Miracle? Mum cure's daughter's brain damage

[crystal sage]

As the thread I posted earlier seems to have'disappeared' unless someone else can find it for me???

I have restarted it....

" Ralda's Daughter Abbie had suffered brain damage after being dangerously ill with wild measles encephalitis...

Years later when Abbie had a backyard fall and her mother was cleaning the wound.. Ralda tried to calm down her screams by explaining to her daughter the importance of cleaning the wound...and that everything heals if you give it the right treatment...

That got Ralda James thinking... can she find the right treatment to cure her daughter???

The Adelaide mum didn't don a white coat...and take to the laboratory...she instead turned to her local library and then her local supermarket and finally her suburban kitchen.

After extensive reading Ralda discovered that Abbies brain damage was caused by the destruction of myelin,the sheath surrounding nerve cells in the brain that aids in the transmission of nerve impulses. " I knew I needed to find a way to restore the myeline'"she says..

She was determined to have a go...

After 4 months of research and looking at the backs of packets in the supermarkets ( she stresses she isn't a doctor or a scientist and didn't look at any other research into restoring myelin as she figured it would be available if they knew how) she reasoned she knew what myelin was and used the ingredients from supermarket shelves to make her own concotion...

She cut out all diet drinks and dark coloured soft drinks..increased Abbies diet of full-fat dairy and waited to see what would happen..

About a week later she got a noise out of her...four months later she was talking..( Abbie was about 7 at this time) each day Ralda gave her miracle reciepe...and each day brought staggering improvements..Suddenly she was palying sport..talking away happily and laughing again...Ralda had borught her little girl back !!!!!!!"

[crystal sage]

"Vitamin B12 is vital for making DNA, RNA and is vital for myelin sheath production, this insulates nerves and keeps the nervous system calm and balanced. It is also needed for cell division. It is needed for red cell production (oxygen carrying system) and energy production. Superfood is particularly rich in B12, so vital for vegans and vegetarians who don't have meat sources."

http://www.herbs-hands-healing.co.uk/Super...tionalinfo.html

"Cholesterol is distributed in the body, especially in the bile, blood, brain tissue, liver, kidneys, adrenal glands, and myelin sheaths or nerve fibers."

http://www.kingdomhealth.net/

Edited December 12, 2006 by crystal sage

[crystal sage]

Another interesting article on Stimulating remyelination

http://www.bio.net/hypermail/neuroscience/...ber/029728.html

There is a lot of research going on in demyelinating diseases,

which inthe long run may be successful. But do we have to wait

passively? Is there nothing we can do now, immediately?

Are there any substances AVAILABLE NOW, which do

stimulate remyelination in demyelinating diseases?

I did a literature research, and I found quite a number of

substances, which might possibly stimulate remyelination

by different pathways. Theremay even be MORE of those

substances. On the other hand I realise, that a lot of this is

speculation, but speculation based on in vitro research,

based on animal research or based on extrapolation from

related research.

Here are my candidates (in no particular order):

-immunoglobulins;

-DHEA and/or progesterone;

-Insulin-like Growth Factor-1 (IGF-1) and other nerve growth

factors or substances, which stimulate the body's own

production of these factors;

-1,25-Dihydroxyvitamin D3 (vitamin D);

-retinoic acid (vitamin A);

-catalase and factors, which stimulate the production of this

enzyme (like NGF e.g.);

-vitamin B6;

-NAC;

-combinations of NAC with progesterone, vitamin C, or

Trolox, a water-soluble vitamin E analogue;

-different free radical scavengers, vitamin E and idebenone;

-arginine;

-myo-inositol;

-cysteine and cystine;

-antioxidants;

-electrical (magnetic) stimulation?

-cyclophosphamide;

-polyunsaturated fatty acids;

-deprenyl

-thiamin (vitamin B1)

I have compiled the following excerpts from medical articles, in

which I found these substances and their possible effect on

remyelination. And I should very much like to hear about

experience with these and other substances.

Rolf Busch

(Hamburg/Germany)

(Hamburg/Germany)

---------------------------------------------------------------

The restoration of MS patients to full health will ultimately be a

two step process. The first step being the development of an

effective treatment or cure for MS and the second the application

of therapeutic strategies designed to repair the existing damage

to myelin. ...this second step (is) known as remyelination.

