A place for Lyme Treatment www.envita.com
Apr 28, 2014
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If you've been diagnosed with fibromyalgia, you know better than anyone the pain, frustration and anxiety associated with this difficult to define disease. Ask anyone what the worst part about fibromyalgia (FMS) is and they might list the numbness, pain, difficulty sleeping, irritable bowel syndrome and the persistent depression – or they might say the worst part is simply not knowing the cause.
Some experts believe FMS is related to "illness," trauma or just plain stress. Others link the condition to hormonal disturbances and chemical imbalances affecting the nervous system. Still other researchers blame genetic ties or claim there is no explanation at all. But what if there was an option D, "all of the above?" Clinical experience and in-depth testing have begun to point to Lyme disease complex, coinfections and weakened immunity, which could answer that question.
Some experts believe FMS is related to "illness," trauma or just plain stress. Others link the condition to hormonal disturbances and chemical imbalances affecting the nervous system. Still other researchers blame genetic ties or claim there is no explanation at all. But what if there was an option D, "all of the above?" Clinical experience and in-depth testing have begun to point to Lyme disease complex, coinfections and weakened immunity, which could answer that question.
Lyme Disease and Fibromyalgia - The Surprising Connection
What is Lyme Disease?
Lyme disease is most famously transferred through insect bites, particularly ticks. As a cousin to syphilis, it may spread from a mother to her fetus or through sexual contact, but this connection has not yet been proven.
Lyme is characterized by a spirochete infection called Borrelia, which is a tube-like bacterium that works by releasing bacterial lipoproteins (BLPs). These BLPs are a type of neurotoxin that lead to memory problems; hormonal imbalances; burning neurological pain; generalized inflammation; gastrointestinal discomfort and numbness; not to mention symptoms like swollen lymph nodes; fever and chills; headache and stiff neck; muscle and joint paint; and the most common symptom, lack of energy.
A spirochete is covered in antigens, which act like fingerprints, identifying itself to the immune system. When your Killer T Cells find these antigens, they know to destroy the invading bacteria. However, when the borrelia spirochete burrows into the body, its antigens are smeared over healthy tissue, which the killer T cells attack because they cannot differentiate between healthy and unhealthy tissue. When this happens, it's called an "autoimmune disease." This is one explanation that may describe why borrelia and its coinfections can be commonly found in autoimmune and rheumatic disease patients.
The more the spirochete moves through the body, the more BLPs it releases, impairing the immune system, creating inflammations, irritations and wreaking havoc to the peripheral and central nervous systems and the entire neural endocrine system. As a result, Lyme disease and its coinfections can be associated with more than 300 other diseases, including chronic fatigue syndrome and numerous autoimmune diseases.
Lyme is characterized by a spirochete infection called Borrelia, which is a tube-like bacterium that works by releasing bacterial lipoproteins (BLPs). These BLPs are a type of neurotoxin that lead to memory problems; hormonal imbalances; burning neurological pain; generalized inflammation; gastrointestinal discomfort and numbness; not to mention symptoms like swollen lymph nodes; fever and chills; headache and stiff neck; muscle and joint paint; and the most common symptom, lack of energy.
A spirochete is covered in antigens, which act like fingerprints, identifying itself to the immune system. When your Killer T Cells find these antigens, they know to destroy the invading bacteria. However, when the borrelia spirochete burrows into the body, its antigens are smeared over healthy tissue, which the killer T cells attack because they cannot differentiate between healthy and unhealthy tissue. When this happens, it's called an "autoimmune disease." This is one explanation that may describe why borrelia and its coinfections can be commonly found in autoimmune and rheumatic disease patients.
The more the spirochete moves through the body, the more BLPs it releases, impairing the immune system, creating inflammations, irritations and wreaking havoc to the peripheral and central nervous systems and the entire neural endocrine system. As a result, Lyme disease and its coinfections can be associated with more than 300 other diseases, including chronic fatigue syndrome and numerous autoimmune diseases.
Linking Fibromyalgia and Lyme Disease Complex
As you can see, early stages of Lyme disease complex can be very difficult to diagnose, even with a blood test. In addition to physical examination results, most doctors will rely on environmental factors such as exposure to ticks and medical history (according to Medscape, only 25-30% of patients recall a tick bite.) But let's go back to fibromyalgia. Some of these symptoms certainly overlap, especially muscle pain and fatigue, but is there a link?
According to one author on Fibromyalgia.com, "…long-term joint problems can be activated and this can lead to a central sensitization syndrome (the central pain amplifier being turned up) … I still can't give you a positive "yes" or "no" but I suspect there is a potential for a link."
Also, consider the connection between Chronic Fatigue Syndrome (CFS) and FMS through the Hypothalamic-pituitary-adrenal axis. Don't let that long string of words confuse you – the HPA is merely a communication network of direct influences and feedback interactions between the hypothalamus, the pituitary gland and the adrenal gland. Think of it as an Internet connection in your brain that controls the master hormones of the body. In many cases, abnormal levels of certain chemicals that are regulated by the HPA axis have been proposed as a potential cause of CFS.
The way this relates to Lyme disease complex is quite interesting. Patients can contract an infection at any point in their lifetime, but the symptoms can very well lay dormant until the individual is weakened (immune compromised), usually by a traumatic experience such as a major injury, giving birth, receiving a vaccine or even extreme emotional trauma such as divorce or death. Such trauma will undoubtedly affect the HPA axis, however, how much will vary depending on the patient.
The HPA axis is where experts have argued there is a genetic link to FMS. However, with infections, it may be less genetic and more epigenetic, which means an outside influence changes gene expression, which is typically seen in cancerous cells.
Let's bring it all back – Chronic Lyme disease complex can affect the Hypothalamic-pituitary-adrenal axis in two ways: via neurotoxins and epigenetic shifts. So if imbalances in the HPA axis can lead to Chronic Fatigue Syndrome, depression, insomnia and generalized pain, all of which is related to fibromyalgia, then it seems there is a strong link from Lyme disease complex and its coinfections to FMS.
According to one author on Fibromyalgia.com, "…long-term joint problems can be activated and this can lead to a central sensitization syndrome (the central pain amplifier being turned up) … I still can't give you a positive "yes" or "no" but I suspect there is a potential for a link."
Also, consider the connection between Chronic Fatigue Syndrome (CFS) and FMS through the Hypothalamic-pituitary-adrenal axis. Don't let that long string of words confuse you – the HPA is merely a communication network of direct influences and feedback interactions between the hypothalamus, the pituitary gland and the adrenal gland. Think of it as an Internet connection in your brain that controls the master hormones of the body. In many cases, abnormal levels of certain chemicals that are regulated by the HPA axis have been proposed as a potential cause of CFS.
The way this relates to Lyme disease complex is quite interesting. Patients can contract an infection at any point in their lifetime, but the symptoms can very well lay dormant until the individual is weakened (immune compromised), usually by a traumatic experience such as a major injury, giving birth, receiving a vaccine or even extreme emotional trauma such as divorce or death. Such trauma will undoubtedly affect the HPA axis, however, how much will vary depending on the patient.
The HPA axis is where experts have argued there is a genetic link to FMS. However, with infections, it may be less genetic and more epigenetic, which means an outside influence changes gene expression, which is typically seen in cancerous cells.
Let's bring it all back – Chronic Lyme disease complex can affect the Hypothalamic-pituitary-adrenal axis in two ways: via neurotoxins and epigenetic shifts. So if imbalances in the HPA axis can lead to Chronic Fatigue Syndrome, depression, insomnia and generalized pain, all of which is related to fibromyalgia, then it seems there is a strong link from Lyme disease complex and its coinfections to FMS.
Finding the Proper Treatment
You may find that treating Lyme disease complex is not easy at all. If it's caught early, antibiotics may nip the problem in the bud. However, this is rarely the case, if Lyme disease is detected at all. Second, the oral antibiotics are usually administrated in a 4-to-6 week period, meaning once that treatment ends, the borrelia will make a comeback, causing the patient to relapse. Furthermore, the antibiotics do not strengthen the immune system and do little to address the coinfections, the secondary infections, the BLP neurotoxins or strip away the protective biofilm, which is a sludge produced by the bacteria to protect itself from antibiotics.
Sometimes patients will include supplements with their antibiotics. In this scenario, the infection will be brought down a little and the supplements will slightly increase the immune system. But again, if the immune system is completely established and all the infections are brought down to lower levels, relapse will occur.
The Lyme disease complex involves a multitude of infections that may also include other complications such as chemical and heavy metal toxicities. If you really want to nuke Lyme disease and its coinfections, it's ideal to have a combination of advanced immunotherapy, aggressive natural antiviral, antifungal, IV antibiotics and biodetoxification. When this is provided by the properly trained integrative physician in a customized treatment plan, these therapies will help bring the patient back to optimal health.
The final step is utilizing the biodetoxification process in order to rid the body of the neurotoxins and the BLPs. Ultimately the neurotoxins are competing with every nerve and hormone receptor within the patient's body. Follow-up care may involve hormone balancing, neurotransmitter and immune system support.
If you or anyone you know is suffering from fibromyalgia, chronic fatigue, autoimmune disease or Lyme disease, please pass this article on.
