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http://www.thestarphoenix.com/health/Effect+antidepressants+placebos+similar/330\

7896/story.html

Effect of antidepressants, placebos similar

By Mark Lemstra, The StarPhoenix July 22, 2010

We could save $2 billion a year on health-care costs in Saskatchewan

while actually improving health outcomes if we adopt evidence-based

protocols.

To do so, we need to go line by line through budgets to find about $40

million of efficiencies in each of about 50 areas.

This is the second article in a five-part series on depression. The

first one discussed how there is no medical test to diagnose depression;

the interview scales have no known validity or reliability because there

is no comparative gold standard; the varying interview scales result in

different diagnostic conclusions; and almost every life reaction is

considered a symptom for depression -- including things such as

indecisiveness, inability to concentrate, changes in weight or sleeping

pattern.

None of this is very scientific.

From 1952 to 1980, the Diagnostic Statistical Manual of Mental

Disorders (DSM) described mental disorders as reactions to environmental

events such as the death of a loved one.

To make depression seem more medical, the editors of the DSM published a

revision in 1980, dismissing environmental influences as causative events.

A small group of practitioners voted and agreed that depression should

no longer be diagnosed if the symptoms were caused by factors such as

bereavement, substance use or other medical conditions.

Although this purely medical concept is obviously good for

pharmaceutical companies, it ignores the reality that almost all cases

of depression are triggered by stressful life events.

So let's review the medical or biological basis for depression.

Numerous theories have been suggested, including noradrenalin

abnormalities, cortisol excess, hippocampal insufficiency and

neurotrophic factor.

All have been dismissed. The latest theory is neurotransmitter

deficiency with a focus on serotonin, although norepinephrine and

dopamine are also included.

The problem with this latest theory is that it, too, cannot be backed up

by data. Molecular Psychiatry published a literature review of all

papers that studied what happens when you lower neurotransmitter levels.

It found that depletion did not result in depression.

In other words, low levels of serotonin, norepinephrine or dopamine do

not cause depression.

If low levels of serotonin do not result in depression, what is the

medical basis for providing someone with a medication such as a

selective serotonin re-uptake inhibitor that alters the levels of

serotonin in the brain?

Some might suggest that we should ignore discrediting the theoretical

basis, because antidepressants work in the real world.

Let's test this theory.

A literature review published in the Cochrane Collaboration found that

antidepressants were no more effective than active placebos in treating

depression.

The lead author and renowned psychiatrist of this study followed up with

an editorial in the Canadian Journal of Psychiatry, titled: " Are

antidepressants as effective as claimed? No, they are not effective at all. "

The editorial argued that any effects observed by treatment with

antidepressants should be attributed to the sedative nature of the

medication, not an actual change in the depressed mood.

This makes sense, because the surveys that patients complete to diagnose

and monitor depression include questions on sleeping difficulty.

The author concluded that it is wrong to persuade people that their

thoughts and feelings originate from a biological deficiency, saying

these efforts prevent us from finding real solutions to the complex

problems we face in our lives.

A completely separate research group published another literature review

in Prevention and Treatment, comparing antidepressants to placebos. This

group reviewed 47 studies and found the effects of antidepressants were

clinically negligible in comparison to that of placebos.

At this point, it is important to clarify that antidepressants actually

have a small clinical benefit. It's just that this benefit is no better

than the benefit of swallowing placebos.

Hopelessness is a central feature of depression, and the promise of

relief with a pill provides the hope that is so desperately needed.

Let's forget the evidence for a second and talk common sense. If

antidepressants work, why is the prevalence of depression not decreasing?

Between 1981 and 2000, spending on antidepressants in Canada rose to

$543.4 million a year from $31.4 million, with no change in the

prevalence of depression at 4.8 per cent.

Would it be so wrong to expect a disease prevalence reduction of even

one per cent for the extra half a billion dollars we spend annually?

Next week's article will discuss how antidepressant drug studies are

funded, selective participant admission criteria, selective reporting of

results, buried results and conflicts of interest. It just might shake

your confidence in pharmaceutical companies.

