Sushi
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Here is another interesting one on how the immune system works in terms of LDI--short, 6 min, good analogies.
Low Dose Antigens / Immunotherapy (LDA/LDI) Lyme
- Thread starter Lemnia
- Start date
Hi @Vitalic, I think you might find interesting and plenty of evidence in the article I wrote on LDI, Lyme and CFS, that will for sure give answer to some of your questions:
http://www.sfc-em-investigacion.com/download/file.php?id=359
As for the homeopathic "issue". Well, actually most conditions treated with LDI need an average dose of 6C (1C=1:100 dilution). This is still a very diluted dose, but EPD ("old" version of LDI) has shown in some solid papers (blinded, against placebo) that at these doses, it worked even better than normal specific-antigen-based-immunotherapy for allergies--for instance raising the number of CD8+ cells.
Moreover, I made the maths and some paper showed how dilutions of 8C did promote an efector response (for the regulatory response expected from LDI, the doses must be way lower).
But, let's be realistic. Yes, the range of doses for Lyme patients is incredibly wide: some need a dilution of 25 C, while others need 4C... So..what is going on here? We go from homeopathy to real molecular science? Even in the same patient, whose first dose is 15C and has to work it up until say 6C over time, as he/she gets better?
I really don't have an answer as for why we, ME/CFS patients with Lyme disease might need so diluted doses... I really don't know. But I have been put in bed for weeks after a dose of 21 C (yes, 1:10 ^42 dilution). The "flare" was stronger than the herx I got from ABX... And believe me, it was not placebo... (I'm not that masochistic!
Just showing facts,
Hope it helps,
Sergio
http://www.sfc-em-investigacion.com/download/file.php?id=359
As for the homeopathic "issue". Well, actually most conditions treated with LDI need an average dose of 6C (1C=1:100 dilution). This is still a very diluted dose, but EPD ("old" version of LDI) has shown in some solid papers (blinded, against placebo) that at these doses, it worked even better than normal specific-antigen-based-immunotherapy for allergies--for instance raising the number of CD8+ cells.
Moreover, I made the maths and some paper showed how dilutions of 8C did promote an efector response (for the regulatory response expected from LDI, the doses must be way lower).
But, let's be realistic. Yes, the range of doses for Lyme patients is incredibly wide: some need a dilution of 25 C, while others need 4C... So..what is going on here? We go from homeopathy to real molecular science? Even in the same patient, whose first dose is 15C and has to work it up until say 6C over time, as he/she gets better?
I really don't have an answer as for why we, ME/CFS patients with Lyme disease might need so diluted doses... I really don't know. But I have been put in bed for weeks after a dose of 21 C (yes, 1:10 ^42 dilution). The "flare" was stronger than the herx I got from ABX... And believe me, it was not placebo... (I'm not that masochistic!
Just showing facts,
Hope it helps,
Sergio
Last edited:
Dufresne
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@serg1942
Do you think the flare is actually the result of your immune system going after borrelia. I've used 30-90X borrelia dilutions in the past and experienced clear die-off reactions. I wonder if it might be the case that some doses increase immunity to the antigen while others decrease it. Because I can't imagine what else this 'flare' could be?
Do you think the flare is actually the result of your immune system going after borrelia. I've used 30-90X borrelia dilutions in the past and experienced clear die-off reactions. I wonder if it might be the case that some doses increase immunity to the antigen while others decrease it. Because I can't imagine what else this 'flare' could be?
junkcrap50
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Hi @Vitalic, I think you might find interesting and plenty of evidence in the article I wrote on LDI, Lyme and CFS, that will for sure give answer to some of your questions:
http://www.sfc-em-investigacion.com/download/file.php?id=359
As for the homeopathic "issue". Well, actually most conditions treated with LDI need an average dose of 6C (1C=1:100 dilution). This is still a very diluted dose, but EPD ("old" version of LDI) has shown in some solid papers (blinded, against placebo) that at these doses, it worked even better than normal specific-antigen-based-immunotherapy for allergies--for instance raising the number of CD8+ cells.
Moreover, I made the maths and some paper showed how dilutions of 8C did promote an efector response (for the regulatory response expected from LDI, the doses must be way lower).
But, let's be realistic. Yes, the range of doses for Lyme patients is incredibly wide: some need a dilution of 25 C, while others need 4C... So..what is going on here? We go from homeopathy to real molecular science? Even in the same patient, whose first dose is 15C and has to work it up until say 6C over time, as he/she gets better?
I really don't have an answer as for why we, ME/CFS patients with Lyme disease might need so diluted doses... I really don't know. But I have been put in bed for weeks after a dose of 21 C (yes, 1:10 ^42 dilution). The "flare" was stronger than the herx I got from ABX... And believe me, it was not placebo... (I'm not that masochistic!
