Re: Detoxification of Biotoxins in Chronic Neurotoxic Syndrome

[Guest guest]

Anita Kessler, here in Las Vegas, took her son to this clinic in

Pennsylvania. Both she and her son were sick from her implants. It

was quite an involved process, but in the end, I am not sure she

stayed with them, but I think she found a local doctor to use

homeopathy and they had some success with that. Anita has not been in

contact. I need to get in touch with her. She buys raw milk from the

same woman I do.

Interestingly, her son is unable to consume homogenized, pasteurized

milk at all, without side effects. However, he can consume gallons of

raw milk and thrive!

Patty

>

> The Detoxx System: Detoxification of Biotoxins in Chronic Neurotoxic

Syndrome

>

>

> By , M.D., 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,

> to 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 s 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

> CytokinesOnce 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 1993, Tsukamoto 1995, Abordo et al 1997,Rajora

et al 1997,

> Brettelal 1989, Hassen et al 1999, son 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 ToxicityInadequate

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 (son 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 (son 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 ( 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 for this Article

> Neal Speight, M.D. may be reached at Center For Wellness in

Charlotte, NC.

> 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

>

>

http://articles.mercola.com/sites/articles/archive/2003/08/09/detoxification-b

> iotoxins.aspx

> The Detoxx System: Detoxification of Biotoxins in Chronic Neurotoxic

> Syndrome - Articles

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

> **************

> New MapQuest Local shows what's happening at your destination.

> Dining, Movies, Events, News & amp; more. Try it out

> (http://local.mapquest.com/?ncid=emlcntnew00000002)

>