Many types of organisms produce substances that are toxic to humans. These include dinoflagellates found in estuaries and the ocean, cyanobacteria (blue-green
algae) found in fresh water, fungi (mold) found in indoor air and outdoors, and some types of bacteria. Our initial research on acute and chronic,
biotoxin-induced illness associated a complex of non-specific symptoms and deficits in visual contrast sensitivity with exposure to estuaries inhabited by the
fish-killing dinoflagellate, Pfiesteria piscicida, and other toxic dinoflagellates in the toxic Pfiesteria complex (1-8). Treatment for this illness, called
Possible Estuary Associated Syndrome (PEAS) by the US Centers for Disease Control and Prevention (CDC; 9), according to our protocol was associated with
recovery of vision and resolution of symptoms. Subsequent research indicated that this paradigm generalizes to chronic illness thought to be caused by toxins
from a marine dinoflagellate, Ciguatera (Chronic Ciguatera Seafood Poisoning), cyanobacteria such as Cylindrospermopsis and Microcystis, various species of
fungi such as Stachybotrys, Aspergillus, Penicillium, and Fusarium, and by spiders such as the Brown Recluse. Our research also suggested that toxins from
tick-borne pathogens such as Borrelia burgdorferi (Lyme disease organism) and Babesia microti may cause chronic illness even after the spirochetes or
intracellular protozoa (also called apicomplexans) have been killed by antibiotics. These biotoxins don't just affect the nervous system. They trigger
release of inflammatory agents in the body that can inflame almost any organ and cause multiple-system symptoms." The theory, and that's where
Shoemaker and Hudnell's theory begins, with biotoxins in the body that some people - as many as 10 million Americans - cannot naturally eliminate,
resulting in many chronic illnesses. The two men believe these poisonous chemical compounds continually circuit the human body, shuttling from nerve to muscle
to brain to sinus to G.I. tract and other organs, triggering the familiar symptoms. These symptoms are similar to those caused by infectious agents, and so is
the effect they have on nerve, muscle, lung, intestines, brain and sinus, say the researchers. Shoemaker and Hudnell say the compounds are manufactured by a
growing number of microorganisms that thrive in our ecosystem due to changes in the human habitat. And although the pathogens differ, Shoemaker and Hudnell say
the biotoxins they produce all do their damage by setting off a similar "exaggerated inflammatory response" in humans. While hiding out in fatty
tissues where blood-borne disease-fighters can't get at them, they trick the body's immune system into launching attacks against joints, muscles,
nerves and brain. There is increasing evidence to show these attacks are carried out by a newly discovered group of molecules, the "pro-inflammatory
cytokines," and that the destruction they cause is linked to recent surges in the rates of heart disease, obesity and diabetes. Illnesses once blamed
solely on diet and life-style choices are now being shown to have an inflammatory basis. And while infections cause a cytokine response from white blood cells,
especially macrophages, the cytokine response to neurotoxins comes from fat cells. "The body can turn off the macrophage cytokine response, so that the
achiness, fever, headache and fatigue of a cold will go away, but there's no negative feedback that stops the cytokine response from fat cells," says
Shoemaker. "So the illness doesn't self-heal." Cholestyramine (CSM) is an FDA-approved medication which has been used to safely lower elevated
levels of cholesterol for more than 20 years. It isn't absorbed; if it's not taken with food, it binds cholesterol, bile salts and biological toxins
from bile in the small intestine, and then the CSM-toxin complex is excreted harmlessly.
My CFS/LDA Dr. recently tested me for neurotoxins and I turned up positive. I just had a phone consultation with Dr. S….. www.neurotoxins.com and my CFS/LDA Dr. These were the recommendations that Dr.S gave us: I would not start CSM (cholestyramine) until you had some special tests done. Levels of MSH, MMP9, 24 hour urine for porphyrins, HLA DR by PCR, the minimum. suspect will find help there. Give us your fax#, I'll fax the info re blood tests and consult when results are in. CSM is extraordinarily hard on multiple food intolerant patients. Use must be justified by cause. He also said in his phone consult that people with Celiac Sprue like conditions often have difficulty with the CSM. It can be done, but he wants to make sure that that is the direction we need to go before I am subjected to the treatment. My CFS Dr. was agreeable to ordering the tests through Esoterix Labs and consulting with Dr. S about the results.