Myelin is synthesised by a specialised cell in the CNS called an

oligodendrocyte. Oligodendrocytes develop from progenitor

(immature) cells that proliferate in a region of the brain called

the sub-ventricular zone.These progenitor cells migrate to the

regions of the brain that are to be myelinated, where they

differentiate (mature) into myelin producing oligodendrocytes.

Remyelination Promoted by Growth Factors

While the two growth factors mentioned above (FGF and PDGF)

do not stimulate mature oligodendrocytes to divide, FGF is

ableto increase the myelin forming potential of mature

oligodendrocytes even when tested on human cells. Similar

effects have been observed when using insulin-like growth

factor-1 (IGF-1). Growth factors such as PDGF, neurotrophin-3

and ciliary neurotrophic factor are able to increase the survival

of mature oligodendrocytes. Thus, the administration of these

growth factors to MS patients as therapeutic agents may protect

oligodendrocytes from destruction as well as promote

remyelination.

Conclusion

A number of strategies are currently being developed to promote

remyelination. The advances in the past few years have been

significant and offer tremendous hope. In the short term the

application of treatments that promote remyelination may slow

disease progression in MS patients and help prevent some of

the incapacitating symptoms. In the longer term,once an

effective treatment has been developed for MS, such

treatment may help MS patients regain function of those

deficits caused by this debilitating disease 1.

But regenerating myelin may also be beneficial

in demyelinating diseases for which no effective treatment has

been developed (e.g., multiple sclerosis). Indeed, the new myelin

may well be able to withstand new attack by the primary

demyelinating agent, either permanently or for long periods of

time.

Immunoglobulins. The results of the immunoglobulin (IgG)

placebo-controlled trial conducted by Drs. Rodriguez and

Noseworthy at the Mayo Clinic will be available by year end.

Progesterone. Dr. Etienne Baulieu has recently shown that

progesterone stimulates remyelination in the rat PNS 2.

Another treatment showing promise is intravenous

immunoglobulin (IVIg) therapy. Animal studies have shown this

treatment may not only decrease exacerbations and neurological

disability, but may also hold the potential for myelin repair.

With respect to remyelination, different types of growth factors

are being tested with animal models. Human trials are expected

to begin in 1998 3.

(There is) evidence that growth factors may have a role in

promoting CNS remyelination by enhancing the survival and

stimulating the proliferation and recruitment of remyelinating

oligodendrocytes 4.

"Glial cell line-derived neurotrophic factor (GDNF) has

significant therapeutic potentials, in particular for

neurodegenerative disorders... our results indicate that 1,25-

(OH)2 D3 is effective at concentrations as low as 10(-10) M and

that retinoic acid has additive effects. These data indicate that

1,25-(OH)2 D3 is a potent inducer of GDNF expression and

suggest that 1,25-(OH)2 D3 may contribute to the regulation of

GDNF in vivo 5."

...this study indicates that clinically significant remyelination is

possible in human CNS 6.

The occurrence of remyelination depends upon the intensity and

time of exposition to the demyelinating agent. Remyelination in

the CNS with complete restoration of conduction may be

made by oligodendrocytes or Schwann cells which invade

the CNS when astrocytes are destroyed 7.

The limiting factor to remyelination is the persistence of the

demyelinating agent.

Nevertheless the demonstration that the process occurs leads

to increasing hope that clinically useful remyelination may be

encouraged in the future either by more carefully controlling the

extent of demyelination or by finding ways of stimulating

oligodendrocyte proliferation and access to the axon 8.

...the use of immunosuppression, immunoglobulins, protein

growth factors, and glial cell transplantation are the primary

experimental therapies designed to promote CNS remyelination

9.

Basic FGF and PDGF are known to stimulate their proliferation

and delay their differentiation. Lack or excess of retinoic acid

(RA) has been known for a long time to alter brain development

suggesting that this compound is involved in normal brain

development. Here we report that RA partially inhibits both

the proliferation and the differentiation of oligodendrocyte

precursor cells 10.

These findings indicate that IGF-I is a potent inducer of

brain growth and myelination in vivo.

Taken together, these in vivo studies indicate that IGF-I can

influence the development of most, if not all, brain regions, and

suggest that the cerebral cortex and cerebellum are especially

sensitive to IGF-I actions. IGF-I's growth-promoting in vivo

actions result from its capacity to increase neuron number,

at least in certain populations, and from its potent stimulation

of myelination 11.

[crystal sage]

Studies show that good diet is important for Remyelination... eg in cases of MS to prevent future osteoperosis...yet extensive studies in these areas have not been done!!! Why???

