Low-Dose Immunotherapy (LDI)

immune systemArticle Written by Ty Vincent, MD  Townsend Letter June 1, 2017
www.townsendletter.com

Low-dose immunotherapy is an expanded application of LDA (low-dose allergy therapy), treatment made available to practitioners in the US by W. A. Shrader, MD, for the resolution of allergies and select autoimmune disorders. An earlier version of that technique, EPD (enzyme-potentiated desensitization), has been used in the field of integrative medicine since it was developed in the 1960s by Leonard McEwen, MD, an allergist in the UK. These techniques have been applied very successfully in the treatment of more than 60 indications, primarily allergy, asthma, and chemical sensitivities; autoimmune disorders including rheumatoid arthritis, systemic lupus, and ankylosing spondylitis; and other select immune-mediated conditions.

The efficacy of EPD was confirmed in a study conducted from 1993 to 2001 by Drs. Shrader and McEwen involving approximately 10,500 patients and more than 100 participating physicians. The study, which documented 68,428 treatment regimens (comprised of over 175,000 EPD injections), found that 76% of patients reported excellent, very good, or good health outcomes. Only 2% reported adverse effects, with 14% indicating a fair response and 8% indicating no change. LDA is virtually the only option currently available to prevent the occurrence of life-threatening reactions or death as a result of acute food allergy.

When I took the LDA training in 2008, I was amazed by the effectiveness of this approach. Within a year or two, I began to realize that the applications for this technique were much broader than the initial conditions for which it was indicated. Since that time, my contribution to this form of immunotherapy has been to apply the same technique to a much greater range of other immune-mediated conditions, including a number of disorders that had previously been thought to be "infections." In the process, I discovered changes in the technique that have made the treatment easier to use and in some cases yield faster results. In my practice and teaching, I now use sublingual antigens, rather than subcutaneous injections, and have found the oral dosing to be equally effective. Our research has also shown that "fresh" antigens are not essential, so LDI dosages can be sent directly to the patient through the mail to self-administer in their own home, rather than requiring repeated office visits to the physician for subcutaneous injections, significantly reducing the cost of therapy. Over the past nine years, I have expanded the application of this approach to the treatment of an additional 40 indications, including numerous difficult-to-treat autoimmune disorders.

An Epidemic of Immunological Illness

Autoimmune disease and allergies have increased dramatically over the last thirty years. Autism, for example, is an immunological illness in the vast majority of cases. In total, the incidence of immune-mediated illness has reached epidemic proportions.

Although the focus in healthcare tends to be on cancer and heart disease (still the leading killers), autoimmune disease and severe allergic disorders can cause decades of suffering in those who are afflicted. This has resulted in an incredible burden of chronic illness that persists for millions and millions of people. These diseases typically do not kill patients, but their quality of life is terrible. Given the debilitating nature of conditions such as rheumatoid arthritis, multiple sclerosis, and Crohn's disease, other categories of disease pale by comparison in terms of disability and compromised quality of life.

People with conditions such as Lyme disease are often not properly diagnosed for many years, if ever. They are given a diagnosis of fibromyalgia or chronic fatigue syndrome and are marginalized by our healthcare system and our psychiatric system. Practitioners and family members assume that these patients have a psychosomatic disorder, but in reality, they have some type of chronic inflammatory response that their immune system is propagating against them. They will suffer for decades if no one is able to correct that.

Breakthroughs in Treatment

All these conditions can be treated with a high rate of success using LDA and LDI. Both therapies involve a form of immunotherapy enhanced by a minute dose of the enzyme beta glucuronidase (10-13), paired with miniscule doses of various allergens (10-6 to 10-17) to stimulate the production of T-suppressor cells (T regulator or T reg cells). The therapy is thought to actively "switch off" helper cells erroneously misidentifying commensals as allergens. Clinically, LDA encompasses the antigens produced for food, environmental, and chemical allergens, and I still use those myself. I have also developed additional antigen formulations that are available to practitioners for the treatment of a range of diagnoses. Additionally, I have developed an approach to this therapy using "autologous" antigen samples derived from the patients themselves, to treat conditions that do not respond to any of the standardized mixtures.

