My New Theory about CFS (really cool!)
Over the past few weeks I have started developing theory that CFS and closely related conditions are primarily a prolonged subliminal, biologically-induced fight-flight response, caused by a chronic biotoxin load, with differentiation of responses based on genetics. I do not mean the type of fight-flight in which a person is frightened by a thought or stress event, but rather a subclinical (or subconscious) form, where a physiological fight-flight, or panic-type response is triggered by certain chemicals in isolation of any anxiety-provoking stimulus. Therefore, the term ‘panic’ or ‘panic/anxiety’ in this theory generally refers to a fight-flight response that is primarily chemically triggered.
Research shows that subclinical panic/anxiety (the fight-flight response) can be chemically induced in a large subset of the population, and is not always an emotionally or intellectually-based phenomenon. It is a biological form of panic/anxiety that may accompany exposure to chemical triggers, which I here hypothesize may be more common among people with genetic biotoxin detox pathway errors. This includes people who have poor detoxification of biotoxins produced by molds, fungi, certain bacterial and parasitic infections, and also some artificial biotoxins such as organophosphates (pesticides).
Because of the poor detoxification, the infections or exposures to biotoxins need not be extreme. For example, a person with these types of genetic problems may have a very low-level chronic infection of a biotoxin-producing organism, a level of infection that may actually be common in the population. However, people who can detoxify these biotoxins never develop the symptoms of CFS, while those genetically predisposed to not detox well will sooner or later become chronically ill. Perhaps a trigger event occurs, such as an illness or life-stressor, and stress can lower the immune response which may allow a small surge in the biotoxin load, overloading their detoxification pathways. Additionally, recent research suggests that some people with CFS may have genetic immune system defects that lead to a higher load of biotoxin-producing infections. Since there is not much you can do to correct the genetics involved, if you have these problems it is critical to continuously treat any exposure to biotoxins. And that is where we begin.
Is subclinical biotoxin-triggered panic/anxiety a major cause of CFS?
I believe that biotoxins may be the chemical trigger for a subliminal chronic panic/anxiety state that can become a major cause of the major symptoms of CFS. I must credit Dr. Ritchie Shoemaker with some of the ideas behind this theory [1]. He has pioneered the clinical treatment of genetic biotoxin pathway errors in his studies of mold illnesses. However, his protocol does not address the possibility of a profound anxiety/panic response to the biotoxin load, nor the possible effects of such a response. Therefore, when I discovered (accidentally) some surprising similarities between the physiological strains involved in both CFS and Panic/Anxiety disorder, I decided to study the issue to determine whether other treatments, combined with those recommended by Dr. Shoemaker, might be important.
As I conducted a search of panic disorder research I found more and more evidence that the two are closely related. Such as the fact that chemically-induced panic may produce no overtly recognizable panic/anxiety symptoms, but still have all of the physiologic effects [2]. Thus there are subtypes of panic, including those who sense an anxiety state and those who do not. This is consistent with the variation in anxiety sensation in CFS. Or the fact that many of the deficiencies of chronic anxiety/panic match those found in CFS, including magnesium, B12, B6, serotonin, and GABA. Also, several up-regulations that occur during panic/anxiety are glutathione [3], hydrocortisone [4] and diastolic heart function [5], issues also involved in CFS. Coagulation increases under a panic/anxiety load, there may be immune suppression, and tension will limit blood-flow to the gut region, lowering gut immune functions, all common problem areas with CFS. Therefore, the question about similarity of the conditions seemed to have a sold answer. There are close similarities in physiological response, suggesting that CFS may be strange type of Panic/Anxiety, perhaps provoked by a biotoxin load and leading over time to exhausted glutathione, adrenal and diastolic heart function.
