Repost of SSRIs and Autism

[Guest guest]

Here's another repost of a Duke University study w/

comments quoted from Dr G - not particularly related

to previous discussions, but I thought you'd find them

interesting: (I apologize how the copying/pasting

skews up the spacing)

These are Dr. Goldberg's comments, then the study

follows...

" As far as the ³goal² of the Paxil / Prozac (or any

SSRI), the recent

announcement by Dr. DeLong (see posting at end of this

response), helps

confirm what has been my ongoing experience. Using the

SSRI¹s (I would say

the whole course of treatment together) I¹ve literally

realized a child¹s

brain is maturing, evolving over time. This is

consistent with the idea of

establishing better function in an area ³compromised²

(as seen on NeuroSPECT

scans). The tissue could not evolve in a healthy

manner, IF it were damaged

to begin with. "

ANTIDEPRESSANTS CAN BREAK THROUGH THE WALL OF MANY

CHILDREN'S AUTISM, DUKE

RESEARCHERS SAY DURHAM, N.C. - Many autistic children

may actually suffer

from a genetically linked depression that is treatable

with antidepressants

such as Prozac (fluoxetine), according to Dr.

DeLong, a Duke

University Medical Center pediatric neurologist. In an

article in the March

23 issue of the journal Neurology, DeLong presents a

new hypothesis that

about two-thirds of children with the most common form

of infantile autism

actually have a treatable, genetically linked,

early-onset form of severe

depression. The argument is based on recent genetic

analyses, behavioral

studies and brain chemistry and imaging analyses on

autistic children by

researchers at Duke and several other institutions.

The research was funded

by the and Sara Goldberg Charitable Trust and

the Duke Children's

Telethon. " Several lines of evidence are now coming

together to form a

cohesive picture of the biological basis of a disease

that has long baffled

the medical community, " said DeLong. " Genetic and

brain imaging studies, as

well as a re-examination of the classical symptoms of

autism, all point to

the conclusion that many autistic children have an

inherited disease that we

know how to treat. " Children with autism appear to be

prisoners of their own

minds because they are unable to learn the language or

social skills

necessary to get along in the world. Autism is

actually a spectrum of

disorders with similar symptoms, said DeLong. Children

who develop autism,

usually in the second year of life, lose the ability

to interact with people

or their environment and don't speak or use language,

even though many have

normal intelligence. While some autism is caused by

diseases or injury to

certain areas of the developing brain, most cases of

autism have no known

cause, and of these so-called idiopathic cases, DeLong

asserts that 70

percent now appear to be an inherited form of an

affective disorder, such as

manic depression or obsessive-compulsive disorder.

" Many years ago I noticed

that if you look carefully at the symptoms of autism,

they look very much

like those of depression and manic depression, " said

DeLong. " These children

show none or the cheerfulness or spontaneity of normal

children. And they

often have extreme moods swings, tantrums and

excessive fearfulness. " DeLong

has identified several lines of evidence that together

show a distinct

subgroup of autistic children who have a genetic

disease that can be treated

with anti-depressive medications. When researchers

examine the brains of

children with idiopathic autism, they find very low

levels of the

neurotransmitter serotonin on the left side of the

brain in the area

responsible for language. Serotonin is also important

in influencing mood

and is low in people with clinical depression. " In the

developing brains of

children, serotonin not only acts as a transmitter of

information, but it is

also an agent of development that influences growth in

the brain, " said

DeLong. " When serotonin levels in the left hemisphere

of the brain don't

reach a critical level in early childhood, one might

expect to see the

symptoms we see in autism: blunting of the child's

cognitive, social and

emotional development. " Studies of people in which the

connection between

the left and right hemispheres of the brain are split

surgically to relieve

symptoms of epilepsy, so-called " split brain "

experiments, show the left

hemisphere is responsible for language and reasoning

skills, while the right

hemisphere is responsible for visual-spatial skills,

musical ability and

some types of rote memorization. Serotonin levels in

the right hemisphere of

most idiopathic autistic children are normal and their

visual and spatial

skills are also normal. In fact, some autistic savants

show a type of

overcompensation on the right side of the brain that

gives them

extraordinary abilities in math computation, music or

artistic skills. When

the researchers studied older children and adolescents

diagnosed with manic

depression, they found these children also have

greater visual-spatial

abilities and lower language skills, although the

differences were not as

great as in autistic children. All these lines of

evidence led DeLong to try

treating autistic children with Prozac and other

specific serotonin

re-uptake inhibitors (SSRIs). These medications, well

known for treating

depression, work by making more serotonin available to

the brain.