Just showing facts,
Hope it helps,
Sergio
Wow, this is incredible research and very well put together. Thank you! I haven't read it entirely yet, but skimmed it and it looks great. This is very helpful to me as I was excited about LDI, but then lost hope as it turned out to be more homeopathy. I'll be reading this with great interest and will be sending it to my doctor. To help the our cause, you may consider sending it to Ty Vincent himself so that he may put it on his website and help spread the word.
Hi @Dufresne, do you mean you took borrelia antigens at a 1:10^50 and at a 1:10^90 dilutions? Both are really low!!! The 1:10^50 seems to be necessary for some few very very sick people, but I have never heard of anyone having to go as low as 1:10^90 for any LDI/LDA antigen…Did you take it sublingually or intradermally?
In reply to your question: A flare caused by LDI feels like Herx, but the mechanism I think is different. The Herx happens when you take an antimicrobial agent and kill bacteria (or other pathogens), and then proteins of the dead bacteria go to the bloodstream, where both the innate and the acquired immune system engage with these proteins and mount an attack toward the bacteria (the immune response has nothing to do--as probably you know-- with the bacteria being alive—it just react towards specific proteins).
In the case of the response observed with LDI, we should better call it a “flare” to distinguish it from the typical Herx, because what occurs is different, as you are not killing pathogens directly with an antimicrobial substance. The only mechanism I know that could explain this reaction is as follows: your immune system, mainly the acquired one, has been “taught” to recognize the bacteria antigens, and to mount a given response (ideally Th1 for viruses and intracelular pathogens, Th2 for parasites and extracellular bacteria, Th17 for mucosae pathogens…) when encountering the bacteria.
The problem in ME/CFS as well we in chronic Lyme disease (this is clearly shown in the literature) is that we have a wrongly set immune system, consisting in a Th1 depressed response, an exacerbated anti-inflammatori Th2 response, a depressed inflammatory Th17 , a depressed innate response (NKs) but over-active at the same time (complement), an acquired response that is at the same time depressed (the Th1, Th17, the low activation of M1 macrophages…) and over active: polyclonal B and T cells, lack of non-pathogen-specific Tregs, etc. As a result of this picture, reactive species rises and autoimmune processes occur (mainly by molecular mimicry but also buy other means). This is not “random”. This picture is pretty much the same in all conditions where some cells misbehave (it is very known in malignant cells as well as in chronically infected cells). Funny thing is that, even though there’s no pathogen shown to cause ME/CFS (yet), the immune profile found is the same one I have just described (it varies over time--hence the need of longitudinal trials!-- and with the severity), so it is to be expected that chronic intracelular infections probably play an etiological role (at least at the beginning, as this wrongly sent immune response can perpetuate itself without the actual presence of the initial trigger).—Ok, note that it is the immune system deployed as I have explained what causes the symptoms in both ME/CFS and chronic Lyme disease (not the bacteria!), as shown by the literature.
So, what are we doing when giving say borrelia, or yeast or EBV antigens with LDI? Ok, let’s forget about very weak dilutions where I have no idea what happens there (maybe they contain enough dead bacteria to still promote the pursued response, or perhaps certain “homeophathic mechanisms” I don’t know about play a role): If the dose is too high, the circulating T cells specific for that pathogen (meaning you have been infected by it!) recognizes the bacteria, and mounts the wrong inflammatory and effector acquired response, that at the end causes our symptoms, so in the case of taking a too strong dose, we are causing a flare.
On the other hand, when you take too a weak dose, you just don’t promote any response. BUT, there seems to be a “proper dose” that actually seems not to stimulate the T inflammatory effector response of the flare, but rather, the antigens inoculated are taken up by the dendritic cells of the mucosae, they travel to the lymph nodes, and they present these antigens to the T naïve cells (part of the acquired immune response that has not yet been “trained”). If the dose is the right one, and the signals around are the needed ones, they will become Treg cells specific for the inoculated pathogen . I guess specific B cells are also formed. The T regs go out to the circulation and tissues and slow down the overactive part of the immune response. At the same time, it is my guess that a proper immune response (Th1, inflammatory Th17) is also formed over time, so that eventually, all this leads to a switch of the immune profile, from the pathological one towards the healthy one.
Note that this mechanism has been partially observed in other conditions (chronic infectious diseases and autoimmune conditions linked to pathogens) treated with similar therapies (but with much higher doses), and I am extrapolating these results and the basic immunology to what might happen with LDI. However, a different mechanism seems unlikely to me in light of the available evidence.
Hope it helps!