© Copyright © The StarPhoenix

Read more:

http://www.thestarphoenix.com/health/Effect+antidepressants+placebos+similar/330\

7896/story.html#ixzz0uS4rd5On

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Share on other sites

Guest guest

http://www.thestarphoenix.com/health/Effect+antidepressants+placebos+similar/330\

7896/story.html

Effect of antidepressants, placebos similar

By Mark Lemstra, The StarPhoenix July 22, 2010

We could save $2 billion a year on health-care costs in Saskatchewan

while actually improving health outcomes if we adopt evidence-based

protocols.

To do so, we need to go line by line through budgets to find about $40

million of efficiencies in each of about 50 areas.

This is the second article in a five-part series on depression. The

first one discussed how there is no medical test to diagnose depression;

the interview scales have no known validity or reliability because there

is no comparative gold standard; the varying interview scales result in

different diagnostic conclusions; and almost every life reaction is

considered a symptom for depression -- including things such as

indecisiveness, inability to concentrate, changes in weight or sleeping

pattern.

None of this is very scientific.

From 1952 to 1980, the Diagnostic Statistical Manual of Mental

Disorders (DSM) described mental disorders as reactions to environmental

events such as the death of a loved one.

To make depression seem more medical, the editors of the DSM published a

revision in 1980, dismissing environmental influences as causative events.

A small group of practitioners voted and agreed that depression should

no longer be diagnosed if the symptoms were caused by factors such as

bereavement, substance use or other medical conditions.

Although this purely medical concept is obviously good for

pharmaceutical companies, it ignores the reality that almost all cases

of depression are triggered by stressful life events.

So let's review the medical or biological basis for depression.

Numerous theories have been suggested, including noradrenalin

abnormalities, cortisol excess, hippocampal insufficiency and

neurotrophic factor.

All have been dismissed. The latest theory is neurotransmitter

deficiency with a focus on serotonin, although norepinephrine and

dopamine are also included.

The problem with this latest theory is that it, too, cannot be backed up

by data. Molecular Psychiatry published a literature review of all

papers that studied what happens when you lower neurotransmitter levels.

It found that depletion did not result in depression.

In other words, low levels of serotonin, norepinephrine or dopamine do

not cause depression.

If low levels of serotonin do not result in depression, what is the

medical basis for providing someone with a medication such as a

selective serotonin re-uptake inhibitor that alters the levels of

serotonin in the brain?

Some might suggest that we should ignore discrediting the theoretical

basis, because antidepressants work in the real world.

Let's test this theory.

A literature review published in the Cochrane Collaboration found that

antidepressants were no more effective than active placebos in treating

depression.

The lead author and renowned psychiatrist of this study followed up with

an editorial in the Canadian Journal of Psychiatry, titled: " Are

antidepressants as effective as claimed? No, they are not effective at all. "

The editorial argued that any effects observed by treatment with

antidepressants should be attributed to the sedative nature of the

medication, not an actual change in the depressed mood.

This makes sense, because the surveys that patients complete to diagnose

and monitor depression include questions on sleeping difficulty.

The author concluded that it is wrong to persuade people that their

thoughts and feelings originate from a biological deficiency, saying

these efforts prevent us from finding real solutions to the complex

problems we face in our lives.

A completely separate research group published another literature review

in Prevention and Treatment, comparing antidepressants to placebos. This

group reviewed 47 studies and found the effects of antidepressants were

clinically negligible in comparison to that of placebos.

At this point, it is important to clarify that antidepressants actually

have a small clinical benefit. It's just that this benefit is no better

than the benefit of swallowing placebos.

Hopelessness is a central feature of depression, and the promise of

relief with a pill provides the hope that is so desperately needed.

Let's forget the evidence for a second and talk common sense. If

antidepressants work, why is the prevalence of depression not decreasing?

Between 1981 and 2000, spending on antidepressants in Canada rose to

$543.4 million a year from $31.4 million, with no change in the

prevalence of depression at 4.8 per cent.

Would it be so wrong to expect a disease prevalence reduction of even

one per cent for the extra half a billion dollars we spend annually?

Next week's article will discuss how antidepressant drug studies are

funded, selective participant admission criteria, selective reporting of

results, buried results and conflicts of interest. It just might shake

your confidence in pharmaceutical companies.