Eg how vitamin A is very important.....

http://neurology.health-cares.net/multiple...s-nutrition.php

"MULTIPLE SCLEROSIS AND NUTRITION

Stefan Schwarz; Hans Leweling Source: Multiple Sclerosis, Feb. 2005, Vol 11, No. 1, pp. 24-32

Benefits from any particular diet in multiple sclerosis (MS) have not yet been proven. It is, however frequently stated that malnutrition may potentially exacerbate the symptoms of MS. There is some evidence that a high intake of saturated fat increases the incidence of MS. Epidemiological studies imply that unsaturated fatty acids may have a possible effect on the course of MS. However, the results of controlled studies are ambiguous. A meta-analysis of three small controlled clinical trials suggests a benefit from linoleic acid. Intake of Vitamin D is associated with a lower incidence of MS. In MS, the risk of osteoporosis is high, and prophylactic vitamin D and calcium should be considered at an early stage. The role of minerals, trace elements, antioxidants, vitamins or fish oil is unclear. The possible relationships between diet and MS have not been subjected to adequate study. It seems possible that in the future, diets or dietary supplements may become recommended forms of treatment for MS."

http://www.fortnet.org/NCMSN/0405.html

Also and interesting fact mentioned by my Naturapath once was that the body is designed to heal itself...this is how I understood it..in my scattered way... LOL!!... eg when there is an injury the body heat increases in that area..inflamation accurs preparing the affected area and readying it for the body's natural healing response... that many people automatically take anti-inflamatories etc... which then in effect blocks off the bodies call signal and communication system of organizing it's own repair team to heal!!!

So this next article rang a bell too!!!!

"INFLAMMATION STIMULATES REMYELINATION IN AREAS OF CHRONIC DEMYELINATION

Foole A.K., Blakeman, W.F., Brain, 2005 Mar., 128/181,34,J Neurol Sci 2005 Feb 15;228(2):161-6.

A major challenge in multiple sclerosis research is to understand the cause or causes of remyelination failure and to devise ways of ameliorating its consequences. This requires appropriate experimental models. Although there are many models of acute demylenation, at present there are few suitable models of chronic demyelination. The taiep rat is a myelin mutant that shows progressive myelin loss and, by 1 year of age, its CNS tissue has many features of chronic areas of demyelination in multiple sclerosis: chronically demyelinated axons present in an astrocytic environment in the absence of acute inflammation. Using the taiep rat and a combination of X-irradiation and cell transplantation, it has been possible to address a number of questions concerning remyelination failure in chronic multiple sclerosis lesions, such as whether chronically demyelinated axons have undergone changes that render them refractory to remyelination and why remyelination is absent when oligidodendrocyte progenitor cells (OPCs) are present. Our experiments show that i) transplanted OPCs will not population OPC-containing areas of chronic demyelination; (ii) myelination competent OPCs can repopulate OPC-depleted chronically demyelinated astrocytosed tissue, but this repopulation does not result in remyelination-closely resembling the situation found in some multiple sclerosis plaques; and (iii) the induction of acute inflammation in this non-remyelinating situation results in remyelination. Thus, we can conclude that axonal changes induced by chronic demyelination are unlikely to contribute to remyelination failure in multiple sclerosis. ....

'Rather, remyelination fails either because OPCs fail to repopulation areas of demyelination or because if OPCs are present they are unable to generate remyelinating oligodendrocytes owing to the presence of inhibitory factors and/or a lack of the stimuli required to activate these cells to regenerate remyelinating oligodendrocytes. This non-remyelinating situation can be transformed to a remyelinating one by the induction of acute inflammation.'"

Edited December 12, 2006 by crystal sage

[crystal sage]