- See more at: http://www.envita.com/lyme-disease/the-surprising-link-between-fibromyalgia-and-lyme-disease#sthash.K1kvWNjm.dpufSometimes patients will include supplements with their antibiotics. In this scenario, the infection will be brought down a little and the supplements will slightly increase the immune system. But again, if the immune system is completely established and all the infections are brought down to lower levels, relapse will occur.
The Lyme disease complex involves a multitude of infections that may also include other complications such as chemical and heavy metal toxicities. If you really want to nuke Lyme disease and its coinfections, it's ideal to have a combination of advanced immunotherapy, aggressive natural antiviral, antifungal, IV antibiotics and biodetoxification. When this is provided by the properly trained integrative physician in a customized treatment plan, these therapies will help bring the patient back to optimal health.
The final step is utilizing the biodetoxification process in order to rid the body of the neurotoxins and the BLPs. Ultimately the neurotoxins are competing with every nerve and hormone receptor within the patient's body. Follow-up care may involve hormone balancing, neurotransmitter and immune system support.
If you or anyone you know is suffering from fibromyalgia, chronic fatigue, autoimmune disease or Lyme disease, please pass this article on.
Neurotoxic Disorders: Lyme, Coinfections, Molds, and Petrochemicals
Apr 25, 2014
Wayne C. Anderson, ND:Neurotoxic Disorders: Reactivity to Lyme, Coinfections, Molds, and Petrochemicals
interview by Nancy Faass
interview by Nancy Faass
Introduction
We originally thought of Lyme disease as primarily an infection caused by the spirochete Borrelia burgdorferi. In the decades that followed, researchers began identifyingother tick-borne bacteria and toxins that frequently accompany Lyme infections. We have come to realize that the symptoms which we once described as "Lyme disease" frequently involve other bacteria, such as Babesia, Bartonella, Ehrlichia, or Mycoplasma, or rarer species such as the Rickettsia group or tularemia. Transmitted in the digestive tract of ticks or fleas, these pathogens may be carried by cats, rats, mice, deer, and other animals, depending on the microbe. These pathogenic bacteria are among the smallest known life-forms on earth. Unlike most bacteria, they are harbored within the cell as a virus would be or within the interstices between the cells, making it difficult for the immune system to dislodge them.
Certain types of toxigenic mold can also be a major factor in neurotoxic conditions. Petrol-based pesticides, insecticides, and solvents are a third major contributor to neurotoxic inflammation. The extensive neurotoxic effects of pesticides, for example, have been well documented. Heavy metals are sludge toxins with some of the same neurotoxic effects as petrol-based chemicals. Mercury, lead, cadmium, and arsenic involve similar neurotoxic mechanisms of action and can cause similar symptoms.
Microbes and toxins stored in fat tissue: Lyme, molds, and petrol-based chemicals all contain lipid molecules. The lipid molecules in the structure of the pathogens and toxins are attracted to the fat in our bodies (lipophilic) and can become embedded in that fat tissue and persist.
Neurological inflammation: These neurotoxins are particularly attracted to the lipids in the myelin sheath, which surrounds all the nerves in the body. Once they are absorbed into the myelin sheath, although they do not destroy it, they accumulate and can serve as chronic irritants to the underlying nerve. Similarly, the brain contains high fat content – 50% fat and 50% nerve. When these toxins are absorbed into fatty tissue of the brain, they can irritate nerve cells within the brain and impair brain function.
We originally thought of Lyme disease as primarily an infection caused by the spirochete Borrelia burgdorferi. In the decades that followed, researchers began identifyingother tick-borne bacteria and toxins that frequently accompany Lyme infections. We have come to realize that the symptoms which we once described as "Lyme disease" frequently involve other bacteria, such as Babesia, Bartonella, Ehrlichia, or Mycoplasma, or rarer species such as the Rickettsia group or tularemia. Transmitted in the digestive tract of ticks or fleas, these pathogens may be carried by cats, rats, mice, deer, and other animals, depending on the microbe. These pathogenic bacteria are among the smallest known life-forms on earth. Unlike most bacteria, they are harbored within the cell as a virus would be or within the interstices between the cells, making it difficult for the immune system to dislodge them.
Certain types of toxigenic mold can also be a major factor in neurotoxic conditions. Petrol-based pesticides, insecticides, and solvents are a third major contributor to neurotoxic inflammation. The extensive neurotoxic effects of pesticides, for example, have been well documented. Heavy metals are sludge toxins with some of the same neurotoxic effects as petrol-based chemicals. Mercury, lead, cadmium, and arsenic involve similar neurotoxic mechanisms of action and can cause similar symptoms.
Microbes and toxins stored in fat tissue: Lyme, molds, and petrol-based chemicals all contain lipid molecules. The lipid molecules in the structure of the pathogens and toxins are attracted to the fat in our bodies (lipophilic) and can become embedded in that fat tissue and persist.
Neurological inflammation: These neurotoxins are particularly attracted to the lipids in the myelin sheath, which surrounds all the nerves in the body. Once they are absorbed into the myelin sheath, although they do not destroy it, they accumulate and can serve as chronic irritants to the underlying nerve. Similarly, the brain contains high fat content – 50% fat and 50% nerve. When these toxins are absorbed into fatty tissue of the brain, they can irritate nerve cells within the brain and impair brain function.
Intracellular Bacteria and Toxins
Many of these intracellular pathogens proliferate very slowly, over months, years, or even decades. They gain access to the body's cells through a simple process and can remain for years.
Step 1. Toxic build-up: Following exposure, the toxin is absorbed through the cell membrane and penetrates the cell. Our own cell membranes consist of two layers of fat (bilipid), which normally provide very effective gatekeeper functions, allowing into the cell what should be allowed as a nutrient and repelling what should be rejected as a toxin. However, because the pathogens also contain lipid molecules, they confuse the gatekeeper mechanism of cell membranes, penetrating the cell wall, and essentially hijacking the cell.
Step 2. Immune reactions: The immune system is activated and tries to destroy or remove the toxins harbored within the cell, but frequently cannot do so. When the system cannot break up or destroy these microbes, inflammation results. As these efforts by the immune system become more and more intense, activity shifts from cellular immunity to antibody production. This frantic immune activity is often associated with the symptoms of autoimmune conditions.
Step 3. Attempts at detoxification: Neurotoxins are typically detoxified through the methylation pathway. This pathway involves numerous genetic strands that all coordinate to remove waste from within the cell, through the cell membrane, to move toxins back into the bloodstream.
If toxins build up within the cell, the cell's function is diminished. These irritants can dysregulate the mitochondria, lowering energy production by the cell. No matter where the cell is located in the body, there will be reduced function or even lack of function. If the toxic cells are stored in muscle tissue, that may be experienced as weakness, pain, or an array of symptoms resembling fibromyalgia. If the toxins have accumulated within the brain, that will create symptoms related to functional neurological deficits such as impaired memory, cognitive processing, and brain fog, as well as mood instability resulting in depression or anxiety.
Initially these toxins do not damage the cells: they primarily compromise the function of cells. The function of entire systems may also be compromised, particularly systems that maintain homeostasis – the brain and nervous system, as well as the immune and endocrine systems and the gut. Ultimately, the neurotoxic disorders also result in inflammation. However, before inflammation is apparent, there will be a compromise in function. Clinically, we often note this in retrospect, because many patients are able to compensate for the lack of function for a time, without any evidence of inflammation.
Many of these intracellular pathogens proliferate very slowly, over months, years, or even decades. They gain access to the body's cells through a simple process and can remain for years.
Step 1. Toxic build-up: Following exposure, the toxin is absorbed through the cell membrane and penetrates the cell. Our own cell membranes consist of two layers of fat (bilipid), which normally provide very effective gatekeeper functions, allowing into the cell what should be allowed as a nutrient and repelling what should be rejected as a toxin. However, because the pathogens also contain lipid molecules, they confuse the gatekeeper mechanism of cell membranes, penetrating the cell wall, and essentially hijacking the cell.
Step 2. Immune reactions: The immune system is activated and tries to destroy or remove the toxins harbored within the cell, but frequently cannot do so. When the system cannot break up or destroy these microbes, inflammation results. As these efforts by the immune system become more and more intense, activity shifts from cellular immunity to antibody production. This frantic immune activity is often associated with the symptoms of autoimmune conditions.
Step 3. Attempts at detoxification: Neurotoxins are typically detoxified through the methylation pathway. This pathway involves numerous genetic strands that all coordinate to remove waste from within the cell, through the cell membrane, to move toxins back into the bloodstream.
If toxins build up within the cell, the cell's function is diminished. These irritants can dysregulate the mitochondria, lowering energy production by the cell. No matter where the cell is located in the body, there will be reduced function or even lack of function. If the toxic cells are stored in muscle tissue, that may be experienced as weakness, pain, or an array of symptoms resembling fibromyalgia. If the toxins have accumulated within the brain, that will create symptoms related to functional neurological deficits such as impaired memory, cognitive processing, and brain fog, as well as mood instability resulting in depression or anxiety.
Initially these toxins do not damage the cells: they primarily compromise the function of cells. The function of entire systems may also be compromised, particularly systems that maintain homeostasis – the brain and nervous system, as well as the immune and endocrine systems and the gut. Ultimately, the neurotoxic disorders also result in inflammation. However, before inflammation is apparent, there will be a compromise in function. Clinically, we often note this in retrospect, because many patients are able to compensate for the lack of function for a time, without any evidence of inflammation.