In my experience, LDI can be roughly 90% successful when properly applied. If the patient remains engaged and is a good communicator, we have an excellent chance of dramatically recovering their health with no drugs, no side effects, and no toxicity. They typically will not need most of the other diverse therapies they have been doing to maintain some semblance of wellness. LDI has the potential to replace all of that treatment with a single, very safe therapeutic technique.

Autologous Therapy for Ulcerative Colitis

One of the major discoveries with this technique has been the use of autologous LDI for people with autoimmune-type phenomena who are reacting to microorganisms within their body's ecosystem. The beauty of the autologous LDI concept is that you do not have to identify the organism that is causing the reactivity. This is especially helpful for complex conditions such as inflammatory bowel disease, irritable bowel syndrome, SIBO, and in some cases, inflammatory arthritis.

When I began expanding the applications of LDI, I treated a patient with ulcerative colitis who was having more than a dozen bloody bowel movements a day and a great deal of abdominal pain – despite medical therapies, prescription drugs, and numerous alternative therapies from a clinic that specialized in this condition. In his case, we used a sample of his own stool, I diluted it out to a 6c dilution (one part per trillion), sterilized it through a millipore filter, and gave it to him as an antigen. This completely eliminated his symptoms. After the first dose, his symptoms stopped 100% within just a few days.

We gave him a few more doses on the two-month cycle, and he was asymptomatic for a year. That was a dramatic discovery for me. In his case, I did not have to identify the target antigen. I just had to have a good suspicion as to the source of that antigen and how to manipulate it using this technique.

Since then, I have found success using that concept with samples from the mouth and throat, the urinary tract, and the skin. In the case of a patient with chronic eye inflammation, I simply had him collect a sample of fluid from his eye, using a piece of wet gauze, and desensitized him with that fluid. I discovered this aspect of the technique more than six years ago and have worked with over one hundred patients, using autologous LDI as a broad concept technique. At this point, I am in a position to train other providers in the use of this approach, based on years of experience with a broad range of patients. We are now fine-tuning the technique to deliver these concepts to practitioners, so they will not have to go through the same process of discovery that I went through over the years.

New Paradigms in Lyme Disease Treatment

tickLyme disease is a good example of the expanded applications of LDI. Lyme patients are among the most complex people I treat. One person might have a great deal of prominent joint pain and peripheral nerve symptoms such as numbness and tingling in their feet. The next person may have headaches, brain fog, and night sweats. So, the condition is very protean, and it requires a great deal of time to carefully document the symptoms of each individual. The patient must observe their own specific symptoms with every dose of LDI and report back as to whether the symptoms improved, got worse, or stayed the same. This is a constant process of working through the different doses of antigen until you get a significant response, and then you must work with that, within the guidelines and time schedule inherent in this technique.

Many of the Lyme patients that I have helped in the last few years came to us after years of antibiotic therapies and various integrative modalities of treatment. At this point, many have spent their whole life savings, typically a hundred thousand dollars or more, trying to get well. Some have been overseas, traveling to as many as ten different countries in their efforts to heal. For many of those people, nothing ever really made a difference. In most cases, we have been able to put their symptoms into remission with very good success.

Perspectives on the Infectious Model of Lyme Disease

Having worked with LDI for several years, I have effectively treated more than one hundred patients with Lyme disease, located all over the world. In my experience, borrelia and the "coinfections" tend to trigger immune-mediated inflammatory disorders rather than true infections. A growing body of research also indicates that these organisms are common commensals. In the patients I am seeing, the Lyme disease process is much more like an allergy than an infection.

Consider acne as a comparable example. Although acne is treated as an infection, this is not actually an infectious process because everyone carries that same bacteria, Propionibacterium acnes. The defining difference between having acne or not does not rest on whether the bacteria are present – it rests upon whether or not one has an adverse immune response to those bacteria. The same scenario appears to be true with Lyme disease. If you test people with dark field microscopy, DNA-probe technology, or sensitive blood culture techniques, you will find that most completely healthy, asymptomatic people are walking around with multiple species of borrelia, bartonella, babesia, ehrlichia, and anaplasma. All these species of Lyme and the co-infections are present in totally healthy individuals.

