Re: Gene Influences Antidepressant Response

[Guest guest]

At least they are consistent with the word " may " . when I see that in an

article I know they are full of it. I researched mental health genes in the

press back into the eighties. They found it but then later someone else

found something else and on and on. It's the words " may " " could " " believe "

that you can spot in a second.

Jim

They don't even know how antidepressants work - by their own admission on

all the patient warnings they " think " or " believe " SSRI's blah, blah, blah.

And now they are claiming to know which genes make which person respond

which way? Bullsh*t!

Terry

http://www.nih.gov/news/pr/mar2006/nimh-15.htm

Gene Influences Antidepressant Response

Whether depressed patients will respond to an antidepressant depends, in

part, on which version of a gene they inherit, a study led by scientists at

the National Institutes of Health (NIH) has discovered. Having two copies of

one version of a gene that codes for a component of the brain's

mood-regulating system increased the odds of a favorable response to an

antidepressant by up to 18 percent, compared to having two copies of the

other, more common version.

Since the less common version was over 6 times more prevalent in white

than in black patients - and fewer blacks responded - the researchers

suggest that the gene may help to explain racial differences in the outcome

of antidepressant treatment. The findings also add to evidence that the

component, a receptor for the chemical messenger serotonin, plays a pivotal

role in the mechanism of antidepressant action.

The study, authored by National Institute of Mental Health (NIMH)

researchers Francis J. McMahon, M.D., Silvia Buervenich, Ph.D., and Husseini

Manji, M.D., along with collaborators at several other institutions, was

posted online March 8 and will appear in the May, 2006 American Journal of

Human Genetics.

" This discovery brings us closer to the day when clinicians will be able

to offer treatment options and medications that are tailored and

personalized to be optimally effective for individual patients, " said NIH

Director Elias A. Zerhouni, M.D.

However, the findings cannot yet guide treatment decisions.

" To our knowledge, this is the first demonstration of significant,

replicated association between genetic variation and outcome of

antidepressant treatment, " added Manji, director of the NIMH's Mood and

Anxiety Disorders Program.

In the initial phase of the NIMH-funded STAR*D (Sequenced Treatment

Alternatives for Depression) trial, about 47 percent of the 2,876

participants experienced some improvement with the serotonin selective

reuptake inhibitor (SSRI) citalopram (Celexa). The NIH scientists set out to

find genetic factors that might help to explain why some patients fared

better than others.

They screened genetic material from 1,953 of the STAR*D patients, a sample

with a higher percentage of responders (69 percent), in part because

patients who were doing well tended to stay in contact longer and were more

likely to allow a blood sample to be drawn. The researchers looked for

associations between treatment response and 768 known sites of variability

in 68 suspect genes - sites where letters in the genetic code vary across

individuals.

They found the strongest connection in the gene that codes for the

serotonin 2A receptor, one of several proteins to which serotonin binds when

brain cells communicate.

Located on cells in the brain's thinking center (cortex), the serotonin 2A

receptor regulates circuits implicated in depression. Antidepressants,

including citalopram, reduce the number of serotonin 2A receptors in animal

cortex over the course of a few weeks - the same time-frame required for the

drugs to work in humans - suggesting that the receptors are important in the

drugs' mechanism of action.

Everyone inherits two copies of the serotonin 2A receptor gene, one from

each parent. A tiny glitch in the gene's chemical sequence results in some

people having an adenine (A) at the same point that other people have a

guanine (G). So an individual can have gene types AA, AG or GG. Overall, the

prevalence of the A version was 38 percent, compared to 62 percent for the G

version in this sample. Fourteen percent had AA gene type, 43 percent AG and

43 percent GG. Since the site of variation is located in a stretch of

genetic material with no known function, the researchers suspect that it may

be just a marker for a still-undiscovered functional variation nearby in the

gene.

Based on scores on a depression rating scale, close to 80 percent of

patients who had AA responded to the antidepressant, compared to about 62

percent of those with GG. Thus, patients with the AA gene type were 16-18

percent more likely to benefit from the medication. Even patients with AG

showed some increased benefit.

But this only applied to white patients, in whom the A version was more

than six times more frequent than in black patients. There was no

significant association between gene type and treatment outcome in black

patients, who tended to fare less well in the trial overall.

" We now have to consider genetic factors as well as psychosocial issues in

our attempts to explain why antidepressants do not help our black patients

as much as they should, " McMahon said. " The new findings help make a

compelling case for a key role of the serotonin 2A receptor in the mechanism

of antidepressant action. "

Also participating in the study were: A. Rush and Madhukar Trivedi,

University of Texas Southwestern Medical Center; Gonzalo Laje, NIMH; Dennis

Charney, Mount Sinai Hospital; Lipsky, National Institute on Alcohol

Abuse and Alcoholism (NIAAA); , a Sorant, and

Papanicolaou, National Human Genome Research Institute (NHGRI); Maurizio

Fava, Massachusetts General Hospital; and Wisniewski, University of

Pittsburgh.

NIMH, NIAAA and NHGRI are part of the National Institutes of Health (NIH),

the Federal Government's primary agency for biomedical and behavioral

research. NIH and CDC are components of the U.S. Department of Health and

Human Services.

The National Institutes of Health (NIH) - The Nation's Medical Research

Agency - includes 27 Institutes and Centers and is a component of the U.S.

Department of Health and Human Services. It is the primary federal agency

for conducting and supporting basic, clinical and translational medical

research, and it investigates the causes, treatments, and cures for both

common and rare diseases. For more information about NIH and its programs,

visit http://www.nih.gov.