Progression of Neurotoxic Disorders
In the past, Lyme-literate clinicians thought in terms of a staged disease. However, I have come to believe that to think in terms of detailed stages can be a distraction. When an initial acute infection is not fully resolved, neurotoxic illness can progress with tremendously varied presentation. That said, there are two subsequent patterns of development that are noteworthy: rapid or gradual progression.
Rapid progression: Approximately 15% of the patients whom I see appear to have some form of genetic vulnerability to neurotoxins. In these patients, unresolved Borrelia or coinfections can evolve into a second stage with intense emergent symptoms, which can become extremely debilitating within a year or two.
Gradual progression: As many as 85% of my patients with unresolved Borrelia and neurotoxic infections tend to have conditions that develop slowly over years or even decades. For these patients, the infection is exacerbated much later in their lives, typically following some type of catastrophic event that reduces or suppresses immune function. Immune suppression could be emotional, resulting from a divorce or the death of a loved one or could be primarily physical, such as an accident, an injury, a major infection, menopause, or andropause.
The illness will take an individual course and presentation, influenced by the patient's genetics, comorbidities, emotional stresses, and general level of health. As a result, more dysfunction is observed in some people and less in others.
In the past, Lyme-literate clinicians thought in terms of a staged disease. However, I have come to believe that to think in terms of detailed stages can be a distraction. When an initial acute infection is not fully resolved, neurotoxic illness can progress with tremendously varied presentation. That said, there are two subsequent patterns of development that are noteworthy: rapid or gradual progression.
Rapid progression: Approximately 15% of the patients whom I see appear to have some form of genetic vulnerability to neurotoxins. In these patients, unresolved Borrelia or coinfections can evolve into a second stage with intense emergent symptoms, which can become extremely debilitating within a year or two.
Gradual progression: As many as 85% of my patients with unresolved Borrelia and neurotoxic infections tend to have conditions that develop slowly over years or even decades. For these patients, the infection is exacerbated much later in their lives, typically following some type of catastrophic event that reduces or suppresses immune function. Immune suppression could be emotional, resulting from a divorce or the death of a loved one or could be primarily physical, such as an accident, an injury, a major infection, menopause, or andropause.
The illness will take an individual course and presentation, influenced by the patient's genetics, comorbidities, emotional stresses, and general level of health. As a result, more dysfunction is observed in some people and less in others.
Systemic Effects
The typical features of neurotoxic illness bear much in common. We now realize that to speak of Lyme disease in isolation is in a sense simplistic, because these are shared mechanisms triggered by a number of similar toxins and pathways.
Load dependent: Neurotoxic disorders tend to wear down the immune system due to their chronic presence and persistent nature. If the patient's exposures are minor and the tick bite contained a weak strain of bacteria, the load is not great, and the immune system can simply fight it off. However, if there is compromise in any of the immune mechanisms, additional opportunistic infections can develop. If one contracts Lyme first and then has a mold exposure, that mold is going to have a greater impact. When a patient has 3 parts Lyme and 3 parts mold, he or she is 6 parts sick.
Neurologic effects: One of the commonalities of the neurotoxic pathogens is that they all produce some form of toxin that affects the brain and nervous system. Due to the nerve to fat ratio, there is a disproportionately greater effect on nerve tissue and the inflammation that they cause tends to be more exacerbated in the nervous system.
The typical features of neurotoxic illness bear much in common. We now realize that to speak of Lyme disease in isolation is in a sense simplistic, because these are shared mechanisms triggered by a number of similar toxins and pathways.
Load dependent: Neurotoxic disorders tend to wear down the immune system due to their chronic presence and persistent nature. If the patient's exposures are minor and the tick bite contained a weak strain of bacteria, the load is not great, and the immune system can simply fight it off. However, if there is compromise in any of the immune mechanisms, additional opportunistic infections can develop. If one contracts Lyme first and then has a mold exposure, that mold is going to have a greater impact. When a patient has 3 parts Lyme and 3 parts mold, he or she is 6 parts sick.
Neurologic effects: One of the commonalities of the neurotoxic pathogens is that they all produce some form of toxin that affects the brain and nervous system. Due to the nerve to fat ratio, there is a disproportionately greater effect on nerve tissue and the inflammation that they cause tends to be more exacerbated in the nervous system.
Autoimmune Reactions
The toxins trigger an inflammatory response, stimulating the release of both anti-inflammatory and pro-inflammatory cytokines, generated by the immune system in its attempts to restore balance and reduce inflammation. As the system becomes upregulated, that typically causes a greater predominance of pro-inflammatory cytokines and autoimmune symptoms. This is the immune system spinning out of control – what would normally be a protective process becomes unproductive as the system becomes overwhelmed.
The most successful bacteria shut down certain aspects of immune function to assure their own survival and proliferation. In the case of Borrelia, the microbe can also cloak itself and effectively hide from the immune system. When these mechanisms are in play, the immune system may fail in its attempts to rid the body of the pathogens.
Unfortunately, it is the efforts of the immune system that result in the patient's symptoms, which may be diagnosed as an autoimmune condition. This is the misfiring of the immune system, in its attempts to deal with toxins or microbes, harbored within the body's cells. In cases of Hashimoto's, we believe that the immune system may be combating infection or toxins within the thyroid. In this excessive response, the immune system eventually targets normal tissue of the thyroid, creating an elevated antibody level. I also believe that rheumatoid arthritis and even gluten intolerance can be caused by this type of exacerbated immune reaction.
When autoimmune disease is present, there can be value in reframing our view of immune function. If we focus on the challenge of combating these elusive stealth bacteria, we recognize the immune system as our ally. The system becomes our partner and one of the goals of patient care is to support immune function.
The toxins trigger an inflammatory response, stimulating the release of both anti-inflammatory and pro-inflammatory cytokines, generated by the immune system in its attempts to restore balance and reduce inflammation. As the system becomes upregulated, that typically causes a greater predominance of pro-inflammatory cytokines and autoimmune symptoms. This is the immune system spinning out of control – what would normally be a protective process becomes unproductive as the system becomes overwhelmed.
The most successful bacteria shut down certain aspects of immune function to assure their own survival and proliferation. In the case of Borrelia, the microbe can also cloak itself and effectively hide from the immune system. When these mechanisms are in play, the immune system may fail in its attempts to rid the body of the pathogens.
Unfortunately, it is the efforts of the immune system that result in the patient's symptoms, which may be diagnosed as an autoimmune condition. This is the misfiring of the immune system, in its attempts to deal with toxins or microbes, harbored within the body's cells. In cases of Hashimoto's, we believe that the immune system may be combating infection or toxins within the thyroid. In this excessive response, the immune system eventually targets normal tissue of the thyroid, creating an elevated antibody level. I also believe that rheumatoid arthritis and even gluten intolerance can be caused by this type of exacerbated immune reaction.
When autoimmune disease is present, there can be value in reframing our view of immune function. If we focus on the challenge of combating these elusive stealth bacteria, we recognize the immune system as our ally. The system becomes our partner and one of the goals of patient care is to support immune function.
Laboratory Testing
Disclaimer: It is important to indicate that this is simply a report of my clinical experience and by no means reflects the broader picture. These observations are drawn from the patients seen in my practice. In addition, there can be regional differences in the symptoms triggered and also differences from one subspecies of microbe to another.
Disclaimer: It is important to indicate that this is simply a report of my clinical experience and by no means reflects the broader picture. These observations are drawn from the patients seen in my practice. In addition, there can be regional differences in the symptoms triggered and also differences from one subspecies of microbe to another.
In the medical system, physicians are trained to diagnose primarily using laboratory testing. In fact, without confirmative lab results, a doctor is on shaky ground to make a diagnosis. That has been a major problem with Lyme disease, since to date there have not been any laboratory tests that are completely conclusive. Currently we have testing for fewer than 5% of the neurotoxic pathogens that have been identified by researchers.
Today, antibody testing is the gold standard for Lyme and the coinfections. Since antibody levels vary based on the relative severity of the infection and the length of time that the patient has been infected, they can serve as a good marker. However, they are not a direct measure of the organism, but rather an indication of the body's response to the organism. Antibodies have been identified for Babesia, Bartonella, Ehrlichia, and Mycoplasma, but there are a surprising number of subspecies, and more are identified every year.
Today, antibody testing is the gold standard for Lyme and the coinfections. Since antibody levels vary based on the relative severity of the infection and the length of time that the patient has been infected, they can serve as a good marker. However, they are not a direct measure of the organism, but rather an indication of the body's response to the organism. Antibodies have been identified for Babesia, Bartonella, Ehrlichia, and Mycoplasma, but there are a surprising number of subspecies, and more are identified every year.
State of the testing: In terms of Babesia, we have the ability to test for two Babesia organisms, but more than 100 strains have currently been identified. For Bartonella, there are tests for two strains, although at least 26 have been identified. For Mycoplasma, there is only one test at this time, although hundreds of strains of Mycoplasma have been identified. Note that it takes years to develop a single test for a pathogen, and the researchers are discovering these microbes so quickly that the lab assessments cannot keep up.
