacerbation).

My symptoms finished at around 6.00pm after 8 hours of waiting; but I was not allowed to have a D-Lactic Assay for 18 hours the following day after my symptoms had ceased altogether; I told the Doctor who collected my blood that it would be a waste of time because my symptoms had stopped altogether while I was waiting for an Assay; he told me that the Assay would only be used as a baseline, but the result was used later in a statement that I did not have D-lactic acidosis; Although my diagnosing Consultant is still backing my diagnosis; it is beginning to feel as though I am under attack and is all deliberate. It is now causing me anxiety and depression. I do not know if I can take much more; once I gain total resistance I will not want to go on living; I spent tortured months frequently unwell to obtain an Assay for FMT. But even if there was no D-lactate there are other Metabolites/Organic Acids capable of causing similar Neurotoxicity and Acidosis;

There are a number of other Organic Acids that are reported to cause symptoms similar to D-lactic acidosis by the American Journal of Nutrition JN; this means that a D-lactic assay may not be the only holy grail.

D-Lactate in Human and Ruminant Metabolism
Julia B. Ewaschuk, Jonathan M. Naylor, Gordon A. Zello
The Journal of Nutrition, Volume 135, Issue 7, July 2005, Pages 1619–1625,

01 July 2005
Article history

Alternatively, other products of excess microbial fermentation may yield these symptoms; possibilities include formate, succinate, histamine, tyramine, endotoxins, and ethanol, although the latter was not found in the blood of SBS patients (53,57,67).

eg, Histamine Intolerance and Mast Cell Activation.

Elevated circulating levels of succinate in human obesity are linked to specific gut microbiota
Carolina Serena 1 2, Victoria Ceperuelo-Mallafré 1 2, Noelia Keiran 1 2, Maria Isabel Queipo-Ortuño 3 4, Rosa Bernal 4 5, Ricardo Gomez-Huelgas 4 5, Mireia Urpi-Sarda 6 7, Mónica Sabater 4 8, Vicente Pérez-Brocal 9 10, Cristina Andrés-Lacueva 6 7, Andres Moya 9 10 11, Francisco J Tinahones 3 4, Jose Manuel Fernández-Real 4 8, Joan Vendrell 12 13 14, Sonia Fernández-Veledo 15 16
Affiliations expand
Free PMC article
Gut microbiota-related metabolites are potential clinical biomarkers for cardiovascular disease (CVD). Circulating succinate, a metabolite produced by both microbiota and the host, is increased in hypertension, ischemic heart disease, and type 2 diabetes. We aimed to analyze systemic levels of succinate in obesity, a major risk factor for CVD, and its relationship with gut microbiome. We explored the association of circulating succinate with specific metagenomic signatures in cross-sectional and prospective cohorts of Caucasian Spanish subjects. Obesity was associated with elevated levels of circulating succinate concomitant with impaired glucose metabolism. This increase was associated with specific changes in gut microbiota related to succinate metabolism: a higher relative abundance of succinate-producing Prevotellaceae (P) and Veillonellaceae (V), and a lower relative abundance of succinate-consuming Odoribacteraceae (O) and Clostridaceae (C) in obese individuals, with the (P + V/O + C) ratio being a main determinant of plasma succinate. Weight loss intervention decreased (P + V/O + C) ratio coincident with the reduction in circulating succinate. In the spontaneous evolution after good dietary advice, alterations in circulating succinate levels were linked to specific metagenomic signatures associated with carbohydrate metabolism and energy production with independence of body weight change. Our data support the importance of microbe-microbe interactions for the metabolite signature of gut microbiome and uncover succinate as a potential microbiota-derived metabolite related to CVD risk.

Rev Endocr Metab Disord

. 2019 Dec;20(4):439-447.
doi: 10.1007/s11154-019-09513-z.