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

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

Bring photos to life! New PhotoMail makes sharing a breeze.

[Guest guest]

At least they are consistent with the word " may " . when I see that in an

article I know they are full of it. I researched mental health genes in the

press back into the eighties. They found it but then later someone else

found something else and on and on. It's the words " may " " could " " believe "

that you can spot in a second.

Jim

They don't even know how antidepressants work - by their own admission on

all the patient warnings they " think " or " believe " SSRI's blah, blah, blah.

And now they are claiming to know which genes make which person respond

which way? Bullsh*t!

Terry

http://www.nih.gov/news/pr/mar2006/nimh-15.htm

Gene Influences Antidepressant Response

Whether depressed patients will respond to an antidepressant depends, in

part, on which version of a gene they inherit, a study led by scientists at

the National Institutes of Health (NIH) has discovered. Having two copies of

one version of a gene that codes for a component of the brain's

mood-regulating system increased the odds of a favorable response to an

antidepressant by up to 18 percent, compared to having two copies of the

other, more common version.

Since the less common version was over 6 times more prevalent in white

than in black patients - and fewer blacks responded - the researchers

suggest that the gene may help to explain racial differences in the outcome

of antidepressant treatment. The findings also add to evidence that the

component, a receptor for the chemical messenger serotonin, plays a pivotal

role in the mechanism of antidepressant action.

The study, authored by National Institute of Mental Health (NIMH)

researchers Francis J. McMahon, M.D., Silvia Buervenich, Ph.D., and Husseini

Manji, M.D., along with collaborators at several other institutions, was

posted online March 8 and will appear in the May, 2006 American Journal of

Human Genetics.

" This discovery brings us closer to the day when clinicians will be able

to offer treatment options and medications that are tailored and

personalized to be optimally effective for individual patients, " said NIH

Director Elias A. Zerhouni, M.D.

However, the findings cannot yet guide treatment decisions.

" To our knowledge, this is the first demonstration of significant,

replicated association between genetic variation and outcome of

antidepressant treatment, " added Manji, director of the NIMH's Mood and

Anxiety Disorders Program.

In the initial phase of the NIMH-funded STAR*D (Sequenced Treatment

Alternatives for Depression) trial, about 47 percent of the 2,876

participants experienced some improvement with the serotonin selective

reuptake inhibitor (SSRI) citalopram (Celexa). The NIH scientists set out to

find genetic factors that might help to explain why some patients fared

better than others.

They screened genetic material from 1,953 of the STAR*D patients, a sample

with a higher percentage of responders (69 percent), in part because

patients who were doing well tended to stay in contact longer and were more

likely to allow a blood sample to be drawn. The researchers looked for

associations between treatment response and 768 known sites of variability

in 68 suspect genes - sites where letters in the genetic code vary across

individuals.

They found the strongest connection in the gene that codes for the

serotonin 2A receptor, one of several proteins to which serotonin binds when

brain cells communicate.

Located on cells in the brain's thinking center (cortex), the serotonin 2A

receptor regulates circuits implicated in depression. Antidepressants,

including citalopram, reduce the number of serotonin 2A receptors in animal

cortex over the course of a few weeks - the same time-frame required for the

drugs to work in humans - suggesting that the receptors are important in the

drugs' mechanism of action.

Everyone inherits two copies of the serotonin 2A receptor gene, one from

each parent. A tiny glitch in the gene's chemical sequence results in some

people having an adenine (A) at the same point that other people have a

guanine (G). So an individual can have gene types AA, AG or GG. Overall, the

prevalence of the A version was 38 percent, compared to 62 percent for the G

version in this sample. Fourteen percent had AA gene type, 43 percent AG and

43 percent GG. Since the site of variation is located in a stretch of

genetic material with no known function, the researchers suspect that it may

be just a marker for a still-undiscovered functional variation nearby in the

gene.

Based on scores on a depression rating scale, close to 80 percent of

patients who had AA responded to the antidepressant, compared to about 62

percent of those with GG. Thus, patients with the AA gene type were 16-18

percent more likely to benefit from the medication. Even patients with AG

showed some increased benefit.

But this only applied to white patients, in whom the A version was more

than six times more frequent than in black patients. There was no

significant association between gene type and treatment outcome in black

patients, who tended to fare less well in the trial overall.

" We now have to consider genetic factors as well as psychosocial issues in

our attempts to explain why antidepressants do not help our black patients

as much as they should, " McMahon said. " The new findings help make a

compelling case for a key role of the serotonin 2A receptor in the mechanism

of antidepressant action. "

Also participating in the study were: A. Rush and Madhukar Trivedi,

University of Texas Southwestern Medical Center; Gonzalo Laje, NIMH; Dennis

Charney, Mount Sinai Hospital; Lipsky, National Institute on Alcohol

Abuse and Alcoholism (NIAAA); , a Sorant, and

Papanicolaou, National Human Genome Research Institute (NHGRI); Maurizio

Fava, Massachusetts General Hospital; and Wisniewski, University of

Pittsburgh.

NIMH, NIAAA and NHGRI are part of the National Institutes of Health (NIH),

the Federal Government's primary agency for biomedical and behavioral

research. NIH and CDC are components of the U.S. Department of Health and

Human Services.

The National Institutes of Health (NIH) - The Nation's Medical Research

Agency - includes 27 Institutes and Centers and is a component of the U.S.