Literally hundreds of intracellular bacteria have been identified by the researchers, with many strains and tremendous species diversity within these pathogen groups. Currently in the literature, the most reliable source of information is the veterinarians, who are tracking the subspecies of Bartonella. Essentially, we are learning that these microtoxic pathogens are much vaster than we ever imagined.
Literally hundreds of intracellular bacteria have been identified by the researchers, with many strains and tremendous species diversity within these pathogen groups. Currently in the literature, the most reliable source of information is the veterinarians, who are tracking the subspecies of Bartonella. Essentially, we are learning that these microtoxic pathogens are much vaster than we ever imagined.
Cultures: Lab cultures are considered the most reliable form of testing in the infectious disease community. However, culturing Borrelia bacteria has proven very difficult and very expensive. Consequently, there has not been a commercially available culture, and thus Lyme diagnosis and treatment have had minimal importance in the scientific community, because there is no confirmatory testing. In fact, a range of tests have been developed, but they have also fallen short because there are so many spirochetes in the body that are nonpathogenic. The tests have not been able to differentiate a nonpathogenic spirochete from the pathogenic Borrelia spirochete. In terms of testing for other sources of neurotoxic illness, much of the testing for molds, petrol-based chemicals, and heavy metals is also unreliable. The good news is that within the past five months, the Advanced Systems Lab has developed a culture test for Borrelia using serum. The new test, which costs less than $600, involves DNA sequencing.
Chemicals: Urinalysis is available for chemicals, but the clinician must have a strong suspicion of which chemical to test for, because each test is specific to a particular chemical. Otherwise we are looking for a needle in a haystack. There are many thousands of petrol-based chemicals in the environment, so although there are panels of tests available for chemicals, unless the clinician has a strong suspicion of the probable exposure, there is no way to identify it.
Heavy metals: We do have good laboratory testing for metals, in the form of challenge testing using oral or IV chelating agents, collecting urine over 6 hours. Hair analysis can be done, but is less specific.
Environmental Relative Moldiness Index (ERMI): In terms of mold, we do not have a good test to evaluate levels of mold within the body: we can measure mold antibodies, but these tend to be variable. However, there is an effective test to evaluate mold within the home: the ERMI test. This assay is an evaluation of dust in the home and has been found to be a very accurate measure of the level of mold in the home environment.
Western blot antibody testing: Antibodies have been identified for Borrelia, Bartonella, Babesia, Ehrlichia, and Mycoplasma. Although the antibodies are not a direct measure of the organism, they do reflect the body's response to the organism.
Public health departments use the western blot antibody test to confirm that a patient is Lyme/Borrelia positive or negative. This test has been the gold standard, so it is important to point out that not all western blots are equal. Integrative practitioners have relied on IGeneX for highly accurate and comprehensive testing, including the western blot, which IGeneX has refined to be much more accurate. Commercial western blot testing provided by LabCorp, Quest, and other labs tends to be less accurate. However, the mainstream medical community seems to discount IGeneX because it has so many positive test results. If one goes to Kaiser with an IGeneX positive, it will not accept the test result. For the record, IGeneX has passed the most stringent laboratory evaluations by the most stringent regulatory agencies. These assessments always show a high level of statistical significance and accuracy, confirmed in double-blind evaluations.
Public health departments use the western blot antibody test to confirm that a patient is Lyme/Borrelia positive or negative. This test has been the gold standard, so it is important to point out that not all western blots are equal. Integrative practitioners have relied on IGeneX for highly accurate and comprehensive testing, including the western blot, which IGeneX has refined to be much more accurate. Commercial western blot testing provided by LabCorp, Quest, and other labs tends to be less accurate. However, the mainstream medical community seems to discount IGeneX because it has so many positive test results. If one goes to Kaiser with an IGeneX positive, it will not accept the test result. For the record, IGeneX has passed the most stringent laboratory evaluations by the most stringent regulatory agencies. These assessments always show a high level of statistical significance and accuracy, confirmed in double-blind evaluations.
Frylab antibody testing: The Frylab, directed by Stephen Fry, is doing very good work in developing antibody testing, which uses blood smears and looks for elements in the blood that can be suggestive of Bartonella and Mycoplasma. Fry's work includes testing using several different staining techniques.
PCR testing: PCR testing is provided by IGeneX and other labs as well. PCR can be very accurate, providing an evaluation based on just a few pieces of the genetic material of pathogens such as Borrelia or the coinfections. We do have PCR profiles on these microbes. The challenge is that the DNA of the pathogen must be present in that specific blood sample for the test to be positive, so there are many false negative tests as a result of PCR. However, when a PCR is positive, that is a highly accurate result.
Evaluation of cytokine levels: Neuroscience Laboratories has a very interesting test that evaluates cytokine levels associated with Borrelia, so the test is only for Borrelia. The lab cross-references antibody activity with elevated cytokine levels. Again, this is not a direct measure of the bacteria, but it can serve as a fingerprint indicating that the bacteria are present because it identifies the specific cytokines that are elevated.
Immune fluorescent testing: IGeneX also has a useful immune fluorescence test that involves staining the blood. If there is even a minute piece of genetic material in that blood, it will stain with a fluorescent illumination. The lab is able to image that fluorescent illumination and identify the organism as present or not.
Fluorescent immune sensitivity: Fluorescent immune sensitivity is now available for Bartonella and Babesia. Although this is an interesting test, it has limitations. As an analogy, think of sitting on a lake in a boat with a bucket. If one dips the bucket into the water, and there are fish in the bucket, clearly there are fish in the lake. However, the key question is, if there are no fish in the bucket, does this mean that there are no fish in the lake?
CD-57: LabCorp is the one lab that does a good CD-57. It is worth mentioning that in the past clinicians have tracked Lyme using the CD-57 (natural killer cell receptors on the surface of the lymphocytes). There can be some usefulness in this test, but again, it is limited because it is an indirect marker. It can be correlated with symptoms as a marker of how well the innate immune system is functioning. However, we are realizing that there are other factors that can affect the CD-57, so it is not a definitive test for Lyme. Although this test apparently indicates Borrelia, it is possible that these markers also reflect the presence of certain viruses and perhaps even mold. Consequently, the CD-57 is not completely conclusive, but can provide another aspect of the picture.
Indirect measures of Borrelia: There are a number of tests which use markers in the blood that serve as general indicators of inflammation, based on the work of Richie Shoemaker, MD. These markers can be useful in determining whether the inflammation is being caused by a neurotoxin. The tests do not differentiate the source, but because neurotoxins have similar mechanisms of action, they also affect certain lab values in terms of inflammation or dysregulation of the body's systems, particularly in relation to the immune, endocrine, and nervous systems. These tests include:
- evaluation for complement components 3a and 4a
- MSH (melanocyte-stimulating hormone)
- VEGF (vascular endothelial growth factor)
- MMP9 (matrix metallopeptidase)
Ultimately, testing depends on cost. It becomes very expensive to perform the lab work, so the choice of testing depends on the patient's funds. Clinicians certainly welcome all the information that they can get.
Symptom Patterns
Our goal as practitioners is to accumulate as much information as possible regarding the health of the individual patient who sits in front of us. Identification of symptom patterns associated with the presence of specific pathogens can be useful in developing a hypothesis. These patterns are also helpful in testing that hypothesis with a challenge protocol.
The series of symptom presentations provided here are general, because every patient will be a little different in relation to how he or she manifests symptoms. Each patient's symptoms will reflect that individual's genetic vulnerabilities and health history. In my own practice, I use the following process to develop and assess patients.
Our goal as practitioners is to accumulate as much information as possible regarding the health of the individual patient who sits in front of us. Identification of symptom patterns associated with the presence of specific pathogens can be useful in developing a hypothesis. These patterns are also helpful in testing that hypothesis with a challenge protocol.
The series of symptom presentations provided here are general, because every patient will be a little different in relation to how he or she manifests symptoms. Each patient's symptoms will reflect that individual's genetic vulnerabilities and health history. In my own practice, I use the following process to develop and assess patients.
- Gather as much information as possible: take a detailed history, ask key questions, perform a physical exam, and evaluate all relevant lab work.
- Create a hypothesis regarding the presumed pathogen.
- Challenge the patient with a therapeutic intervention that is as specific as possible to the suspected pathogen, making note of aggravated symptoms if the hypothesis is correct.
- Evaluate the patient's response to the therapeutic challenge.
- Moderate the challenge dosage to minimize discomfort to the patient.
Borrelia
Borrelia burgdorferi is the specific bacterial spirochete associated with Lyme disease. It is important to treat acute Borrelia infections aggressively with antibiotics before they deepen and compromise immune function, enabling other opportunistic infections.
Borrelia burgdorferi is the specific bacterial spirochete associated with Lyme disease. It is important to treat acute Borrelia infections aggressively with antibiotics before they deepen and compromise immune function, enabling other opportunistic infections.
