Very Encompassing Article on the Lyme epidemic, and diseases it causes

[Guest guest]

This is a must read. It talks about so much, how the lyme epidemic started, how it causes disease and the diseases it causes, including autism.

Heidi N

================BEGIN QUOTE============================================

_http://www.wddty.com/03363800369405675265/lyme-disease-a-leaky-brain.html_

(http://www.wddty.com/03363800369405675265/lyme-disease-a-leaky-brain.html)

Lyme disease: a leaky brain

Lyme disease is still barely recognized by orthodox medicine, but new,

explosive evidence links this worldwide epidemic with certain types of mental

illness, including autism.

The first cases of Lyme disease (LD) occurred in the US, but it’s now

acknowledged to be a worldwide problem. Britain had its first official death due to

LD in December 2005: “liver disease due to Lyme sepsisâ€, according to the

autopsy. In May of this year, a 38-year-old British pro-fessor committed

suicide after developing dementia brought about by LD. It’s particularly prevalent

at this time of the year—late spring and early summer.

The number of diagnosed cases of Lyme disease are now rising—and not just

because doctors are finally beginning to recognize it, but also possibly as a

result of global warming. And, as with many new-disease discoveries, a whole

raft of previously mysterious conditions are now being laid at the door of LD,

including chronic fatigue (CFS/ME), multiple sclerosis (MS) and even autism.

Could we be witnessing the start of a new epidemic? “Many of the diseases

that are considered incurable by conven-tional medicine may have some kind of

Lyme component,†says American alternative practitioner Dr Lee Cowden.

What is Lyme disease? In essence, it’s a kind of malaria, although it

emerges not from the swampy jungle, but from temperate forests. Like malaria, the

disease is transmitted by being bitten by a blood-feeding creature—in the case

of LD, not by an insect, but a tick, an arachnid, that lives on animals such

as cattle, birds and even mice, but primarily deer.

Where it all began

Lyme disease first appeared more than 30 years ago as a mysterious disease

outbreak in an American town called Lyme, in Connecticut. In the spring of

1975, there was a cluster of cases of what appeared to be juvenile arthritis.

Children as young as 10 began to develop severe joint pain. Doctors from nearby

Yale University were called in

to investigate, and were puzzled by the appearance of odd rashes on the

children’s skin. Months of detective work finally led the doctors to connect the

symptoms to a disease that had first been described in Europe almost a

century before as ‘sheep-tick fever’.

After years of further detective work, researchers traced the illness to a

rogue spirochaetes bacterium in the patients’ blood known as Borrelia

burgdorferi—hence, the alternative name of ‘Lyme borreliosis’. But where had it

come from? Already alerted to the fact that it might be due to a tick bite, the

scientists began a hunt among the local animal population. The Borrelia

microorganism was finally tracked down to a tick of the genus Ixodes that lives on

deer. This tiny arachnid—related to mites, spiders and scorpions, having

eight legs—has a correspondingly tiny mouth, so its bite is rarely felt, which

may be one reason why it was able to elude detection for so long. Ixodes is

also cleverly able to inject its prey with a local anaesthetic, further

disguising its attack. In fact, most victims of Lyme disease have no idea they were

ever on the tick’s hit list.

In fact, it’s likely that Ixodes has to remain undetected because it’s

believed to be an inefficient feeder. It needs to be plugged in to its prey for

hours to obtain sufficient nourish-ment. One indication of this is the

probability that B. burgdorferi is not transmitted until the tick has been attached

for at least 12 hours.

Initially, medicine treated the disease just like any other bacterial

infection—with antibiotics. These appeared to work, and doctors patted themselves

on the back for having put paid so easily to this novel disease. But the story

hasn’t turned out to be that simple.

Although this medical field is still relatively small, there is already a

schism appearing among LD clinic-ians; indeed, some would call it a war. One

army of experts believe that Lyme disease can be easily cured by a short course

of antibiotics, whereas the opposing side says no, LD is a complex,

potentially long-term illness (see box, page 6).

The problems begin with the diag-nosis. If LD is spotted early on, then

antibiotics can prove helpful. But, in practice, LD turns out to be very

diffi-cult to diagnose (see box, page 8), and the later stages of the disease are

much harder to treat with the usual drugs.

