Low-Dose Immunotherapy (LDI), Part 1 is online.
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Low-dose immunotherapy is relevant to virtually any condition that has an immunological, inflammatory basis. This encompasses an extremely broad range of chronic illness, including the following:
- Autism spectrum disorders;
- Chronic fatigue syndrome and fibromyalgia syndrome;
- Crohn's disease, IBS, parasitic inflammation, SIBO, ulcerative colitis, yeast sensitivity;
- Food allergies and sensitivities;
- Lyme disease and other coinfections, including those triggered by Babesia, Bartonella, Ehrlichia, and Mycoplasma;
- Multiple sclerosis;
- Reactions caused by Clostridia and Streptococcus, as well as those due to the Epstein-Barr virus and herpes simplex;
- Responses to environmental allergens including animal dander, chemicals, molds, and pollen;
- Rheumatoid arthritis and other inflammatory arthritic conditions; and
- Skin disorders of all types including acne, dandruff, discoid lupus, eczema, hidradenitis, psoriasis, pyoderma gangrenosum, rosacea, tinea, and all manner of unexplained dermatitis conditions.
This therapy, initially termed EPD (enzyme-potentiated desensitization), was developed by a British allergist, Leonard McEwen, MD, in the 1960s. Here in the US, that treatment (known as LDA) was modified by W.A. Shrader, MD, who conducted extensive clinical trials to gain permission from the FDA for American use. I apply essentially the same treatment protocol and the same concepts and have discovered new antigens to use in the same manner. Modifying the protocol, we get better responses, more quickly, that are sustained longer. To date, I have been able to successfully address over 40 autoimmune or inflammatory conditions with this technique. Additionally, the use of autologous antigens has yielded encouraging success in the treatment of persistent disorders of the skin, joints, nervous system, conjunctiva, sinuses, mouth, GI tract, bladder, and vagina. Prior to this therapy, there was no effective intervention for some of these conditions. (For more information on clinical outcomes achieved with this treatment, see part 1 of this article, "Low-Dose Immunotherapy," Townsend Letter, June 2017.)
In clinical practice, I spend at least an hour with every new patient, with three primary goals in mind. The first is to determine whether or not there is an immunological basis for their symptoms. If there is, I must identify the underlying target antigen(s) that is triggering the excessive immune activity. Frequently there is more than one trigger, so I develop a list of possible suspects and decide which antigen to prescribe first, using a diagnostic process of elimination. The third question is the starting dosage or dilution to use for that specific individual. Ultimately these are the primary considerations on the initial visit: Is this an immunological issue? If so, which antigen should be given first—and at what dosage? This becomes an iterative process to determine additional antigenic target(s) and the proper dosage of each antigen to neutralize that immune response.
The process involves giving a diluted sublingual dosage of one particular antigen (or a mixture of related antigens such as Borrelia and the coinfections) and then tracking the response to that antigen or antigenic mix. The patient needs to pay attention to the particular symptoms that occur in response to each dose and report back to me as to whether their symptoms got better, worse, or stayed the same. This means working through different dosages of that antigen or antigen mixture until the patient has a significant improvement, and then working with that dilution within the rules and the time schedule inherent in this technique. The experience of the practitioner helps to sort through the variables more efficiently.
Differentiation of LDI from Conventional Allergy Treatment
For decades, conventional allergists have treated hay fever and other allergy conditions using dilutions of the very antigen to which the patient is reacting. However, the dilution range used is stronger than LDI, relatively speaking, and initially must be given by injection twice a week. Conventional dilutions typically range from one part per million to as high as one in ten.
In the approach I take to LDI, the antigen is almost always administered sublingually. Microbial samples are procured from a sample warehouse and include bacteria, fungi, viruses, and parasites that have been inactivated via electron beam irradiation to assure that there is no possibility of infection. To treat acne, for example, I often employ an inert sample of Propionibacterium acnes, along with a collection of other skin bacteria, all diluted to a strength of approximately one trillion to one (6C), a typical dosage in LDI. When we give acne patients the right dilution of the appropriate bacterial mixture, their acne will resolve quickly and dramatically, often within a week.