- transmission: most common tick-borne disease in North America; various species worldwide
- major symptoms: fatigue, pain, immune suppression
- exhaustive fatigue, achiness, poor stamina
- insomnia, nonrestorative sleep
- moderate to severe joint pain or sore muscles
- frequent severe headaches, disabling memory problems, poor concentration, ADHD
- depression, anger, overwhelm, panic, or bipolar syndrome
- minor injuries that can take months to heal
- for 85%, varied symptoms that develop gradually over a period of years
- for 15%, neurologic symptoms resembling multiple sclerosis, Parkinson's, dementia, or Alzheimer's
Bartonella
In a patient with Bartonella, pain is almost always the primary symptom: predominant complains are joint pain and headaches. Bartonella settles in the joints with pain that tends to migrate, affecting different joints at various times. This pain is frequently mistaken for arthritis in its intensity. Headaches, which are often severe, range from sharp piercing pain to dull occipital pain. Typically other neurotoxic infections (Babesia, Ehrlichia, and Mycoplasma) tend to penetrate deep within the body. In contrast, Bartonella tends to linger on the surface and causes symptoms involving the skin and mucus membranes. When a patient presents with chronic pain, headaches, swollen lymph nodes, and sore throat, consider Bartonella.
In a patient with Bartonella, pain is almost always the primary symptom: predominant complains are joint pain and headaches. Bartonella settles in the joints with pain that tends to migrate, affecting different joints at various times. This pain is frequently mistaken for arthritis in its intensity. Headaches, which are often severe, range from sharp piercing pain to dull occipital pain. Typically other neurotoxic infections (Babesia, Ehrlichia, and Mycoplasma) tend to penetrate deep within the body. In contrast, Bartonella tends to linger on the surface and causes symptoms involving the skin and mucus membranes. When a patient presents with chronic pain, headaches, swollen lymph nodes, and sore throat, consider Bartonella.
- transmission: cats (cat scratch or a bite), tick bites
- clinical prevalence: the most frequently observed coinfection
- primary complaint: pain, particularly joint pain or headaches
- cognitive, memory, and mood problems, but not as extreme as Babesia
- hot and feverish, although actual temperature is often normal
- can cause swollen lymph nodes and congested lymphatic system; sore throat
- acne-like skin lesions, skin streaking, or stria
- neuropathy involving the feet, particularly the toes
- pain, burning sensations, or discomfort on the soles of the feet
- can involve the liver and spleen; may elevate liver enzymes slightly
Babesia
Babesia can cause emotional symptoms that resemble every diagnosis in the DSM-IV due to inflammation of the brain. Another classic symptom of Babesia is dysfunction of the autonomic nervous system with symptoms such heart palpitations (which are not a problem of the heart but due to autonomic regulation of the heart) or shortness of breath (which is not a problem of the lungs, but due to oxygen saturation levels). As a clinician, I do not rely on any one symptom. These are symptom patterns, so when a patient is diagnosed with carpel tunnel and also has severe brain fog, mood instability, and night sweats, then I begin thinking in terms of Babesia.
Babesia can cause emotional symptoms that resemble every diagnosis in the DSM-IV due to inflammation of the brain. Another classic symptom of Babesia is dysfunction of the autonomic nervous system with symptoms such heart palpitations (which are not a problem of the heart but due to autonomic regulation of the heart) or shortness of breath (which is not a problem of the lungs, but due to oxygen saturation levels). As a clinician, I do not rely on any one symptom. These are symptom patterns, so when a patient is diagnosed with carpel tunnel and also has severe brain fog, mood instability, and night sweats, then I begin thinking in terms of Babesia.
- transmission: tick bites, mosquito bites in Asia and Africa, blood transfusions
- anecdotal/clinical prevalence: the coinfection second to Bartonella; when caused by a tick bite, Babesia and Bartonella tend to occur together
- primary complaints: cognitive and memory problems; mood and emotional instability
- depression, anxiety, panic disorder, OCD, ADD
- racing irregular heart rate
- malaria-like symptoms: severe chills, fever, sweats, disoriented thinking
- drenching night sweats or even day sweats
- sudden symptoms of intense flu that can last weeks to months
- carpal tunnel in the wrists or neuropathy in the hands or feet
- hepatomegaly and/or splenomegaly
Ehrlichia
- primary symptoms: any neurological sensation in the extremities
- sciatica, numbness, tingling paresthesia, burning
- less involvement in the brain
Mycoplasma
In cases of Mycoplasma, fatigue is pervasive, resulting in a sense of total exhaustion. All the neurotoxic conditions cause nonrestorative sleep, but debilitating fatigue is a hallmark of Mycoplasma. These disorders also frequently cause inflammation of the fascia (which wraps every muscle in the body), resulting in chronic muscular pain or aching. In sum, if the patient is utterly exhausted with symptoms of joint pain, tender fascia, or skin irritations, consider Mycoplasma.
In cases of Mycoplasma, fatigue is pervasive, resulting in a sense of total exhaustion. All the neurotoxic conditions cause nonrestorative sleep, but debilitating fatigue is a hallmark of Mycoplasma. These disorders also frequently cause inflammation of the fascia (which wraps every muscle in the body), resulting in chronic muscular pain or aching. In sum, if the patient is utterly exhausted with symptoms of joint pain, tender fascia, or skin irritations, consider Mycoplasma.
- primary symptom: extreme, debilitating fatigue
- fibromyalgia-like pain or symptoms: muscular pain or aching throughout the body
- joint pain; tight shoulders or tight hips
- inflammation or involvement of the lungs
- symptoms involving the skin or mucus membranes
Challenge Testing
We have an increased index of suspicion of neurotoxic illness when the patient's symptoms are predominantly neurologic, and have not responded to treatment, with symptoms that could include pain and involve multiple organ systems. If we have made the determination that this patient could have a neurotoxin condition, we need to hypothesize which of these pathogens is likely to be dominant (which has the immune system's attention at the moment). The response of the immune system will be reflected in the patient's symptomatic presentation. Developing a hypothesis involves pattern recognition, connecting the dots between signs and symptoms that would otherwise seem unrelated. Once we have developed a hypothesis, we test the theory with a challenge protocol. The challenge agent selected is an antibiotic, antimicrobial, botanical, or homeopathic remedy that has been shown to reduce symptoms associated with that particular pathogen. The therapeutic variable could include one of the following:
We have an increased index of suspicion of neurotoxic illness when the patient's symptoms are predominantly neurologic, and have not responded to treatment, with symptoms that could include pain and involve multiple organ systems. If we have made the determination that this patient could have a neurotoxin condition, we need to hypothesize which of these pathogens is likely to be dominant (which has the immune system's attention at the moment). The response of the immune system will be reflected in the patient's symptomatic presentation. Developing a hypothesis involves pattern recognition, connecting the dots between signs and symptoms that would otherwise seem unrelated. Once we have developed a hypothesis, we test the theory with a challenge protocol. The challenge agent selected is an antibiotic, antimicrobial, botanical, or homeopathic remedy that has been shown to reduce symptoms associated with that particular pathogen. The therapeutic variable could include one of the following:
- a prescription antibiotic or antimicrobial
- herbal product or formula that is sensitive and specific enough to elicit a predictable patient response
- a homeopathic nosode specific to the microbe
Theory of Challenge Testing
In this approach, the practitioner uses a single, specific therapeutic variable as a challenge and then evaluates the patient's response. In the past I have used antibiotics for Borrelia and the coinfections. I now find that herbal protocols are also effective in challenge testing. In my experience the botanical extracts contained in the Byron White Formulas are gentle, yet strong enough to provoke a highly specific immune response: a Herxheimer reaction. The formulas are invaluable tools in challenge testing. I also use them extensively as a form of immune support. (Immune support protocols are included at the end of the article.)
In this approach, the practitioner uses a single, specific therapeutic variable as a challenge and then evaluates the patient's response. In the past I have used antibiotics for Borrelia and the coinfections. I now find that herbal protocols are also effective in challenge testing. In my experience the botanical extracts contained in the Byron White Formulas are gentle, yet strong enough to provoke a highly specific immune response: a Herxheimer reaction. The formulas are invaluable tools in challenge testing. I also use them extensively as a form of immune support. (Immune support protocols are included at the end of the article.)
Note: The botanical extracts can be powerful immune system modulators and restoratives, so they should only be provided under the supervision of a practitioner who is familiar with their use.
Case study: Consider the case of a patient whose symptom pattern suggests an infection by a pathogen in the Babesia family. At this point we need to test that hypothesis. One way to confirm that this patient has Babesia is to challenge him with a Babesia-specific immune variable. In my practice, I use a botanical 1:1 extract, the Byron White Formula A-BAB. Dosage is highly individual, and I typically begin patients on one or two drops, supervising them carefully to assure their comfort level. If the therapeutic variable triggers an intensification of that symptom pattern, that is preliminary confirmation of the hypothesis.
Herxheimer response: In this example, if the patient does have a Babesia-like infection, the botanical extract will typically result in a die-off reaction or Herxheimer response. A Herx often indicates more die-off than the body can detoxify, which results in an activation of symptoms. In the past we thought that the greater the Herx response, the more we were helping the patient. We believed that it was desirable to have a significantly aggravated response. We now realize that an intense Herx is probably confusing to the immune system and may only be creating more havoc.
Dosage in challenge testing: In my experience, the progressive rate of increase in dosage is different for each patient. If the patient is highly sensitive, I initially begin with one or two drops and definitely go slower; if she is a hardy, healthy individual, I will probably increase the dosage somewhat faster. The process involves gradually increasing the dosage, and monitoring the patient's symptoms for an aggravated response. If a Herx response is observed, I take that as a preliminary confirmation of the hypothesis.