I began to see things in this way as I became aware of the Lyme problem in my population of patients in Alaska, which is interesting, since Lyme disease is thought not to exist in Alaska. I was seeing people who had chronic inflammatory problems with no clear cause. I would treat them with antibiotics and some would get better, some would get worse, and some here and there would go into remission – typical response patterns. Then I tried treating with homeopathic remedies, and I got a certain amount of positive response once again, but still no significant progress for most patients. Based on the response to these therapies and the way the disease seemed to behave, it occurred to me that it was more like an allergy or an autoimmune disorder than an infection.

To test my theory, in the summer of 2014, I developed a mixture of bacteria that included eight species of borrelia, seven species of bartonella, and a single species of babesia. I began giving that mixture as an LDI solution, starting at the "6C" dilution, to all the patients I suspected might have Lyme disease. The first 40 cases nearly all responded to this quite significantly. Approximately half initially got worse and I had to make the dilution weaker, but many of them had complete resolution of their symptoms once their ideal dose was found. The results were quite dramatic, and the experience solidified for me the theory that Lyme disease is an immune activation syndrome. It clearly involves an immunological intolerance or an autoimmune reaction, as a few others have theorized before me.

Among these Lyme patients, I saw people who had been on antibiotics for years. In some cases, the antibiotics would control their symptoms for a while; but when the drug was stopped, some would immediately relapse. That is not how infection works. Even the worst true infections, such as endocarditis and osteomyelitis, tend to resolve completely with just six weeks of intravenous antibiotic therapy. Lyme patients will be given multiple antibiotics for many years on end with poor success and often serious negative effects. What I discovered by using LDI with Lyme disease patients confirmed my suspicion that the real issue is the immune response. Now that we have this tool, it is no longer necessary to treat Lyme with antibiotics after the initial month of antibiotics following a bug bite or onset of symptoms.

Over the past few years, I have modified my broad-spectrum Lyme mixture to include 74 total species in a formulation with borrelia, bartonella, babesia, and ehrlichia/coxiella. I have refined the therapeutic technique even more in order to segregate out antigens category by category, to isolate the most relevant of these four genera. Each set of antigens is isolated within its own genus, so I can identify which symptoms are corresponding to which category of antigen. That way I can give patients the different genera at different concentrations based on their symptom response patterns. It is very common for these complex patients to need a different dosage/dilution for one genus versus another. It has been educational and very encouraging to find that people with these constellations of horrible chronic symptoms can, in many cases, become completely asymptomatic without resorting to antibiotics or antimicrobial therapies. LDI therapy simply reestablishes immunological harmony and tolerance to organisms that have probably always lived within our bodies. It is possible that these bacterial organisms are a gift from our mothers at birth, if not beforehand.

Underlying Triggers in MS and RA

Most autoimmune conditions appear to have diverse triggers; but in some disorders, specific triggers are more prevalent. With multiple sclerosis, about 90% of the MS patients I see actually seem to have a more advanced neurological version of "Lyme disease." I say that because for most of these people, we can get their symptoms to go into complete remission using the LDI Lyme antigen mixture.

Early on, I had patients who had been diagnosed with multiple sclerosis; but because they had other Lyme-ish symptoms, I tried giving them the Lyme LDI mix, and all of their MS symptoms resolved. Some of the MS patients using the LDI antigens for years have had repeated MRI brain scans, and most of their brain lesions have gone away. There is a small population that does not seem to respond, so there must be more than one antigen causing these symptoms. With rheumatoid arthritis, 90% respond to the Proteus antigen; and for the rest, the trigger is something else. I have found success for most of those patients using an autologous oral LDI antigen.

