The Born Free Protocol

[mariovitali]

Thanks for replying, @mariovitali. A Merry Christmas to you too.
I assume you are referring to my comment when you mention 'negative bias'. Yes, I do have a negative bias against promoters of unevidenced protocols who go all over social media encouraging very sick and desperate people to follow complicated and expensive protocols with no research evidence to support them and that have made some people sicker, and moreover claiming without evidence that his protocol can treat all sorts of other conditions.

The negative bias I was referring to was the fact that in your comment you chose to leave out "red flags" I mentioned in the thread related to BF protocol namely the fact that different versions of the protocols exist, that it makes the assumption that all patients are the same, that it has no warnings for specific patient groups having certain conditions (e.g. hemochromatosis) and whether these patients could also follow it. Yes, you could say that I did not mention out several other red flags such as the claims that it is applicable to so many other conditions and many others but in your comment and by leaving out the criticisms I made, it seems that I am supporting Leisk. This is the negative bias I was referring to.

In a nutshell the idea of my thread was "There are several red flags about this protocol but let's see if it indeed worked for some people, why this might be the case and why it may be dangerous".

The rest of your twitter thread mentions your own experimentation and use of unnamed supplements. Again, not useful information for readers. And you make some comments about the BF protocol, presumably based on bits and pieces from your own unreplicated researches.

"Unreplicated researches" : It seems that you repeatedly disregard my posts in this very forum by writing this. We have SEVERAL instances of my findings being later identified and this is exactly the reason why I have not "closed the books" since so many years and I am still here trying to show the obvious. The liver dysfunction (Chris Ponting), ER Stress (Hwang et. al), Bile acid metabolism disruption (Naviaux et. al), LXR (Hanson et. al) are all replicated findings. @Jonathan Edwards were you in the LSHTM in 2018 and the presentation I gave? If yes, do you recall me discussing all of the above?

And since you said the following @Jonathan Edwards :

this sentence itself as often used by those who prefer positive bias

So you are calling all of my previous findings a positive bias? Fair enough, Thank you. However, it seems to me that you consistently choose to disregard the fact that I identified these mechanisms years ago and yet you say nothing about it. When the study of @Chris Ponting mentioning liver dysfunction came out , I do not recall you saying "Yes this was mentioned by this guy repeatedly years ago". I did not see that from @Trish either. This is text book negative bias at play, again.

I have much more respect for your own decision not to publicise what you found helped you, with your understanding that your self treatment should not be promoted as a cure for others just on the basis of your anecdote.

I will have to admit this is not true because I did publicise what has helped me [1] after a lot of thinking and after making sure I mentioned all the warnings. Allow me to explain why I did so by giving a timeline.

December 2015 : I write an email to a number of researchers listing my regimen (yes it was just supplements). The email -shown in [1]- mentioned liver dysfunction, bile acid metabolism dysregulation, endoplasmic reticulum stress. (Note : Do we have evidence that these are taking place in MECFS? Yes we have)

Years are passing by (2016-2017) and I see concepts I identified earlier coming out : Bile acids then Phospholipid deficiency. I knew that a supplement I was taking was Choline. Choline by the way is important for cell membranes. @TamaraRC posted a theory on how cell membrane integrity can be crucial for MECFS.

2018 : I presented my theory to LSHTM. I am sure that a lot of researchers were asking "Who is this guy and what is he doing here". In that presentation [2] mentions about Fibroscans showing liver issues, ER Stress and Hemochromatosis (which appears in GWAS candidate genes as a condition given HFE Gene. @Chris Ponting ) . @Trish I recall no comments from you on this along the way in the sense that you knew that someone has been talking about this and yet you chose to refrain from posting any sort of supporting comments. This is another example of negative bias.

Years passing by and we have then ER Stress coming out (Hwang et. al). I also knew that I have been taking TUDCA which is a textbook compound for ER Stress amelioration. The moment this took place I knew that I had to go public as much as I can because that finding increased my confidence that whatever I was doing was showing up in research, repeatedly. I refrained from posting the whole regimen but then decided to post it all with repeated warnings that this should not be tried.