Now that I knew the conditions had many common points, I worked through possibility that an extended period of panic/anxiety, provoked by a relentless biotoxin load, could in fact produce the multi-stage developmental pathway of CFS. For example, with CFS there is often high adrenal function for a time, followed by a crash. This is what we would also expect with prolonged panic/anxiety, based on Selye’s work with adrenal exhaustion. Diastolic heart dysfunction has recently been identified clinically in CFS. In the case of prolonged panic/anxiety, we would expect that the heart would adapt to accommodate the diastolic load. This would be a natural response to keep out of heart failure, and would actually be an adaptation and not necessarily a dysfunction. Logically, the victim of a long-term biotoxin-based anxiety/panic syndrome would be both agitated and fatigued, which is also typical of many CFS cases. The similarities between the developmental pathway of CFS and the hypothetical result of prolonged biotoxin-induced panic/anxiety were too compelling to ignore. I have not found any other explanation for CFS that can so thoroughly match the data as this hypothesis. The strain of long-term biotoxin load combined with a long-term panic/anxiety response could certainly be responsible for a majority of the problems and dysfunctions found in CFS research. The more I learn about biotoxin illness and panic/anxiety, the better this all fits together. Even if this hypothesis only is correct for a subset of people with CFS, it certainly is a large subset, and so I decided to attempt to create a treatment plan based solely on this hypothesis.
How can we treat this?
If biotoxin-induced panic/anxiety is the cause of CFS, then what is an ideal treatment? I believe the logical treatment of a biotoxin-induced panic form of CFS would be to first support the deficiencies that result from a chronic panic/anxiety response. Once those deficiencies were addressed, the major secondary problems of the disorder should be treated. For example, if the person has hypercoagulation resulting from the chronic subclinical fight/flight condition, or from the biotoxin-producing infection, then any coagulation load must be reduced and removed from the vascular system. Additionally, if key organ or glandular systems are down-regulated then they must be supported (but probably only conservatively as there is still a biotoxin load and over-supporting those systems could increase toxicity levels). Once these secondary issues were being addressed, then detoxification of biotoxin load could be gradually boosted. Then, with better biotoxin detox, it might finally be safe to treat the biotoxin sources (including removing environmental exposure and treating any toxic infections), and clean up any remaining biotoxins. The final task would be to repair the free radical damage and gradually recondition the body up to normal functional responses, giving time for systems to adapt to wellness. I think those are the main goals. They are far from simple goals, but they are also not as complex and expensive as some current treatments for CFS that either focus on just one aspect of the illness, or attempt to prop-up nearly every major physiological function.
If this hypothesis is correct, then our primary task is to solve the biotoxin load, resolve the damage from the prolonged panic/anxiety state, and support healing. But this is not a straightforward task. A confounding problem in treating CFS as a biotoxin-induced panic/anxiety problem is that the biologic panic/anxiety response will worsen if the biotoxin load increases during treatment. In fact, Shoemaker identifies this as the cause of the ‘herx’ phenomenon, as the biotoxin load triggers the releases of inflammatory cytokines (immune cells). Additionally, if the person with CFS perceives the physiologic panic/anxiety state and overreacts, this produces an amplified feed-back loop because of the toxic state of the nervous system. Perhaps this is the cause of the exaggerated emotional swings sometimes seen during treatment of biotoxin-producing infections, such as Lyme disease. Therefore, we must also treat any subclinical panic/anxiety reactions to the treatments themselves, to avoid amplifying any panic/anxiety or related symptoms.
I am working on a meta-protocol that would address CFS and Lyme from the viewpoint of a subclinical fight-flight, or panic/anxiety reaction to biotoxins. I hope to post on this topic again soon!
References
[1] Shoemaker RC. (2005). Mold warriors: Fighting America’s hidden health threat. Baltimore: Gateway Press, Inc.
[2] Schmid NB, Forsyth JP, Santiago HT, Trakowski JH. (2002). Classification of panic attack subtypes in patients and normal controls in response to biological challenge: implications for assessment and treatment. J Anxiety Disord.;16(6):625-38.
[3] Kuloglu M, Atmaca M, Tezcan E, Ustundag B, Bulut S. (2002). Antioxidant enzyme and malondialdehyde levels in patients with panic disorder. Neuropsychobiology.;46(4):186-9.
[4] Coplan JD, Goetz R, Klein DF, Papp LA, Fyer AJ, Liebowitz MR, Davies SO, Gorman JM. (1998). Plasma cortisol concentrations preceding lactate-induced panic. Psychological, biochemical, and physiological correlates. Arch Gen Psychiatry. Feb;55(2):130-6.
