> > > > > someone posted the following article on another list and I'm copying > > it here....i find that this article explains oh so much > > > > > > > pos for stealth, neurotoxins - in the past had herpes 6 and > > epstein barr - have been laid up for months by bug bites so > something > > is definitely wrong with the immune system - rnasel tested high a > few > > years ago. but i love the explanation of cell membrane > > problems...here's the article: > > "...Healing the membrane is virtually...healing the brain..." > > > > ------------------------------------------ > > NEUROTOXIC SYNDROMES > > ------------------------------------------ > > > > The Detoxx System: > > Detoxification of Biotoxins in Chronic Neurotoxic Syndromes > > > > By John Foster, M.D., Patricia Kane, Ph.D., Neal Speight, M.D. > > > > Chronically ill individuals suffering from neurotoxin exposure > > impacts patient populations with CFIDS, Fibromyalgia, MS, Autism, > > Cardiovascular Disease, Depression, Rheumatoid Arthritis, IBS, > > Infertility, ALS, Parkinsons, Lyme, Toxic Building Syndrome, Estuary > > Associated Syndrome, Psychosis, Diabetes without family Hx, Optic > > Neuritis, Refractory Heavy Metal Toxicity, Pulmonary Hemorrhage, > > Stroke. Patients diagnosed with these chronic illnesses may be > > potentially classified as 'Neurotoxic Membrane Syndrome' (NMS) with > > the endothelial cell membrane as the target of degeneration. > > > > While hypercoagulation involves a myriad of proteins, it is > > ultimately a membrane event, essentially disrupting the > phospholipids > > that structure the membrane. Agglomeration (blocked cellular > exposure > > to blood flow/nutrients and impaired cell-to-cell communication) > > indicates elevation of phospholipase A2 and the uncoupling of > > eicosanoids from the cell membrane causing inflammation. The > > agglomeration that eventually occurs is, in essence, a product of a > > weakened membrane, and ultimately a disturbed red cell fatty acid > > profile. > > > > Clinical Research > > > > We have established a biomedical protocol in our clinics, The > > Haverford Wellness Center in Havertown, PA and The Center for > > Wellness in Charlotte, NC for patients with neurotoxic illness. > > Our biomedical approach is an attempt to reach the systemic nature > of > > these tenacious neurotoxic syndromes and provide clinically proven > > methods that eradicate neurotoxins. Our course of action is that of > > freeing the patient of pervasive symptoms of neurotoxic illness in a > > noninvasive manner that heals the membrane, and ultimately the body > > and brain. > > > > The recent pioneering work of Ritchie Shoemaker, M.D., as > > communicated in his book Desperation Medicine and his peer reviewed > > papers (Shoemaker 2001), lends strong support to a connection > between > > Chronic Fatigue Syndrome, Fibromyalgia, Lyme Disease, Pfiesteria > > infection and that of numerous Neurotoxic Syndromes. > > > > Biotoxins as Neurotoxins > > > > The presentation of biotoxin exposure often parallels neurological > > and psychological impairment due to the interrelationship between > the > > ENS (Enteral Nervous System) and the CNS. The biliary tree, gall > > bladder, and bile formation within the liver serve in the vital > > processes of detoxication (disposal of waste products bilirubin, > > heavy metals, biotoxins, xenobiotics), lipid metabolism, transport > > and digestion (bile acids). Abnormalities of the hepatobiliary > system > > may involve biliary stasis whereby infectious material or biotoxins > > reside within the liver, biliary tree and gall bladder, as a viscous > > suspension in biliary sludge. > > > > Biotoxins as bacteria, viruses, parasites, spirochetes, > > dinoflagelletes, and fungus may be within biliary sludge often > > creating neurotoxins impacting the CNS via the ENS, or the Second > > Brain (gut). The occurrence of biliary sludge may be due to > prolonged > > fasting, low fat intake, high carbohydrate diets or exposure to > > pathogens. Restriction of dietary fat may impair biliary flow which > > would be contraindicated in attempting to clear toxicity as bile is > > paramount to cleansing the body and getting biotoxins and heavy > > metals excreted into the fecal matter. > > > > Neurotoxins are minute compounds between 200-1000 KD (kilodaltons) > > that are comprised of oxygen, nitrogen and sulfate atoms arranged in > > such a way as to make the outside of the molecule fat loving and > > water hating. As such, once it enters the body, it tends to bind to > > structures that are rich in fat such as most of our cells, > especially > > the liver, kidney, and brain. Neurotoxins are capable of dissolving > > in fatty tissue and moving through it, crossing cell membranes > > (transporting against a gradient, particularly