Not knowing what these tests measured and how they would help me, I read through all of the info I could find on Dr. S's work and have pieced together somewhat of a picture.
MSH: (MSH is a hypothalamic neuroregulatory/cytokine regulatory/mucus membrane regulatory hormone.)
In short: MSH stands for "MELANOCYTE-STIMULATING HORMONE". It is one of the hormones of the hypothalamus. Neurotoxin Mediated Illness severely affects the hypothalamus and causes a deficiency in MSH. MSH deficiency causes many problems.
Most notable:
1) is the effect it has on decreasing Melatonin production, which causes a crippling sleep disorder. Once Neurotoxin therapy is initiated, MSH increases and so does Melatonin production and sleep.
2) It causes an imbalance in mucus regulation and an overproduction of mucus ensues With Neurotoxin therapy, mucus regulation stabilizes and mucus expectoration ensues abundantly and the overproduction is corrected.
3) It is a hormone critical to the functionality of all the other hormones.
In essence, it's importance can not be emphasized enough.
The HLA DR by PCR is a typing of immune response genes, that can show individual susceptibility to particular neurotoxins. These are not found in controls. In other words, they're beginning to crack the genetic code to show that some people are genetically predisposed to get certain chronic fatiguing illnesses. He has found there are unique HLA genes in his CFS patients; that his Sick Building Syndrome patients have at least three unique triplets of gene biomarkers; his Post-Lyme patients have two; and that these gene-types are quite different from each other. CFS is an illness that includes a genetic susceptibility to particular neurotoxins, which trigger cytokines associated with carrying CNS (chronic neurotoxins), that produce nerve, hormone and immune system dysfunction in the ventromedial nucleus of the hypothalamus. Dr. S is looking at HLA DR genotype analyzed by PCR that contains the standard 2 triplets. One being DRB1-4, DQ-8 and DRB4-53 is the ciguatera genotype. Dr. Hokama's work with ciguatoxin (actually, there are at least 8 types of ciguatoxin) might bring insight into ciguatera (a toxin found in warm water ocean fish) as a source of a chronic fatiguing illness. His other triplet was the multisusceptible DRB1-14, DQ-5, DRB3-52B. These patients are readily affected by Lyme, mold, coag neg Staph, BG algae and dinoflagellates. We also know that the 4-3-3-53 genotype is a particularly rough genotype to have. These people go on to develop what I consider as true CFS, as we can't find a logical source for their illness, except that they develop hypothalamic deficiencies after a cytokine mediated illness, especially Coxsackie, mono, ECHO B27 and possibly mono. The use of HLA DR4 indicating Lyme would simply lump all of these patients as "Lyme." I hope that those who have the DR4 to go and have the more precise assay of HLA DR by PCR.
MMP-9 is activated by cytokine effect; cytokine effects are activated by biological toxin activity. Any result over 400 is cause for concern regarding "active delivery" by MMP-9 of inflammatory elements from the blood into tissues including joint, nerve, muscle and brain.
We are seeing the results of serial MMP-9 testing over the course of treatment shows an endpoint that is highly correlated with resolution of symptoms due to cytokines.
Patients with low MMP-9 values and symptoms need to look to abnormalities in hormonal pathways, especially MSH, that may have been damaged previously by cytokine effects. Low MMP-9 indicates a reduced inflammatory process in illness. Patients with high MMP-9 show an active inflammatory process for which cytokine reduction is necessary.
MMP-9 tells us a great deal if it is high or changing with treatment. We are seeing a significant clinical benefit from lowering of MMP9 with pioglitazone (Actos) and the no amylose diet, with the diet alone showing some lowering of MMP-9.
MMP9 changes hyperacutely with exposure, flares dramatically in antibiotic-induced Herxheimer reactions in Lyme patients, shows remarkable correlation with central nervous system involvement with coagulase negative Staph and a subset (need more data on speciation of risk factors here) of mold patients.