[5] Koszycki D, Zachardko RM, Le Melledo JM, Bradwein J. (1998). Behavioral, cardiovascular, and neuroendocrine profiles following CCK-4 challenge in healthy volunteers: a comparison of panickers and nonpanickers. Depress Anxiety.;8(1):1-7.
Read more!
Research shows that subclinical panic/anxiety (the fight-flight response) can be chemically induced in a large subset of the population, and is not always an emotionally or intellectually-based phenomenon. It is a biological form of panic/anxiety that may accompany exposure to chemical triggers, which I here hypothesize may be more common among people with genetic biotoxin detox pathway errors. This includes people who have poor detoxification of biotoxins produced by molds, fungi, certain bacterial and parasitic infections, and also some artificial biotoxins such as organophosphates (pesticides).
Because of the poor detoxification, the infections or exposures to biotoxins need not be extreme. For example, a person with these types of genetic problems may have a very low-level chronic infection of a biotoxin-producing organism, a level of infection that may actually be common in the population. However, people who can detoxify these biotoxins never develop the symptoms of CFS, while those genetically predisposed to not detox well will sooner or later become chronically ill. Perhaps a trigger event occurs, such as an illness or life-stressor, and stress can lower the immune response which may allow a small surge in the biotoxin load, overloading their detoxification pathways. Additionally, recent research suggests that some people with CFS may have genetic immune system defects that lead to a higher load of biotoxin-producing infections. Since there is not much you can do to correct the genetics involved, if you have these problems it is critical to continuously treat any exposure to biotoxins. And that is where we begin.
Is subclinical biotoxin-triggered panic/anxiety a major cause of CFS?
I believe that biotoxins may be the chemical trigger for a subliminal chronic panic/anxiety state that can become a major cause of the major symptoms of CFS. I must credit Dr. Ritchie Shoemaker with some of the ideas behind this theory [1]. He has pioneered the clinical treatment of genetic biotoxin pathway errors in his studies of mold illnesses. However, his protocol does not address the possibility of a profound anxiety/panic response to the biotoxin load, nor the possible effects of such a response. Therefore, when I discovered (accidentally) some surprising similarities between the physiological strains involved in both CFS and Panic/Anxiety disorder, I decided to study the issue to determine whether other treatments, combined with those recommended by Dr. Shoemaker, might be important.
As I conducted a search of panic disorder research I found more and more evidence that the two are closely related. Such as the fact that chemically-induced panic may produce no overtly recognizable panic/anxiety symptoms, but still have all of the physiologic effects [2]. Thus there are subtypes of panic, including those who sense an anxiety state and those who do not. This is consistent with the variation in anxiety sensation in CFS. Or the fact that many of the deficiencies of chronic anxiety/panic match those found in CFS, including magnesium, B12, B6, serotonin, and GABA. Also, several up-regulations that occur during panic/anxiety are glutathione [3], hydrocortisone [4] and diastolic heart function [5], issues also involved in CFS. Coagulation increases under a panic/anxiety load, there may be immune suppression, and tension will limit blood-flow to the gut region, lowering gut immune functions, all common problem areas with CFS. Therefore, the question about similarity of the conditions seemed to have a sold answer. There are close similarities in physiological response, suggesting that CFS may be strange type of Panic/Anxiety, perhaps provoked by a biotoxin load and leading over time to exhausted glutathione, adrenal and diastolic heart function.
Now that I knew the conditions had many common points, I worked through possibility that an extended period of panic/anxiety, provoked by a relentless biotoxin load, could in fact produce the multi-stage developmental pathway of CFS. For example, with CFS there is often high adrenal function for a time, followed by a crash. This is what we would also expect with prolonged panic/anxiety, based on Selye’s work with adrenal exhaustion. Diastolic heart dysfunction has recently been identified clinically in CFS. In the case of prolonged panic/anxiety, we would expect that the heart would adapt to accommodate the diastolic load. This would be a natural response to keep out of heart failure, and would actually be an adaptation and not necessarily a dysfunction. Logically, the victim of a long-term biotoxin-based anxiety/panic syndrome would be both agitated and fatigued, which is also typical of many CFS cases. The similarities between the developmental pathway of CFS and the hypothetical result of prolonged biotoxin-induced panic/anxiety were too compelling to ignore. I have not found any other explanation for CFS that can so thoroughly match the data as this hypothesis. The strain of long-term biotoxin load combined with a long-term panic/anxiety response could certainly be responsible for a majority of the problems and dysfunctions found in CFS research. The more I learn about biotoxin illness and panic/anxiety, the better this all fits together. Even if this hypothesis only is correct for a subset of people with CFS, it certainly is a large subset, and so I decided to attempt to create a treatment plan based solely on this hypothesis.