with potassium) > > disrupting the electrical balance of the cell itself. > > > > As fat soluble neurotoxins move through the cells of the body from > > the GI tract to sinus to lung to eye to muscle, to joint to nerve, > > whereby they eventually enter the liver and the bile. Once > > neurotoxins bind with bile they have access to the liver, the body > > is poisoned over and over again as the bile is re-circulated (first > > released into the intestine to digest fats, and then reabsorbed). > > > > Neurotoxins cause damage by disrupting sodium and calcium channel > > receptors, attacking enzyme reactions involved in glucose production > > thereby disrupting energy metabolism in the cell, manufacturing > > renegade fatty acids as saturated very long chain, odd chain and > > branched chain fatty acids impairing membrane function, stimulating > > enzymes (PLA2) which uncouple essential fatty acids from the cell > > membrane and impairing the function of the nuclear receptor PPAR > > gamma which partially controls transcription (the conversion of > > instructions held in our DNA to RNA which then leads to translation > > or protein production in the cell). > > > > Heavy Metals reside in Fatty Tissue with Biotoxins > > > > Heavy metals are also lipid soluble and often compound the removal > of > > biotoxins (Aschner et al 1990, 1998; Dutzak 1991). As has been > > observed by many clinicians, often as the patients' heavy metal > > toxicity is addressed they are faced with the additional > complication > > of the presence of biotoxins. Biotoxins and heavy metal exposure > > co-exist within the cell membrane and fatty tissue requiring > > consideration for both types of toxicity in regard to patient > > intervention. > > > > By stabilizing glutathione we in turn impact metallothionein markers > > (Nordberb and Nordberb 2000, Ebadi et al 1995, Sato et al 1995, > > Kerper et al 1996, Susanto et al 1998), glycoaminoglycans or GAGS > > (Klein 1992), methylation, sulfation, hepatic and renal function as > > we introduce treatment protocols for detoxication with gentle, > > natural modalities that unload cellular toxicity safely. GSH > infusion > > by fast IV push has been a remarkable tool to unload the body burden > > of heavy metals and neurotoxins in both pediatric and adult > > populations, without side effects. > > > > Renegade fatty acids as Neurotoxin Markers > > > > Renegade fats as very long chain fats (VLCFAs) that are over > > expressed, disrupt the membrane structure. There is a beautiful > > geometry to the membrane that is highly sensitive to the size of the > > lipid chains. The overall width of the fatty acid portion of the > > membrane is ~3 ½ nm which must be maintained for stability. > > Saturated > > or monounsaturated fatty acids with a length of 16 or 18 carbons and > > polyunsaturated fatty acids of 18 to 22 carbons are preferred to > > permit the structure to maintain optimal horizontal fluidity. > VLCSFAs > > that range from 20 to 26 carbons force the parallel dimensions > > vertically. There simply is not enough room. > > > > The distortion weakens the phosphate bonds that derive their strong > > attraction only as long as the phospholipids are parallel to each > > other on both sides of the membrane. The cell weakness is then > > expressed in leaky attraction to ion channels and receptors which > > marginalize cell cytosol fluids and electrolytes with the only > option > > as early cell death. > > > > The Brain is Comprised of 60% Fat > > > > To view the brain beyond its architecture as a biological > > orchestration of the physical and chemical constituents necessary > for > > performance, we cannot begin to conceptualize without considering > the > > importance of fatty acids as the human brain is 60% lipid. Dendrites > > and synapses are up to 80% in lipid content. Although Arachidonic > > acid (AA) has been given a negative association, it is the most > > prominent essential fatty acid in the red cell and comprises 12% of > > the total brain and 15.5% of the body lipid content. > > > > If AA is depleted by overdosing with marine or flax oil establishing > > the balance of the EFAs is profoundly impaired. Often both > > prostaglandin one and two series relating to omega six metabolism > are > > compromised when flax and marine oils are overdosed or lipid intake > > is insufficient. When AA, the lead eicosanoid of the body, is > > suppressed due to excess intake of omega 3, toxicity or disease the > > control circuitry of the body is impaired as is clearly viewed in > the > > patient's presentation. > > > > Arachidonic acid is preferentially wasted in states of heavy metal > > toxicity (Tiin and Lin, 1998) and has been observed to be sharply > > suppressed in RBC lipid analysis in states of heavy metal toxicity > > (Kane, clinical observation 1997-2002). > > > > The fatty acid cleaving enzyme PLA2 > > > > In states of toxicity via biotoxins or heavy metals there is a > > dramatic elevation in Phospholipase A2 (PLA2) activity (Verity et al > > 1994) Increases in PLA2 activity result in premature uncoupling of > > the essential fatty acids (EFAs) from phospholipids in the cell > > membrane. Accelerated loss of EFA places the patient in a severely > > compromised position as that of inflammation which results from the > > promiscuous release of AA in the presence of an overexpression of > > PLA2. Carbohydrate consumption, as one of the most profound > > stimulators of PLA2, must be restricted to control the insulin > > response and the subsequent loss of EFAs. > > > > Phospholipids and Neurons > > > > Phospholipids, cholesterol, cerebrosides, gangliosides and > sulfatides > > are the lipids most predominant in the brain residing within the > > architectural bilayers (Bazan et al 1992). The phospholipids and > > their essential fatty acid components provide second messengers and > > signal mediators. In essence, phospholipids and their essential > fatty > > acid components play a vital role in the cell signaling systems in > > the neuron. The functional behavior of neuronal membranes largely > > depends upon the ways in which individual phospholipids are aligned, > > interspersed with cholesterol, and associated with proteins. > > > > All neurotransmitters are wrapped up in phospholipid vesicles. The > > release and uptake of the neurotransmitters depends upon the > > realignment of the phospholipid molecules. The nature of the > > phospholipid is a factor in determining how much neurotransmitter or > > metal ion will pass out of a vesicle or be taken back in. > > Phospholipid re-modeling may be accomplished by supplying generous > > amounts of balanced lipids and catalysts via nutritional > intervention > > and the use of intravenous Phospholipid Exchange (IV Phosphatidyl > > choline). > > > > Hypercoagulation and Membrane Integrity > > > > An undesirable course of events in an exposure to biotoxins is > > agglomeration in a hypercoagulation state. The distorted membrane > > with its weakened structure and almost absolute reduced fluidity is > > powerless to resist coagulation. A highly fluid membrane would kick > > off an accumulation of oxidized cholesterol; it would not permit it > > to attach. This is not the case when the membrane is compromised, as > > in much of the patient population affected with neurotoxic illness. > > > > Hypercoagulation is predominantly a non-regulated mass of proteins > > disrupting function. When referencing the artery; hypercoagulation > > invariably involves the plasmic side of the cell and if endothelial > > cells of the vascular system are targeted by a toxin (virus, > > neurotoxin, metal, antibody, etc) , restriction of blood flow > > ultimately results. If a neuron is targeted then signaling is > > disrupted. The presence of neurotoxins invariably involves PLA2, > > which is the "sergeant at arms" monitoring cell membrane health. > > A membrane disturbance(unwanted mass) would trigger PLA2, which > > hydrolyses the release of eicosanoids, which would then induce > > inflammation and call to attention the clean-up committee, i.e. > > macrophages. > > > > Hypercoagulation is a restrictive agglomeration, (mass) that occurs > > principally on the membrane of endothelial cells blocking the flow > of > > vital fluids, blood, bile, etc., with a high causal relationship to > > oxidation, and equally to toxicity, quite often neurotoxins. > Oxidized > > LDL (Sobel et al 2000) is predominantly a membrane disturbing event > > agglomerating and attaching to endothelial cells, while neurotoxins > > can move through the lipid membrane and attack the cell itself. > > > > The Liver as the Center of the Storm > > > > Unhealthy bacteria have been known to colonize the liver and its > > biliary system. These bacteria as well as viruses, spirochetes, > > dinoflagellates, and the like can synthesize very long chain > > saturated or renegade fats (Harrington et al 1968, Carballerira et > > al 1998) that lead to liver toxicity, biliary congestion, impairment > > of prostaglandin synthesis and the release of glutathione (Ballatori > > et al 1990). Lipids vibrate in the cell at millions of times/second. > > The double bonds of the omega 6 and omega 3 lipids are the singing > > backbone of life expressed through their high energy level. > > > > These bonds are their vibratory song, and they absolutely carry a > > tune befitting every act and function in the exercise of life, > > providing all 70 trillion of our cells their flexible nature. When > > renegade fats are over represented in the cell membrane they result > > in off key expression, and