We must recognize that the process by which CFS develops may include an acute neurotoxic event which includes upper respiratory symptoms," says Shoemaker. He believes that the secondary cytokine damage from neurotoxic exposure changes the mucus membranes in the nose, allowing biofilm-forming, slow-growing CNS to release hemolysins (once called delta toxins) that in turn activate a powerful cytokine response. The boost in cytokines disrupts the leptin-MSH production link. This classic, positive feedback system increases cytokines and CNS and reduces MSH. Shoemaker and Hudnell's data show that there's a group of CSM treatment-resistant CFS patients who are coagulase negative Staph (CNS) positive and who have high leptin levels. (Leptin is a hormone made by fat cells that signals the satiety center in the hypothalamus that a person is no longer hungry. Leptin stimulates the production of alpha melanocyte stimulating hormone (MSH), which in turn controls production of endorphins (the body's natural "opiates") and melatonin (which regulates sleep) in the hypothalamus. CFS patients rarely have much MSH.) Eradicating CNS does nothing to the high leptin and low MSH levels in patients with "end-stage CFS," says Shoemaker, but it certainly does in patients who are diagnosed acutely and treated aggressively, preventing irreversible damage to the MSH-manufacturing pathway. CFS patients are the most difficult to treat. They are resistant to a cure with Cholestyramine if their Leptin is high along with a low MSH. They CAN be treated, and get tremendous symptomatic relief, and very often return to the Land of the Living. But the treatment may have to be chronic. Only Dr. Shoemaker and his treatment will tell you this. As it now stands, low MMP9 and illness means not-inflammatory (put the antibiotics and Actos away) and likely simply hormonal. Mid line MMP9 and symptoms, must fix the inflammatory basis and the hormonal. High MMP9, must mega-fix the inflammatory basis.
PORPHYRINS are metabollic markers in the urine that indicate sensitivity from molds, fungi, pollens and chemicals in a patient's environment. If porphyrins are high then one must look to the environment to find the source of neurotoxins. The problem with the mold patients is that so many have been sick or misdiagnosed for so long that their MSH levels are quite low. With low MSH, coag neg Staph grows well; if a given mold patient has a low MSH and a coag neg Staph, what causes the MMP9 to be high? The answer might just be VCS, as visual contrast in coag neg Staph patients is rarely abnormal and it is routinely abnormal in mold patients.
Shoemaker won't yet say that the HLA DR genes or the abnormalities in the leptin/MSH pathway are the "Holy Grail" of CFS research, but he is hoping that his study shows that replacement of MSH improves many (or most!) of the abnormalities of CFS. That study will be done after the animal studies required by the FDA are completed. They hope it will establish an effective MSH dose and the most effective method of MSH delivery
"Patients must have a compatible history, the deficit in VCS, the HLA genotype, an abnormal cytokine response, and the abnormal effects of cytokines on hypothalamic hormones, especially melanocyte stimulating hormone (MSH)," said Shoemaker. "All CFS patients should have the MSH test done."
The team has found particular genotypes of the immune response genes in HLA-DR that show marked consistency within a diagnosis group and marked disparity in other diagnostic groups.
In their study they'll do baseline VCS tests and MSH levels first, and will attempt to show that high levels of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor alpha and leptin improve after treatment. "Most patients improve in two weeks, some with complete abatement of symptoms, but depending on the amount of toxin in your body, it may take longer," says Shoemaker.
There are many kinds of staph, but the one I had when I had staph was staph epi. Following is some info on it:
Staph Epidermidis is a Coagulase Negative Staph. Normally it is considered to be normal flora and not worked up by most labs and considered insignificant by most physicians. It is the research of Dr. Shoemaker that has brought to light it's ability to produce Neurotoxins and it a serious problem and potential cause of Neurotoxin Illness.
With suppressed MSH, the mucus regulation is disrupted and the impacted mucus gives a perfect habitat for this staph to grow. It is a major cause of suppressing MSH and will interfere with effective Neurotoxin therapy. Most labs do not even work up the Coagulase Negative Staphs because they must be cultured for 5 to 6 days instead of 48 hours. Esoterix labs because of the study with Dr. Shoemaker work it up and it's sensitivities to which antibiotics for treatment. If you want the right test done, it must be HLA-DR by PCR.
Dr. Shoemaker has recommended a Compounding Pharmacy specializing is Cholestyramine for those intolerant of sugar, aspartame, and maltodextrin. (Sugar and maltodextrin can stimulate the Neurotoxins and are part of the NO Amylose Diet and Aspartame can stimulate Insulin production). This pharmacist has designed a formulation of the Cholestyramine as per Dr. Shoemaker.