http://content.karger.com/ProdukteDB/produ...ArtikelNr=91917

Dietary polyunsaturated fatty acids (PUFAs) have been postulated as alternative supportive treatment for multiple sclerosis, since they may promote myelin repair. We set out to study the effect of supplementation with n-3 and n-6 PUFAs on OLN-93 oligodendroglia and rat primary oligodendrocyte differentiation in vitro. It appeared that OLN-93 cells actively incorporate and metabolise the supplemented PUFAs in their cell membrane. The effect of PUFAs on OLN-93 differentiation was further assessed by morphological and Western blot evaluation of markers of oligodendroglia differentiation: 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP), zonula occludens-1 (ZO-1) and myelin-associated glycoprotein (MAG). Supplementation of the OLN-93 cells with n-3 and n-6 PUFAs increased the degree of differentiation determined by morphological analysis. Moreover, CNP protein expression was significantly increased by gamma-linolenic acid (GLA, 18:3n-6) supplementation. In accordance with the OLN-93 results, studies with rat primary oligodendrocytes, a more advanced model of cell differentiation, showed GLA supplementation to promote oligodendrocyte differentiation. Following GLA supplementation, increased numbers of proteolipid protein (PLP)-positive oligodendrocytes and increased myelin sheet formation was observed during differentiation of primary oligodendrocytes. Moreover, increased CNP, and enhanced PLP and myelin basic protein expression were found after GLA administration. These studies provide support for the dietary supplementation of specific PUFAs to support oligodendrocyte differentiation and function.

Copyright © 2006 S. Karger AG, Basel

Edited December 12, 2006 by crystal sage

[crystal sage]

"Inflammation stimulates remyelination in areas of chronic demyelination ..."

http://www.pnas.org/cgi/content/full/97/13/7585?ck=nck

[crystal sage]

"during remyelination reverts to that seen during normal development. ... a minor constituent of myelin, is a sialic acid binding lectin with two .."

http://www.ihop-net.org/UniPub/iHOP/gs/122649.html

Biochem J. 1981 May 1; 195(2): 525–528.

Copyright notice

Demonstration of five major glycoproteins in myelin and myelin subfractions.

E E Mena, B W Moore, S Hagen, and H C Agrawal

Abstract

Myelin was found to contain five major glycoproteins with molecular weights of 120000, 95000, 88000, 43000 and 38000. Light myelin contained only 5-7% of the amount of these glycoproteins in whole myelin, whereas heavy myelin and the membrane fraction contained amounts nearly identical with whole myelin. Since all the major and minor glycoproteins, with the exception of 120000-mol-wt. glycoprotein, were detected only after treating the myelin membrane with neuraminidase, N-acetylneuraminic acid is a terminal sugar residue in these glycoproteins.

http://www.pubmedcentral.nih.gov/articlere...i?artid=1162919

[crystal sage]

Lots of info here...and other similar sites.....On the healing powers of Glyconutrients...importantly how vital they are for neural health...

http://www.shirleys-wellness-cafe.com/glyconutrients.htm

http://chetday.com/glyconutrients.htm

[crystal sage]

Lots of info here...and other similar sites.....On the healing powers of Glyconutrients...importantly how vital they are for neural health...

http://www.shirleys-wellness-cafe.com/glyconutrients.htm

http://chetday.com/glyconutrients.htm

Reading Chet's site... they did a rundown on Mannatech!!!My neighbour told me at the beginning of the year how her

Aunt was sold Mannatech for her advanced cancer...and the hard sell tactics she faced... and how the expensive stuff kept arriving even after her( the aunt's) death with hefty bills attatched!!!!

Sorry can't recommend that product!!!

Edited December 12, 2006 by crystal sage

[crystal sage]

http://www.doctorspiller.com/local_anesthetics.htm

The structure of nerve cell membranes

*

Toxicity of local anesthetics

*

Three special cases

o

Bupivicaine

o

Prilocaine

o

Articaine

+

Prolonged numbness and tingling with articaine

*

Table of doses and half life

*

Practical problems arising from injection of local anesthesia

o

Pt does not get numb

+

Field Blocks

+

Major Nerve Blocks

+

S

Pain, Numbness or paresthesia (tingling) after the procedure

+

Injection under the periosteum

o

Nervousness and fast heart beat directly after shot

*

Allergies to dental anesthetics

o

Ester based anesthetics

o

Amine based ansethetics

o

P

Can local anesthetics cause false positive drug tests?

o

Drug testing: Your rights versus the employer

It is estimated that the average dentist administers between 1500 and 2000 injections of local anesthesia each year. By definition, therefore, every dentist is an expert in the field of local anesthesia, which is an extremely good thing, since without the ability to produce profound numbness, modern dentistry would be all but impossible.

The history of local anesthetic agents.