Department of Health and Human Services. It is the primary federal agency

for conducting and supporting basic, clinical and translational medical

research, and it investigates the causes, treatments, and cures for both

common and rare diseases. For more information about NIH and its programs,

visit http://www.nih.gov.

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

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

Bring photos to life! New PhotoMail makes sharing a breeze.

[Guest guest]

At least they are consistent with the word " may " . when I see that in an

article I know they are full of it. I researched mental health genes in the

press back into the eighties. They found it but then later someone else

found something else and on and on. It's the words " may " " could " " believe "

that you can spot in a second.

Jim

They don't even know how antidepressants work - by their own admission on

all the patient warnings they " think " or " believe " SSRI's blah, blah, blah.

And now they are claiming to know which genes make which person respond

which way? Bullsh*t!

Terry

http://www.nih.gov/news/pr/mar2006/nimh-15.htm

Gene Influences Antidepressant Response

Whether depressed patients will respond to an antidepressant depends, in

part, on which version of a gene they inherit, a study led by scientists at

the National Institutes of Health (NIH) has discovered. Having two copies of

one version of a gene that codes for a component of the brain's

mood-regulating system increased the odds of a favorable response to an

antidepressant by up to 18 percent, compared to having two copies of the

other, more common version.

Since the less common version was over 6 times more prevalent in white

than in black patients - and fewer blacks responded - the researchers

suggest that the gene may help to explain racial differences in the outcome

of antidepressant treatment. The findings also add to evidence that the

component, a receptor for the chemical messenger serotonin, plays a pivotal

role in the mechanism of antidepressant action.

The study, authored by National Institute of Mental Health (NIMH)

researchers Francis J. McMahon, M.D., Silvia Buervenich, Ph.D., and Husseini

Manji, M.D., along with collaborators at several other institutions, was

posted online March 8 and will appear in the May, 2006 American Journal of

Human Genetics.

" This discovery brings us closer to the day when clinicians will be able

to offer treatment options and medications that are tailored and

personalized to be optimally effective for individual patients, " said NIH

Director Elias A. Zerhouni, M.D.

However, the findings cannot yet guide treatment decisions.

" To our knowledge, this is the first demonstration of significant,

replicated association between genetic variation and outcome of

antidepressant treatment, " added Manji, director of the NIMH's Mood and

Anxiety Disorders Program.

In the initial phase of the NIMH-funded STAR*D (Sequenced Treatment

Alternatives for Depression) trial, about 47 percent of the 2,876

participants experienced some improvement with the serotonin selective

reuptake inhibitor (SSRI) citalopram (Celexa). The NIH scientists set out to

find genetic factors that might help to explain why some patients fared

better than others.

They screened genetic material from 1,953 of the STAR*D patients, a sample

with a higher percentage of responders (69 percent), in part because

patients who were doing well tended to stay in contact longer and were more

likely to allow a blood sample to be drawn. The researchers looked for

associations between treatment response and 768 known sites of variability

in 68 suspect genes - sites where letters in the genetic code vary across

individuals.

They found the strongest connection in the gene that codes for the

serotonin 2A receptor, one of several proteins to which serotonin binds when

brain cells communicate.

Located on cells in the brain's thinking center (cortex), the serotonin 2A

receptor regulates circuits implicated in depression. Antidepressants,

including citalopram, reduce the number of serotonin 2A receptors in animal

cortex over the course of a few weeks - the same time-frame required for the

drugs to work in humans - suggesting that the receptors are important in the

drugs' mechanism of action.

Everyone inherits two copies of the serotonin 2A receptor gene, one from

each parent. A tiny glitch in the gene's chemical sequence results in some

people having an adenine (A) at the same point that other people have a

guanine (G). So an individual can have gene types AA, AG or GG. Overall, the

prevalence of the A version was 38 percent, compared to 62 percent for the G

version in this sample. Fourteen percent had AA gene type, 43 percent AG and

43 percent GG. Since the site of variation is located in a stretch of

genetic material with no known function, the researchers suspect that it may

be just a marker for a still-undiscovered functional variation nearby in the

gene.

Based on scores on a depression rating scale, close to 80 percent of

patients who had AA responded to the antidepressant, compared to about 62

percent of those with GG. Thus, patients with the AA gene type were 16-18

percent more likely to benefit from the medication. Even patients with AG

showed some increased benefit.

But this only applied to white patients, in whom the A version was more

than six times more frequent than in black patients. There was no

significant association between gene type and treatment outcome in black

patients, who tended to fare less well in the trial overall.

" We now have to consider genetic factors as well as psychosocial issues in

our attempts to explain why antidepressants do not help our black patients

as much as they should, " McMahon said. " The new findings help make a

compelling case for a key role of the serotonin 2A receptor in the mechanism

of antidepressant action. "

Also participating in the study were: A. Rush and Madhukar Trivedi,

University of Texas Southwestern Medical Center; Gonzalo Laje, NIMH; Dennis

Charney, Mount Sinai Hospital; Lipsky, National Institute on Alcohol

Abuse and Alcoholism (NIAAA); , a Sorant, and

Papanicolaou, National Human Genome Research Institute (NHGRI); Maurizio

Fava, Massachusetts General Hospital; and Wisniewski, University of

Pittsburgh.

NIMH, NIAAA and NHGRI are part of the National Institutes of Health (NIH),

the Federal Government's primary agency for biomedical and behavioral

research. NIH and CDC are components of the U.S. Department of Health and

Human Services.

The National Institutes of Health (NIH) - The Nation's Medical Research

Agency - includes 27 Institutes and Centers and is a component of the U.S.