Despite the extensive number of possible triggers, we hope to gain success by applying the concept of cross-reactivity. Within each formulation for borrelia, babesia or bartonella, I have more than 20 individual species. If a patient is reacting to a related species that is not in the mix, there is a good chance immunologically that it will cross-react with species that are present in the antigen formulation. Typically, we get some degree of beneficial response in any case. That has been demonstrated through decades of clinical experience using the LDA food and environmental mixtures, with additional antigens to elicit more cross-reactivity.

Reprogramming Immune Tolerance

In conventional medicine, the strategy for treating autoimmune disease is to disable the immune system using drugs. That is often effective in alleviating symptoms, but this is a double-edged sword. Yes, their autoimmune symptoms may be better, but now they risk having a life-threatening complication because their immune system is not functioning. There is drastically increased risk of fatal infection or cancer when using immunosuppressant drugs, similar to having AIDS; and some of these drugs even cause new autoimmune problems.

With LDI, we reprogram the immune response to promote immune tolerance. This concept is central to LDI. We are re-establishing immunological acceptance or tolerance of the antigen that is triggering the symptoms. The "antigen" can be a food, natural environmental antigen (e.g. mold, pollen, animal), chemical substance, bacterium, virus, fungi or protozoan. In recent years, I have also found that hormones, minerals, and essential nutrients may also act as antigens. The key, once we have identified the right antigen, is to find that magical dilution – the point at which the immune system stops attacking. Those are the keys to success with this approach.

In some cases, I do not possess a standardized sample of the right microbe for a given patient. In that instance, I can often treat them by taking an autologous sample from their own body. For my group of patients with rheumatoid arthritis who do not respond to the Proteus antigen, I found that treating with microbes from the oral cavity works very well. For many people with inflammatory bowel disease, using a sample of their own stool can be miraculous. Samples are diluted and sterilized through a millipore filter before use as autologous LDI. I have successfully treated patients with samples from the mouth, sinuses, bowel, vagina, skin, and conjunctiva.

Mediating Intricate Ecology in GI Disorders

The complexity of GI disorders is usually greater than that of conditions such as rheumatoid arthritis or multiple sclerosis. Crohn's disease, ulcerative colitis, and undifferentiated IBD are typically multifactorial. I have treated dozens of people with these disorders and usually they are not reacting to a single trigger. These are among the more challenging cases I treat, but LDI has a very high success rate nonetheless. Common antigens include the following:

  • Foods. I use the LDA food antigens.
  • Yeast. I have a mixture of yeast species including candida, bakers', and brewers' yeasts.
  • Mycobacteria. In the case of Crohn's disease and ulcerative colitis, there is a documented association involving Mycobacterium avium paratuberculosis. I have a mix that includes that antigen and two additional species of mycobacteria in a formulation that is often effective in IBD cases.
  • Parasites. I have a parasite mixture (all protozoans), which has been dramatically effective in some inflammatory bowel cases.

Autologous Stool: Another approach is to use autologous LDI. When we try the above antigen mixtures and still do not get complete resolution of symptoms, I have patients collect a stool sample and process that into an LDI antigen. The theory is that whatever is inflaming their gut is residing within their gut, so all I need is a sample of it and the right dilution and I can resolve their symptoms. Autologous LDI has been instrumental in resolving inflammatory bowel problems for a number of patients I have treated over the years.

Multiple Issues in Autism

Autism is another good example of a multifactorial immune-mediated condition. For many of these young patients, the condition is primarily caused by some type of immunological inflammatory process. The target organ for their inflammation is primarily the brain, and that can manifest in a wide range of symptoms including learning disabilities, communication problems, stimming behaviors, and other neurological manifestations. Working with colleagues who have larger autism patient populations, we have found that many LDI antigens may work for them. Antigens that are commonly relevant in the autism population include the following:

  • Borrelia, bartonella, babesia, mycoplasma;
  • Herpes simplex, streptococcus, clostridia;
  • Yeast and foods;
  • MMR and DTaP vaccines;
  • Chemical and environmental allergens.