Surprisingly, the first local anesthetic was Cocaine which was isolated from coca leaves by Albert Niemann in Germany in the 1860s. The very first clinical use of Cocaine was in 1884 by (of all people) Sigmund Freud who used it to wean a patient from morphine addiction. It was Freud and his colleague Karl Kollar who first noticed its anesthetic effect. Kollar first introduced it to clinical ophthalmology as a topical ocular (eye) anesthetic. Also in 1884, Dr. William Stewart Halsted was the first to describe the injection of cocaine into a sensory nerve trunk to create surgical anesthesia. Halsted was an eminent surgeon who had been trained in Britain. He was the first to establish formal surgical training for physicians in America. Prior to that time, surgery was a self taught discipline among US physicians. He also invented and pioneered the use of rubber gloves. Unfortunately, much to his own regret, he began to use cocaine himself and became highly addicted to it. At that time, there was no stigma attached to the recreational use of cocaine, and it gained a following among the elites of the day. Arthur Conan Doyle's Sherlock Holmes was supposed to be an addict, and Holmes kept Dr Watson around as a source for his drugs, as well as for the comic relief he provided.

It became fairly obvious fairly quickly that while the anesthetic characteristics of cocaine were desirable, the euphoria and subsequent addiction it produced was not! The turn of the century was a tremendous time of scientific progress, and the new discipline of organic chemistry enabled the synthesis of the first analog of cocaine in 1905. (An analog of a chemical molecule is one in which the original molecule is progressively modified to retain and enhance certain holistic characteristics of the original substance while ridding it of other unwanted characteristics.) The first synthetic local anesthetic was procaine, better remembered today by its trade name, "Novocain".

Novocain was not without its problems. It took a very long time to set (ie. to produce the desired anesthetic result), wore off too quickly and was not nearly as potent as cocaine. On top of that, it is classified as an ester. Esters tend to have a very high potential to cause allergic reactions. It is estimated that about one third of all persons who received it developed at least minor allergic reactions to it. Faced with the legal and ethical difficulties associated with the use of cocaine as a local anesthetic, and with the inefficiencies and allergenicity associated with the use of procaine, it is not surprising that most dentists of the day worked without any local anesthetic at all. (Nitrous oxide gas was available during this period.) Today, procaine is not even available for dental procedures.

The first modern local anesthetic agent was lidocaine (trade name Xylocaine®). It was invented in the 1940s. Prior to its introduction, Nitrous oxide gas (plus alcohol in the form of whiskey) was the major source of pain relief during dental procedures. Lidocaine proved to be so successful that during the 1940s and 1950s the use of nitrous oxide gas as a primary anesthetic agent all but vanished. (Whiskey somehow survived, but it is no longer used on patients.) Today, nitrous oxide is used principally as an anti-anxiety palliative. Lidocaine is in a broad class of chemicals called amides, and unlike ester based anesthetics, amides tend to be hypoallergenic. It sets quickly and when combined with a small amount of epinephrine (adrenalin), it produces profound anesthesia for several hours. Lidocaine is still the most widely used local anesthetic in America today.

Over the next thirty years, a number of other amide local anesthetics were invented, most not differing significantly from lidocaine. The major problem with lidocaine and its analogs is that they cause vasodilation, or the tendency of the local blood vessels to open wider increasing the blood flow in the area. This causes the anesthetic to be absorbed too quickly to take effect. Hence these anesthetics are always mixed with low concentrations of epinephrine which has the opposite effect (ie vasoconstriction) and closes the blood vessels down to keep the anesthesia in position long enough to produce long lasting numbness.

Mepivicaine (Carbocaine®) and prilocaine (Citanest®) have much less vasodilative qualities and hence can be used without the epinephrine vasoconstrictor. The advantage to this is that these anesthetics can be used more safely in patients who are taking medications which may interact negatively with the vasoconstrictor. These drugs include certain blood pressure medications (most notably non selective beta blockers) and tricyclic antidepressants (Elevil® and imipramine are two examples). Carpules that do not contain the vasoconstrictor also do not contain a preservative. This eliminates a possible source of allergic reaction.

How nerves conduct an impulse

The image to the right is a fairly accurate representation of a nerve bundle. (For a detailed explanation of this diagram as well as nerve anatomy and physiology, see my page on Understanding Pain.) If you think of a nerve bundle as an electrical cable, the blue axons represent the "wires" that carry the impulse from the tooth to the ganglion at the other end. The rest of the tissue surrounding the axons represent the "insulation" which separates the various wires in the cable from each other. At this point, the analogy breaks down because, while the insulation in an electrical cable is a passive material that serves only to separate the wires from each other to prevent short circuits, the insulation in a nerve bundle is an active participant in the conduction of the impulse.