What’s more, these antibiotics can sometimes make things even worse. Any

Borrelia bacteria that are not totally killed off by the drugs don’t just

develop resistance—which is bad enough—but also become what is referred to as ‘

cell-wall deficient’. This makes them very elusive as, without walls, they can

hide inside of healthy cells, thereby avoiding direct attack by the drugs

(Infection, 1996; 24: 218–26).

Lyme patients also find that the types of antibiotics used to treat them may

actually exacerbate their symp-toms. This is thought to be the result of

changes due to the drugs in the genetic sequencing of Borrelia, causing them to

release toxins into the body. These toxins often get into the brain and

nervous system, precipitating what is called the Jarisch–Herxheimer reaction

(named after Karl Herx-heimer, the German dermatologist who first observed it). J–

H reactions can be life-threatening, and are seen in one in seven Lyme

borreliosis patients treated.

The leaky brain

In fact, it has also been suggested that LD in itself—whether treated by

antibiotics or not—may be neurotoxic. The idea is that Lyme disease creates

ammonia in the brain, causing a ‘leaky-brain syndrome’. Among the first to

propose the idea was LD specialist Dr Jernigan. As ammonia can alter

permeability of the blood–brain barrier, he says, it would allow large molecules to

reach the brain, causing ‘cerebral allergies’. Jernigan believes that this

may be a major cause of a variety of LD symptoms (Townsend Lett Docs, 2007;

April: 141–8; online only).

Confirmation of this hypothesis has come from animal studies. Using

radioactive tracers, researchers have shown that laboratory animals, when infected by

Borrelia, lose the pro-tection of the blood–brain barrier after just two

weeks (Schutzer SE, ed. Lyme Disease: Molecular and Immunologic Approaches,

Series 6. Current Communications in Molecular and Cell Biology. Plainview, NY:

Cold Spring Harbor Press, 1992).

How does Borrelia do this? It’s thought that the bacteria burrow their way

between the cells of the brain’s outermost membrane, causing a localized

inflammation that, in turn, releases proteins to fight against the bacterial

invasion; this then results in holes in the cerebral membrane. It’s much the same

mechanism as seen in the leaky-gut syndrome but, in this case, it’s

potentially more serious as it involves the brain.

In addition, there is now laboratory evidence that Borrelia can “attach to

or invade human cortical neuronal cellsâ€, say researchers at the National

Center for Infectious Diseases in Colorado, part of the US Centers for Disease

Control and Prevention (CDC). This makes the bacteria difficult to kill by the

immune system (Microbes Infect, 2006; 8: 2832–40). It also helps to explain

why Lyme disease can be both relaps-ing and resistant to treatment.

Incidentally, the spirochaetes bac-terium that causes syphilis has a similar

mode of action and can also lodge in the brain, potentially remain-ing

active for years.

Brain abnormalities

The leaky-brain theory also accounts for some of the highly specific

neur-ological abnormalities found in Lyme patients—including Bell’s palsy,

lymphocytic meningitis, meningo-encephalitis and cranial neuritis—not to mention the

less specific CFS/ME and ‘brain fog’.

“The neurological and psychiatric manifestations of Borrelia are so numerous

that it is called the ‘new great imitator’,†says Dr Frederic Blanc, of the

University of Strasbourg, France. “Every part of the nervous system can be

involved: from central

to peripheral nervous system, and even muscles†(Med Mal Infect, 2007; Mar

8; Epub ahead of print).

In fact, as long as 10 years ago, LD was firmly characterized as a ‘

neuro-psychiatric illness’. Reviewing the whole history of the disease, a team of

psychiatrists at New York’s Colum-bia University found Lyme disease to be

responsible for “a broad range of psychiatric reactionsâ€, including paranoia,

dementia, schizophrenia, bipolar disorder, panic attacks, major depression,

anorexia nervosa and obsessive–compulsive disorder (Am J Psychiatry, 1994; 151:

1571–83). Since then, tests have discovered reduced blood flow in the brains of

chronic LD sufferers, explaining the impaired mental functioning that

afflicts so many victims of the disease (Neuro-psychiatry Clin Neurosci, 2003; 15:

326–32).

The autism connection

The most dramatic mental condition thought to be caused by Lyme disease is

autism. A rare condition 50 years ago, autism now affects one in every 150

American children, according to the latest figures from the CDC.

But why should Lyme disease be implicated? One of the first clues was that

the psychological symptoms of

LD are similar to those of autism.