How can we treat this?
If biotoxin-induced panic/anxiety is the cause of CFS, then what is an ideal treatment? I believe the logical treatment of a biotoxin-induced panic form of CFS would be to first support the deficiencies that result from a chronic panic/anxiety response. Once those deficiencies were addressed, the major secondary problems of the disorder should be treated. For example, if the person has hypercoagulation resulting from the chronic subclinical fight/flight condition, or from the biotoxin-producing infection, then any coagulation load must be reduced and removed from the vascular system. Additionally, if key organ or glandular systems are down-regulated then they must be supported (but probably only conservatively as there is still a biotoxin load and over-supporting those systems could increase toxicity levels). Once these secondary issues were being addressed, then detoxification of biotoxin load could be gradually boosted. Then, with better biotoxin detox, it might finally be safe to treat the biotoxin sources (including removing environmental exposure and treating any toxic infections), and clean up any remaining biotoxins. The final task would be to repair the free radical damage and gradually recondition the body up to normal functional responses, giving time for systems to adapt to wellness. I think those are the main goals. They are far from simple goals, but they are also not as complex and expensive as some current treatments for CFS that either focus on just one aspect of the illness, or attempt to prop-up nearly every major physiological function.
If this hypothesis is correct, then our primary task is to solve the biotoxin load, resolve the damage from the prolonged panic/anxiety state, and support healing. But this is not a straightforward task. A confounding problem in treating CFS as a biotoxin-induced panic/anxiety problem is that the biologic panic/anxiety response will worsen if the biotoxin load increases during treatment. In fact, Shoemaker identifies this as the cause of the ‘herx’ phenomenon, as the biotoxin load triggers the releases of inflammatory cytokines (immune cells). Additionally, if the person with CFS perceives the physiologic panic/anxiety state and overreacts, this produces an amplified feed-back loop because of the toxic state of the nervous system. Perhaps this is the cause of the exaggerated emotional swings sometimes seen during treatment of biotoxin-producing infections, such as Lyme disease. Therefore, we must also treat any subclinical panic/anxiety reactions to the treatments themselves, to avoid amplifying any panic/anxiety or related symptoms.
I am working on a meta-protocol that would address CFS and Lyme from the viewpoint of a subclinical fight-flight, or panic/anxiety reaction to biotoxins. I hope to post on this topic again soon!
References
[1] Shoemaker RC. (2005). Mold warriors: Fighting America’s hidden health threat. Baltimore: Gateway Press, Inc.
[2] Schmid NB, Forsyth JP, Santiago HT, Trakowski JH. (2002). Classification of panic attack subtypes in patients and normal controls in response to biological challenge: implications for assessment and treatment. J Anxiety Disord.;16(6):625-38.
[3] Kuloglu M, Atmaca M, Tezcan E, Ustundag B, Bulut S. (2002). Antioxidant enzyme and malondialdehyde levels in patients with panic disorder. Neuropsychobiology.;46(4):186-9.
[4] Coplan JD, Goetz R, Klein DF, Papp LA, Fyer AJ, Liebowitz MR, Davies SO, Gorman JM. (1998). Plasma cortisol concentrations preceding lactate-induced panic. Psychological, biochemical, and physiological correlates. Arch Gen Psychiatry. Feb;55(2):130-6.
[5] Koszycki D, Zachardko RM, Le Melledo JM, Bradwein J. (1998). Behavioral, cardiovascular, and neuroendocrine profiles following CCK-4 challenge in healthy volunteers: a comparison of panickers and nonpanickers. Depress Anxiety.;8(1):1-7.
Read more!
posted by Kurt at 5:25 PM
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