Gut microbiota-derived succinate: Friend or foe in human metabolic diseases?
Sonia Fernández-Veledo 1 2, Joan Vendrell 3 4 5
Affiliations expand
Free PMC article
There is now a wealth of evidence showing that communication between microbiota and the host is critical to sustain the vital functions of the healthy host, and disruptions of this homeostatic coexistence are known to be associated with a range of diseases including obesity and type 2 diabetes. Microbiota-derived metabolites act both as nutrients and as messenger molecules and can signal to distant organs in the body to shape host pathophysiology. In this review, we provide a new perspective on succinate as a gut microbiota-derived metabolite with a key role governing intestinal homeostasis and energy metabolism. Thus, succinate is not merely a major intermediary of the TCA traditionally considered as an extracellular danger signal in the host, but also a by-product of some bacteria and a primary cross-feeding metabolite between gut resident microbes. In addition to maintain a healthy microbiome, specific functions of microbiota-derived succinate in peripheral tissues regulating host nutrient metabolism should not be rule out. Indeed, recent research point to some probiotic interventions directed to modulate succinate levels in the intestinal lumen, as a new microbiota-based therapies to treat obesity and related co-morbidities. While further research is essential, a large body of evidence point to succinate as a new strategic mediator in the microbiota-host cross-talk, which might provide the basis for new therapeutically approaches in a near future.
Keywords: Metabolism; Microbiota; Succinate.

Your Changing Microbiome - University of Utah!&&p=6c3695a38b38d560JmltdHM9MTY3NjA3MzYwMCZpZ3VpZD0wYzE1YzM1Yy0wMjYxLTZmNzQtMmExMi1kMWRlMDY2MTY5MjUmaW5zaWQ9NTE2NQ&ptn=3&hsh=3&fclid=0c15c35c-0261-6f74-2a12-d1de06616925&psq=Symptoms+of+overproduction+of+Formalate+in+the+microbiome&u=a1aHR0cHM6Ly9sZWFybi5nZW5ldGljcy51dGFoLmVkdS9jb250ZW50L21pY3JvYmlvbWUvY2hhbmdpbmcv&ntb=1
Events like a fever, a course of antibiotics, or new foods can cause sudden shifts in the microbiome, with effects that may last for years or even a lifetime. 3 years - adulthood By age three, a child's microbiome looks a lot like an adult's, and it becomes much more stable.

Gut bacteria imbalance ‘linked to chronic fatigue syndrome’
US scientists said the finding shows only a ‘correlation, not a causation’.
Nilima Marshall
2 days ago

Chronic fatigue syndrome is associated with distinct changes in gut bacteria (Anna Gowthorpe/PA)
(PA Archive).

Patients recently diagnosed with chronic fatigue syndrome have reduced levels of certain types of gut bacteria that support digestive health, research suggests.
Scientists in the US have also found that patients living with the condition, also known as myalgic encephalomyelitis (ME/CFS), for 10 years or longer have differences in blood metabolites – substances made or used when the body breaks down food – compared to those without the disease.

The researchers said their work, published in two separate papers in the journal Cell Host & Microbe, only shows a “correlation, not causation, between these microbiome changes and ME/CFS”.

Julia Oh, an associate professor at the Jackson Laboratory in the US and senior author of one of the two papers, said: “These findings are the prelude to many other mechanistic experiments that we hope to do to understand more about ME/CFS and its underlying causes.”

Some aspects of overproduction of secondary metabolites
WebDifferent approaches used to increase production of secondary metabolites and construct overproducing strains of microorganisms are reviewed. Overproduction of secondary …
  • Author: J. Spížek, P. Tichý
  • Estimated Reading Time: 5 mins
  • Publish Year: 1995
News about Symptoms Of Overproduction Of Formalate In The Mi

The bottom line is changes in normal Gut biodiversity, with both high and low levels of necessary Bacteria in the Microbiome and either over or under production of specific metabolites and organic acids with alteration to the immune system and crosstalk between bacteria and our immune system as hosts and activation of defence systems against the host including MAST Cell Activation; This has to be a product of modern living in the industrial age where there are so many chemical challenges to Microbiota.


Senior Member
Hopefully you have all seen this; but FMT is about to be tested on ME/CFS in trials according to Professor Carding;

Thank God! This could be a lifeline for many with microbiome related disease including ME/CFS.

Then to heal our minds; many will have been through hell, some for decades; I was told aggressively by a Doctor just over a year ago that this was all nonsense and that ME/CFS was a mental health problem!

Radio 4: Today Programme covers Faecal Microbiota Transplantation (FMT) and ME/CFS | The ME Association.

Radio 4: Today Programme Covers Faecal Microbiota Transplantation (FMT) And ME/CFS
February 14, 2023
Radio 4 talks to Professor Carding based at Norwich research park about his plans on a trial of Faecal Microbiota Transplantation (FMT) for people with ME/CFS and the radio presenter mentions it might also help people with Long Covid (00.52.00).