© Copyright © The StarPhoenix

Read more:

http://www.thestarphoenix.com/health/Effect+antidepressants+placebos+similar/330\

7896/story.html#ixzz0uS4rd5On

Link to comment
Share on other sites

Guest guest

http://www.thestarphoenix.com/health/Effect+antidepressants+placebos+similar/330\

7896/story.html

Effect of antidepressants, placebos similar

By Mark Lemstra, The StarPhoenix July 22, 2010

We could save $2 billion a year on health-care costs in Saskatchewan

while actually improving health outcomes if we adopt evidence-based

protocols.

To do so, we need to go line by line through budgets to find about $40

million of efficiencies in each of about 50 areas.

This is the second article in a five-part series on depression. The

first one discussed how there is no medical test to diagnose depression;

the interview scales have no known validity or reliability because there

is no comparative gold standard; the varying interview scales result in

different diagnostic conclusions; and almost every life reaction is

considered a symptom for depression -- including things such as

indecisiveness, inability to concentrate, changes in weight or sleeping

pattern.

None of this is very scientific.

From 1952 to 1980, the Diagnostic Statistical Manual of Mental

Disorders (DSM) described mental disorders as reactions to environmental

events such as the death of a loved one.

To make depression seem more medical, the editors of the DSM published a

revision in 1980, dismissing environmental influences as causative events.

A small group of practitioners voted and agreed that depression should

no longer be diagnosed if the symptoms were caused by factors such as

bereavement, substance use or other medical conditions.

Although this purely medical concept is obviously good for

pharmaceutical companies, it ignores the reality that almost all cases

of depression are triggered by stressful life events.

So let's review the medical or biological basis for depression.

Numerous theories have been suggested, including noradrenalin

abnormalities, cortisol excess, hippocampal insufficiency and

neurotrophic factor.

All have been dismissed. The latest theory is neurotransmitter

deficiency with a focus on serotonin, although norepinephrine and

dopamine are also included.

The problem with this latest theory is that it, too, cannot be backed up

by data. Molecular Psychiatry published a literature review of all

papers that studied what happens when you lower neurotransmitter levels.

It found that depletion did not result in depression.

In other words, low levels of serotonin, norepinephrine or dopamine do

not cause depression.

If low levels of serotonin do not result in depression, what is the

medical basis for providing someone with a medication such as a

selective serotonin re-uptake inhibitor that alters the levels of

serotonin in the brain?

Some might suggest that we should ignore discrediting the theoretical

basis, because antidepressants work in the real world.

Let's test this theory.

A literature review published in the Cochrane Collaboration found that

antidepressants were no more effective than active placebos in treating

depression.

The lead author and renowned psychiatrist of this study followed up with

an editorial in the Canadian Journal of Psychiatry, titled: " Are

antidepressants as effective as claimed? No, they are not effective at all. "

The editorial argued that any effects observed by treatment with

antidepressants should be attributed to the sedative nature of the

medication, not an actual change in the depressed mood.

This makes sense, because the surveys that patients complete to diagnose

and monitor depression include questions on sleeping difficulty.

The author concluded that it is wrong to persuade people that their

thoughts and feelings originate from a biological deficiency, saying

these efforts prevent us from finding real solutions to the complex

problems we face in our lives.

A completely separate research group published another literature review

in Prevention and Treatment, comparing antidepressants to placebos. This

group reviewed 47 studies and found the effects of antidepressants were

clinically negligible in comparison to that of placebos.

At this point, it is important to clarify that antidepressants actually

have a small clinical benefit. It's just that this benefit is no better

than the benefit of swallowing placebos.

Hopelessness is a central feature of depression, and the promise of

relief with a pill provides the hope that is so desperately needed.

Let's forget the evidence for a second and talk common sense. If

antidepressants work, why is the prevalence of depression not decreasing?

Between 1981 and 2000, spending on antidepressants in Canada rose to

$543.4 million a year from $31.4 million, with no change in the

prevalence of depression at 4.8 per cent.

Would it be so wrong to expect a disease prevalence reduction of even

one per cent for the extra half a billion dollars we spend annually?

Next week's article will discuss how antidepressant drug studies are

funded, selective participant admission criteria, selective reporting of

results, buried results and conflicts of interest. It just might shake

your confidence in pharmaceutical companies.