Six years ago, the above-mentioned Columbia University psychiatrists found

that children with Lyme disease have “significantly more cognitive and

psychiatric disturbances . . . resulting in psychosocial and academic impair-mentsâ€

(J Neuropsychiatry Clin Neurosci, 2001; 13: 500–7).

There are other clues, too. As already mentioned, syphilis, which is caused

by a similar spirochaetes as in LD, in the womb is known to cause autism.

Furthermore, autistic children are known to have many metabolic dysfunctions

which are shared by victims of LD, in particular, chronically low counts of CD57

natural-killer (NK) cells.

Of course, scores of theories have been proposed for the cause of autism,

among which vaccine damage is perhaps the best known. But LD may be involved

there, too. “It is possible that the two are conjoined in damage, and the

long-term effects of Borrelia could hamper the body’s ability to mount a

significant, timely response to vaccines,†says Dr Geoffrey Radoff, of the Alternative

Medical Care Center of Arizona. “This could explain the higher incidences of

adverse reactions to vaccinations in children with autism (Townsend Lett

Docs, 2007; April: 78–81; online only).

However, some children appear to be born with autism, so how could Lyme

disease be involved there? Although the research has yet to be done in humans,

studies of farm animals have shown that Borrelia can pass through the placental

barrier into the womb and even into breast milk. This makes it possible for

an infected mother to pass on the disease to her newborn child, in whom it

could present as autism.

Do the numbers stack up? With autism now so widespread, is it likely that so

many children—or their mothers—could have been bitten by a relatively

uncommon tick?

One answer is that ticks, it appears, are not the only cuplrits. Mosquitoes,

fleas and lice may also carry Borrelia (Agric Environ Med, 2002; 9: 257–9),

thus vastly increasing the risk of infection. Another theory is that there

may be

a ‘Borrelia-related complex’ wherein the bacteria pass unnoticed from

generation to generation, and only present when the immune system is under stress.

Autistic children are known to suffer from a plethora of autoimmune and

metabolic disorders (J Autism Dev Disord, 2000; 30: 475–9), and these could turn

latent Borrelia infect-ion into a full-blown attack—with no tick in sight.

Such theories were recently aired at a January 2007 meeting of the newly

formed Lyme-Induced Autism Foundation, held in San Diego. Texas physician Dr

Harvey reported that he had many patients who tested positive for

Borrelia, and yet, “our part of Texas is not an endemic region of Lyme diseaseâ€,

he said. “No patient had the typical skin rash, but most

had been ill for many years, with similarly ill family members.â€

Other delegates agreed. “There may be two forms of Borrelia infection: Lyme

disease and epidemic borrelio-

sis—disease spread directly between humans,†said fellow LD physician Dr

Radoff. “It is quite possible that the prevalence of autoimmune disorders found

in families with autism is an infection that has existed chronically in the

body for years, if not decades.â€

Dr Warren Levin, another LD practitioner, has reported that, in the 10

children with autism he has seen,

all tested positive for Lyme disease.

Predictably, medicine’s knee-jerk reaction to such findings has been to

dismiss them, but one group of researchers is taking them seriously. Yet again,

that pioneering team of psychiatrists at Columbia University, led by Dr

Fallon, has already taken up the challenge and embarked on a huge

epidemiological study of Lyme disease and autism.

Fallon believes that two things will emerge from his study: that regions

with very high rates of Lyme disease will also have higher-than-normal rates of a

utism; and that at least some of those autistic children will respond to LD

therapy.

“In our work with children with LD, we have encountered a few children with

autistic-like disorders,†says Dr Fallon. “When they received intensive

antibiotic therapy, the autistic syn-dromes dramatically improved and, in some

cases, resolved.â€

Tony

==================END QUOTE============================================

Heidi N

More new features than ever. Check out the new AOL Mail!

[Guest guest]

Thank you good post.

>

> This is a must read.  It talks about so much, how the lyme

epidemic started, how it causes disease and the diseases it causes,

including autism.

>

> Heidi N

> ================BEGIN

QUOTE============================================

> _http://www.wddty.com/03363800369405675265/lyme-disease-a-leaky-

brain.html_

> (http://www.wddty.com/03363800369405675265/lyme-disease-a-leaky-

brain.html)

>

> Lyme disease: a leaky brain

>

> Lyme disease is still barely recognized by orthodox medicine, but

new,

> explosive evidence links this worldwide epidemic with certain types

of mental

> illness, including autism.