Sergio
In reply to your question: A flare caused by LDI feels like Herx, but the mechanism I think is different. The Herx happens when you take an antimicrobial agent and kill bacteria (or other pathogens), and then proteins of the dead bacteria go to the bloodstream, where both the innate and the acquired immune system engage with these proteins and mount an attack toward the bacteria (the immune response has nothing to do--as probably you know-- with the bacteria being alive—it just react towards specific proteins).
In the case of the response observed with LDI, we should better call it a “flare” to distinguish it from the typical Herx, because what occurs is different, as you are not killing pathogens directly with an antimicrobial substance. The only mechanism I know that could explain this reaction is as follows: your immune system, mainly the acquired one, has been “taught” to recognize the bacteria antigens, and to mount a given response (ideally Th1 for viruses and intracelular pathogens, Th2 for parasites and extracellular bacteria, Th17 for mucosae pathogens…) when encountering the bacteria.
The problem in ME/CFS as well we in chronic Lyme disease (this is clearly shown in the literature) is that we have a wrongly set immune system, consisting in a Th1 depressed response, an exacerbated anti-inflammatori Th2 response, a depressed inflammatory Th17 , a depressed innate response (NKs) but over-active at the same time (complement), an acquired response that is at the same time depressed (the Th1, Th17, the low activation of M1 macrophages…) and over active: polyclonal B and T cells, lack of non-pathogen-specific Tregs, etc. As a result of this picture, reactive species rises and autoimmune processes occur (mainly by molecular mimicry but also buy other means). This is not “random”. This picture is pretty much the same in all conditions where some cells misbehave (it is very known in malignant cells as well as in chronically infected cells). Funny thing is that, even though there’s no pathogen shown to cause ME/CFS (yet), the immune profile found is the same one I have just described (it varies over time--hence the need of longitudinal trials!-- and with the severity), so it is to be expected that chronic intracelular infections probably play an etiological role (at least at the beginning, as this wrongly sent immune response can perpetuate itself without the actual presence of the initial trigger).—Ok, note that it is the immune system deployed as I have explained what causes the symptoms in both ME/CFS and chronic Lyme disease (not the bacteria!), as shown by the literature.
So, what are we doing when giving say borrelia, or yeast or EBV antigens with LDI? Ok, let’s forget about very weak dilutions where I have no idea what happens there (maybe they contain enough dead bacteria to still promote the pursued response, or perhaps certain “homeophathic mechanisms” I don’t know about play a role): If the dose is too high, the circulating T cells specific for that pathogen (meaning you have been infected by it!) recognizes the bacteria, and mounts the wrong inflammatory and effector acquired response, that at the end causes our symptoms, so in the case of taking a too strong dose, we are causing a flare.
On the other hand, when you take too a weak dose, you just don’t promote any response. BUT, there seems to be a “proper dose” that actually seems not to stimulate the T inflammatory effector response of the flare, but rather, the antigens inoculated are taken up by the dendritic cells of the mucosae, they travel to the lymph nodes, and they present these antigens to the T naïve cells (part of the acquired immune response that has not yet been “trained”). If the dose is the right one, and the signals around are the needed ones, they will become Treg cells specific for the inoculated pathogen . I guess specific B cells are also formed. The T regs go out to the circulation and tissues and slow down the overactive part of the immune response. At the same time, it is my guess that a proper immune response (Th1, inflammatory Th17) is also formed over time, so that eventually, all this leads to a switch of the immune profile, from the pathological one towards the healthy one.
Note that this mechanism has been partially observed in other conditions (chronic infectious diseases and autoimmune conditions linked to pathogens) treated with similar therapies (but with much higher doses), and I am extrapolating these results and the basic immunology to what might happen with LDI. However, a different mechanism seems unlikely to me in light of the available evidence.
Hope it helps!
Sergio
Hi @junkcrap50! Thank you, I'm glad you liked it!. I expended months to elaborate this article, because I wanted to "look" for the underlying mechanism of LDI/LDA, as I had studied the typical specific-antigen-based-immunotherapy used to (most times) cure (or at least to make patients asymptomatic) patients with all sorts of allergies, and had thought that something similar should be doable for us (and then I knew about LDI!)... And not only I found what seems to me like a "universal" mechanism, but also found, much to my surprise, that it perfectly fit with both ME/CFS and chronic Lyme disease etiopathogenesis.
I do understand the reticence towards homeopathy (I am actually studying allopathic medicine, so you can imagine...). But the thing is that this "issue" started to "appear" over time, when some patients very sick could not stand the non-homeopathic doses many other patients were doing well with... So to tell you the truth, I don't care, as long as it works. I still think the mechanism I've explained above might happen anyway with so very low doses. (To test this hypothesis I have tested my mom, who was sick too, and is almost well after just 4 doses of LDI. I will let you know if her improvement correlates with immune lab tests!