© Copyright © The StarPhoenix

Read more:

http://www.thestarphoenix.com/health/Effect+antidepressants+placebos+similar/330\

7896/story.html#ixzz0uS4rd5On

Link to comment
Share on other sites

Guest guest

http://www.thestarphoenix.com/health/Effect+antidepressants+placebos+similar/330\

7896/story.html

Effect of antidepressants, placebos similar

By Mark Lemstra, The StarPhoenix July 22, 2010

We could save $2 billion a year on health-care costs in Saskatchewan

while actually improving health outcomes if we adopt evidence-based

protocols.

To do so, we need to go line by line through budgets to find about $40

million of efficiencies in each of about 50 areas.

This is the second article in a five-part series on depression. The

first one discussed how there is no medical test to diagnose depression;

the interview scales have no known validity or reliability because there

is no comparative gold standard; the varying interview scales result in

different diagnostic conclusions; and almost every life reaction is

considered a symptom for depression -- including things such as

indecisiveness, inability to concentrate, changes in weight or sleeping

pattern.

None of this is very scientific.

From 1952 to 1980, the Diagnostic Statistical Manual of Mental

Disorders (DSM) described mental disorders as reactions to environmental

events such as the death of a loved one.

To make depression seem more medical, the editors of the DSM published a

revision in 1980, dismissing environmental influences as causative events.

A small group of practitioners voted and agreed that depression should

no longer be diagnosed if the symptoms were caused by factors such as

bereavement, substance use or other medical conditions.

Although this purely medical concept is obviously good for

pharmaceutical companies, it ignores the reality that almost all cases

of depression are triggered by stressful life events.

So let's review the medical or biological basis for depression.

Numerous theories have been suggested, including noradrenalin

abnormalities, cortisol excess, hippocampal insufficiency and

neurotrophic factor.

All have been dismissed. The latest theory is neurotransmitter

deficiency with a focus on serotonin, although norepinephrine and

dopamine are also included.

The problem with this latest theory is that it, too, cannot be backed up

by data. Molecular Psychiatry published a literature review of all

papers that studied what happens when you lower neurotransmitter levels.

It found that depletion did not result in depression.

In other words, low levels of serotonin, norepinephrine or dopamine do

not cause depression.

If low levels of serotonin do not result in depression, what is the

medical basis for providing someone with a medication such as a

selective serotonin re-uptake inhibitor that alters the levels of

serotonin in the brain?

Some might suggest that we should ignore discrediting the theoretical

basis, because antidepressants work in the real world.

Let's test this theory.

A literature review published in the Cochrane Collaboration found that

antidepressants were no more effective than active placebos in treating

depression.

The lead author and renowned psychiatrist of this study followed up with

an editorial in the Canadian Journal of Psychiatry, titled: " Are

antidepressants as effective as claimed? No, they are not effective at all. "

The editorial argued that any effects observed by treatment with

antidepressants should be attributed to the sedative nature of the

medication, not an actual change in the depressed mood.

This makes sense, because the surveys that patients complete to diagnose

and monitor depression include questions on sleeping difficulty.

The author concluded that it is wrong to persuade people that their

thoughts and feelings originate from a biological deficiency, saying

these efforts prevent us from finding real solutions to the complex

problems we face in our lives.

A completely separate research group published another literature review

in Prevention and Treatment, comparing antidepressants to placebos. This

group reviewed 47 studies and found the effects of antidepressants were

clinically negligible in comparison to that of placebos.

At this point, it is important to clarify that antidepressants actually

have a small clinical benefit. It's just that this benefit is no better

than the benefit of swallowing placebos.

Hopelessness is a central feature of depression, and the promise of

relief with a pill provides the hope that is so desperately needed.

Let's forget the evidence for a second and talk common sense. If

antidepressants work, why is the prevalence of depression not decreasing?

Between 1981 and 2000, spending on antidepressants in Canada rose to

$543.4 million a year from $31.4 million, with no change in the

prevalence of depression at 4.8 per cent.

Would it be so wrong to expect a disease prevalence reduction of even

one per cent for the extra half a billion dollars we spend annually?

Next week's article will discuss how antidepressant drug studies are

funded, selective participant admission criteria, selective reporting of

results, buried results and conflicts of interest. It just might shake

your confidence in pharmaceutical companies.

© Copyright © The StarPhoenix

Read more:

http://www.thestarphoenix.com/health/Effect+antidepressants+placebos+similar/330\

7896/story.html#ixzz0uS4rd5On

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