The connective tissue that is associated with each neuron is composed of a special material called myelin which is itself made up of the cell bodies of specialized cells called Schwann cells.

The myelin sheath is almost continuous along the entire axon. There are, however tiny breaks in the continuity of the myelin sheath between each succeeding Schwann cell. These breaks are called "nodes of Ranvier". These nodes are quite important in the conduction of an impulse along a nerve axon on its way to the cell body in the ganglion, mostly because their presence along the way speeds the impulse quite a bit.

How a nerve fiber transmits an impulse

Nerves are NOT like electrical wires with electrons traveling their length to transfer information from one end to the other. They are actually complex electro-chemical structures which utilize the electrical potential difference between the fluid inside of the axon, and the fluid that surrounds the axon. The fluid inside the axon (called cytoplasm) contains a high concentration of potassium ions, while the fluid outside contains a high concentration of sodium ions. There is no real difference in electrical potential between a potassium ion and a sodium ion, however, the fact that they exist in different concentrations on either side of the cell membrane sets up an electrochemical pressure gradient between the two. Sodium ions want to flow into the nerve cytoplasm, while the potassium ions want to flow out, but both are prevented from doing so by the presence of the nerve cell membrane.

When a nerve is stimulated, this sets up a chain reaction in which sodium ions begin to penetrate through the nerve cell membrane and flow into the axon, while potassium ions begin to flow out. This activity happens at the nodes of Ranvier. This process is called depolarization of the nerve membrane. The imbalance in the chemical makeup of the extracellular fluid then causes an imbalance in the concentration of sodium ions at the adjacent node which stimulates an identical depolarization at this node as well. This process proceeds from node to node until the impulse reaches the cell body of the nerve in the ganglion where it stimulates a similar cascade in a network of other neurons which make contact with it.

You might think that once all the potassium and sodium ions have exchanged places, the nerve would no longer be able to conduct impulses. The nerve, however, is a living entity and can regenerate the original concentrations of ions using energy from the food you eat in almost the same way that muscle cells use that same energy to cause muscle movement. It does this using proteins embedded in the cell membrane which act as "ion pumps".

Edited December 16, 2006 by crystal sage

[crystal sage]

http://www.doctorspiller.com/local_anesthetics.htm

How local anesthesia interrupts this process

Local anesthetics work to block nerve conduction by reducing the influx of sodium ions into the nerve cytoplasm. If the sodium ions cannot flow into the neuron, then the potassium ions cannot flow out, thus inhibiting the depolarization of the nerve. If this process can be inhibited for just a few nodes of Ranvier along the way, then nerve impulses generated downstream from the blocked nodes cannot propagate to the ganglion. In order to accomplish this feat, the anesthetic molecules must actually enter through the cell membrane of the nerve. Herein lies the differences in the potency, time of onset and duration of the various local anesthetics.

[crystal sage]

"When a nerve is stimulated, this sets up a chain reaction in which sodium ions begin to penetrate through the nerve cell membrane and flow into the axon, while potassium ions begin to flow out. This activity happens at the nodes of Ranvier. This process is called depolarization of the nerve membrane. The imbalance in the chemical makeup of the extracellular fluid then causes an imbalance in the concentration of sodium ions at the adjacent node which stimulates an identical depolarization at this node as well. This process proceeds from node to node until the impulse reaches the cell body of the nerve in the ganglion where it stimulates a similar cascade in a network of other neurons which make contact with it.

You might think that once all the potassium and sodium ions have exchanged places, the nerve would no longer be able to conduct impulses. The nerve, however, is a living entity and can regenerate the original concentrations of ions using energy from the food you eat in almost the same way that muscle cells use that same energy to cause muscle movement. It does this using proteins embedded in the cell membrane which act as "ion pumps"."

http://www.doctorspiller.com/local_anesthetics.htm

But if you read further into his article...and explanations how things work...you may deduce that the residuals of the aneasthetics that can stay in the nerves for up to a year ..prevent/.block the healing...restoring..nutrition to these nerves....Hence!!!! eventual...possible neural damage!!!

Does my reasoning sound right to you!!!

There are many articles on the internet that discuss that the long term affects of some aneasthetics is neural damage..demyelination....!!!!!