In a study reported in the October 1998 issue of the

Journal of

Developmental Medicine and Child Neurology, DeLong and

his colleagues showed

that when 37 autistic children ages three to seven

were treated with Prozac

(fluoxetine) for up to three years, 22 responded well

to the medication,

regaining language abilities, becoming more sociable

and losing obsessive

compulsions such as fixating on a single object for

hours on end. Of those

children who responded to the medication, all had a

family history of a

major depressive disease, such as bipolar disorder.

" It is tempting to say

that autism and manic depression are caused by a

defect in the same gene, "

said DeLong, " and genetic evidence is beginning to

point in that direction. "

Recent studies by DeLong and his colleagues at Duke

point to a gene

somewhere on chromosome 15 as a potential autism gene.

And now several

studies by investigators at other institutions

studying manic depression

have narrowed down their search to the same general

area on chromosome 15 as

well. " While we can't yet definitively say that the

genes are one and the

same, the evidence is tantalizing, and we expect to

have answers in the near

future, " said DeLong. Such genetic studies offer hope

of an earlier

diagnosis, said DeLong, and the development of more

specific medications to

increase the availability of serotonin in the

developing brains of autistic

children offers the hope of even more effective

treatment for the disease.

" Instead of seeing autism as a disease we can't do

anything about, we now

see it as treatable, rather than hopeless, " said

DeLong. " My hope is that

these new lines of research will lead to earlier

identification and earlier

intervention to make autism a highly treatable

disease. "

__________________________________________________

[Guest guest]

Thanks, , these are very interesting and informative. I appreciate your

taking the time to post these.

Repost of SSRIs and Autism

Here's another repost of a Duke University study w/

comments quoted from Dr G - not particularly related

to previous discussions, but I thought you'd find them

interesting: (I apologize how the copying/pasting

skews up the spacing)

These are Dr. Goldberg's comments, then the study

follows...

" As far as the ³goal² of the Paxil / Prozac (or any

SSRI), the recent

announcement by Dr. DeLong (see posting at end of this

response), helps

confirm what has been my ongoing experience. Using the

SSRI¹s (I would say

the whole course of treatment together) I¹ve literally

realized a child¹s

brain is maturing, evolving over time. This is

consistent with the idea of

establishing better function in an area ³compromised²

(as seen on NeuroSPECT

scans). The tissue could not evolve in a healthy

manner, IF it were damaged

to begin with. "

ANTIDEPRESSANTS CAN BREAK THROUGH THE WALL OF MANY

CHILDREN'S AUTISM, DUKE

RESEARCHERS SAY DURHAM, N.C. - Many autistic children

may actually suffer

from a genetically linked depression that is treatable

with antidepressants

such as Prozac (fluoxetine), according to Dr.

DeLong, a Duke

University Medical Center pediatric neurologist. In an

article in the March

23 issue of the journal Neurology, DeLong presents a

new hypothesis that

about two-thirds of children with the most common form

of infantile autism

actually have a treatable, genetically linked,

early-onset form of severe

depression. The argument is based on recent genetic

analyses, behavioral

studies and brain chemistry and imaging analyses on

autistic children by

researchers at Duke and several other institutions.

The research was funded

by the and Sara Goldberg Charitable Trust and

the Duke Children's

Telethon. " Several lines of evidence are now coming

together to form a

cohesive picture of the biological basis of a disease

that has long baffled

the medical community, " said DeLong. " Genetic and

brain imaging studies, as

well as a re-examination of the classical symptoms of

autism, all point to

the conclusion that many autistic children have an

inherited disease that we

know how to treat. " Children with autism appear to be

prisoners of their own

minds because they are unable to learn the language or

social skills

necessary to get along in the world. Autism is

actually a spectrum of

disorders with similar symptoms, said DeLong. Children

who develop autism,

usually in the second year of life, lose the ability

to interact with people

or their environment and don't speak or use language,

even though many have

normal intelligence. While some autism is caused by

diseases or injury to

certain areas of the developing brain, most cases of

autism have no known

cause, and of these so-called idiopathic cases, DeLong

asserts that 70

percent now appear to be an inherited form of an

affective disorder, such as

manic depression or obsessive-compulsive disorder.