Department of Health and Human Services. It is the primary federal agency

for conducting and supporting basic, clinical and translational medical

research, and it investigates the causes, treatments, and cures for both

common and rare diseases. For more information about NIH and its programs,

visit http://www.nih.gov.

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

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

Bring photos to life! New PhotoMail makes sharing a breeze.

[Guest guest]

At least they are consistent with the word " may " . when I see that in an

article I know they are full of it. I researched mental health genes in the

press back into the eighties. They found it but then later someone else

found something else and on and on. It's the words " may " " could " " believe "

that you can spot in a second.

Jim

They don't even know how antidepressants work - by their own admission on

all the patient warnings they " think " or " believe " SSRI's blah, blah, blah.

And now they are claiming to know which genes make which person respond

which way? Bullsh*t!

Terry

http://www.nih.gov/news/pr/mar2006/nimh-15.htm

Gene Influences Antidepressant Response

Whether depressed patients will respond to an antidepressant depends, in

part, on which version of a gene they inherit, a study led by scientists at

the National Institutes of Health (NIH) has discovered. Having two copies of

one version of a gene that codes for a component of the brain's

mood-regulating system increased the odds of a favorable response to an

antidepressant by up to 18 percent, compared to having two copies of the

other, more common version.

Since the less common version was over 6 times more prevalent in white

than in black patients - and fewer blacks responded - the researchers

suggest that the gene may help to explain racial differences in the outcome

of antidepressant treatment. The findings also add to evidence that the

component, a receptor for the chemical messenger serotonin, plays a pivotal

role in the mechanism of antidepressant action.

The study, authored by National Institute of Mental Health (NIMH)

researchers Francis J. McMahon, M.D., Silvia Buervenich, Ph.D., and Husseini

Manji, M.D., along with collaborators at several other institutions, was

posted online March 8 and will appear in the May, 2006 American Journal of

Human Genetics.

" This discovery brings us closer to the day when clinicians will be able

to offer treatment options and medications that are tailored and

personalized to be optimally effective for individual patients, " said NIH

Director Elias A. Zerhouni, M.D.

However, the findings cannot yet guide treatment decisions.

" To our knowledge, this is the first demonstration of significant,

replicated association between genetic variation and outcome of

antidepressant treatment, " added Manji, director of the NIMH's Mood and

Anxiety Disorders Program.

In the initial phase of the NIMH-funded STAR*D (Sequenced Treatment

Alternatives for Depression) trial, about 47 percent of the 2,876

participants experienced some improvement with the serotonin selective

reuptake inhibitor (SSRI) citalopram (Celexa). The NIH scientists set out to

find genetic factors that might help to explain why some patients fared

better than others.

They screened genetic material from 1,953 of the STAR*D patients, a sample

with a higher percentage of responders (69 percent), in part because

patients who were doing well tended to stay in contact longer and were more

likely to allow a blood sample to be drawn. The researchers looked for

associations between treatment response and 768 known sites of variability

in 68 suspect genes - sites where letters in the genetic code vary across

individuals.

They found the strongest connection in the gene that codes for the

serotonin 2A receptor, one of several proteins to which serotonin binds when

brain cells communicate.

Located on cells in the brain's thinking center (cortex), the serotonin 2A

receptor regulates circuits implicated in depression. Antidepressants,

including citalopram, reduce the number of serotonin 2A receptors in animal

cortex over the course of a few weeks - the same time-frame required for the

drugs to work in humans - suggesting that the receptors are important in the

drugs' mechanism of action.

Everyone inherits two copies of the serotonin 2A receptor gene, one from

each parent. A tiny glitch in the gene's chemical sequence results in some

people having an adenine (A) at the same point that other people have a

guanine (G). So an individual can have gene types AA, AG or GG. Overall, the

prevalence of the A version was 38 percent, compared to 62 percent for the G

version in this sample. Fourteen percent had AA gene type, 43 percent AG and

43 percent GG. Since the site of variation is located in a stretch of

genetic material with no known function, the researchers suspect that it may

be just a marker for a still-undiscovered functional variation nearby in the

gene.

Based on scores on a depression rating scale, close to 80 percent of

patients who had AA responded to the antidepressant, compared to about 62

percent of those with GG. Thus, patients with the AA gene type were 16-18

percent more likely to benefit from the medication. Even patients with AG

showed some increased benefit.

But this only applied to white patients, in whom the A version was more

than six times more frequent than in black patients. There was no

significant association between gene type and treatment outcome in black

patients, who tended to fare less well in the trial overall.

" We now have to consider genetic factors as well as psychosocial issues in

our attempts to explain why antidepressants do not help our black patients

as much as they should, " McMahon said. " The new findings help make a

compelling case for a key role of the serotonin 2A receptor in the mechanism

of antidepressant action. "

Also participating in the study were: A. Rush and Madhukar Trivedi,

University of Texas Southwestern Medical Center; Gonzalo Laje, NIMH; Dennis

Charney, Mount Sinai Hospital; Lipsky, National Institute on Alcohol

Abuse and Alcoholism (NIAAA); , a Sorant, and

Papanicolaou, National Human Genome Research Institute (NHGRI); Maurizio

Fava, Massachusetts General Hospital; and Wisniewski, University of

Pittsburgh.

NIMH, NIAAA and NHGRI are part of the National Institutes of Health (NIH),

the Federal Government's primary agency for biomedical and behavioral

research. NIH and CDC are components of the U.S. Department of Health and

Human Services.

