All the makings of a good movie or a great novel? Where do you think writers get their inspiration? I say one week as a fly on the wall inside Big Pharma would give them enough material for a lifetime!
Big Pharma execs and attorneys themselves would make the best authors and screen writers. Not only do the have the knowledge of all of these vile events (and many more) but think of the imagination and forward thinking they must also posses.
From a business standpoint, it is almost admirable and awe-inspiring; the way Big Pharma controls the industry and the world to protect their cash cows. I said almost - if it wasn't for the fact that these loathsome and wicked acts are all too real. People become very creative when it comes to money; and money, of course, is what fuels this hideous beast known as Big Pharma. It stretches out like a multi-tentacled monster controlling, altering or completely blocking every harpoon hurled its direction. Money causes and in-turn enables the beast to infiltrate everywhere, everyone and everything.
Imagine fighting an opponent that knows your next move even before you do. That has anticipated every path that you may use to harm it and has closed those paths down. That has intertwined itself and infiltrated every mean with which you may hope to get any form of a victory.
Yes the beast has thought of that. Whether you are looking for the ultimate goal of destruction, some sort of recourse or just some honest answers from it, the road blocks are already in place.
The beast’s tentacles reach from the White House to your house and everywhere in-between. To the news media, to your government officials, to the school systems, to your doctors, to your pharmacists and to your medicine cabinet. Plus many of its tentacles have off spring that bi-furcate to perform double duty.
The tentacle that encases the FDA, for example comes in the front door promising miracle drugs and a better way of life while, at the same time, coming in the back with inaccurate test results, threats and bribes. The FDA is being used! They are a front for drug dealers with more cash to go around than any third world cartel ever had. If anyone questions Big Pharma, the FDA has placed itself to protect them and even take the fall if need be. Like some over zealous secret service agent taking one for the president they stand between anyone who would dare threaten their leader. Big Pharma just produces it. All the FDA has to do is approve it for use and be the front man. Forget the fact that approval was based on incorrect reporting of the facts; that many members of the FDA have ties that should be considered a conflict of interest or that Big Pharma is paying for all this! Big Pharma runs the FDA. It's no secret. All it takes is money.
The tentacles have a grip on modern medicine too. Not just psychiatry either. We're talking about general practitioners, nurse practitioners and counselors who have all been empowered with mind altering psychotics. There are also the drug distributors, drug reps, salespeople, and pharmacists too. Big Pharma has everything from free lunches and promotional material to cash for prescribing their products more. They hide the truth with false reports, fixed studies, mislabeling of adverse reactions and non-reporting of negative test results. They also use their influence with the FDA and clever advertising to create the perceived need for every person to take their drugs. Most anyone who goes to the doctor today will walk out with "FREE SAMPLES" of the SSRI Antidepressant of the doctors choosing (in other words the one that has courted and wooed the doctor the most in any manner necessary).
How convenient for them to market a drug labeled "Anti-Depressants" that actually cause depression! They also cause a large number of other horrific side effects such as suicide, homicide, diabetes, heart disease, mania and akethisia! The purported cure is making us sick! Selective Serotonin Reuptake Inhibitor (SSRI) Anti-Depressants by definition and by Big Pharma's own admittance raise levels of the "feel good" hormone Serotonin in the brain. Excess serotonin has been proven to cause mental disorders not prevent them! Through all the tests and trials and experiments on people, SSRI's have yet to be proven effective in treating depression. Effectiveness is not a concern of Big Pharma, however. They have positioned their drugs to sell and sell big whether they work or not. In fact the list of off-label prescriptions is growing so rapidly, Big Pharma is assured that this Beast they have created will be nearly impossible to defeat. As many as 75% of the prescriptions written for SSRI's were for treatments not approved by the FDA. SSRI's are being prescribed for such things as pain, insomnia, anxiety, shyness, menstrual discomfort, dementia, restless leg syndrome, eating disorders and many others (most if not all of which are just made up) with little or no proof of effectiveness. In addition, a sub-market is being created for hundreds of other drugs that are used to counter the side effects of the original drug!
It's also extremely convenient for Big Pharma that these drugs are so very difficult to stop taking! Once on them, the worst thing you can do is stop abruptly. Too many times we hear in the news how the person who shot those people, drowned their child, murdered their parents or set themselves on fire recently stopped taking their medication. Big Pharma’s answer is don't stop! What type of sick and twisted company will take someone’s tragedy and spin it to promote the very thing that caused the problem?