I then move to an immune support protocol using the same herbal extract but at a lower dosage, which is increased more gradually. We give just enough of the botanical extract to have a mildly provoking effect and elicit a mild Herx. However, if that response becomes too intense, we stop, and allow those symptoms to subside. The ability to calibrate the dosage with a product such as the Byron White Formulas makes these extracts unique, because they can be adjusted in response to the patient's reaction. The optimal dosage is the specific number of drops that support improvement in that individual patient, gradually reducing symptomatology without provoking a full-blown Herx.
I then move to an immune support protocol using the same herbal extract but at a lower dosage, which is increased more gradually. We give just enough of the botanical extract to have a mildly provoking effect and elicit a mild Herx. However, if that response becomes too intense, we stop, and allow those symptoms to subside. The ability to calibrate the dosage with a product such as the Byron White Formulas makes these extracts unique, because they can be adjusted in response to the patient's reaction. The optimal dosage is the specific number of drops that support improvement in that individual patient, gradually reducing symptomatology without provoking a full-blown Herx.
Case Study: Babesia Infection
This case demonstrates the use of the herbal protocols alone without the need for antibiotics. Note that as a provider, I typically find that I need to ask key questions to identify the patient's complete symptom pattern. In this case, the information obtain through my inquiries is listed under Additional History.
This case demonstrates the use of the herbal protocols alone without the need for antibiotics. Note that as a provider, I typically find that I need to ask key questions to identify the patient's complete symptom pattern. In this case, the information obtain through my inquiries is listed under Additional History.
Patient: 32-year-old female
Chief complaint: Irregular heart rate with shortness of breath and dizziness. Evaluated in ER and by two cardiologists, who found no cardiac pathology.
Patient report: Slow onset of fatigue over the course of one year. Symptoms of restless legs syndrome, resulting in delayed sleep onset. Restless sleep in last year with frequent waking. Unrefreshing sleep. Episodic, low-level headache that can last for days without a known trigger, seems to be worse with poor-quality sleep. Some minor joint pain, no redness or swelling, worse in ankles when walking.
Additional history: Overheated at night, alternating with chill, pulls covers up or throws covers off. Night sweats 3 out of 7 nights, occasionally needs to change nightshirt. More anxious at night. Anxiety states worse during headache episodes. Headaches can be severe if the episode coincides with menses. Episodes of irregular heart rate either at rest or during exercise, which can be worse in the days preceding menses. Shortness of breath experienced independently of irregular heart rate.
Assessment: Patient has a symptom picture that is consistent with that of other patients who respond to A-BAB administration.
Challenge testing: Started A-BAB challenge beginning at lowest dosage two times per day (b.i.d.). Instructed patient to stop if she experienced uncomfortable aggravation of her symptoms, or to quickly decrease the number of drops. Patient will follow up in 2 weeks.
Office visit at 2 weeks: There was a mild Herx response to A-BAB. Suggested that patient continue use with a slow increase in number of drops until she notices a mild increase in symptoms. The patient was advised to hold the dosage at that level for several days and then gradually continue to increase as tolerated.
Office visit at 6 weeks: The patient identified tolerable symptom dosage, and was instructed to continue until symptoms again plateaued and then increase by one drop as tolerated.
Office visit at 12 weeks: After 6 weeks more, patient was symptom free and was advised to maintain the dosage at that level for an additional 30 days. She remained symptom free and discontinued the formula after the additional 30 days.
Chief complaint: Irregular heart rate with shortness of breath and dizziness. Evaluated in ER and by two cardiologists, who found no cardiac pathology.
Patient report: Slow onset of fatigue over the course of one year. Symptoms of restless legs syndrome, resulting in delayed sleep onset. Restless sleep in last year with frequent waking. Unrefreshing sleep. Episodic, low-level headache that can last for days without a known trigger, seems to be worse with poor-quality sleep. Some minor joint pain, no redness or swelling, worse in ankles when walking.
Additional history: Overheated at night, alternating with chill, pulls covers up or throws covers off. Night sweats 3 out of 7 nights, occasionally needs to change nightshirt. More anxious at night. Anxiety states worse during headache episodes. Headaches can be severe if the episode coincides with menses. Episodes of irregular heart rate either at rest or during exercise, which can be worse in the days preceding menses. Shortness of breath experienced independently of irregular heart rate.
Assessment: Patient has a symptom picture that is consistent with that of other patients who respond to A-BAB administration.
Challenge testing: Started A-BAB challenge beginning at lowest dosage two times per day (b.i.d.). Instructed patient to stop if she experienced uncomfortable aggravation of her symptoms, or to quickly decrease the number of drops. Patient will follow up in 2 weeks.
Office visit at 2 weeks: There was a mild Herx response to A-BAB. Suggested that patient continue use with a slow increase in number of drops until she notices a mild increase in symptoms. The patient was advised to hold the dosage at that level for several days and then gradually continue to increase as tolerated.
Office visit at 6 weeks: The patient identified tolerable symptom dosage, and was instructed to continue until symptoms again plateaued and then increase by one drop as tolerated.
Office visit at 12 weeks: After 6 weeks more, patient was symptom free and was advised to maintain the dosage at that level for an additional 30 days. She remained symptom free and discontinued the formula after the additional 30 days.
Case Study: Babesia, Borrelia, and Mold
In this case, we took an integrative approach to patient care, using botanical extracts for challenge testing and immune support and periodic treatment with targeted antibiotics and other medications.
In this case, we took an integrative approach to patient care, using botanical extracts for challenge testing and immune support and periodic treatment with targeted antibiotics and other medications.
Patient: 34-year-old female
Medical History: Previously healthy young woman with progressively worsening symptoms over the last 5 years. Known tick bite, which occurred in a region of the country where Lyme disease is endemic. No complicating comorbidities. No postexertion fatigue. No history of prescription medication use.
As a child, chronic allergies with mild episodic asthma, dysthymic depression, and IBS.
Chief complaint: Unstable mood (both anxious and depressed), problems with cognition, memory processing, and fatigue, as well as difficulty falling asleep and staying asleep
Laboratory testing: Positive IGeneX Western blot IgM and IgG. LabCorp CD-57 level 68. Complement testing: C4a at 8000. HLA-DRB typing positive, indicating mold predisposition.
Patient report: Dizziness, shortness of breath, occipital head pain. Easily overwhelmed, increased problems at work due to difficulty multitasking
Additional review of symptoms: Head pressure, minor low back pain, and mild bilateral neuropathy in the hands. Night sweats, temperature intolerance, and periodic chills. Intermittent diarrhea with multiple food allergies, gas, and bloating. Energy 4/10. Shortness of breath, similar to air hunger.
Assessment: Symptom picture suggests probable coinfection with a Babesia-like organism accompanying a Borrelia infection (confirmed by western blot) and a possible mold component (known susceptibility per HLA typing).
Medical History: Previously healthy young woman with progressively worsening symptoms over the last 5 years. Known tick bite, which occurred in a region of the country where Lyme disease is endemic. No complicating comorbidities. No postexertion fatigue. No history of prescription medication use.
As a child, chronic allergies with mild episodic asthma, dysthymic depression, and IBS.
Chief complaint: Unstable mood (both anxious and depressed), problems with cognition, memory processing, and fatigue, as well as difficulty falling asleep and staying asleep
Laboratory testing: Positive IGeneX Western blot IgM and IgG. LabCorp CD-57 level 68. Complement testing: C4a at 8000. HLA-DRB typing positive, indicating mold predisposition.
Patient report: Dizziness, shortness of breath, occipital head pain. Easily overwhelmed, increased problems at work due to difficulty multitasking
Additional review of symptoms: Head pressure, minor low back pain, and mild bilateral neuropathy in the hands. Night sweats, temperature intolerance, and periodic chills. Intermittent diarrhea with multiple food allergies, gas, and bloating. Energy 4/10. Shortness of breath, similar to air hunger.
Assessment: Symptom picture suggests probable coinfection with a Babesia-like organism accompanying a Borrelia infection (confirmed by western blot) and a possible mold component (known susceptibility per HLA typing).
Immune Support Protocol 1
Protocol: Challenge testing was done using A-BAB, followed by10 weeks of A-BAB in progressively increased dosage as tolerated, followed by 6 weeks of Mepron and Zithromax.
Symptoms improved after 4 months: improvement in symptoms including memory and cognitive processing. Less dizziness, fewer night sweats, chills, or anxiety states. (Symptoms that improved are all typical of a Babesia symptom picture.)
Persisting symptoms: Mild headache, moderate depression (symptoms typically associated with Borrelia). Abdominal gas with bloating (persisting symptom typically of a fungal symptom picture).
Worsening symptoms: Back, neck and shoulder pain, moderate neuropathy hands L>R, moderate to severe bilateral leg muscle aching, and significant fatigue (energy 2/10). (A strong Borrelia-like symptom picture)
Assessment: Babesia symptom picture 70% improved in 4 months of immune support.
Borrelia symptom picture now more dominant; consider Borrelia protocol: Patient's LabCorp CD 57 dropped from 68 to 31 (of 360). Low CD-57 levels associated with a Borrelia symptom picture; the lower the level, the greater the severity.
Protocol: Challenge testing was done using A-BAB, followed by10 weeks of A-BAB in progressively increased dosage as tolerated, followed by 6 weeks of Mepron and Zithromax.