The National Institutes of Health (NIH) - The Nation's Medical Research

Agency - includes 27 Institutes and Centers and is a component of the U.S.

Department of Health and Human Services. It is the primary federal agency

for conducting and supporting basic, clinical and translational medical

research, and it investigates the causes, treatments, and cures for both

common and rare diseases. For more information about NIH and its programs,

visit http://www.nih.gov.

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

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

Bring photos to life! New PhotoMail makes sharing a breeze.

[Guest guest]

This crap really needs to stop, wasting money trying to keep the

races separated. Aren't there enough bi-racial people in this country

now to make this kind of study worthless? Anything to try and explain

why it doesn't work. Could it be there are more black people who are

poor and don't have insurance? Guess they can't afford it anyway so

the explanation is, it doesn't work on them. Sure would like to take

my family and make this idiot's acquaintance and let him explain our

response to antidepressants.

>

> At least they are consistent with the word " may " . when I see that

in an

> article I know they are full of it. I researched mental health

genes in the

> press back into the eighties. They found it but then later someone

else

> found something else and on and on. It's the

words " may " " could " " believe "

> that you can spot in a second.

>

> Jim

>

> They don't even know how antidepressants work - by their own

admission on

> all the patient warnings they " think " or " believe " SSRI's blah,

blah, blah.

> And now they are claiming to know which genes make which person

respond

> which way? Bullsh*t!

> Terry

>

> http://www.nih.gov/news/pr/mar2006/nimh-15.htm

> Gene Influences Antidepressant Response

> Whether depressed patients will respond to an antidepressant

depends, in

> part, on which version of a gene they inherit, a study led by

scientists at

> the National Institutes of Health (NIH) has discovered. Having two

copies of

> one version of a gene that codes for a component of the brain's

> mood-regulating system increased the odds of a favorable response

to an

> antidepressant by up to 18 percent, compared to having two copies

of the

> other, more common version.

> Since the less common version was over 6 times more prevalent in

white

> than in black patients - and fewer blacks responded - the

researchers

> suggest that the gene may help to explain racial differences in the

outcome

> of antidepressant treatment. The findings also add to evidence that

the

> component, a receptor for the chemical messenger serotonin, plays a

pivotal

> role in the mechanism of antidepressant action.

> The study, authored by National Institute of Mental Health (NIMH)

> researchers Francis J. McMahon, M.D., Silvia Buervenich, Ph.D., and

Husseini

> Manji, M.D., along with collaborators at several other

institutions, was

> posted online March 8 and will appear in the May, 2006 American

Journal of

> Human Genetics.

> " This discovery brings us closer to the day when clinicians will

be able

> to offer treatment options and medications that are tailored and

> personalized to be optimally effective for individual patients, "

said NIH

> Director Elias A. Zerhouni, M.D.

> However, the findings cannot yet guide treatment decisions.

> " To our knowledge, this is the first demonstration of significant,

> replicated association between genetic variation and outcome of

> antidepressant treatment, " added Manji, director of the NIMH's Mood

and

> Anxiety Disorders Program.

> In the initial phase of the NIMH-funded STAR*D (Sequenced

Treatment

> Alternatives for Depression) trial, about 47 percent of the 2,876

> participants experienced some improvement with the serotonin

selective

> reuptake inhibitor (SSRI) citalopram (Celexa). The NIH scientists

set out to

> find genetic factors that might help to explain why some patients

fared

> better than others.

> They screened genetic material from 1,953 of the STAR*D patients,

a sample

> with a higher percentage of responders (69 percent), in part because

> patients who were doing well tended to stay in contact longer and

were more

> likely to allow a blood sample to be drawn. The researchers looked

for

> associations between treatment response and 768 known sites of

variability

> in 68 suspect genes - sites where letters in the genetic code vary

across

> individuals.

> They found the strongest connection in the gene that codes for the

> serotonin 2A receptor, one of several proteins to which serotonin

binds when

> brain cells communicate.

> Located on cells in the brain's thinking center (cortex), the

serotonin 2A

> receptor regulates circuits implicated in depression.

Antidepressants,

> including citalopram, reduce the number of serotonin 2A receptors

in animal

> cortex over the course of a few weeks - the same time-frame

required for the

> drugs to work in humans - suggesting that the receptors are

important in the

> drugs' mechanism of action.

> Everyone inherits two copies of the serotonin 2A receptor gene,

one from

> each parent. A tiny glitch in the gene's chemical sequence results

in some

> people having an adenine (A) at the same point that other people

have a

> guanine (G). So an individual can have gene types AA, AG or GG.

Overall, the

> prevalence of the A version was 38 percent, compared to 62 percent

for the G

> version in this sample. Fourteen percent had AA gene type, 43

percent AG and

> 43 percent GG. Since the site of variation is located in a stretch

of

> genetic material with no known function, the researchers suspect

that it may

> be just a marker for a still-undiscovered functional variation

nearby in the

> gene.

> Based on scores on a depression rating scale, close to 80 percent

of

> patients who had AA responded to the antidepressant, compared to

about 62

> percent of those with GG. Thus, patients with the AA gene type were

16-18

> percent more likely to benefit from the medication. Even patients

with AG

> showed some increased benefit.

> But this only applied to white patients, in whom the A version

was more

> than six times more frequent than in black patients. There was no

> significant association between gene type and treatment outcome in

black

> patients, who tended to fare less well in the trial overall.