>

> The first cases of Lyme disease (LD) occurred in the US, but it’s

now

> acknowledged to be a worldwide problem. Britain had its first

official death due to

> LD in December 2005: “liver disease due to Lyme sepsisâ€,

according to the

> autopsy. In May of this year, a 38-year-old British pro-fessor

committed

> suicide after developing dementia brought about by LD. It’s

particularly prevalent

> at this time of the year†" late spring and early summer.

>

> The number of diagnosed cases of Lyme disease are now rising†" and

not just

> because doctors are finally beginning to recognize it, but also

possibly as a

> result of global warming. And, as with many new-disease

discoveries, a whole

> raft of previously mysterious conditions are now being laid at the

door of LD,

> including chronic fatigue (CFS/ME), multiple sclerosis (MS) and

even autism.

> Could we be witnessing the start of a new epidemic? “Many of the

diseases

> that are considered incurable by conven-tional medicine may have

some kind of

> Lyme component,†says American alternative practitioner Dr Lee

Cowden.

>

> What is Lyme disease? In essence, it’s a kind of malaria,

although it

> emerges not from the swampy jungle, but from temperate forests.

Like malaria, the

> disease is transmitted by being bitten by a blood-feeding

creature†" in the case

> of LD, not by an insect, but a tick, an arachnid, that lives on

animals such

> as cattle, birds and even mice, but primarily deer.

>

> Where it all began

>

> Lyme disease first appeared more than 30 years ago as a mysterious

disease

> outbreak in an American town called Lyme, in Connecticut. In the

spring of

> 1975, there was a cluster of cases of what appeared to be juvenile

arthritis.

> Children as young as 10 began to develop severe joint pain. Doctors

from nearby

> Yale University were called in

> to investigate, and were puzzled by the appearance of odd rashes on

the

> children’s skin. Months of detective work finally led the doctors

to connect the

> symptoms to a disease that had first been described in Europe

almost a

> century before as ‘sheep-tick fever’.

>

> After years of further detective work, researchers traced the

illness to a

> rogue spirochaetes bacterium in the patients’ blood known as

Borrelia

> burgdorferi†" hence, the alternative name of ‘Lyme

borreliosis’. But where had it

> come from? Already alerted to the fact that it might be due to a

tick bite, the

> scientists began a hunt among the local animal population. The

Borrelia

> microorganism was finally tracked down to a tick of the genus

Ixodes that lives on

> deer. This tiny arachnid†" related to mites, spiders and scorpions,

having

> eight legs†" has a correspondingly tiny mouth, so its bite is

rarely felt, which

> may be one reason why it was able to elude detection for so long.

Ixodes is

> also cleverly able to inject its prey with a local anaesthetic,

further

> disguising its attack. In fact, most victims of Lyme disease have

no idea they were

> ever on the tick’s hit list.

>

> In fact, it’s likely that Ixodes has to remain undetected because

it’s

> believed to be an inefficient feeder. It needs to be plugged in to

its prey for

> hours to obtain sufficient nourish-ment. One indication of this is

the

> probability that B. burgdorferi is not transmitted until the tick

has been attached

> for at least 12 hours.

>

> Initially, medicine treated the disease just like any other

bacterial

> infection†" with antibiotics. These appeared to work, and doctors

patted themselves

> on the back for having put paid so easily to this novel disease.

But the story

> hasn’t turned out to be that simple.

>

> Although this medical field is still relatively small, there is

already a

> schism appearing among LD clinic-ians; indeed, some would call it a

war. One

> army of experts believe that Lyme disease can be easily cured by a

short course

> of antibiotics, whereas the opposing side says no, LD is a complex,

> potentially long-term illness (see box, page 6).

> The problems begin with the diag-nosis. If LD is spotted early on,

then

> antibiotics can prove helpful. But, in practice, LD turns out to be

very

> diffi-cult to diagnose (see box, page 8), and the later stages of

the disease are

> much harder to treat with the usual drugs.

>

> What’s more, these antibiotics can sometimes make things even

worse. Any

> Borrelia bacteria that are not totally killed off by the drugs

don’t just

> develop resistance†" which is bad enough†" but also become what is

referred to as ‘

> cell-wall deficient’. This makes them very elusive as, without

walls, they can

> hide inside of healthy cells, thereby avoiding direct attack by the

drugs

> (Infection, 1996; 24: 218†" 26).