With LDI, I am now able to prescribe 99% of the doses sublingually and that works as effectively as injections. In my practice, 95% of the people I see respond to sublingual doses just as they would if the antigen were injected. Perhaps 4% need a stronger sublingual dosage in order to benefit. Then there are a rare handful of individuals who do not seem to get a response unless we inject the antigen. Of the more than 1,000 people we have treated using these various techniques, only 1% still receive LDI by injection.
Effective sublingual administration was first reported by Gus Kotsanis, MD, a physician with a large clinic in Texas who sees children with autism spectrum diagnoses. It is well known that autistic kids are commonly afflicted by food and environmental allergies. He found, as many of us have, that those in the autism community benefit greatly from the LDA technique. When he experimented with sublingual antigens to achieve a better rate of compliance, he found that the degree of effectiveness was virtually the same.
Regarding autism and Lyme disease, we have discovered that for a large percentage of the autism population, the Lyme bacterium is one of the target antigens causing their inflammatory responses. The broad-spectrum Lyme/coinfection mixture that I have developed contains 74 total species in a formulation that includes Borrelia, Bartonella, Babesia, Ehrlichia, and Coxiella. This mixture of antigens has worked miraculously for some of the children and adults on the autism spectrum and also for those with symptoms of Lyme disease or coinfections.
Selecting the Initial Treatment Antigen
The choice of the first antigens to test with a given patient should be based primarily on an extensive history. I look for patterns in the symptoms they exhibit and clues in the circumstances surrounding the onset of their chronic problems. Often the most important information is how the patient responded to prior treatments, particularly if any form of antimicrobial therapy was used. The more clinical experience and better understanding of pathophysiology the practitioner has, the better they will be at sorting through the possibilities.
Some clinicians in the integrative medicine community use muscle testing, autonomic response testing, or bio-energetic devices. Although those techniques seem to have a certain degree of success in determining the right antigen, they are only marginally better than good clinical assessment, and they are not very successful at determining the right dosage or dilution for antigens. For instance, the difference between the Epstein-Barr virus and Candida yeast is significant, so that technique is fairly effective at differentiating between those two agents. However, if the antigen is Candida, for example, those technologies are not as useful in determining the difference between two dilutions, for example an 18C and a 21C dosage. The technology is unable to identify the dosage that will be most appropriate for a given patient.
Across clinical medicine, a variety of immunotherapy techniques are employed to desensitize patients to various antigens. In LDI and LDA, the strongest concentrations we typically use range from one part per hundred million to one part per trillion, depending on the antigen. Some antigens, such as yeast or Lyme organisms, may require far weaker dilutions, as far out as ten to the 80th. Once the right dosage is found, it need only be taken once every seven weeks. Conventional immunotherapy, in contrast, uses injections that are usually one part per ten thousand or stronger, given twice a week. Provocation/neutralization, a desensitization technique commonly applied in environmental medicine, might use dilutions as strong as 1:125, and the dosage can be taken every day if needed to neutralize symptoms as soon as they return.
At a dilution of approximately one part per million, a change seems to occur in which the interaction between patient and antigen shifts from being purely molecular to more of an energetic phenomenon. Even at stronger concentrations of an LDI antigen such as 10-10 or 10-12, the effect is likely a harmonic interaction rather than a molecular interaction. The belief is that we continue to lose molecules as the antigen mixture becomes more dilute until we reach 10-24. If you dilute a substance 10-24 or further, you theoretically have eliminated all the molecules from that dilution. These solutions are described as dilutions beyond Avogadro's number, because the antigen is no longer detectable by scanning electron microscopy. (Avogadro's number refers to the number of atoms in one molecule of any given substance.) What is still functioning in the dilution is thought to be the harmonic signature or the vibrational frequency of that substance. When an antigen is diluted out to 10-24 (12C) or beyond, theoretically that is energy medicine, which is the basis not only of LDI, but also of constitutional homeopathic prescribing.