> " We now have to consider genetic factors as well as psychosocial

issues in

> our attempts to explain why antidepressants do not help our black

patients

> as much as they should, " McMahon said. " The new findings help make a

> compelling case for a key role of the serotonin 2A receptor in the

mechanism

> of antidepressant action. "

> Also participating in the study were: A. Rush and Madhukar

Trivedi,

> University of Texas Southwestern Medical Center; Gonzalo Laje,

NIMH; Dennis

> Charney, Mount Sinai Hospital; Lipsky, National Institute on

Alcohol

> Abuse and Alcoholism (NIAAA); , a Sorant, and

> Papanicolaou, National Human Genome Research Institute (NHGRI);

Maurizio

> Fava, Massachusetts General Hospital; and Wisniewski,

University of

> Pittsburgh.

> NIMH, NIAAA and NHGRI are part of the National Institutes of

Health (NIH),

> the Federal Government's primary agency for biomedical and

behavioral

> research. NIH and CDC are components of the U.S. Department of

Health and

> Human Services.

> The National Institutes of Health (NIH) - The Nation's Medical

Research

> Agency - includes 27 Institutes and Centers and is a component of

the U.S.

> Department of Health and Human Services. It is the primary federal

agency

> for conducting and supporting basic, clinical and translational

medical

> research, and it investigates the causes, treatments, and cures for

both

> common and rare diseases. For more information about NIH and its

programs,

> visit http://www.nih.gov.

>

> ---------------------------------

>

>

> ---------------------------------

>

> Bring photos to life! New PhotoMail makes sharing a breeze.

>

>

[Guest guest]

I was just wondering what they would consider a favorable response?

Lets see, what are our chocies? Mania, hypomania, depersonalization,

aggitation, agression, suicide, murder. That doesn't cover all of

them but, those are the ones I could think of.

Peggy

emn i.sone

> >

> > At least they are consistent with the word " may " . when I see that

> in an

> > article I know they are full of it. I researched mental health

> genes in the

> > press back into the eighties. They found it but then later

someone

> else

> > found something else and on and on. It's the

> words " may " " could " " believe "

> > that you can spot in a second.

> >

> > Jim

> >

> > They don't even know how antidepressants work - by their own

> admission on

> > all the patient warnings they " think " or " believe " SSRI's blah,

> blah, blah.

> > And now they are claiming to know which genes make which person

> respond

> > which way? Bullsh*t!

> > Terry

> >

> > http://www.nih.gov/news/pr/mar2006/nimh-15.htm

> > Gene Influences Antidepressant Response

> > Whether depressed patients will respond to an antidepressant

> depends, in

> > part, on which version of a gene they inherit, a study led by

> scientists at

> > the National Institutes of Health (NIH) has discovered. Having

two

> copies of

> > one version of a gene that codes for a component of the brain's

> > mood-regulating system increased the odds of a favorable response

> to an

> > antidepressant by up to 18 percent, compared to having two copies

> of the

> > other, more common version.

> > Since the less common version was over 6 times more prevalent

in

> white

> > than in black patients - and fewer blacks responded - the

> researchers

> > suggest that the gene may help to explain racial differences in

the

> outcome

> > of antidepressant treatment. The findings also add to evidence

that

> the

> > component, a receptor for the chemical messenger serotonin, plays

a

> pivotal

> > role in the mechanism of antidepressant action.

> > The study, authored by National Institute of Mental Health

(NIMH)

> > researchers Francis J. McMahon, M.D., Silvia Buervenich, Ph.D.,

and

> Husseini

> > Manji, M.D., along with collaborators at several other

> institutions, was

> > posted online March 8 and will appear in the May, 2006 American

> Journal of

> > Human Genetics.

> > " This discovery brings us closer to the day when clinicians

will

> be able

> > to offer treatment options and medications that are tailored and

> > personalized to be optimally effective for individual patients, "

> said NIH

> > Director Elias A. Zerhouni, M.D.

> > However, the findings cannot yet guide treatment decisions.

> > " To our knowledge, this is the first demonstration of

significant,

> > replicated association between genetic variation and outcome of

> > antidepressant treatment, " added Manji, director of the NIMH's

Mood

> and

> > Anxiety Disorders Program.

> > In the initial phase of the NIMH-funded STAR*D (Sequenced

> Treatment

> > Alternatives for Depression) trial, about 47 percent of the 2,876

> > participants experienced some improvement with the serotonin

> selective

> > reuptake inhibitor (SSRI) citalopram (Celexa). The NIH scientists

> set out to

> > find genetic factors that might help to explain why some patients

> fared

> > better than others.

> > They screened genetic material from 1,953 of the STAR*D

patients,

> a sample

> > with a higher percentage of responders (69 percent), in part

because

> > patients who were doing well tended to stay in contact longer and

> were more

> > likely to allow a blood sample to be drawn. The researchers

looked

> for

> > associations between treatment response and 768 known sites of

> variability

> > in 68 suspect genes - sites where letters in the genetic code

vary

> across

> > individuals.

> > They found the strongest connection in the gene that codes for

the

> > serotonin 2A receptor, one of several proteins to which serotonin

> binds when

> > brain cells communicate.

> > Located on cells in the brain's thinking center (cortex), the

> serotonin 2A

> > receptor regulates circuits implicated in depression.

> Antidepressants,

> > including citalopram, reduce the number of serotonin 2A receptors

> in animal

> > cortex over the course of a few weeks - the same time-frame

> required for the

> > drugs to work in humans - suggesting that the receptors are

> important in the

> > drugs' mechanism of action.