The compounding Pharmacist, Denis Katz, Rph., President of Hopkinton Drug, Inc. is very experienced with Cholestyramine and has been working and studying it for years. He is highly recommended. He can be contacted at:
Denis Katz, RPh., Hopkinton Drug, Inc., 52 Main St., Hopkinton, Mass., 01748, Phone#: 800-439-4441, Fax#: 508-435-5983, Compounding Pharmacist Specializing in Cholestyramine
Dr. S's tests can be ordered by your physician from Esoterix Labs. He must set up an account with them, you cannot do it:
Esoterix Labs, Inc.
7540 Louis Pasteur, Suite 200
San Antonio, TX 78229-4008
1-800-661-4118
www.esoterix.com
I haven't taken the tests yet and then it will be sometime before the results come in…it should be interesting to see where I am in all of this. I found a communication from a lady who took Cholestyramine and found this to be interesting. She says:
"The first several great Smokies stool tests I did all showed a max dysbiosis of 20. 6 weeks after starting cholestyramine it went down to 10 and a month or so after adding Primal Defense went down to 6 - optimal is probably under 3 (am guessing from the color coded graph). I never really had any gut symptoms but if the gut is unhealthy - "leaky" - nutrients aren't going to be absorbed very well and more junk will leak into the blood stream. If Shoemaker is correct and the neurotoxins are in the fatty tissues then whenever bile is dumped in the gut so are the neurtotoxins - hence dydbiosis; so by taking the neurotoxins out of the gut it has a chance to heal and you can start to properly absorb the myriads of supplements you take (I take anyway!).Anyway, that's how I see it!"
I think this may be the reason why I have never been able to get my GUT to heal. Anyway all of the tests are covered by medicare and it will be interesting to see what my results are !!!
I hope this is informative for all of you,
Sarah
My CFS/LDA Dr. recently tested me for neurotoxins and I turned up positive. I just had a phone consultation with Dr. S….. www.neurotoxins.com and my CFS/LDA Dr. These were the recommendations that Dr.S gave us: I would not start CSM (cholestyramine) until you had some special tests done. Levels of MSH, MMP9, 24 hour urine for porphyrins, HLA DR by PCR, the minimum. suspect will find help there. Give us your fax#, I'll fax the info re blood tests and consult when results are in. CSM is extraordinarily hard on multiple food intolerant patients. Use must be justified by cause. He also said in his phone consult that people with Celiac Sprue like conditions often have difficulty with the CSM. It can be done, but he wants to make sure that that is the direction we need to go before I am subjected to the treatment. My CFS Dr. was agreeable to ordering the tests through Esoterix Labs and consulting with Dr. S about the results.
Not knowing what these tests measured and how they would help me, I read through all of the info I could find on Dr. S's work and have pieced together somewhat of a picture.
MSH: (MSH is a hypothalamic neuroregulatory/cytokine regulatory/mucus membrane regulatory hormone.)
In short: MSH stands for "MELANOCYTE-STIMULATING HORMONE". It is one of the hormones of the hypothalamus. Neurotoxin Mediated Illness severely affects the hypothalamus and causes a deficiency in MSH. MSH deficiency causes many problems.
Most notable:
1) is the effect it has on decreasing Melatonin production, which causes a crippling sleep disorder. Once Neurotoxin therapy is initiated, MSH increases and so does Melatonin production and sleep.
2) It causes an imbalance in mucus regulation and an overproduction of mucus ensues With Neurotoxin therapy, mucus regulation stabilizes and mucus expectoration ensues abundantly and the overproduction is corrected.
3) It is a hormone critical to the functionality of all the other hormones.
In essence, it's importance can not be emphasized enough.