Radio Presenter
Could there be hope in a science park here in Norwich for people with ME, indeed for other conditions such as Long Covid that seemed mysterious and damaging and ill understood. What's being investigated is Faecal Microbiota Transplantation (FMT) essentially injecting people with faecal matter, with poo.
I went to see, Professor Simon Carding at his lab at the Quadram Institute at the University of East Anglia medical school.
Professor Carding
We are looking at and an aerobic cabinet, which allows us to work with microbes in the absence of oxygen to try and replicate the conditions under which a lot of microbes in your gut exist.
Radio Presenter
Tell us specifically about what you're doing with faecal matter and the idea of injecting it, which sounds. To put it mildly. Crazy, gross. But it isn't?
Professor Carding
No. So it's not new. I mean, it's coming to the sort of popular press quite recently, but he actually dates back to the fourth century as part of Chinese medicine. Very recently in the last 10 years, we started to use it, adopted it in the NHS to treat a very nasty infection caused by Clostridium, difficile, or C difficile.
And this is now becoming a frontline form of treatment for patients that have recurrent episodes of infection by this potentially life-threatening infection.
Radio Presenter
So what's actually done what, what is involved?
Professor Carding
We select donors and this is broadly similar to the process we use to select blood donors. So, they provide blood samples, they fill in health questionnaires, the stool is taken and examine for the presence of any potential pathogens, as we want to exclude those. So, we select the donors on a strict criteria and we then take a stool sample and then we can basically emulsify it, put it into a syringe and then deliver that through a tube through the nose or through a colonoscope.
Increasing over, we're looking at encapsulating the stool, so we can actually use capsule delivery, which would be a real significant change in the way FMT delivered, opening up for treatment for a variety of patients and diseases.
Radio Presenter
A variety of diseases, which is why it's fascinating. So at the moment, you've explained what it is used for. How, why might that variety be?
Professor Carding
The thing to bear in mind here is that about 90%, maybe even all human diseases are associated with changes and the composition of your gut microbes. So lots of diseases now, opening up to the possibility of using FMT as a treatment, inflammatory bowel disease, irritable bowel disease but neurological diseases, dementias and cancers.
These are all opportunities to test the application of FMT is a treatment.
Radio Presenter
Fascinated by the idea that neurological diseases could be treated in this way.
Professor Carding
Yes. So my particular interest here is Myalgic Encephalomyelitis, ME, previously known as Chronic Fatigue Syndrome.
And we are planning FMT trial in patients with ME because they have disturbances in their gut microbes that causes lots of conditions throughout the body.
Radio Presenter
There are no treatment for ME are there? Is that, are you looking at potentially coming up with treatments in a reasonable kind of timeframe? Is that a realistic possibility, realistic hope for what you're doing here?
Professor Carding
That's certainly our aim is to understand more about the causes of ME, so we can develop more effective treatments. So few patients make a full recovery. There's clearly an urgent need to develop new therapies.
Radio Presenter
It's not around the corner, but it is a pathway?
Professor Carding
Absolutely. It's a pathway. Yes, collectively, I think there's some real hope here, that working together we will be able to develop new therapies.
Certainly in the next few years, I would hope.
Radio Presenter
More widely, we are much more aware now aren't we about the link that there is between our guts and our, and our brains actually, and the way we are much more generally.
Professor Carding
We're talking about the gut-brain axis here, the bi-directional communication between the brain and the gut and microbes play important part in that communication pathway. Because they can interact with all the neurons that are present in our gut, the immune system, that's present in our gut and the hormonal system that is present in our gut. So just being close to all these sensory systems allows them to influence a whole range of physiology, organ systems and we're particularly interested in how it may influence the brain.
Radio Presenter
And if that is the case, It, it sort of changes, doesn't it in a really fundamental way, the way in which at least in the west medicine has regarded a kind of division between what's going on down there and your stomach and what's happening in the rest of you.
Professor Carding
Yeah. So I think it's fair to say that China, Asian countries have had much more serious interest in FMT in using it, dating back as I said to the fourth century. We're only just becoming converts to the potential. There are questions that remain to be answered such. What's the best way for screening donors to make it absolutely safe? What is the best route of delivery?
So there's still some research done, but I think the potential is huge.
Radio Presenter
Professor Simon carding. Thank you very much.
Professor Carding
You're welcome. Thank you.
Other Information
More information about FMT for ‘Clostridioides difficile'
NICE: Faecal microbiota transplant for recurrent Clostridioides difficile infection