> > Everyone inherits two copies of the serotonin 2A receptor gene,

> one from

> > each parent. A tiny glitch in the gene's chemical sequence

results

> in some

> > people having an adenine (A) at the same point that other people

> have a

> > guanine (G). So an individual can have gene types AA, AG or GG.

> Overall, the

> > prevalence of the A version was 38 percent, compared to 62

percent

> for the G

> > version in this sample. Fourteen percent had AA gene type, 43

> percent AG and

> > 43 percent GG. Since the site of variation is located in a

stretch

> of

> > genetic material with no known function, the researchers suspect

> that it may

> > be just a marker for a still-undiscovered functional variation

> nearby in the

> > gene.

> > Based on scores on a depression rating scale, close to 80

percent

> of

> > patients who had AA responded to the antidepressant, compared to

> about 62

> > percent of those with GG. Thus, patients with the AA gene type

were

> 16-18

> > percent more likely to benefit from the medication. Even patients

> with AG

> > showed some increased benefit.

> > But this only applied to white patients, in whom the A version

> was more

> > than six times more frequent than in black patients. There was no

> > significant association between gene type and treatment outcome

in

> black

> > patients, who tended to fare less well in the trial overall.

> > " We now have to consider genetic factors as well as

psychosocial

> issues in

> > our attempts to explain why antidepressants do not help our black

> patients

> > as much as they should, " McMahon said. " The new findings help

make a

> > compelling case for a key role of the serotonin 2A receptor in

the

> mechanism

> > of antidepressant action. "

> > Also participating in the study were: A. Rush and Madhukar

> Trivedi,

> > University of Texas Southwestern Medical Center; Gonzalo Laje,

> NIMH; Dennis

> > Charney, Mount Sinai Hospital; Lipsky, National Institute

on

> Alcohol

> > Abuse and Alcoholism (NIAAA); , a Sorant, and

>

> > Papanicolaou, National Human Genome Research Institute (NHGRI);

> Maurizio

> > Fava, Massachusetts General Hospital; and Wisniewski,

> University of

> > Pittsburgh.

> > NIMH, NIAAA and NHGRI are part of the National Institutes of

> Health (NIH),

> > the Federal Government's primary agency for biomedical and

> behavioral

> > research. NIH and CDC are components of the U.S. Department of

> Health and

> > Human Services.

> > The National Institutes of Health (NIH) - The Nation's Medical

> Research

> > Agency - includes 27 Institutes and Centers and is a component of

> the U.S.

> > Department of Health and Human Services. It is the primary

federal

> agency

> > for conducting and supporting basic, clinical and translational

> medical

> > research, and it investigates the causes, treatments, and cures

for

> both

> > common and rare diseases. For more information about NIH and its

> programs,

> > visit http://www.nih.gov.

> >

> > ---------------------------------

> >

> >

> > ---------------------------------

> >

> > Bring photos to life! New PhotoMail makes sharing a breeze.

> >

> >

[Guest guest]

Hi,

I am wondering why I posted the original.

I don't disagree with anything that has been said

about the issues.

john

--- Peggy Rose <rpggyr@...> wrote:

> I was just wondering what they would consider a

> favorable response?

> Lets see, what are our chocies? Mania, hypomania,

> depersonalization,

> aggitation, agression, suicide, murder. That doesn't

> cover all of

> them but, those are the ones I could think of.

>

> Peggy

>

>

> emn i.sone

> > >

> > > At least they are consistent with the word

> " may " . when I see that

> > in an

> > > article I know they are full of it. I researched

> mental health

> > genes in the

> > > press back into the eighties. They found it but

> then later

> someone

> > else

> > > found something else and on and on. It's the

> > words " may " " could " " believe "

> > > that you can spot in a second.

> > >

> > > Jim

> > >

> > > They don't even know how antidepressants work -

> by their own

> > admission on

> > > all the patient warnings they " think " or

> " believe " SSRI's blah,

> > blah, blah.

> > > And now they are claiming to know which genes

> make which person

> > respond

> > > which way? Bullsh*t!

> > > Terry

> > >

> > > http://www.nih.gov/news/pr/mar2006/nimh-15.htm

> > > Gene Influences Antidepressant Response

> > > Whether depressed patients will respond to an

> antidepressant

> > depends, in

> > > part, on which version of a gene they inherit, a

> study led by

> > scientists at

> > > the National Institutes of Health (NIH) has

> discovered. Having

> two

> > copies of

> > > one version of a gene that codes for a component

> of the brain's

> > > mood-regulating system increased the odds of a

> favorable response

> > to an

> > > antidepressant by up to 18 percent, compared to

> having two copies

> > of the

> > > other, more common version.

> > > Since the less common version was over 6 times

> more prevalent

> in

> > white

> > > than in black patients - and fewer blacks

> responded - the

> > researchers

> > > suggest that the gene may help to explain racial

> differences in

> the

> > outcome

> > > of antidepressant treatment. The findings also

> add to evidence

> that

> > the

> > > component, a receptor for the chemical messenger

> serotonin, plays

> a

> > pivotal

> > > role in the mechanism of antidepressant action.

> > > The study, authored by National Institute of

> Mental Health

> (NIMH)

> > > researchers Francis J. McMahon, M.D., Silvia

> Buervenich, Ph.D.,

> and

> > Husseini

> > > Manji, M.D., along with collaborators at several

> other

> > institutions, was

> > > posted online March 8 and will appear in the

> May, 2006 American

> > Journal of

> > > Human Genetics.