" Many years ago I noticed

that if you look carefully at the symptoms of autism,

they look very much

like those of depression and manic depression, " said

DeLong. " These children

show none or the cheerfulness or spontaneity of normal

children. And they

often have extreme moods swings, tantrums and

excessive fearfulness. " DeLong

has identified several lines of evidence that together

show a distinct

subgroup of autistic children who have a genetic

disease that can be treated

with anti-depressive medications. When researchers

examine the brains of

children with idiopathic autism, they find very low

levels of the

neurotransmitter serotonin on the left side of the

brain in the area

responsible for language. Serotonin is also important

in influencing mood

and is low in people with clinical depression. " In the

developing brains of

children, serotonin not only acts as a transmitter of

information, but it is

also an agent of development that influences growth in

the brain, " said

DeLong. " When serotonin levels in the left hemisphere

of the brain don't

reach a critical level in early childhood, one might

expect to see the

symptoms we see in autism: blunting of the child's

cognitive, social and

emotional development. " Studies of people in which the

connection between

the left and right hemispheres of the brain are split

surgically to relieve

symptoms of epilepsy, so-called " split brain "

experiments, show the left

hemisphere is responsible for language and reasoning

skills, while the right

hemisphere is responsible for visual-spatial skills,

musical ability and

some types of rote memorization. Serotonin levels in

the right hemisphere of

most idiopathic autistic children are normal and their

visual and spatial

skills are also normal. In fact, some autistic savants

show a type of

overcompensation on the right side of the brain that

gives them

extraordinary abilities in math computation, music or

artistic skills. When

the researchers studied older children and adolescents

diagnosed with manic

depression, they found these children also have

greater visual-spatial

abilities and lower language skills, although the

differences were not as

great as in autistic children. All these lines of

evidence led DeLong to try

treating autistic children with Prozac and other

specific serotonin

re-uptake inhibitors (SSRIs). These medications, well

known for treating

depression, work by making more serotonin available to

the brain.

In a study reported in the October 1998 issue of the

Journal of

Developmental Medicine and Child Neurology, DeLong and

his colleagues showed

that when 37 autistic children ages three to seven

were treated with Prozac

(fluoxetine) for up to three years, 22 responded well

to the medication,

regaining language abilities, becoming more sociable

and losing obsessive

compulsions such as fixating on a single object for

hours on end. Of those

children who responded to the medication, all had a

family history of a

major depressive disease, such as bipolar disorder.

" It is tempting to say

that autism and manic depression are caused by a

defect in the same gene, "

said DeLong, " and genetic evidence is beginning to

point in that direction. "

Recent studies by DeLong and his colleagues at Duke

point to a gene

somewhere on chromosome 15 as a potential autism gene.

And now several

studies by investigators at other institutions

studying manic depression

have narrowed down their search to the same general

area on chromosome 15 as

well. " While we can't yet definitively say that the

genes are one and the

same, the evidence is tantalizing, and we expect to

have answers in the near

future, " said DeLong. Such genetic studies offer hope

of an earlier

diagnosis, said DeLong, and the development of more

specific medications to

increase the availability of serotonin in the

developing brains of autistic

children offers the hope of even more effective

treatment for the disease.

" Instead of seeing autism as a disease we can't do

anything about, we now

see it as treatable, rather than hopeless, " said

DeLong. " My hope is that

these new lines of research will lead to earlier

identification and earlier

intervention to make autism a highly treatable

disease. "

__________________________________________________

[Guest guest]

The article listed in the Duke PR release mentioned in the previous email

(thanks, ) as appearing Neurology March 23 isn't this year--it's

from 1999. Here is the complete citation:

DeLong GR.

Autism: new data suggest a new hypothesis.

Neurology. 1999 Mar 23;52(5):911-6.

PMID: 10102405

The finding of depression or bipolar illness in family members of many

children with autism led to the idea of using an SSRI (fluoxetine

primarily) to treat the children. Many respond very nicely.

Bob Delong has continued to investigate the

autism/serotonin/depression/SSRI relationship--here is a very recent

article with its abstract:

J Neuropsychiatry Clin Neurosci. 2004 Spring;16(2):199-213.