if strong enough, may spell cellular > death > > and apoptosis. Healing the outer leaflet of the membrane (Schachter > > et al 1983), comprised primarily of phosphatidylcholine, with > > phospholipid therapy, is our highest priority in addressing chronic > > illness and hypercoagulation. > > > > The Visual Contrast Sensitivity Test > > > > Our clinical approach is to first confirm that neurotoxin mediated > > illness could in fact be a problem for the patient via the Visual > > Contrast Sensitivity test that isolates deficits in velocity of flow > > in retinal capillaries. If the patient scores poorly on this test > > then the evaluation may include screening for cytokine elevations > > followed by coagulation and red blood cell lipid testing through > > Johns Hopkins/interpretation through BodyBio. (For pediatric > patients > > the Heidelberg Retinal Tomogram Flow Meter Evaluation may be > > performed in place of the Visual Contrast Test by an > > ophthalmologist.) > > > > Neurotoxins and Cytokines > > > > Once neurotoxins enter the cell they move toward the nucleus turning > > on indirectly the production of cytokines such as TNF alpha, IL6, > and > > IL-1Beta (Shrief and Thompson 1993, Tsukamoto 1995, Abordo et al > > 1997, Rajora et al 1997, Brettelal 1989, Hassen et al 1999, Davidson > > 2001). TNF alpha will stimulate macrophages in the body > (macrophages) > > to become active. The white cells are also induced to gather in the > > area of the cytokine (TNF alpha) release. In addition, TNF alpha > > induces endothelial cell adhesion. > > > > Endothelial cells which line the blood vessels of the body become > > "sticky" in conjunction with the increase in white cells. Increased > > blood viscosity results in restricted blood flow in neurotoxic > > patients leading to fatigue and discomfort, and quite possibly > > disturbed toxic photoreceptor lipid structures that become > > compromised with subsequent reduction in visual performance. > > > > The cellular impact of biotoxin and heavy metal burdens results in > > disturbed prostaglandin synthesis, poor cellular integrity, > decreased > > GSH levels (DeLeve and Kaplowitz 1990, Dentico et al 1995, Hayter et > > al 2001, Miles et al 2000, Nagai et al 2002, Zalups and Barfuss > 1995, > > Watanabe et al 1988, Fernandez-Checa et al 1996), significant > > suppression of omega 6 arachidonic acid and marked elevation of > > Renegade fats and ultimately with demyelination (depressed DMAs). > > The presence of VLCFAs are evidence of peroxisomal dysfunction and > > suppression of the beta oxidation of lipids and cellular > respiration. > > > > Renegade fats (VLCSFAs, Odd Chains, Branched Chains) are represented > > as an increase in fat content in the brain as discovered in stroke > > patients examined by Stanley Rapoport, Chief of the Laboratory of > > Neuroscience at the NIH. Biotoxins and heavy metals are lipid > soluble > > thus the effect upon cellular processes and hepatobiliary function > is > > often gravely deranged. Often, patients do not possess a gross > burden > > of toxins but rather a burden that has a finite impact upon the cell > > by blocking receptor sites such as G proteins, which act as a relay > > system through the cell. > > > > Peroxisomes, most prevalent in the liver and kidney, are organelles > > within the cell that play a crucial role in clearing xenobiotics and > > the third phase of detoxification. Peroxisomes are intimately > > involved in cellular lipid metabolism (Bentley et al 1993, Mannaerts > > and Van Veldhoven 1992, Luers et al 1990, Leiper 1995) as in the > > biosynthesis of fatty acids via ß-oxidation involving > > physiologically > > important substrates for VLCFAs, thromboxanes, leukotrienes and > > prostaglandins. > > > > The creation of a prostaglandin is an oxidative event (Diczfalusy > > 1994). Inappropriate use of antioxidants (mega-dosing) will inhibit > > ß-oxidation, the production of prostaglandins and cellular > > metabolism, thus the liberal use of potent antioxidants would be > > contraindicated in the buildup of Renegade fats as VLCFAs, Odd Chain > > and Branched Chains (Akasaka et al 2000) which are the hallmark of > > toxicity (Kane and Kane 1997, Kane 1999, Kane 2000, Roels et al > 1993, > > Rustan et al 1992). > > > > Peroxisomal oxidation enzymes are suppressed by elevation of > > cytokines such as TNFalpha (Beier et al 1992). Individuals with > > immune, CNS, cardiac, GI and endocrine disorders often present with > > complex xenobiotics involving disturbances in the cytochrome P450 > > superfamily (hepatic detoxification difficulties) which parallels > > disturbances in peroxisomal function. > > > > The cytochrome P450's are responsible for the biotransformation of > > endogenous compounds including fatty acids, steroids, > prostaglandins, > > leukotrienes