> > > " This discovery brings us closer to the day

> when clinicians

> will

> > be able

> > > to offer treatment options and medications that

> are tailored and

> > > personalized to be optimally effective for

> individual patients, "

> > said NIH

> > > Director Elias A. Zerhouni, M.D.

> > > However, the findings cannot yet guide

> treatment decisions.

> > > " To our knowledge, this is the first

> demonstration of

> significant,

> > > replicated association between genetic variation

> and outcome of

> > > antidepressant treatment, " added Manji, director

> of the NIMH's

> Mood

> > and

> > > Anxiety Disorders Program.

> > > In the initial phase of the NIMH-funded STAR*D

> (Sequenced

> > Treatment

> > > Alternatives for Depression) trial, about 47

> percent of the 2,876

> > > participants experienced some improvement with

> the serotonin

> > selective

> > > reuptake inhibitor (SSRI) citalopram (Celexa).

> The NIH scientists

> > set out to

> > > find genetic factors that might help to explain

> why some patients

> > fared

> > > better than others.

> > > They screened genetic material from 1,953 of

> the STAR*D

> patients,

> > a sample

> > > with a higher percentage of responders (69

> percent), in part

> because

> > > patients who were doing well tended to stay in

> contact longer and

> > were more

> > > likely to allow a blood sample to be drawn. The

> researchers

> looked

> > for

> > > associations between treatment response and 768

> known sites of

> > variability

> > > in 68 suspect genes - sites where letters in the

> genetic code

> vary

> > across

> > > individuals.

> > > They found the strongest connection in the

> gene that codes for

> the

> > > serotonin 2A receptor, one of several proteins

> to which serotonin

> > binds when

> > > brain cells communicate.

> > > Located on cells in the brain's thinking

> center (cortex), the

> > serotonin 2A

> > > receptor regulates circuits implicated in

> depression.

> > Antidepressants,

> > > including citalopram, reduce the number of

> serotonin 2A receptors

> > in animal

> > > cortex over the course of a few weeks - the same

> time-frame

> > required for the

> > > drugs to work in humans - suggesting that the

> receptors are

> > important in the

> > > drugs' mechanism of action.

> > > Everyone inherits two copies of the serotonin

> 2A receptor gene,

> > one from

> > > each parent. A tiny glitch in the gene's

> chemical sequence

> results

> > in some

> > > people having an adenine (A) at the same point

> that other people

> > have a

> > > guanine (G). So an individual can have gene

> types AA, AG or GG.

> > Overall, the

> > > prevalence of the A version was 38 percent,

> compared to 62

> percent

> > for the G

> > > version in this sample. Fourteen percent had AA

> gene type, 43

> > percent AG and

> > > 43 percent GG. Since the site of variation is

> located in a

> stretch

> > of

> > > genetic material with no known function, the

> researchers suspect

> > that it may

> > > be just a marker for a still-undiscovered

> functional variation

> > nearby in the

> > > gene.

> > > Based on scores on a depression rating scale,

> close to 80

> percent

> > of

> > > patients who had AA responded to the

> antidepressant, compared to

> > about 62

> > > percent of those with GG. Thus, patients with

> the AA gene type

> were

> > 16-18

> > > percent more likely to benefit from the

> medication. Even patients

> > with AG

> > > showed some increased benefit.

> > > But this only applied to white patients, in

> whom the A version

> > was more

> > > than six times more frequent than in black

> patients. There was no

> > > significant association between gene type and

> treatment outcome

> in

> > black

> > > patients, who tended to fare less well in the

> trial overall.

> > > " We now have to consider genetic factors as

> well as

> psychosocial

> > issues in

> > > our attempts to explain why antidepressants do

> not help our black

> > patients

> > > as much as they should, " McMahon said. " The new

> findings help

> make a

> > > compelling case for a key role of the serotonin

> 2A receptor in

> the

> > mechanism

> > > of antidepressant action. "

> > > Also participating in the study were: A.

> Rush and Madhukar

> > Trivedi,

> > > University of Texas Southwestern Medical Center;

> Gonzalo Laje,

> > NIMH; Dennis

> > > Charney, Mount Sinai Hospital; Lipsky,

> National Institute

> on

> > Alcohol

> > > Abuse and Alcoholism (NIAAA); ,

> a Sorant, and

> >

> > > Papanicolaou, National Human Genome Research

> Institute (NHGRI);

> > Maurizio

> > > Fava, Massachusetts General Hospital; and

> Wisniewski,

> > University of

> > > Pittsburgh.

> > > NIMH, NIAAA and NHGRI are part of the National

> Institutes of

> > Health (NIH),

> > > the Federal Government's primary agency for

> biomedical and

> > behavioral

> > > research. NIH and CDC are components of the U.S.

> Department of

> > Health and

> > > Human Services.

> > > The National Institutes of Health (NIH) - The

> Nation's Medical

> > Research

> > > Agency - includes 27 Institutes and Centers and

> is a component of

> > the U.S.

> > > Department of Health and Human Services. It is

> the primary

> federal

> > agency

> > > for conducting and supporting basic, clinical

> and translational

> > medical

> > > research, and it investigates the causes,

> treatments, and cures

> for

> > both

> > > common and rare diseases. For more information

> about NIH and its

> > programs,

> > > visit http://www.nih.gov.

> > >

> > > ---------------------------------

> > >

> > >

> > > ---------------------------------

> > >

> > > Bring photos to life! New PhotoMail makes

> sharing a breeze.

> > >

> > > [Non-text portions of this message have been

> removed]

> > >

> > >

> > >

> > >

> > >