Even our children are under direct attack by the tentacles of Big Pharma. When they go to school they are subjected to hundreds of other people who are on these medications. Any student or staff member on SSRI's has the potential to be a ticking bomb. What's more, when the ticking stops you don't know if they will implode or explode. Now our children are even being screened in the schools for potential disorders which, of course, are automatically treated with SSRI Anti-Depressants and other medications. 90% of our kids who have gone through the screening process walk out with a prescription! "Teen Screen" is supported, financially and otherwise, by Big Pharma in an effort to create more paying customers. Their goal is to screen all school age children; millions of which will end up on psychiatric drugs!
Big Pharma is also trying to create patients in the womb! Another would be victim is the pregnant mother and her unborn child. The latest of the beast’s efforts to control the world is "The Mothers Act" Bill which would have Government mandated testing of as many pregnant women and new mothers as possible for depression and then treat them with antidepressants! This is despite the myriad of studies showing a link between antidepressants and violence, abortion and birth defects. Being pregnant or a new mom is stressful enough without being on a medication that has been proven to make people "crazy"! There are worse things than depression! On December 8, 2005, the FDA issued a public health advisory to report that women who take Paxil in early pregnancy are at an approximately 2-fold increased risk of having an infant born with a cardiac defect compared to the general population. Another study finds that infants exposed to SSRI's in late pregnancy showed a 6-times greater risk of developing the lung disorder known as persistent pulmonary hypertension of the newborn (PPHN), a condition that, despite treatment, results in the death of approximately 10 to 20 percent of affected infants.
Alert the public you say? Why not just tell them the truth about what Big Pharma is doing? They surely will not allow this to continue once they know, right? The beast has thought of that too. As always, we've been beaten to the punch. There's another tentacle that has already alerted the public! And they're telling us more nearly every day about the dangers of SSRI Anti-Depressants. They tell us this horrific news and reveal unconsciousable side effects but they do it with smiley faces and cartoon characters to create a rosy public perception. They use direct to consumer advertising to boost this perception to a point where the drugs are revered. So many organizations, such as ours, "The COPES Foundation", "The International Coalition for Drug Awareness" and many others are continually making attempts to educate the public of the horrors of Big Pharma and the caustic chemicals they promote but they ALREADY KNOW! They know because their best bud, Big Pharma, told them so! They don't see the mealy beast for what it is. They feel the tentacle around them but think it's comforting! They think it protects them! They don't know they are victims! Victims of Deceit, of Corruption, of Death and of Criminals with Forward thinking.
Big Pharma has high ranking politicians, high powered lawyers, decision making officials in psychiatry, coveted news media and others in positions of power in place to defend it when needed. These tentacles seem to act separately and independently until called upon and then seamlessly become a part of the beast putting in or taking out legislation as need be; thwarting any attempts of litigation with counter suits, invasions of privacy and threats; inventing new illnesses and spewing the lies and propaganda of the drug companies to the unsuspecting public.
Don't they care that people are killing themselves and others because of these medications? I think they do. Not for the normal, humanitarian reasons however. We see it as the loss of a loved one. The loss of our daughter, someone’s mother, someone’s sister. They see it is a loss of revenue! They care because each person who dies is one less potential customer. One less person to feed the thriving beast.
What is to be done? Do we keep throwing stones just to see them be swatted away? Do we continue to tell people the information they don't want to hear? Do we alienate our friends and family by imposing this pile of information on them? Do we talk to legislators and the news media (those that may have not gotten wrapped in tentacles yet)? YES to all of the above. What options do we have? We won't sit idle. Others may but we won't. Remember what I said? People become very creative when it comes to money. The key to this is people. People have the power. Unfortunately, people are not as strong as we would like them to be. We've learned they can be a down right disapointment. But maybe things will be different. We will be here to support each other. We will not fade away! We will work together against the beast. I have to believe we will make a difference. I KNOW we WILL make a difference. For Sarina, for our family, for your families and for the world. I was going to say I've learned not to expect too much from people but that would be inaccurate. Now, more than ever, I expect so very much from all of us. Give me and the world a reason to hope. A reason to believe. WE WILL NOT BACK DOWN!
