Herxheimer reactions are an unavoidable and necessary result of Inflammation Therapy (IT).
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Chronically ill patients are carrying a heavy load of intracellular pathogens by the time they become symptomatic because the Th1/Th17 infection has been growing, unhindered, for most of a patient's life. The immune system response when these intracellular bacteria are recognized and killed causes a similar immune cascade.
Immunopathology
Immunopathology is a term, similar to Herxheimer, used by the scientific community. It describes all the collateral pathological effects on the body (e.g., hormonal, endocrine, cell death and blood count changes) caused by the immune system during normal function.
Intracellular bacteria
WirostkoIt’s normal for the body to generate an immune response when challenged by foreign matter such as microbes and allergens. Research has led to the hypothesis that this reaction in chronically ill patients is triggered by cell wall deficient, polymorphic L-form microbes. It is believed these intracellular bacteria have learned to live inside the macrophages (phagocytes) of the immune system. Apparently, they fail to be destroyed by the phagocytes which are supposed to kill them because they have adapted mechanisms to prevent being identified by the immune system.
When the intraphagocytic bacteria are killed by the immune system, the cells they lived in also die (apoptosis). As the immune system tries to clear up this cellular debris, it releases a host of inflammatory molecules which, along with the toxins released by the bacteria as they die, cause a rise in symptoms in the area in which the bacteria are being killed.
Identifying the bacteria
It’s difficult (and unnecessary) to determine which of the many species of intracellular mycoplasma might be responsible for individual Th1/Th17 inflammatory diseases. These bacteria are difficult to see even with an electron microscope, very slow growing and tedious to culture. This is only done in a research lab and makes it impractical to cross-match species to find the appropriate antibiotics.
Thus, the elicitation of a Herxheimer reaction is a key component of IT to determine, by therapeutic probe, which antibiotics are effective.
Identifying the Herxheimer reaction
Herxheimer symptoms are varied, may be unexpected, subjective or objective. Patients report that a Herxheimer reaction makes them feel as though their disease symptoms have suddenly gotten worse. They may describe reactivation of previous symptoms, exacerbation of current symptoms, or new symptoms. The onset of herxing is from 1-2 hrs to 10 days after the antibiotic/s are administered. Patients who have received other therapies prior to starting IT may have delayed or reduced Herxheimer reactions.
The intensity of the reaction is thought to be dependent on many factors; location of the inflammation, appropriateness of the antibiotic/s, the antibiotic dosage, the presence of immunosuppressants, the level of 25 hydroxyvitamin-D and the prophylactic dosing schedule of Benicar used to interrupt the inflammatory cascade.
Herxheimer symptoms usually wax and wane with antibiotic administration but dramatic waxing and waning of symptoms doesn’t always happen. An increase in symptoms may be constant for varying intervals. Patients with effective detoxification and elimination systems may not experience significant aggravation of symptoms.
Herxheimer symptoms usually wax and wane with antibiotic administration but dramatic waxing and waning of symptoms doesn’t always happen. An increase in symptoms may be constant for varying intervals. Patients with effective detoxification and elimination systems may not experience significant aggravation of symptoms.
Most, if not all, symptoms experienced while on IT are due to Th1/Th17 inflammation, although patients are still susceptible to acute infections (e.g., bacterial, viral, etc.). Patients may correctly attribute any or all symptoms as being due to immunopathology and not a progression of the disease.
Since chronically ill patients are believed to have acquired many different species of intracellular bacteria over a long period of time, the effectiveness of a different antibiotic combination probe with a positive Herxheimer reaction demonstrates the presence of another species, or of bacteria previously hidden within tissues poorly perfused by the antibiotics.
Patients will continue to experience Herxheimer reactions as long as effective antibiotic therapy continues. Trial and error with carefully selected antibiotic combinations provokes a resumption of herxing when symptoms have subsided.
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New symptoms
IT doesn’t create new inflammation because it can't make bacteria appear where there weren't any bacteria before. When patients experience new symptoms they haven't had before, it's probably because the therapy is exposing more bacteria.
Without therapy, these hidden bacteria would not remain hidden for ever. Eventually they would multiply to the point where they reveal themselves in new symptoms. If patients stop therapy prematurely, not only will the 'new' symptoms remain and worsen, but also further new symptoms will gradually develop, just as they would have done if the patient had never started IT.
Most symptoms have been reported by other patients on IT. The exact molecular mechanism for them is obscure and a topic best left to the scientists. The simple explanation is that Th1/Th17 inflammation during the disease process and during Herxheimer reactions affects a wide variety of biochemical processes.
The disease process causes symptoms and patients with chronic inflammatory diseases are systemically ill. Likely, no part of the body has escaped some damage even if it isn’t readily apparent.
Wanting to know specifically why certain symptoms occur is micromanaging the process and unnecessary. It’s best not to try to fit every symptom into a category (herx, hormone readjustment, old symptom revisited, etc.). If patients are patient with the therapeutic process and have confidence it will work, they will eventually forget they ever had these symptoms.
Herxheimer symptoms versus disease progression
Most disease symptoms progress slowly. Herxheimer symptoms usually flare quickly. If the underlying cause of chronic illness, intracellular bacteria, is being eliminated it is unlikely the disease process is progressing.
’Side effects’
Herxheimer symptoms are not a 'side effect' of IT medications. Herxheimer symptoms are caused by the disease process, not directly by Benicar or the antibiotics.
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Managing expected Herxheimer reactions
Herxheimer reactions are an unavoidable part of the long journey to recovery. Although herxing is often unpredictable, it can be managed with the correct use of Benicar, the judicious choice of antibiotic combinations, careful antibiotic dosing schedules, adjustment of antibiotic dosing and palliative medications. IT does not require eliciting a more severe herxing than a patient can tolerate in order to eliminate the bacteria.
As the number of dying bacteria is reduced with subsequent antibiotic doses, effective treatment requires increasing doses and changing antibiotic combinations to continue eliciting a Herxheimer response. The occurrence of herxing is seen as evidence of continuing elimination of these very persistent bacteria. Details of Herxheimer symptom management are in our Library of Information.
How to reduce disability caused by Herxheimer reactions
Patients can help lessen the disability experienced during Inflammation Therapy if they:
Minimize exposure to other sources of toxins, including airborne chemicals and pollutants, food containing additives or other chemicals, unnecessary medications, poor water etc.
Maximize the quality of food, water and air.
Avoid unnecessary stress.
Rest during the day, especially if experiencing sleep problems at night.
Keep a perspective that symptoms, though unpleasant, are rarely life threatening and will diminish with time.
Remember that intracellular bacteria can influence thinking (psychological symptoms) and may encourage counterproductive activities.
Therapeutic efficacy
The patient is expected to experience episodic Herxheimer reactions as long as antibiotic therapy is needed. The gradual resolution of symptoms has been noted to require months or years depending on the extent of Th1/Th17 inflammation. The Herxheimer reaction is a key component in evaluating the efficacy of each IT antibiotic, antibiotic combination or dosing schedule. The lack of a Herxheimer reaction when disease symptoms are still present signals a need for a change in dosing schedule or antibiotic.
Remission is determined by absence of symptoms, both objective and subjective.