>

> Lyme patients also find that the types of antibiotics used to treat

them may

> actually exacerbate their symp-toms. This is thought to be the

result of

> changes due to the drugs in the genetic sequencing of Borrelia,

causing them to

> release toxins into the body. These toxins often get into the brain

and

> nervous system, precipitating what is called the

Jarisch†" Herxheimer reaction

> (named after Karl Herx-heimer, the German dermatologist who first

observed it). J†"

> H reactions can be life-threatening, and are seen in one in seven

Lyme

> borreliosis patients treated.

>

> The leaky brain

>

> In fact, it has also been suggested that LD in itself†" whether

treated by

> antibiotics or not†" may be neurotoxic. The idea is that Lyme

disease creates

> ammonia in the brain, causing a ‘leaky-brain syndrome’. Among

the first to

> propose the idea was LD specialist Dr Jernigan. As ammonia

can alter

> permeability of the blood†" brain barrier, he says, it would allow

large molecules to

> reach the brain, causing ‘cerebral allergies’. Jernigan

believes that this

> may be a major cause of a variety of LD symptoms (Townsend Lett

Docs, 2007;

> April: 141†" 8; online only).

>

> Confirmation of this hypothesis has come from animal studies. Using

> radioactive tracers, researchers have shown that laboratory

animals, when infected by

> Borrelia, lose the pro-tection of the blood†" brain barrier after

just two

> weeks (Schutzer SE, ed. Lyme Disease: Molecular and Immunologic

Approaches,

> Series 6. Current Communications in Molecular and Cell Biology.

Plainview, NY:

> Cold Spring Harbor Press, 1992).

>

> How does Borrelia do this? It’s thought that the bacteria burrow

their way

> between the cells of the brain’s outermost membrane, causing a

localized

> inflammation that, in turn, releases proteins to fight against the

bacterial

> invasion; this then results in holes in the cerebral membrane.

It’s much the same

> mechanism as seen in the leaky-gut syndrome but, in this case,

it’s

> potentially more serious as it involves the brain.

>

> In addition, there is now laboratory evidence that Borrelia can

“attach to

> or invade human cortical neuronal cellsâ€, say researchers at the

National

> Center for Infectious Diseases in Colorado, part of the US Centers

for Disease

> Control and Prevention (CDC). This makes the bacteria difficult to

kill by the

> immune system (Microbes Infect, 2006; 8: 2832†" 40). It also helps

to explain

> why Lyme disease can be both relaps-ing and resistant to treatment.

>

> Incidentally, the spirochaetes bac-terium that causes syphilis has

a similar

> mode of action and can also lodge in the brain, potentially remain-

ing

> active for years.

>

> Brain abnormalities

>

> The leaky-brain theory also accounts for some of the highly

specific

> neur-ological abnormalities found in Lyme patients†" including

Bell’s palsy,

> lymphocytic meningitis, meningo-encephalitis and cranial

neuritis†" not to mention the

> less specific CFS/ME and ‘brain fog’.

>

> “The neurological and psychiatric manifestations of Borrelia are

so numerous

> that it is called the ‘new great imitator’,†says Dr Frederic

Blanc, of the

> University of Strasbourg, France. “Every part of the nervous

system can be

> involved: from central

> to peripheral nervous system, and even muscles†(Med Mal Infect,

2007; Mar

> 8; Epub ahead of print).

> In fact, as long as 10 years ago, LD was firmly characterized as a

‘

> neuro-psychiatric illness’. Reviewing the whole history of the

disease, a team of

> psychiatrists at New York’s Colum-bia University found Lyme

disease to be

> responsible for “a broad range of psychiatric reactionsâ€,

including paranoia,

> dementia, schizophrenia, bipolar disorder, panic attacks, major

depression,

> anorexia nervosa and obsessive†" compulsive disorder (Am J

Psychiatry, 1994; 151:

> 1571†" 83). Since then, tests have discovered reduced blood flow in

the brains of

> chronic LD sufferers, explaining the impaired mental functioning

that

> afflicts so many victims of the disease (Neuro-psychiatry Clin

Neurosci, 2003; 15:

> 326†" 32).

>

> The autism connection

>

> The most dramatic mental condition thought to be caused by Lyme

disease is

> autism. A rare condition 50 years ago, autism now affects one in

every 150

> American children, according to the latest figures from the CDC.