In case you miss it, in [2] below it shows how machine learning identified ABCA1 (identified by PrecisionLife in 2025) back then. ABCA1 along with CH25H (also identified later by PrecisionLife) was specifically mentioned in my presentation in 2018 as well. In [3] a thread on how previous work I did identified several genes being identified in 2025 by precisionLife.

@EndME and @Suffolkres are you following this? Any comments?

Of course if anyone on this forum believes I am a fake, delusional or a liar (or perhaps all 3) then please do say this so this can be also included for future reference. And by the way the total funds I received for all of this is so far $0.

It's free so this is all crap, right? Unfortunately, moving things forward is not only about funding.


Thread on my recovery , the email I sent. Observe my reluctance to post all the regimen and my repeated warnings.
[1] : https://threadreaderapp.com/thread/1678408083834298368.html

Presentation at EUROMENE Thread :
[2] : https://www.s4me.info/threads/presentation-at-euromene-london-uk.5760/

Thread related to PrecisionLife and my earlier findings
[3] : https://threadreaderapp.com/thread/1997005812838076483.html

 

[Jonathan Edwards]

The liver dysfunction (Chris Ponting), ER Stress (Hwang et. al), Bile acid metabolism disruption (Naviaux et. al), LXR (Hanson et. al) are all replicated findings.

@mariovitali, I appreciate your enthusiasm for liver and bile issues and your attempts to make sense of things but, no, I don't think these are what we would call replicated findings.

The main replicating finding of Beentjes et al was that nearly all people with ME/CFS have normal liver tests, as has been noted many times. There was a very small statistical shift in values for a population but one cannot build a causal mechanism on that. It est you can say that there is a faint clue to something that might be indirectly linked to a mechanism. For liver test all you need is a low level of Kupffer cell activation to get changes. And slight shifts in liver function tests, glucose tolerance and CRP (the things licked up if I remember) all all just the sort of things that are likely to be picked up for confounding reasons relating to population selection.

The other main reason I say little about these aspects is that I see no obvious way to implicate them in an explanation for ME/CFS symptoms.

 

[EndME]

@EndME and @Suffolkres are you following this? Any comments?

I think we're talking at cross purpose here. My comments are all just about the Born Free Protocol. I indeed misunderstood what you meant with "negative bias" but it wouldn't change any of my comments about the protocol.

Beyond that I see little point in having lengthy discussions on "whether specific things worked for some people" unless there is special evidence that it did, which in this case there isn't (see also the Rituximab trials).

 

[mariovitali]

@mariovitali, I appreciate your enthusiasm for liver and bile issues and your attempts to make sense of things but, no, I don't think these are what we would call replicated findings.

Thank you for your reply, I see one aspect of confusion on my behalf here. My mistake. When I mentioned replicated findings I meant that specific medical concepts that have been identified as being important in -say 2016- have been found later (say 2023) by published research.

The main replicating finding of Beentjes et al was that nearly all people with ME/CFS have normal liver tests, as has been noted many times. There was a very small statistical shift in values for a population but one cannot build a causal mechanism on that. It est you can say that there is a faint clue to something that might be indirectly linked to a mechanism. For liver test all you need is a low level of Kupffer cell activation to get changes. And slight shifts in liver function tests, glucose tolerance and CRP (the things licked up if I remember) all all just the sort of things that are likely to be picked up for confounding reasons relating to population selection.

Thank you for clarifying this. I must admit I do not quite understand and I would prefer that I make no assumptions here. Are you proposing that the study by Beentjes et.al regarding the existence of a combination of liver dysfunction and insulin intolerance and elevated CRP in MECFS do not provide us with any useful information regarding MECFS pathology ?

The other main reason I say little about these aspects is that I see no obvious way to implicate them in an explanation for ME/CFS symptoms.

I assume that by "these aspects" you mean the identification of ABCA1, CH25H, LXR, Endoplasmic Reticulum stress, Choline deficiency and others. First of all, I believe that we cannot rule out that easily the potential importance of concepts having being identified more than one time (not making the same mistake as with "replicated findings"). If we disregard the potential relevance of these concepts, would you be still talking about confirmation bias on my part?