and vitamins as well as the detoxification of exogenous > > compounds resulting in substantial alterations of P450s (Guengerich > > 1991) as xenobiotics may turn off or greatly reduce the expression > of > > constitutive isoenzymes (Sharma et al 1988). > > > > Targeted Nutritional Intervention for Toxicity > > > > Inadequate stores of arachidonic acid can compromise P450 function > > (McGiff 1991). Oral application of hormones such as pregnenolone, > > DHEA (Di Santo et al 1996, Ram et al 1994, Rao et al 1993) or > thyroid > > stimulate peroxisomal proliferation and the ß-oxidation of > > Renegade > > fats as would nutrients (riboflavin, pyruvate, manganese) and > > oxidative therapies. > > > > Anti-oxidants slow cellular metabolism and must remain in the proper > > balance with all the essential nutrients and substrates (lipids, > > protein) to maintain metabolic equilibrium. Removal of renegade fats > > in the diet is accomplished by the avoidance of mustard, canola oil > > (Naito et al 2000), peanuts and peanut oil which contain VLCSFAs > that > > can challenge patients with liver and CNS toxicity. > > > > The oral use of butyrate, a short 4-carbon chain fatty acid, is of > > striking benefit (Fusunyan et al 1998, Segain et al 1983, Yin et al > > 2001) in mobilizing renegade fats, lowering TNFalpha, sequestering > > ammonia, and clearing biotoxins. > > > > In states of toxicity it is paramount to stabilize omega 6 fatty > > acids and the lead eicosanoid (Attwell et al 1993) Arachidonic acid > > (AA) before introducing omega 3 lipids. There exists a crucial > > balance between omega 6 and omega 3 fatty acids in human lipid > > metabolism which has only recently been brought into clearer focus > > through the work of Yehuda (1993, 1994, 1995, 1998, 2000, 2002). His > > development of the SR-3 (specific ratio of omega 6 to omega 3) has > > revealed that the optimum ratio of omega 6 to omega 3 FAs is 4:1. > > > > AA, the lead eicosanoid, must be stable first along with the other > w6 > > EFAs before w3 fatty acids are introduced and balanced. Clinicians > > are often met with poor patient outcomes when merely administering > > omega 3 lipids without first introducing omega 6 fatty acids, > > stabilizing the structural lipids, increasing the fat content of the > > diet, stimulating the ß-oxidation of renegade fatty acids, > > flushing > > of the gall bladder/biliary tree and supporting digestion of fats > > with bile salts and lipase. > > > > The manipulation of lipid distortion involves two basic essential > > fats: omega 6 and omega 3. The body loses its ability to metabolize > > fats in states of toxicity and therefore becomes depleted in the > > eicosanoids and prostaglandins. Essential fatty acids are the > > precursors to the regulatory prostaglandins which are "local > > hormones" providing the communication controlling all cell to cell > > interactions. The human cell membrane cannot be supported nor its > > function controlled without respect to lipid substrate, yet fatty > > acid metabolism has been poorly delineated in the medical > literature. > > > > An optimum balance of fatty acids make up the dynamic membrane. The > > membrane of every living cell and organelle is composed of two fatty > > acid tails facing each other. This bilipid layer is so minute (3.5 > > nanometers) that it would take 10,000 membranes layered on top of > > each other to make up the thickness of this paper. Yet the dynamics > > that occur within this tiny envelope with organelles prancing up and > > down the cytoskeleton microtubules is a microcosm that is a > challenge > > for the human mind to envision. Mercury toxicity damages the > > microtubule structure of the cell. All cells must synthesize > > molecules and expel waste. > > > > All cells must create, through gene expression, the proteins needed > > for cellular gates embedded in the membrane as ion channels and > > receptors. The ultimate control of how those peptides behave rests > > with the character of the membrane while the integrity of the > > membrane rests with the structural (oleic, stearic, palmitic, > > cholesterol) and essential lipids (omega 6, omega 3). Without > control > > of membrane function through lipid manipulation, detoxication is > > compromised. In essence, the life of the cell is intimately tied to > > health of the membrane and the health of the entire organism. > > > > Our clinical protocol is to initiate treatment with changing the > > patients' overall diet, addressing the lipid balance and especially > > the outer lipid leaflet of the cell membrane through fatty acid > > therapy and the addition of supplementation targeted towards > > dissolving fibrin, clearing the liver/biliary tree, and healing the > > cell membrane. Patient progress is evaluated