[crystal sage]

http://jnnp.bmj.com/cgi/content/full/64/4/563

[crystal sage]

Thyroid hormone administration enhances remyelination in chronic demyelinating inflammatory disease

http://www.pnas.org/cgi/content/full/101/4...ournalcode=pnas

[crystal sage]

Inflammation and Remyelination in the Central Nervous System

A Tale of Two Systems

http://ajp.amjpathol.org/cgi/content/full/164/5/1519

[frogfish]

...you may deduce that the residuals of the aneasthetics that can stay in the nerves for up to a year ..prevent/.block the healing...restoring..nutrition to these nerves....Hence!!!! eventual...possible neural damage!!!

Does my reasoning sound right to you!!!

There are many articles on the internet that discuss that the long term affects of some aneasthetics is neural damage..demyelination....!!!!!

I doubt this plays a significant role in demyelination. In MS, demyelination happens in the CNS, including glia. Glia lack a synapse, so neuron growth (led by glia) is inhibited. Heavy metals have shown to been a major cause of this.

Most Anesthetics agents are molecular compunds, having no metals present.

[crystal sage]

I doubt this plays a significant role in demyelination. In MS, demyelination happens in the CNS, including glia. Glia lack a synapse, so neuron growth (led by glia) is inhibited. Heavy metals have shown to been a major cause of this.

Most Anesthetics agents are molecular compunds, having no metals present.

Like the Mercury etc in some of the fillings and found in some vaccinations???

http://www.cfsdoc.org/mercury.htm

http://www.evenbetternow.com/environmental-toxicity.html

http://www.add-adhd-help-center.com/Chelation/edta.htm

http://www.downtoearth.org.in/full6.asp?fo..._id=7&sid=1

[crystal sage]

oxic Drugs, Chemicals and Heavy Metals in the Workplace

Heavy metals usually target an organ or structure, therefore the configuration is characteristic to the area of damage. Lead causes a demyelination of ...

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Gulf War and Health:

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Heavy Metals

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[PPT]

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File Format: Microsoft Powerpoint - View as HTML

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[PPT]

Possible Connection of Heavy Metal Toxicity and Autism

File Format: Microsoft Powerpoint - View as HTML

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To determine if there was evidence of heavy metal deposition in other organs, ... Neuropathological studies have shown demyelination of the corticospinal ...

adc.bmjjournals.com/cgi/content/full/83/5/439 - Similar pages

Trace element (nutritional) theory of "mad cow" disease

Demyelination has been observed in deer with copper deficiency (Geisel et al., 1997; ... Heavy metals and/or Cu deficiency may damage the integrity of the ...

bse.airtime.co.uk/copper.htm - 26k - Cached - Similar pages

[frogfish]

Like the Mercury etc in some of the fillings and found in some vaccinations???

But they are rarely used in vaccinations anymore, and the amount found in vaccines were small

[crystal sage]

Is Academic Medicine for Sale?

Former editor of the New England Journal of Medicine (NEJM), Dr. Marcia Angell, struggled to bring the attention of the world to the problem of commercializing scientific research in her outgoing editorial titled "Is Academic Medicine for Sale?" Angell called for stronger restrictions on pharmaceutical stock ownership and other financial incentives for researchers. She said that growing conflicts of interest are tainting science. She warned that, "When the boundaries between industry and academic medicine become as blurred as they are now, the business goals of industry influence the mission of medical schools in multiple ways." She did not discount the benefits of research but said a Faustian bargain now existed between medical schools and the pharmaceutical industry.

Excerpt: Death by Medicine, by Gary Null PhD, Carolyn Dean MD ND, Martin Feldman MD, Debora Rasio MD, Dorothy Smith PhD

http://www.medicinefreeliving.com/Research.htm

http://www.medicinefreeliving.com/Articles...%20MEDICINE.pdf

[crystal sage]

But they are rarely used in vaccinations anymore, and the amount found in vaccines were small

maybe only in the wealthier countries....

http://www.downtoearth.org.in/full6.asp?fo..._id=7&sid=1

Boston Globe Online / Nation | World / Lives Lost

It is a system often lacking in basic technology, a system that regularly dispenses outdated medicines or spoiled vaccines, a system so widely despised and ...

www.boston.com/globe/nation/packages/lives_lost/cambodia.shtml - 44k - Cached - Similar pages

http://www.boston.com/globe/nation/package.../cambodia.shtml

http://www.pcrm.org/resources/education/re.../research1.html

The Ethical Landscape

Ethical issues in human research generally arise in relation to population groups that are vulnerable to abuse. For example, much of the ethically dubious research conducted in poor countries would not occur were the level of medical care not so limited. Similarly, the cruelty of the Tuskegee experiments clearly reflected racial prejudice. The NIH experiments on short children were motivated to counter a fundamentally social problem, the stigma of short stature, with a profitable pharmacologic solution. The unethical military experiments during the Cold War would have been impossible if GIs had had the right to abort assignments or raise complaints. As we address the ethical issues of human experimentation, we often find ourselves traversing complex ethical terrain. Vigilance is most essential when vulnerable populations are involved.