With many chronic conditions, one difficulty lies in the fact that symptoms caused by different antigens can look very similar. This is very common in autism. To determine which antigens to use, the provider must ask a great many questions. Some of these patients have digestive problems. Some have symptoms such as rashes, fevers, or swollen lymph nodes, as well as psychological symptoms like OCD tendencies. To determine which antigens are going to fit, it is essential to develop a comprehensive list of specific symptoms. A great deal of clinical experience goes into making good decisions early on, and not every clinician has the patience and diligence to master this technique. An experienced practitioner can figure out difficult cases eventually if they are thorough and get communication from the family or the patient. Through experience, one gets better and better over time, able to get to the right answer quicker. I equate using LDI to playing a piano. When you first sit in front of a piano, you are more likely to make "noise" than music. With practice and experience, you will be able to make music for your patients using LDI.

Modified Allergy Protocol

Allergies have skyrocketed in the last few years, reflected in the number of children in the public school system who need to have an Epi-Pen and emergency measures in place. More and more people now have life-threatening allergies not only to peanuts and shellfish, but also to common foods such as corn, strawberries, or coconut. The low-dose antigen (LDA) mixes have been extremely successful in eliminating those allergy problems for people. I have modified the LDA protocol to a certain degree and gotten even better results in people with the most severe cases, finding that some people need to take the antigens in even more diluted form in order to achieve a good response. Those highly sensitive patients cannot tolerate the standard LDA concentrations without a severe flare of symptoms. I have also used certain foods in isolation such as corn, wheat, egg, or milk with people who have severe reactions to that particular substance. Again, one of the keys to success is achieving the right dilution.

Conclusion

Ultimately, one of my goals is that this therapy (and the underlying concepts) become standard of care for people with autoimmune disorders. This approach is safe, efficacious, inexpensive, and user-friendly. LDI can now be administered in the home using sublingual low-dose antigen formulations, and treatment is often successful for disabling conditions for which there are currently no other effective form of therapy. Although I can only treat a thousand people in my own practice, if I can train a thousand other physicians to do this, then we can treat a million people. There is strength in numbers, and great power in knowledge.

Infection, Commensals, and Tolerance

The concept of infection requires a particular interaction between an organism and the host. By definition, when a true infection is present, the organism has been found in a location within the body where it does not belong. The mere presence of the organism within that tissue site causes a predictable and reproducible immune-inflammatory reaction that is necessary to protect the host and eradicate the invasive organism. Common examples of routine infections include bladder infections with E. coli or pneumonia with Streptococcus pneumoniae. Both the E. coli and S. pneumoniae organisms are common in human beings; they live within the bowels and nasal/sinus passages respectively. They only become "infections" if they enter a body compartment where they do not belong (the bladder or the lungs in these scenarios). The other essential feature of a true infection is that it can be cured by a relatively short course of antimicrobial therapy.

Certain organisms are truly foreign and seem to have a more intense inherent virulence or immune reactivity when encountered by the human immune system. They do not reside normally anywhere in the body and are always attacked when they are encountered there. Examples include the Ebola virus, salmonella, and typhoid organisms. However, even those rules are not absolute because many organisms thought to be obligate pathogens have a certain asymptomatic carriage rate. Humans have been forced to co-evolve with microbes since there were first humans; and our tolerance for these organisms improves over time with persistent colonization or exposure. In part, that is related to the fact that highly "susceptible" or highly "reactive" (the difference is very blurry) individuals will all die off fairly quickly after the introduction of a new pathogen, leaving only more "tolerant" individuals behind. Examples of such microbial culling include the cholera pandemics of the past, measles, tuberculosis, influenza, and others. Different strains of influenza have certainly demonstrated highly variable rates of immune reactivity. This was evidenced by the pandemic of 1918 that killed millions of people and, also, by the way in which a typical strain of the virus killed a significant percentage of the Alaskan native people upon introduction to that immunologically naive population. It is not clear why certain pathogens are more immunogenic than others, just as it is not clear why certain foods such as peanuts and shellfish are more inherently allergenic than others. Why are those foods frequently lethal allergens, rather than rice or olives, for example, which are more common in the human diet?