through the Visual > > Contrast Test and repeat lab evaluation. > > > > Blood thinning agents such as Heparin and Warfarin increase blood > > flow around the blocked endothelium, however, reconstituting > membrane > > fluidity can directly address coagulation in a natural restorative > > way. Vibrant healthy membranes will not permit agglomeration. The > > high polyunsaturated lipids with a preponderance of > > phosphatidylcholine on the plasmic surface precludes undesirable > > clumping to occur. Treatment modalities should address dissolving > > fibrin and healing the cell membrane. > > > > Spreading Infection > > > > It has been suggested that the use of heparin will address > > hypercoagulation. Recent data from JAMA (Stephenson 2001) indicates > > that the use of low dose heparin may transform a 'benign fungal > > infection into a toxic shock-like reaction'. This research was > > presented at the 39th annual meeting of the Infectious Diseases > > Society of America in 2001 by Margaret K. Hostetter, M.D. of Yale > > University School of Medicine (Hostetter 2001 and San-Blas et al > > 2000). > > > > Hostetter and colleagues found that Candida albicans can attach to > > host cells and form invasive hyphae. Low dose heparin utilized in > > procedures for hospitalized patients through the practice of heparin > > in intravascular catheters may transform C. albicans into a > > life-threatening pathogen. Hostetter was able to identify a gene, > > INT1, encoding a C. albicans surface protein, Intlp, which was > linked > > with adhesion, the ability to grow filaments and ultimately > virulence > > of C. albicans of a systemic nature. > > > > The use of heparin raises the cytokines TNF alpha and IL-6 > > (Stephenson 2001) in addition to Phospholipase A2 (Mudher et al > 1999; > > Kern et al 2000; Farooqui 1999; Verity et al 1994). Biotoxins which > > form neurotoxins, may create a state of hypercoagulation from the > > rise in TNF alpha. Consequently, the use of heparin may exacerbate > > the hypercoagulation and the neurotoxic condition. The source of the > > problem- biotoxins, which have formed neurotoxins creating a state > of > > hypercoagulation, must be addressed from the context of the > > underlying neurotoxic condition and healing the cell membrane. > > > > Evidence Based Clinical Protocols > > > > By stabilizing lipid status with intravenous Phospholipid exchange > > and oral EFA supplementation we have remarkable tools to unload the > > body burden of neurotoxins (Jenkins et al 1982, Cariso et al 1983, > > Jaeschke et al 1987, Kolde et al 1992) in both pediatric and adult > > populations, without side effects. Oral use of phospholipids in a > > Liver Flush is also an effective intervention in addressing > > neurotoxic syndromes. > > > > Through isolating individual fatty acids and dimethylacetyls in red > > cells we can now examine the cellular integrity/structure, fluidity, > > the formation of renegade fats that impair membrane function, > > myelination status, and the intricate circuitry of the > > prostaglandins. The systemic health of the individual patient may > > reached and targeted nourishment utilized through evidence based > > intervention which may yield positive patient outcomes. > > > > Healing the membrane is virtually healing the brain. > > > > References and additional information, see: > > http://www.mercola.com/2003/aug/9/detoxification_biotoxins.htm > > > > Neal Speight, M.D. may be reached at Center For Wellness in > > Charlotte, > > NC. Patricia Kane, Ph.D. at the Haverford Wellness Center in > > Havertown, > > PA. or to obtain the 'The Detoxx Book: Detoxification of Biotoxins > > in > > Chronic Neurotoxic Syndromes' at 888.320.8338 or 856.825.8338 > > > > ---------- > > ©Copyright Dr. Joseph Mercola, 2003. All Rights Reserved. This > > content may be copied in full, as long as copyright, contact, and > > creation information is given, only if used only in a not-for-profit > > format. If possible, I would also appreciate an endorsement and > > encouragement to subscribe to the newsletter. If any other use is > > desired, written permission is required. > > > > Community e-mail Addresses: > > > > Post Message : [email protected] > > Contact List Owner : [email protected] > > > > To change your subscription options for the List, send an empty > > message to: > > > > Unsubscribing : > [email protected] > > No Mail ( temporary ) : [email protected] > > Daily Digest : [email protected] > > Indivdual Messages : [email protected] > (Default) > > > > For Research on Chronic Fatigue Syndrome ( CFS ), visit the List's > > Website at: http://www.cfsresearch.org/ > > > > > > > Lyme Aid's main website can be found at: > http://groups.yahoo.com/group/Lyme-Aid . You can
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