 

[Jonathan Edwards]

Are you proposing that the study by Beentjes et.al regarding the existence of a combination of liver dysfunction and insulin intolerance and elevated CRP in MECFS do not provide us with any useful information regarding MECFS pathology ?

In short, yes. The data are overwhelmingly negative on these issues. The tiny positive signal looks to me to be either an artefact or something so indirectly relevant that it does not help us.

 

[mariovitali]

I think we're talking at cross purpose here. My comments are all just about the Born Free Protocol. I indeed misunderstood what you meant with "negative bias" but it wouldn't change any of my comments about the protocol.

Beyond that I see little point in having lengthy discussions on "whether specific things worked for some people" unless there is special evidence that it did, which in this case there isn't (see also the Rituximab trials).

Well, in the case of Witney Dafoe and the amazing change of his symptoms we could say that we look at individual elements from patient recoveries (like myself) and then see whether we find any commonalities. I will add my two cents here. If indeed the GWAS results suggest brain and glutamatergic synapses involvement we can see some commonalities. Both Witney and myself refrained from glutamate. Witney via medication (Attivan upregulates GABA) and myself by avoiding anything with glutamate (shown in the sources I linked above related to my recovery).

I cannot prove if Leisk has mashed up several findings and theories and used every supplement known to man to address all of these findings. If I would be able to prove it, I would write about it. Can we see any commonalities here ? Taurine (which he uses and I used) ameliorates ER Stress. He also mentions Phosphatidylcholine in his regimen. Could it be possible that first By Attivan (which has helped Witney considerably) and then by using compounds we know that have specific effects (Phospahtidylcholine in cell membranes, Taurine/TUDCA for ER Stress) we are able to stop a vicious cycle ?

Do I believe that these supplements can stop MECFS ? Far from it , because for so many years I have been proposing that we are looking at different conditions that negatively affect the liver. Not everyone has Wilson's, Gilbert's or hemochromatosis or a mutation on a condition called palmitoyltransferase deficiency. No Taurine or TUDCA will help these patients alone. https://www.s4me.info/threads/metabolic-conditions-and-the-liver.47788/

All I am asking is that the information posted here does not go unnoticed for another 10 years.

 

[Trish]

Thank you @mariovitali for responding to my question and clarifying your views.

I'm afraid you are expecting more from me than I can manage. I simply have neither the capacity in time and energy, nor the background depth of knowledge to examine your research methodology to assess whether it is a valid process for investigation biomechanisms of a specific disease or not.

I therefore decided long ago to step away from trying to make sense of your work. Whatever you found would need to be re-explored and replicated anyway by more direct methods, so seemed to me to take us no further forward.

But we are talking here about Leisk's protocol. I repeat that I have seen no attempt by Leisk to set up the clinical trial he talked of a few years ago. Instead we see someone using what I consider unethical promotion of unevidenced treatment that can cause harm. In this context a few anecdotes claiming efficacy are of no more use than anecdotes of efficacy of ear seeds, homeopathy or thinking happy thoughts.

 

[Peter T]

Well, in the case of Witney Dafoe and the amazing change of his symptoms we could say that we look at individual elements from patient recoveries (like myself) and then see whether we find any commonalities.

I too had had misinterpreted what you meant by ‘negative bias’ as relating to the Born Free protocol in general or even our more general scepticism of any unevidenced treatments, and now I appreciate you are taking a more nuanced approach. But I still argue we should approach all individual recovery anecdotes with caution.

I agree that we should ideally examine patterns of reported as potential sources of information about our condition. You obviously appreciate the problems around basing treatment on anecdote. Unfortunately cherry picking recovery stories that suit a particular approach risks encouraging people down dangerous paths, especially when those involve high profile individuals like Garner or Whitney.