).Well, I am a patient of Dr. Ty, and he knows I am eager to know the details of LDI mechanims. However he doesn't seem to care much, as long as the therapy works--and that is fine with me, as he is focusing on improving the outcomes of the therapy for his patients-- So I'm not sure he'd like to show my theory on how LDI works as the way LDI might work, because I think he is also coming to think that homeopathic mechanism have to play a key role...hey! but feel free to forward the article to him! it's fine with me!
Best!
Sergio
Jesse2233
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Is this effective for non-Lyme CFS/ME?
Sushi
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It has shown efficacy for ME/CFS that has either a viral or bacterial component. I get really notable symptom relief for a couple of weeks after a dose. The doctor is trying to increase the length of time it lasts for me by tweaking dosing.
Jesse2233
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Interesting, thanks Sushi. How large is your dose and what is the symptom relief like?
Sushi
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It is nearly impossible to describe the "size" of the dose as it isn't in mgs but rather is a dilution given in the quantity of .o4 ml. As far as symptom relief, when I get an effective dose it relieves symptoms across the board.
junkcrap50
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To Sushi or anyone else ,
I am most interested in LDI for my sister who has textbook PANDAS. She has undergone all the testing I have (for textbook CFS) and the only thing that shows up is PANDAS antibodies and clinical history & symptoms of PANDAS. I think LDI would be very effective for her.
Thank you for any help.
- Does anyone know the best way to get LDI?
- Do I have to go to Alaska and visit Ty Vincent? That's way out of my price range and I can't afford it.
- How do I get my doctor LDI "trained" or "approved" so that he can prescribe/sell LDI?
- Does Ty Vincent's office have a list of US doctors or contacts that sell his version of LDI?
- Can I buy LDI straight from Ty Vincent's office?
- From where dose Ty Vincent acquire his LDI solutions ? I know Dr. Shrader who does LDA (slightly different than LDI) gets his solutions from a pharmacy in Utah.
I am most interested in LDI for my sister who has textbook PANDAS. She has undergone all the testing I have (for textbook CFS) and the only thing that shows up is PANDAS antibodies and clinical history & symptoms of PANDAS. I think LDI would be very effective for her.
Thank you for any help.
Sushi
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- Dr. Vincent has moved to Hawaii (he was moving back and forth between Alaska (where he had a brick and mortar practice) and Hawaii, where he had a Skype practice. He now only has a Skype practice. Anyone can make an appointment through http://www.globalimmunotherapy.com/
No one can "buy" it anywhere as you need to consult with a doctor to embark on this treatment. Then the doctor will supply the antigens that seem appropriate for the individual.
Dr. Vincent uses both LDA (now from a different pharmacy--College Pharmacy no longer supplies it) and LDI. He makes the solutions of LDI himself. I don't know where he buys the raw materials.
Dr. Vincent trains other doctors in the use of LDI/LDA. His office could tell you how to put your doctor in touch with him.
So does Dr. Vincent prescribe LDI from a video chat? I know that this may be the wave of the future, but is it ethical, at least to prescribe a pain medication ? is LDN a controlled substance?
My healthcare provider, a large medical center has this service. I have no idea what type of medical issues the video chat entails.
I need to look up this info. Maybe it should be the subject of a thread?
If this is too off topic, let me know. Thanks!
Edit. I just realized ldn is used to block thr effects of narcotics.
My healthcare provider, a large medical center has this service. I have no idea what type of medical issues the video chat entails.
I need to look up this info. Maybe it should be the subject of a thread?
If this is too off topic, let me know. Thanks!
Edit. I just realized ldn is used to block thr effects of narcotics.
Sushi
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You have an hour plus appointment with him by Skype. And yes, it is legal and ethical. He doesn't (and can't) prescribe drugs without an in-person consult but he can prescribe LDI (which is not a drug).
I think you saw this but it is LDI not LDN. LDN is a prescription medication though not a "controlled substance."
Sushi
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I actually found that Skype was a great medium for a medical consult. We had a full head and shoulders view of each other and it felt like being in the same room. After this first consult, we report to him by filling out a report for each dose and he analyzes your report and replies by email.
knackers323
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How is everyone doing on this treatment?
Hanna
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@Sushi and the others pioneers in LDI , any news about the outcomes of this treatment ?
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Wow... I was seriously considering EPD for a long time, from around 2000 for several years, but it seemed to be falling out of favour by then. Isn't this something Dr Myhill uses, or has used? So sorry to hear about the negative effect it had on your health.
Sushi
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A few have had pretty spectacular results--remission. Most of us have had mixed results, such as feeling great for a week or so after a dose and then the benefit fading or difficulty in finding the right antigen and dose level. I have had some great results and some with no effect and a few where I felt worse for a few days. There is a lot of exploration needed (at this stage) to get consistent results.