Symptoms improved after 4 months: improvement in symptoms including memory and cognitive processing. Less dizziness, fewer night sweats, chills, or anxiety states. (Symptoms that improved are all typical of a Babesia symptom picture.)
Persisting symptoms: Mild headache, moderate depression (symptoms typically associated with Borrelia). Abdominal gas with bloating (persisting symptom typically of a fungal symptom picture).
Worsening symptoms: Back, neck and shoulder pain, moderate neuropathy hands L>R, moderate to severe bilateral leg muscle aching, and significant fatigue (energy 2/10). (A strong Borrelia-like symptom picture)
Assessment: Babesia symptom picture 70% improved in 4 months of immune support.
Borrelia symptom picture now more dominant; consider Borrelia protocol: Patient's LabCorp CD 57 dropped from 68 to 31 (of 360). Low CD-57 levels associated with a Borrelia symptom picture; the lower the level, the greater the severity.
Immune Support Protocol 2
Protocol: Rocephin IV 2 gm b.i.d., 4 days on 3 off, with doxycycline 100 mg, 2 tablets 2× per day, and Actigall.
Response after 2 months: Resolved symptoms included reduced back, neck, and shoulder pain. No headache, pressure, or occipital head pain
Improved but persistent symptoms: Moderate neuropathy in hands improved to mild. Mild bilateral muscle aches. Sleep improved but still restless. Fatigue (energy 4/10) associated with a Borrelia symptom picture.
Worsening symptoms: Shortness of breath, asthma-like symptoms, severe abdominal bloating and gas. Dark mood with flat affect. Sinus congestion and mild sore throat (symptoms associated with a fungal symptom picture).
Assessment: Inflammation more superficial with much of the mucous membranes involved. Neurological symptoms much improved, with only remaining neuropathy in hands, now bilateral. Borrelia symptom picture improved; dominant mold presentation persisting.
Unresolved: Are the abdominal bloating and gas related to the mold symptom picture, or a result of the antibiotics, or both?
Protocol: Rocephin IV 2 gm b.i.d., 4 days on 3 off, with doxycycline 100 mg, 2 tablets 2× per day, and Actigall.
Response after 2 months: Resolved symptoms included reduced back, neck, and shoulder pain. No headache, pressure, or occipital head pain
Improved but persistent symptoms: Moderate neuropathy in hands improved to mild. Mild bilateral muscle aches. Sleep improved but still restless. Fatigue (energy 4/10) associated with a Borrelia symptom picture.
Worsening symptoms: Shortness of breath, asthma-like symptoms, severe abdominal bloating and gas. Dark mood with flat affect. Sinus congestion and mild sore throat (symptoms associated with a fungal symptom picture).
Assessment: Inflammation more superficial with much of the mucous membranes involved. Neurological symptoms much improved, with only remaining neuropathy in hands, now bilateral. Borrelia symptom picture improved; dominant mold presentation persisting.
Unresolved: Are the abdominal bloating and gas related to the mold symptom picture, or a result of the antibiotics, or both?
Immune Support Protocol 3
Protocol: With the probable dominant mold symptom picture, a recommendation of 3 months on Byron White Formula A-FNG for fungal conditions
Response: This patient was sensitive to a small dosages starting at 1 to 2 drops a day. Immune support was carefully guided to avoid aggravation of her symptoms, and gradually increased in response to patient tolerance. After 3 months she continued protocol with resolved depression, and less shortness of breath (common mold symptom picture).
Protocol: With the probable dominant mold symptom picture, a recommendation of 3 months on Byron White Formula A-FNG for fungal conditions
Response: This patient was sensitive to a small dosages starting at 1 to 2 drops a day. Immune support was carefully guided to avoid aggravation of her symptoms, and gradually increased in response to patient tolerance. After 3 months she continued protocol with resolved depression, and less shortness of breath (common mold symptom picture).
Immune Support Protocol 4
Persisting symptoms: The patient continued to experience unresolved muscle aches and neuropathy, similar to a Lyme symptom picture.
Protocol: In the final immune support protocol, patient used A-Lyme Complex for one month with improvement. The goal was to continue unloading the Borrelia without additional adverse effect on the gut. A-L Complex was stopped after 30 days of additional use with no relapse in improved symptoms.
Persisting symptoms: The patient continued to experience unresolved muscle aches and neuropathy, similar to a Lyme symptom picture.
Protocol: In the final immune support protocol, patient used A-Lyme Complex for one month with improvement. The goal was to continue unloading the Borrelia without additional adverse effect on the gut. A-L Complex was stopped after 30 days of additional use with no relapse in improved symptoms.
Interventions and Patient Care
The discussion of antibiotics and botanicals is relatively limited for a number of reasons, which include the potential severity of neurotoxic disorders and the tremendous sensitivity of many patients with Borrelia and/or coinfections. In patient care for these conditions, a particular antibiotic will heal one patient and worsen the symptoms of the next. A single drop of an herbal extract will hardly be noticed by most patients, yet in a highly sensitive patient can provoke symptoms. Ultimately, this reflects the tremendous variation in both patient health and biochemical individuality.
The discussion of antibiotics and botanicals is relatively limited for a number of reasons, which include the potential severity of neurotoxic disorders and the tremendous sensitivity of many patients with Borrelia and/or coinfections. In patient care for these conditions, a particular antibiotic will heal one patient and worsen the symptoms of the next. A single drop of an herbal extract will hardly be noticed by most patients, yet in a highly sensitive patient can provoke symptoms. Ultimately, this reflects the tremendous variation in both patient health and biochemical individuality.
Wayne Anderson, ND, initially practiced in a busy community-based family medical center, for more than 20 years, treating individuals and families from birth to old age. The focus of his practice gradually shifted to a search for effective interventions for patients experiencing chronic illness. Located in an area where Lyme disease was endemic, he became aware of the prevalence of chronic Lyme and related conditions and came to realize the important role that they were playing in many of the chronic health disorders of his patients.
Ten years ago, he left family practice to work with Eric Gordon, MD, in a practice using both conventional and integrative medicine. Dr. Anderson is a dedicated clinician whose work emphasizes immune support for patients with chronic and neurologic health conditions, including those with Lyme disease and/or Lyme coinfections.
Ten years ago, he left family practice to work with Eric Gordon, MD, in a practice using both conventional and integrative medicine. Dr. Anderson is a dedicated clinician whose work emphasizes immune support for patients with chronic and neurologic health conditions, including those with Lyme disease and/or Lyme coinfections.
http://www.townsendletter.com/
Resources for providers
Sources for botanical extracts and training in botanical protocols:
Sources for botanical extracts and training in botanical protocols:
- Information, periodic training sessions, and patient consultations, available atwww.WayneAnderson.com.
- Forthcoming workshop on Lyme disease with Dr. Joseph Burrascano, American College for the Advancement of Medicine; May 5, 2012, San Diego, California.
- Byron White Formulas currently offers 28 biotargeted herbal formulas for practitioners, as well as practitioner education, including teleconferences, consultations, and numerous articles on the in-depth utilization of the formulas. Contact: ByronWhiteFormulas@gmail.com; www.ByronWhiteFormulas.com.
- BioResource serves as distributor for five major Byron White Formulas. Teleclasses on the formulas are available on CD and via download athttp://www.bioresourceinc.com/teleclass.
Can We Domesticate Germs
Apr 23, 2014
Instead of trying to kill these bacteria, parasites, and viruses we should basically control the way the evolve and this in return allows a more symbiotic relationship for everyone. Basically the gist is these bacteria, parasites, and viruses can make an entire generation in one day. They're constantly evolving and ahead of us. They communicate to tell the others what to watch out for so they can be prepared for the next assult. So think about it, basically by the time they figure out an antibiotic that will kill your current strain of BB but by the time it's dicovered it's not that relevant because the bacteria already upgraded while you were discovering. So in the book he discusses malaria as an example.. He said it used to be bad in Alabama, people dying and such, so they started slowly implementing mosquito nets around every house in the state. By the time they got to the last house, the strain that infected people was weak and produced so little toxins, the rate of malaria decreased, and now to this day peope in Alabama still have antibodies to malaria, but the strain doesn't make them ill. I personally think us tearing down the forests, changing the terrain and forcing us to live with the wild life has caused Lyme Disease to reach more people, and because of that it's evolved due to how many more are producing and it's just a huge issue. So anyway, the solution that's worked for treating my lyme, which has been in remission for months now, was simply to find a way to live with these critters but not allow them to suck me dry. If you can make your terrain undesirable they will not be allowed to thrive and produce as many toxins which is what is making you sick. Same for parasites/viruses. This whole kill, kill, kill approach will never get us anywhere. Many of these viruses and bacteria have been around since before the dinosaurs. They're thinking they might play an important role in our survival either. Watch this video if you're interested as it explains it a lot better...... Maggie Rumfelt
Evolutionary biologist Paul Ewald drags us into the sewer to discuss germs. Why are some more harmful than others? How could we make the harmful ones benign? Searching for answers, he examines a disgusting, fascinating case:...
TED|BY PAUL EWALD
Thug Kitchen Asparagus Risotto, watch out for deliciousness and foul language.
Asparagus is a solid stand-alone veggie with all its vitamin K and folate but paired with this creamy risotto? HOT DAMN it takes this spring staple to another level.