We have missed a golden opportunity with Covid to study whole populations, trying to establish if there are any biological differences between those that develop ME/CFS type Long Covid and those that do not, but also to see if there are any biochemical or physiological differences between those that subsequently recover and those that do not. Given the enormous variation between and within individuals with ME/CFS, and given that so many of us try a wide assortment of of interventions it is inevitable that by chance alone there will be fortuitous coincidences.

I understand you may feel confident in the association for yourself between what you have tried and your improvements.

I know for myself with my gluten intolerance that when I am gluten free, reintroducing gluten always results a specific pattern of deterioration, with those symptoms overlapping with the symptoms involved in PEM. So for myself I feel confident eliminating gluten from my diet avoids the negative consequences of eating gluten. However, though this means my health is better when I am gluten free, I can not go on to say being gluten free improves my underlying ME/CFS. Similarly I suffer from B12 deficiency, and when in deficit B12 supplementation causes an improvement in my fatigue levels and in my brain fog, but a maintenance dose does not result in an ongoing improvement in my underlying ME/CFS, just avoids the negative consequences of further deficit.

For me looking at many varied recovery stories in the round, none of which so far involve interventions having universal success, the only commonality we see is that they were all improving, so unless you postulate sub groups, isn’t the more likely explanation that increasing activity allows the individual to trial the intervention and reinforces their ongoing commitment to that intervention rather than the intervention itself treats the underlying condition.

To use recovery stories, you need to take on of two approaches, the best is to take a whole population, follow up and see what the differences are between those smaller numbers that subsequently improve or recover and those larger numbers that do not. Unfortunately this would involve large numbers of subjects and potentially following them up over many years.

Alternatively, as you do, we could look at apparent groupings of recovered or recovering individuals, which of themselves tell us nothing conclusive, but use them as a hint about where to focus other research. Though you obviously feel that has offered clues, many of us remain sceptical that this so far has provided any useful leads. Perhaps the only reliable data we have so far relates to DecodeME’s findings, so it may be that we should look at the genetics of those who report recovery compared to those who do not, though given the problems around diagnosis extreme care would need to be taken in identifying the ‘recovered’ cohort.

 

[mariovitali]

Thank you @mariovitali for responding to my question and clarifying your views.

I'm afraid you are expecting more from me than I can manage. I simply have neither the capacity in time and energy, nor the background depth of knowledge to examine your research methodology to assess whether it is a valid process for investigation biomechanisms of a specific disease or not.

Thank you, I totally understand. I do not want to derail the thread so I will not comment further. Let's say I have been trying to identify the pros and cons of this methodology.

I therefore decided long ago to step away from trying to make sense of your work. Whatever you found would need to be re-explored and replicated anyway by more direct methods, so seemed to me to take us no further forward.

I agree. If you look at a thread earlier I linked, I propose that there may be patients with key metabolic defects and this needs to be looked at. I also mentioned ER Stress 10 years ago. Isn't it A SHAME THAT NO ONE DID NOTHING ??? Yes , I am screaming right now. Where we would be right now if someone took this seriously ? I do understand, someone out of nowhere sends an email and talks about ER Stress. I find it hard to accept how any researcher would treat this email seriously. However...things are definitely not the same when a methodology appears (note the word 'appears' - I am being very careful) to REPEATEDLY identify earlier key concepts to MECFS. And more importantly, are these theories utter nonsense or not despite that there is no understanding of the methodology.

But we are talking here about Leisk's protocol. I repeat that I have seen no attempt by Leisk to set up the clinical trial he talked of a few years ago. Instead we see someone using what I consider unethical promotion of unevidenced treatment that can cause harm. In this context a few anecdotes claiming efficacy are of no more use than anecdotes of efficacy of ear seeds, homeopathy or thinking happy thoughts.

Understood. Again, my thread was trying to show the red flags (I should have done better here) but on the same time have people investigate how any information presented in BF protocol has any sort of scientific evidence. If for example he would mention TUDCA being used, then this would have scientific evidence since ER Stress appears to be a key mechanism in MECFS and we know that TUDCA does reduce ER Stress in humans.