The HLA DR by PCR is a typing of immune response genes, that can show individual susceptibility to particular neurotoxins. These are not found in controls. In other words, they're beginning to crack the genetic code to show that some people are genetically predisposed to get certain chronic fatiguing illnesses. He has found there are unique HLA genes in his CFS patients; that his Sick Building Syndrome patients have at least three unique triplets of gene biomarkers; his Post-Lyme patients have two; and that these gene-types are quite different from each other. CFS is an illness that includes a genetic susceptibility to particular neurotoxins, which trigger cytokines associated with carrying CNS (chronic neurotoxins), that produce nerve, hormone and immune system dysfunction in the ventromedial nucleus of the hypothalamus. Dr. S is looking at HLA DR genotype analyzed by PCR that contains the standard 2 triplets. One being DRB1-4, DQ-8 and DRB4-53 is the ciguatera genotype. Dr. Hokama's work with ciguatoxin (actually, there are at least 8 types of ciguatoxin) might bring insight into ciguatera (a toxin found in warm water ocean fish) as a source of a chronic fatiguing illness. His other triplet was the multisusceptible DRB1-14, DQ-5, DRB3-52B. These patients are readily affected by Lyme, mold, coag neg Staph, BG algae and dinoflagellates. We also know that the 4-3-3-53 genotype is a particularly rough genotype to have. These people go on to develop what I consider as true CFS, as we can't find a logical source for their illness, except that they develop hypothalamic deficiencies after a cytokine mediated illness, especially Coxsackie, mono, ECHO B27 and possibly mono. The use of HLA DR4 indicating Lyme would simply lump all of these patients as "Lyme." I hope that those who have the DR4 to go and have the more precise assay of HLA DR by PCR.
MMP-9 is activated by cytokine effect; cytokine effects are activated by biological toxin activity. Any result over 400 is cause for concern regarding "active delivery" by MMP-9 of inflammatory elements from the blood into tissues including joint, nerve, muscle and brain.
We are seeing the results of serial MMP-9 testing over the course of treatment shows an endpoint that is highly correlated with resolution of symptoms due to cytokines.
Patients with low MMP-9 values and symptoms need to look to abnormalities in hormonal pathways, especially MSH, that may have been damaged previously by cytokine effects. Low MMP-9 indicates a reduced inflammatory process in illness. Patients with high MMP-9 show an active inflammatory process for which cytokine reduction is necessary.
MMP-9 tells us a great deal if it is high or changing with treatment. We are seeing a significant clinical benefit from lowering of MMP9 with pioglitazone (Actos) and the no amylose diet, with the diet alone showing some lowering of MMP-9.
MMP9 changes hyperacutely with exposure, flares dramatically in antibiotic-induced Herxheimer reactions in Lyme patients, shows remarkable correlation with central nervous system involvement with coagulase negative Staph and a subset (need more data on speciation of risk factors here) of mold patients.
We must recognize that the process by which CFS develops may include an acute neurotoxic event which includes upper respiratory symptoms," says Shoemaker. He believes that the secondary cytokine damage from neurotoxic exposure changes the mucus membranes in the nose, allowing biofilm-forming, slow-growing CNS to release hemolysins (once called delta toxins) that in turn activate a powerful cytokine response. The boost in cytokines disrupts the leptin-MSH production link. This classic, positive feedback system increases cytokines and CNS and reduces MSH. Shoemaker and Hudnell's data show that there's a group of CSM treatment-resistant CFS patients who are coagulase negative Staph (CNS) positive and who have high leptin levels. (Leptin is a hormone made by fat cells that signals the satiety center in the hypothalamus that a person is no longer hungry. Leptin stimulates the production of alpha melanocyte stimulating hormone (MSH), which in turn controls production of endorphins (the body's natural "opiates") and melatonin (which regulates sleep) in the hypothalamus. CFS patients rarely have much MSH.) Eradicating CNS does nothing to the high leptin and low MSH levels in patients with "end-stage CFS," says Shoemaker, but it certainly does in patients who are diagnosed acutely and treated aggressively, preventing irreversible damage to the MSH-manufacturing pathway. CFS patients are the most difficult to treat. They are resistant to a cure with Cholestyramine if their Leptin is high along with a low MSH. They CAN be treated, and get tremendous symptomatic relief, and very often return to the Land of the Living. But the treatment may have to be chronic. Only Dr. Shoemaker and his treatment will tell you this. As it now stands, low MMP9 and illness means not-inflammatory (put the antibiotics and Actos away) and likely simply hormonal. Mid line MMP9 and symptoms, must fix the inflammatory basis and the hormonal. High MMP9, must mega-fix the inflammatory basis.
PORPHYRINS are metabollic markers in the urine that indicate sensitivity from molds, fungi, pollens and chemicals in a patient's environment. If porphyrins are high then one must look to the environment to find the source of neurotoxins. The problem with the mold patients is that so many have been sick or misdiagnosed for so long that their MSH levels are quite low. With low MSH, coag neg Staph grows well; if a given mold patient has a low MSH and a coag neg Staph, what causes the MMP9 to be high? The answer might just be VCS, as visual contrast in coag neg Staph patients is rarely abnormal and it is routinely abnormal in mold patients.