>

> But why should Lyme disease be implicated? One of the first clues

was that

> the psychological symptoms of

> LD are similar to those of autism.

>

> Six years ago, the above-mentioned Columbia University

psychiatrists found

> that children with Lyme disease have “significantly more

cognitive and

> psychiatric disturbances . . . resulting in psychosocial and

academic impair-mentsâ€

> (J Neuropsychiatry Clin Neurosci, 2001; 13: 500†" 7).

>

> There are other clues, too. As already mentioned, syphilis, which

is caused

> by a similar spirochaetes as in LD, in the womb is known to cause

autism.

> Furthermore, autistic children are known to have many metabolic

dysfunctions

> which are shared by victims of LD, in particular, chronically low

counts of CD57

> natural-killer (NK) cells.

>

> Of course, scores of theories have been proposed for the cause of

autism,

> among which vaccine damage is perhaps the best known. But LD may be

involved

> there, too. “It is possible that the two are conjoined in damage,

and the

> long-term effects of Borrelia could hamper the body’s ability to

mount a

> significant, timely response to vaccines,†says Dr Geoffrey

Radoff, of the Alternative

> Medical Care Center of Arizona. “This could explain the higher

incidences of

> adverse reactions to vaccinations in children with autism (Townsend

Lett

> Docs, 2007; April: 78†" 81; online only).

>

> However, some children appear to be born with autism, so how could

Lyme

> disease be involved there? Although the research has yet to be done

in humans,

> studies of farm animals have shown that Borrelia can pass through

the placental

> barrier into the womb and even into breast milk. This makes it

possible for

> an infected mother to pass on the disease to her newborn child, in

whom it

> could present as autism.

>

> Do the numbers stack up? With autism now so widespread, is it

likely that so

> many children†" or their mothers†" could have been bitten by a

relatively

> uncommon tick?

>

> One answer is that ticks, it appears, are not the only cuplrits.

Mosquitoes,

> fleas and lice may also carry Borrelia (Agric Environ Med, 2002; 9:

257†" 9),

> thus vastly increasing the risk of infection. Another theory is

that there

> may be

> a ‘Borrelia-related complex’ wherein the bacteria pass

unnoticed from

> generation to generation, and only present when the immune system

is under stress.

> Autistic children are known to suffer from a plethora of autoimmune

and

> metabolic disorders (J Autism Dev Disord, 2000; 30: 475†" 9), and

these could turn

> latent Borrelia infect-ion into a full-blown attack†" with no tick

in sight.

>

> Such theories were recently aired at a January 2007 meeting of the

newly

> formed Lyme-Induced Autism Foundation, held in San Diego. Texas

physician Dr

> Harvey reported that he had many patients who tested

positive for

> Borrelia, and yet, “our part of Texas is not an endemic region of

Lyme diseaseâ€,

> he said. “No patient had the typical skin rash, but most

> had been ill for many years, with similarly ill family members.â€

>

> Other delegates agreed. “There may be two forms of Borrelia

infection: Lyme

> disease and epidemic borrelio-

> sis†" disease spread directly between humans,†said fellow LD

physician Dr

> Radoff. “It is quite possible that the prevalence of autoimmune

disorders found

> in families with autism is an infection that has existed

chronically in the

> body for years, if not decades.â€

>

> Dr Warren Levin, another LD practitioner, has reported that, in the

10

> children with autism he has seen,

> all tested positive for Lyme disease.

>

> Predictably, medicine’s knee-jerk reaction to such findings has

been to

> dismiss them, but one group of researchers is taking them

seriously. Yet again,

> that pioneering team of psychiatrists at Columbia University, led

by Dr

> Fallon, has already taken up the challenge and embarked on a huge

> epidemiological study of Lyme disease and autism.

>

> Fallon believes that two things will emerge from his study: that

regions

> with very high rates of Lyme disease will also have higher-than-

normal rates of a

> utism; and that at least some of those autistic children will

respond to LD

> therapy.

>

> “In our work with children with LD, we have encountered a few

children with

> autistic-like disorders,†says Dr Fallon. “When they received

intensive

> antibiotic therapy, the autistic syn-dromes dramatically improved

and, in some

> cases, resolved.â€

>

> Tony

> ==================END

QUOTE============================================

> Heidi N

>

______________________________________________________________________

__

> More new features than ever. Check out the new AOL Mail ! -

http://webmail.aol.com

>