Unnecessary Drugs Mean Unnecessary Experiments

A widespread ethical problem, although one that has not yet received much attention, is raised by the development of new pharmaceuticals. All new drugs are tested on human volunteers. There is, of course, no way subjects can be fully apprised of the risks in advance, as that is what the tests purport to determine. This situation is generally considered acceptable, provided volunteers give “informed” consent. Many of the drugs under development today, however, offer little clinical benefit beyond those available from existing treatments. Many are developed simply to create a patentable variation on an existing drug. It is easy to justify asking informed, consenting individuals to risk limited harm in order to develop new drug therapies for a condition from which they are suffering or for which existing treatments are inadequate. The same may not apply when the drug being tested offers no new benefits to the subjects because they are healthy volunteers, or when the drug offers no significant benefits to anyone because it is essentially a copy of an existing drug.

Manufacturers, of course, hope that animal tests will give an indication of how a given drug will affect humans. However, a full 70 to 75 percent of drugs approved by the Food and Drug Administration for clinical trials based on promising results in animal tests, ultimately prove unsafe or ineffective for humans.2 Even limited clinical trials cannot reveal the full range of drug risks. A U.S. General Accounting Office (GAO) study reports that of the 198 new drugs which entered the market between 1976 and 1985, 102 (52 percent) caused adverse reactions that premarket tests failed to predict.3 Even in the brief period between January and August 1997, at least 53 drugs currently on the market were relabeled due to unexpected adverse effects.4

[pbarosso]

wow! i am the only other poster on this thread! sage, you have managed to own this thread!

[jeceris]

As the thread I posted earlier seems to have'disappeared' unless someone else can find it for me???

I have restarted it....

" Ralda's Daughter Abbie had suffered brain damage after being dangerously ill with wild measles encephalitis...

there was no need to re-start this ridiculous ramble.

ralda is you, you are ralda, and if i were you i'd stop going on about myelin sheath degredation and start looking into chemical imbalances.

it might help you to get some insight.

[crystal sage]

As the thread I posted earlier seems to have'disappeared' unless someone else can find it for me???

I have restarted it....

" Ralda's Daughter Abbie had suffered brain damage after being dangerously ill with wild measles encephalitis...

there was no need to re-start this ridiculous ramble.

ralda is you, you are ralda, and if i were you i'd stop going on about myelin sheath degredation and start looking into chemical imbalances.

it might help you to get some insight.

I have olive skin...dark hair ,brown eyes....and at least 10 years on Ralda... Of my thousands of posts..not just this site of course...why would I make this one thing up???

I'm proud of Ralda... of not giving up when the doctors did....and using a sensible well researched methods of healing with good nutrition...

Ir you read up on MS and other demyelination diseases...you find that good nutrition is vital.... yet they themselves have admited as per some of the earlier quoted articles on this topic..that the benefits of nutrition and healing have not really been studied...as they can not really be patented perhaps????

What would happen to all the research funds... potential profits...if they found that clever purpose created smoothies can heal lots of illnesses????

Unless the recipient has some allergies to say strawberries ..or dairy...etc... I don't see any possible side affect to these healing aids...just as excercise.. tai chi or meditation..or miotherapy, sacral therapy...acupunctere...reflexology..massage ...can assist in healing....

We should have more people like her in this world....

Edited December 20, 2006 by crystal sage

[ice2]

I have been watching to see if this thread would disappear, crystal and I live in different states

I told Abbie what has been said,

her reply was "well I am real and you are my mum".

We had our photo in the Woman's Day with our REAL names printed in the text.

I had to supply Woman Day with Abbie's medical reports in writing,

before they would print anything.

I have in writing from medical specialists

MRI report of Demyelination

neurologist and other specialists reports which state in writing confirming permanent brain damage

MRI report of a normal brain scan, myelin repaired.

now that I have posted again lets see if the thread stays

I can't wait to post what has been happening....