 

[mariovitali]

I too had had misinterpreted what you meant by ‘negative bias’ as relating to the Born Free protocol in general or even our more general scepticism of any unevidenced treatments, and now I appreciate you are taking a more nuanced approach. But I still argue we should approach all individual recovery anecdotes with caution.

Thank you Peter. Just to say that in my response I did not have the time to explain what I mean by "negative bias" and the right context. Yes I agree, every single recovery needs to be screened in order to avoid any false claims.

I agree that we should ideally examine patterns of reported as potential sources of information about our condition. You obviously appreciate the problems around basing treatment on anecdote. Unfortunately cherry picking recovery stories that suit a particular approach risks encouraging people down dangerous paths, especially when those involve high profile individuals like Garner or Whitney.

Yes. Again, I was refraining all of these years to post details of my recovery because I did not want from people to start experimenting.

We have missed a golden opportunity with Covid to study whole populations, trying to establish if there are any biological differences between those that develop ME/CFS type Long Covid and those that do not, but also to see if there are any biochemical or physiological differences between those that subsequently recover and those that do not. Given the enormous variation between and within individuals with ME/CFS, and given that so many of us try a wide assortment of of interventions it is inevitable that by chance alone there will be fortuitous coincidences.

Totally agree.

I understand you may feel confident in the association for yourself between what you have tried and your improvements.

Yes there is one key detail here however. The interventions I made appeared to be the ones needed in order to lower ER Stress, support cell membranes and lower oxidative stress. There is more on this and I will be sharing a Youtube video.

I know for myself with my gluten intolerance that when I am gluten free, reintroducing gluten always results a specific pattern of deterioration, with those symptoms overlapping with the symptoms involved in PEM. So for myself I feel confident eliminating gluten from my diet avoids the negative consequences of eating gluten. However, though this means my health is better when I am gluten free, I can not go on to say being gluten free improves my underlying ME/CFS. Similarly I suffer from B12 deficiency, and when in deficit B12 supplementation causes an improvement in my fatigue levels and in my brain fog, but a maintenance dose does not result in an ongoing improvement in my underlying ME/CFS, just avoids the negative consequences of further deficit.

For me looking at many varied recovery stories in the round, none of which so far involve interventions having universal success, the only commonality we see is that they were all improving, so unless you postulate sub groups, isn’t the more likely explanation that increasing activity allows the individual to trial the intervention and reinforces their ongoing commitment to that intervention rather than the intervention itself treats the underlying condition.

I agree. My research suggests that there is no Single Point Of Failure. It is a mixture of unfortunate metabolic+immune inefficiencies.

To use recovery stories, you need to take on of two approaches, the best is to take a whole population, follow up and see what the differences are between those smaller numbers that subsequently improve or recover and those larger numbers that do not. Unfortunately this would involve large numbers of subjects and potentially following them up over many years.

Alternatively, as you do, we could look at apparent groupings of recovered or recovering individuals, which of themselves tell us nothing conclusive, but use them as a hint about where to focus other research. Though you obviously feel that has offered clues, many of us remain sceptical that this so far has provided any useful leads.

Agreed. I like the example here of the metabolic issues thread I posted earlier. Do you think that anyone will care? Speaking of metabolic issues, Gilbert's is consider a "benign" syndrome. Is this really so ? https://europepmc.org/article/MED/8097856 . I am not suggesting it is, all I am doing is asking for someone to look at this. No one did so far.

Perhaps the only reliable data we have so far relates to DecodeME’s findings, so it may be that we should look at the genetics of those who report recovery compared to those who do not, though given the problems around diagnosis extreme care would need to be taken in identifying the ‘recovered’ cohort.

I would like to ask someone -as I do not have the knowledge- whether the GWAS study would be able to identify that several MECFS patients have metabolic issues -say- in Urea cycle. I very much doubt this is possible but an expert should give an answer.

 

[Peter T]

Yes there is one key detail here however. The interventions I made appeared to be the ones needed in order to lower ER Stress, support cell membranes and lower oxidative stress. There is more on this and I will be sharing a Youtube video.