Autism and familial major mood disorder: are they related?

DeLong R.

Division of Pediatric Neurology, Department of Pediatrics, Duke University

Medical Center, Durham, NC 27710, USA.

Family history studies of autism consistently reveal a large subgroup with

a high incidence of major mood disorder in family members, suggesting the

two entities are related clinically and genetically. This review examines

this concept, comparing current clinlical and biological knowledge of

autism and major mood disorder, and advances the hypothesis that this

subgroup of autism represents an early-life phenotype of major mood

disorder. If confirmed, this hypothesis would suggest that the basic

biological defects determining major mood disorders may have prominent

neurodevelopmental and cognitive dimensions. Testing of the hypothesis

will depend on genetic studies.

Publication Types:

Review

PMID: 15260372

S G Kahler

--

Office:

G. Kahler, MD

Professor, Division of Clinical Genetics Department of Pediatrics

University of Arkansas for Medical Sciences

email KahlerG@...

Office Phone 501-364-2966

Fax 501-364-1564

Pager (alphanumeric) 501-395-7865

Mail:

Division of Clinical Genetics

Slot 512-22

Arkansas Children's Hospital

800 Marshall St.

Little Rock, AR 72202-3591

Home:

NEW EMAIL sgkahler@...

91 Pebble Beach Dr.

Little Rock, AR 72212

phone 501-227-7609 (AFTERNOONS AND EVENINGS)

efax 610-771-7268

mobile 501-773-1688 (ALL TIMES)

Using Opera's revolutionary e-mail client: http://www.opera.com/m2/

[Guest guest]

Dr Kahler!

welcome back! We miss you in Baltimore!

Ack- you moved to Arkansas?

They don't have crabs, boardwalk fries or Fischers

popcorn!

doris

maryland

>

> The article listed in the Duke PR release mentioned in the previous

email

> (thanks, ) as appearing Neurology March 23 isn't this year--it's

> from 1999. Here is the complete citation:

>

> DeLong GR.

> Autism: new data suggest a new hypothesis.

> Neurology. 1999 Mar 23;52(5):911-6.

> PMID: 10102405

>

> The finding of depression or bipolar illness in family members of many

> children with autism led to the idea of using an SSRI (fluoxetine

> primarily) to treat the children. Many respond very nicely.

>

>

> Bob Delong has continued to investigate the

> autism/serotonin/depression/SSRI relationship--here is a very recent

> article with its abstract:

>

> J Neuropsychiatry Clin Neurosci. 2004 Spring;16(2):199-213.

> Autism and familial major mood disorder: are they related?

>

> DeLong R.

>

> Division of Pediatric Neurology, Department of Pediatrics, Duke

University

> Medical Center, Durham, NC 27710, USA.

>

> Family history studies of autism consistently reveal a large

subgroup with

> a high incidence of major mood disorder in family members,

suggesting the

> two entities are related clinically and genetically. This review

examines

> this concept, comparing current clinlical and biological knowledge of

> autism and major mood disorder, and advances the hypothesis that this

> subgroup of autism represents an early-life phenotype of major mood

> disorder. If confirmed, this hypothesis would suggest that the basic

> biological defects determining major mood disorders may have prominent

> neurodevelopmental and cognitive dimensions. Testing of the hypothesis

> will depend on genetic studies.

>

> Publication Types:

> Review

>

> PMID: 15260372

>

>

>

>

> S G Kahler

> --

>

> Office:

>

> G. Kahler, MD

> Professor, Division of Clinical Genetics Department of Pediatrics

> University of Arkansas for Medical Sciences

>

> email KahlerG@...

> Office Phone 501-364-2966

> Fax 501-364-1564

> Pager (alphanumeric) 501-395-7865

>

> Mail:

>

> Division of Clinical Genetics

> Slot 512-22

> Arkansas Children's Hospital

> 800 Marshall St.

> Little Rock, AR 72202-3591

>

>

>

>

>

> Home:

>

> NEW EMAIL sgkahler@...

>

> 91 Pebble Beach Dr.

> Little Rock, AR 72212

> phone 501-227-7609 (AFTERNOONS AND EVENINGS)

> efax 610-771-7268

> mobile 501-773-1688 (ALL TIMES)

>

>

>

> Using Opera's revolutionary e-mail client: http://www.opera.com/m2/

>