Shoemaker won't yet say that the HLA DR genes or the abnormalities in the leptin/MSH pathway are the "Holy Grail" of CFS research, but he is hoping that his study shows that replacement of MSH improves many (or most!) of the abnormalities of CFS. That study will be done after the animal studies required by the FDA are completed. They hope it will establish an effective MSH dose and the most effective method of MSH delivery
"Patients must have a compatible history, the deficit in VCS, the HLA genotype, an abnormal cytokine response, and the abnormal effects of cytokines on hypothalamic hormones, especially melanocyte stimulating hormone (MSH)," said Shoemaker. "All CFS patients should have the MSH test done."
The team has found particular genotypes of the immune response genes in HLA-DR that show marked consistency within a diagnosis group and marked disparity in other diagnostic groups.
In their study they'll do baseline VCS tests and MSH levels first, and will attempt to show that high levels of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor alpha and leptin improve after treatment. "Most patients improve in two weeks, some with complete abatement of symptoms, but depending on the amount of toxin in your body, it may take longer," says Shoemaker.
There are many kinds of staph, but the one I had when I had staph was staph epi. Following is some info on it:
Staph Epidermidis is a Coagulase Negative Staph. Normally it is considered to be normal flora and not worked up by most labs and considered insignificant by most physicians. It is the research of Dr. Shoemaker that has brought to light it's ability to produce Neurotoxins and it a serious problem and potential cause of Neurotoxin Illness.
With suppressed MSH, the mucus regulation is disrupted and the impacted mucus gives a perfect habitat for this staph to grow. It is a major cause of suppressing MSH and will interfere with effective Neurotoxin therapy. Most labs do not even work up the Coagulase Negative Staphs because they must be cultured for 5 to 6 days instead of 48 hours. Esoterix labs because of the study with Dr. Shoemaker work it up and it's sensitivities to which antibiotics for treatment. If you want the right test done, it must be HLA-DR by PCR.
Dr. Shoemaker has recommended a Compounding Pharmacy specializing is Cholestyramine for those intolerant of sugar, aspartame, and maltodextrin. (Sugar and maltodextrin can stimulate the Neurotoxins and are part of the NO Amylose Diet and Aspartame can stimulate Insulin production). This pharmacist has designed a formulation of the Cholestyramine as per Dr. Shoemaker.
The compounding Pharmacist, Denis Katz, Rph., President of Hopkinton Drug, Inc. is very experienced with Cholestyramine and has been working and studying it for years. He is highly recommended. He can be contacted at:
Denis Katz, RPh., Hopkinton Drug, Inc., 52 Main St., Hopkinton, Mass., 01748, Phone#: 800-439-4441, Fax#: 508-435-5983, Compounding Pharmacist Specializing in Cholestyramine
Dr. S's tests can be ordered by your physician from Esoterix Labs. He must set up an account with them, you cannot do it:
Esoterix Labs, Inc.
7540 Louis Pasteur, Suite 200
San Antonio, TX 78229-4008
1-800-661-4118
www.esoterix.com
I haven't taken the tests yet and then it will be sometime before the results come in…it should be interesting to see where I am in all of this. I found a communication from a lady who took Cholestyramine and found this to be interesting. She says:
"The first several great Smokies stool tests I did all showed a max dysbiosis of 20. 6 weeks after starting cholestyramine it went down to 10 and a month or so after adding Primal Defense went down to 6 - optimal is probably under 3 (am guessing from the color coded graph). I never really had any gut symptoms but if the gut is unhealthy - "leaky" - nutrients aren't going to be absorbed very well and more junk will leak into the blood stream. If Shoemaker is correct and the neurotoxins are in the fatty tissues then whenever bile is dumped in the gut so are the neurtotoxins - hence dydbiosis; so by taking the neurotoxins out of the gut it has a chance to heal and you can start to properly absorb the myriads of supplements you take (I take anyway!).Anyway, that's how I see it!"
I think this may be the reason why I have never been able to get my GUT to heal. Anyway all of the tests are covered by medicare and it will be interesting to see what my results are !!!
I hope this is informative for all of you,
Sarah