I wonder if some confusion arose, @mariovitali , because you were raising issues in part tangential to this thread, so I was wondering if it would be worth starting a specific thread(s) on what you see as the key issue(s) involved. (I could not see any relevant existing threads, but I do cognitively struggle searching amongst the large number of possible alternatives.) For example I could not find anything relating to ER stress. Is this a topic you would like to see specific discussion on?

Alternatively there are a couple of threads on what future research we would like to see relating to ME/CFS.

 

[Suffolkres]

Thank you, I totally understand. I do not want to derail the thread so I will not comment further. Let's say I have been trying to identify the pros and cons of this methodology.

I agree. If you look at a thread earlier I linked, I propose that there may be patients with key metabolic defects and this needs to be looked at. I also mentioned ER Stress 10 years ago. Isn't it A SHAME THAT NO ONE DID NOTHING ??? Yes , I am screaming right now. Where we would be right now if someone took this seriously ? I do understand, someone out of nowhere sends an email and talks about ER Stress. I find it hard to accept how any researcher would treat this email seriously. However...things are definitely not the same when a methodology appears (note the word 'appears' - I am being very careful) to REPEATEDLY identify earlier key concepts to MECFS. And more importantly, are these theories utter nonsense or not despite that there is no understanding of the methodology.


Understood. Again, my thread was trying to show the red flags (I should have done better here) but on the same time have people investigate how any information presented in BF protocol has any sort of scientific evidence. If for example he would mention TUDCA being used, then this would have scientific evidence since ER Stress appears to be a key mechanism in MECFS and we know that TUDCA does reduce ER Stress in humans.

'Isn't it A SHAME THAT NO ONE DID NOTHING ???'
Slightly confused. Double negative, n'est pas?!
Do you mean someone did something ...????

As for me, re. any comments?
Professionally, I am not a scientist nor a medic.
I worked in Specialist education and am a carer for 2 with ME diagnosis. IN 1996 and 2006.
On a personal level, pursuing any 'treatments' or alternative approaches in the UK is a very, very dangerous dangerous game. With young people.
I know from my own bitter experience around 2000, falling foul of the local paediatric service in Suffolk for even daring to ask questions about my child's diagnosis and situation.

A local friend fared worse....(Panorama 1999, Sick and Tired. Matthew Hill.) Child x
We were both regarded as harming parents.
I dared to ask for a second opinion.
Not an alternative practitioner, but a very highly regarded former NHS Essex based consultant paediatrician who had new and novel approaches to food intolerance and allergy. Bless him RIP, AF!
I did take advised from nutritional herbalists and other alternative practitioners who were extremely helpful, re diet and vitamin deficiency. And we did see progress and relief of symptoms.
I secured specialist testing from Biolab who found high levels of toxic chemicals in my son's blood...
unexplained exposures. save for living 4 metres next to sprayed and chemically treated farmland. Sugar beet products Lindane, which persist in the environment, blow as dust and can enter via inhalation, or sprays can impact via the olfactory Pathway direct across blood brain barrier to impact the brain.

Chemicals implicated in Parkinsons disease via this possible mechanism?
Despite seeking best qualified advisers, I was viewed locally with suspicion......
My GP was good.

Irony is, the nature of my work, with very complex vulnerable young people, meant I was highly safeguarding trained and had enhanced DBS clearance..
Made no difference, mattered not a jot to local Services......
Still happening in UK.

Even adults are not immune nor can prevent invoking the Mental Capacity Act (2005)..
So what do I think?
Interesting though your findings may be, no matter how sincere and worthy you may be, any prospective client needs to understand the dangers of going against established, Governmentally endorsed practice, or possibly face the most terrible personal risks and consequences when the state can and will intervene and take control.
What you say is an interesting intellectual exercise, but it will have no bearing at all on NHS Services under the control of individuals within NHS England, who will remain unnamed but would have a field day with what you propose…
So, whilst interesting, it will have little relevance or merit for the majority, and may prove catastrophic for families if misconstrued by statutory services. And likely misconstrued, it will be.