Using dilutions in the homeopathic range of the harmonic spectrum, such as a trillion to one or further, there seems to be a longer lasting effect on the immune response. For these doses, we must follow a different set of rules, and, as described, we find that we must delay the administration of the next dose by seven weeks or longer. Due to that essential seven-week window, the theory is that we are causing a tolerance reaction mediated by regulatory T lymphocytes. These particular lymphocytes are thought to live approximately 50 to 60 days, and a new dosage provides the educational signal to sustain that response. That is the working hypothesis behind LDA and LDI.
Contrasting LDI dosages with homeopathic remedies, note that dilutions in LDI are described literally. The higher the number of an LDI dilution (30C vs 6C), the more diluted the antigen, and the "weaker" the dose. In contrast, with homeopathic treatment, the more diluted remedies are referred to as "stronger" dosages. A homeopathic remedy of 30C is considered stronger than one of 6C, despite the fact that the 30C is much more diluted. In LDI terminology, the 6C dosage is much "stronger" than 30C, by a dilution difference of 48 zeros.
Timeline and Titration
Once an antigen dose is taken by the patient, one of three types of responses will occur:
- If it is too weak, that dilution will do nothing and they will have no change in their symptoms. At that point, they can take the next stronger dosage at least ten days later.
- If the dosage is on target, their symptoms will improve for some length of time. The same beneficial dose may be repeated, but one must wait at least seven weeks to reset the immune response. The immune system appears to have some form of memory function that is responsible for the necessity of waiting seven weeks. Only weaker "booster" doses may be taken within that seven-week period.
The titration process may initially require a series of doses every ten days to learn where your patient responds. How many doses it takes depends on how far off the starting dose was. The ideal dosage for the patient cannot be known in advance. Consequently, it can take months of dose titration or even a year until you determine the optimal effective dose. It is also possible to start in the middle of the range of dilutions or at a strong "diagnostic" dose. These are all style points that should be thoroughly discussed with the patient.
- The dose may be too strong and cause a "flare" or worsening of their symptoms (whatever symptoms tend to be chronically associated with that antigen). The good news associated with a flare is that you have found the correct antigen for their treatment. In that event, they must wait at least seven weeks as a washout period, and back off to a weaker dose for the next cycle. How far to back off correlates fairly well with how long the flare lasts. The rule of thumb is that the appropriate dosage is diluted roughly 1C for every week that the flare persists. (Most dose titration proceeds by increments of 100:1 denoted by the letter C (100 in Roman numerals). Dilutions are often prepared in 1C increments (for example 30C, 31C, etc.). A flare that lasts three weeks, caused by an antigen of 30C strength, is therefore replaced by one diluted of 33C, taken after a full seven weeks from the initial dose.
A flare can also result if the patient inadvertently takes the proper dose of antigen before the seven-week washout has transpired. Consider the example of desensitizing someone to a milk allergy or to peanuts. If you find the right dilution of that specific antigen and give it every seven weeks, the person will find that they can eat dairy products or peanuts with no reaction. However, if you give them that food dilution at six weeks instead of waiting the full seven weeks, when they try to consume dairy products or peanuts again, they may have a temporary reaction that is worse than those they had before they initiated treatment. That is also true with all the autoimmune and chronic inflammatory disorders that we have treated, including Crohn's disease, Lyme disease, and multiple sclerosis. When someone flares because they have taken a dose prematurely, you do not need to modify the dose; they just have to wait the full seven weeks before taking the next dosage.
The seven-week washout period required between doses to "reset" the immune system was initially worked out by Leonard McEwen, MD, more than 50 years ago. In 2015, I began experimenting with that timeline. Through clinical research, I found that it is not necessary to wait seven weeks between doses if you are going progressively stronger in an attempt to find an effective dose (i.e. 30C, 29C, 28C, etc.). Additionally, it is not necessary to wait seven weeks if you are giving a significantly weaker dose after improvement, once the previous dose has worn off. I call the first situation "dose titration" and the second situation, "booster dosing."
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