SPRING ASPARAGUS RISOTTO
enough for 4 people
2 tablespoons olive oil
1/3 cup chopped shallots or yellow onion
3 cloves garlic, minced
1 cup Arborio rice*
½ cup white wine
¼ teaspoon salt
4 ½ cups vegetable broth
1 bunch asparagus, about 1 pound
½ teaspoon lemon zest
1 teaspoon olive oil
¼ cup minced chives
pepper to taste
Warm up the veggie broth in a medium pot until it gently simmers then turn off the heat. Chop up the shallots, garlic, and asparagus. You’ll want the asparagus in pieces about an inch long, like bite-sized. Cut off the tough ends because those woody sons of bitches will ruin everything.
In a large skillet or pot with a wide bottom, heat up the 2 tablespoons of oil over a medium heat. Add the shallots and sauté them around until they start to look kinda golden, about 2-3 minutes. Add the garlic and rice and sauté until the rice smells toasted and starts looking like it absorbed some of the oil, about 2 more minutes. This helps make your risotto all creamy SO DON’T SKIP THIS SHIT. Add the white wine and salt to the pot and cook until most of the wine has evaporated and you scraped whatever bits of shallot got stuck to the bottom of the pot, like a minute or 2. Drink the rest wine because... well, that shits already open. Might as well.
Now add 2 cups of the warm broth, stir, and lower the heat so that the pot is at a simmer, uncovered. Stir every couple of minutes until most of the broth has absorbed into the rice, about 7-10 minutes. You don’t need to stand there and stir it the whole fucking time; whoever started that rumor about cooking risotto is a goddamn liar. Just stir it every minute or two while you clean up or troll the internet. Add another 2 cups of warm broth at this point, and do that whole stir and simmer thing again for another 7 minutes or until the rice tastes slightly undercooked and there’s still broth in the pot. Now dump in the asparagus and cook until it’s tender and the rice looks like its sitting in a creamy gravy, about 5 more minutes. If it starts looking a little dry before everything is tender, just add some more of the broth a tablespoon at a time to fix that shit.
When the rice and asparagus taste on point, turn off the heat; add the lemon zest, remaining oil, half the chives, and a little pepper. Taste and add more salt, pepper, or whateverthefuck you want. Serve right away and top with the remaining chives.
* This kind of rice is starchy as hell, so it will make your risotto the extra creamy and delicious. If you can’t find it don’t worry about it, just grab a short grain rice.
Raw coconut lime blueberry tart
Apr 17, 2014
This sounds so good I just had to spread the word......
Ingredients
- CRUST
- 3 full TBSP coconut butter
- 2 flat TBSP mashed blueberries
- FILLING
- meat of 1 young coconut
- zest and juice of 1 lime
- 2 TBSP raw honey or maple syrup (or 3 TBSP if you prefer it sweeter)
- 2 TBSP coconut oil
- TOPPING
- chia seeds
- edible flowers – no need to be fancy: go for rosemary flowers, basil flowers or dry lavender buds
Instructions
- Line your cake dish with cling film.
- Mix the ingredients for the crust in a bowl. They can easily be mixed with a spoon.
- Press the crust in the cake dish and form your crust. It will be soft at this stage, but it firms up well in the fridge.
- Pop the cake pan in the fridge.
- Add the ingredients for the filling to a blender and whiz up for few seconds, until it becomes smooth and silky. Taste at this point to see if it’s sweet enough for you.
- Scoop the filling into the cake pan. Depending on how much coconut meat your coconut has, you might have an extra spoon or two of filling left, but I’m pretty sure you know what to do with that.
- Pop the cake in the fridge to firm up.
- Serve with chia seeds and edible flowers.
Notes
This recipe makes 1 small 9-10cm cake.
http://talesofakitchen.com/
Can Cannabis help treat Lyme?
Apr 16, 2014
Going through the medical system with Lyme disease is like being a ball in an old fashioned pinball game machine. The standard of care treatment of antibiotics and pharmaceuticals forever is risking serious adverse events, or at least reducing one’s immune system protections. But now at least one natural solution has surfaced for Lyme disease – marijuana.
The Borrelia burgdorferi bacteria (Lyme disease), whether from tick bites or not, are responsible for a disease that has spread worldwide after being first discovered in Lyme, Connecticut. The Borrelia bacteria are motile (capable of motion) spirochetes, heavily armored, and DNA equipped so they can worm their ways deeply into all sorts of tissue and resist antibiotics.
All this with usually no solution, but just more complications. Cannabis come to the rescue.
Smoking Cannabis and Lyme Success
Alexis, diagnosed with late-stage Lyme Disease, is an example of someone using mainstream solutions for her Lyme disease to no avail. She was on antibiotics long enough for her gastrointestinal tract to be damaged and to be hospitalized with hemorrhagic colitis.
She was taken off antibiotics and put on several strong pain prescriptions that were barely effective while putting her into lower emotional states. Then she tried smoking marijuana.
That routine handled most of her nausea, enabled her to eat well enough to avoid wasting away, helped her sleep better, and eased her pain while elevating her mood. She maintains that marijuana has been the best thing for her Lyme disease.
Alexis wrote, “In the hospital, I have needed to have morphine or lorazepam through an IV to accomplish what smoking two grams of cannabis does on the comfort of my couch, in a fraction of the time.” But Alexis is looking for a long-term solution.
Cannabis Oil Remission Success
Some have discovered that cannabis oil may be the solution for Lyme disease. Cannabis oil is a highly concentrated substance that’s extracted and reduced from large amounts of cannabis with a beneficial balance of THC and othe cannabinoids.
What do you do when you’re sick and everything you’ve been told about proper treatment was wrong? What would you do if, in the interest of feeling “okay”, you let your doctor pump you full of medications, all for naught? Like most people who have been through fruitless medical treatments, Lyme disease sufferer Shelley M. White, got fed up and started researching for herself. What she found out about her Lyme disease and potential treatments changed her life.
Shelley found a tick behind her ear at the age of 14. Seven years later, after a variety of health problems, she was diagnosed with Lyme disease, Mycoplasma, Bartonella, Lupus, and Babesia. She had multiple seizures every single day and was put through the ringer with conventional medical treatments. It wasn’t until she tried treating her symptoms with marijuana that she found relief.
“Desperately searching for answers, I stumbled across what turned out to be one of the most profound facts I have ever learned,” Shelley writes. “Marijuana contains one of the most potent anticonvulstants in the world. Controversy over the subject was meaningless at that point, as the herb offered a possible solution to one of my most debilitating symptoms.”She began with smoking, which didn’t only make her feel better, it actually eliminated her seizures completely. Now, she makes her own cannabis oil, which she takes throughout the day. Similar to how marijuana has helped children overcome ‘untreatable’ seizures and how one woman used cannabis juice to replace 40 medications, the effects have been nothing short of amazing.
“After only a month of taking it I was able to return to work and school, and began to drive and have a social life again. Now, I am finally planning to move out and be independent for the first time in years. Basically, I am returning to a lifestyle that I was once unsure I would ever see again thanks to the immense healing power of cannabis oil.”
As researchers with the University of Reading and GW Pharmaceuticals in the U.K. recently found, rats and mice treated with one of 100 non-psychoactive cannabinoids had fewer seizures, less severe seizures, and a lower mortality rate when compared with animals given a placebo. Because the compound was non-psychoactive, people who want the benefits without the “high” could reap similar benefits.
Cannabis has a wealth of healing compounds, some of which we are only beginning to understand. The many benefits of this plant should be reason enough to make it available to all who need it, without fear of jail time or arrest. Until that day comes, however, some are still willing to risk it all for relief and healing.
It has become increasingly available in states that allow medical marijuana, but it’s also available “underground”.
Another young lady suffering from Lyme disease, Shelley White’s Lyme Disease was so debilitating that she had endured at least 10 seizures daily for a year and a half. She began smoking marijuana from a pipe and then switched to inhaling it through a vaporizer. Just from that, her seizures had stopped. Then she decided to go to the next level of using cannabis oil.
After a month of the oil, she was able to return to work and school. At the time of writing her story, she was happy to announce that she could now move out and live on her own and enjoy a normal social life.
An internet radio show called “High Noon” interviewed a couple of Lyme disease victims who had been using cannabis oil successfully, Pamela Baily and Lisa Sikes. Listen here.
One of the underground pioneers of cannabis oil who followed Rick Simpson has reported that more Lyme Disease sufferers have come to cannabis oil recently with mostly successful results.
WHAT IT IS LIKE TO HAVE LYME DISEASE
04/03/2014 · by Shelley M. White ·
Imagine everything that’s old always feels new.
Imagine what was once familiar is now unfamiliar.
Imagine waking up to an existence more surreal than your dreams.
Imagine losing everything rendering nothing as everything.
Imagine all of your lies meeting your truth.
Imagine you would die to live what you once considered a nightmare.
Imagine becoming so alone, that you are no longer lonely.
Imagine suffocating in order to take your first breath.
Imagine consciously lingering on the brink of the unconscious mind.
Imagine you live where darkness meets light.
Imagine dying, to finally be alive.
Imagine you are me, and that I am you.
Read more: http://naturalsociety.com/cannabis-can-conquer-lyme-disease-2/#ixzz2z3xq6XQZ
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