The difference between "infection" and an immune-based chronic disorder targeting a specific microorganism is a critical paradigm shift. Consider the example of Streptococcus pyogenes, the bacterium that causes strep throat. S. pyogenes is commonly a true pathogen and an "infectious" bacterial species, meaning that it tends to cause a predictable inflammatory response in the vast majority of humans upon inoculation. Probably 90% of people will develop a fever, terrible sore throat, swollen tonsils, fatigue, and other symptoms within a few days of colonization. However, up to 10% of people will have none of those symptoms and will simply "carry" the organism with no reactivity. That is an example of variable individual "tolerance" for this particular microbe, and it means those tolerant carriers will spread the infection to others unknowingly. Another manifestation of differential tolerance for this organism is evidenced by the fact that strep is known to trigger at least four very different types of "autoimmune" reactions, including rheumatic fever, post-streptococcal glomerulonephritis (technically an immune-complex disease, but bear with me), guttate psoriasis, and PANDAS. These conditions affect very different systems in the body through a distant or systemic immune response that is somewhat unique to the individual, based on genetic susceptibility and the degree to which the immune system is dysfunctional.

Generally speaking, the human immune system has become increasingly dysfunctional due to accumulated environmental toxins within our species over time, and the resulting epigenetic changes that have ensued. Allergies and autoimmune diseases have skyrocketed in recent decades, and I believe this is a response to the environmental pollution we have inflicted upon ourselves and future generations. The result in terms of immune function is that the immune system has developed increasing difficulty in distinguishing "friend" from "enemy" and has begun to attack harmless substances such as foods, plant pollens, and commensal microbes with increasing regularity. The vast majority of autoimmune diseases can be shown to be initiated by an immune attack on some type of internal microorganism, part of our normal flora, which then cross-reacts with the host tissue in some manner due to a lack of appropriate discrimination. Another relevant term is "molecular mimicry" (things look more similar the worse your vision becomes). The fundamental problem is a loss of immune tolerance, which underlies all allergic and autoimmune response, and most chronic inflammatory conditions.

When someone with the high-risk HLA genotype for a disease becomes colonized with the relevant triggering microbe, and then some form of stressor agitates the immune system, an autoimmune disease can ensue. Most patients with rheumatoid arthritis, for example, are actually reacting to bacteria within the genus Proteus, cross-reacting with their joint tissues due to their HLA type. Every autoimmune disease seems to have those same components: molecular mimicry between a host tissue and microorganism, with the inflammatory response set off by some sort of immune-stimulating event. That event can be something like a true infection, a vaccine, physical trauma, intense psychological stress, or a drastic hormonal change (childbirth, for example, is an extremely common "catalytic event").

In my experience, chronic "Lyme disease" fits this model extremely well. Borrelia organisms and other bacteria thought to be "co-infections" appear to actually be commensal flora, not true pathogens. I say this because sensitive detection techniques such as blood cultures or PCR testing will demonstrate the presence of these organisms within the vast majority of completely healthy adults. That means they are not true pathogens, and the disease associated with them is not an "infection" in the true sense of the word. Consequently, we have to presume the virulence of the organisms themselves is not the issue, and the disease process rests entirely upon the host immune response. I believe this is why LDI has been so effective in treating chronic conditions due to borrelia, bartonella, babesia, candida, mycoplasma, and numerous other microbes. This is also the reason that taking antibiotics for years still fails to solve the problem for the great majority of those who are afflicted. The "infection model" of Lyme disease does not correlate with the growing evidence, and the "immune response" model at this point seems more relevant.

The keys to success with LDI for autoimmune and chronic inflammatory conditions are to properly identify the triggering organisms or agents and to find the ideal neutralizing dose for that antigen. If you can determine those two things, you can make 90% or more of these people well to a significant degree. At this point, I have hundreds of Lyme disease patients all around the world; many have responded dramatically to this therapy and no longer need any kind of antimicrobial treatment whatsoever. For me, that has been very eye-opening.

Source Article
Article Written by Ty Vincent, MD  June 1, 2017
Townsend Letter


© 2020 Light Your Sparkle, LTD
All Rights Reserved
website build | design: InCreation