Brian Milke
Father of Sarina Angel
COPES Foundation
Sunday, February 24, 2008
Saturday, February 23, 2008
Dr Tracy on Post Partum Depression and The Mothers Act.
Post Partum Depression is not a difficult problem to address. Simple dietary changes along with rest cure the majority of cases. The remainder are hormonal in nature.
For those of you who have read my book you have seen the study in the beginning section which declares that science has known for decades that most mental illness is caused by blood sugar imbalances. This should not surprise us much because initially what was done to "cure" mental illness was to throw the patient into insulin shock. These drugs we are now told "cure" mental illness are designed to do basically the same thing with a pill, thus the high diabetic rate produced by them all.
Since so many women go into gestational diabetes we need to stop and think how many more must be going into the beginning stages of pancreatic malfunction which is manifested in symptoms of hypoglycemia or low blood sugar. Depression is generally one of the first symptoms we see with low blood sugar. Therefore it should be clear that the majority of the cases of Post Partum stem from exhaustion and hypoglycemia brought on by the stress of the pregnancy and/or labor and delivery.
There is great concern over Post Partum Psychosis as the blood sugar becomes even more disrupted as it is ignored as a cause, yet with the addition of antidepressants which interfere even more with the blood sugar balance, the chances of suffering Post Partum Psychosis jumps by TEN FOLD (Read the package insert)!
The drugs they are planning to give all these young mothers who are screened and show signs of depression during and/or after pregnancy are the same drugs that Melanie Stokes (the mother the Mother's Act was named after) was taking when she jumped to her death. Her death was one of four suicides by young mothers in the Chicago area in a very short time period. Of the four three were taking antidepressants which we know at least double the rate of suicide. (Data was not available for the fourth mother.)
These so called antidepressant medications also produce miscarriage and serious birth defects for which the manufacturers are facing close to a couple of hundred lawsuits currently that I am familiar with.
This law is nothing more than additional intrusion into the lives of Americans and an attempt by the drug industry to drum up more customers. Clearly they are targeting the unborn in an attempt to get them hooked on their drugs before they ever get a chance to take their first breath! They can never seem to get enough money!
Far fetched? Not at all. Look how many mothers were prescribed amphetamines in the late 60's early 70's to make sure these mothers did not gain too much weight during pregnancy. Although that is shocking to us now to hear, it happened. And now those babies are living in a world where meth=amphetamine has been of America's worst illegal drug problems.
I had a neighbor who became addicted to amphetamines in the womb in this way who has suffered from this addiction his entire life. How many more were and who has bothered to investigate? I believe that this medical practice of drugging these mothers was a huge contributor to this meth problem that has cost this country so much, not only in finances, but in lost lives and lost productive lives. Are we ready to relive that history with these antidepressants that work so similarly to LSD or PCP?
Go to "www.drugawareness.org" to learn more about the dangers of these drugs. And find below some additional information from Amy Philo who is working hard to get more information out on the impact of this bill. Then we ask that you please rush to the following link to sign the petition against implementing this act into law. The Senate is meeting on this very soon:
"http://www.thepetitionsite.com/1/stop-the-dangerous-and-invasive-mothers-act"
Ann Blake Tracy, Ph.D., Executive Director,
International Coalition For Drug Awareness
Website: "www.drugawareness.org" &
"www.ssristories.com"
Author: Prozac: Panacea or Pandora? - Our Serotonin Nightmare
& CD or audio tape on safe withdrawal: "Help! I Can't Get
Off My Antidepressant!"
Order Number: 800-280-0730
FROM AMY:
The Mother's Act is the new Teen Screen program but this time for new
mothers instead of teens. I found this on the ICSPP website "http://www.icspp.org/" with regard to Teen Screen. It says that 90% of Teen Screen Subjects walked out with a prescription. Now multiply that by the millions with all the new moms we have each year. CAN YOU IMAGINE WHAT IS GOING TO HAPPEN NEXT IF THE MOTHER'S ACT IS SIGNED INTO LAW?!!! Teen Screen is not even GOVERNMENT MANDATED...THE MOTHER'S ACT WOULD BE. CAN YOU IMAGINE WHAT WILL HAPPEN IF THE MOTHERS ACT GOES THROUGH????????? GOD HELP US ALL!!!
To a New Jersey newspaper where the Mother's Act is already in place:
I am aware that the mental health screening program in your state has been an utter disaster with moms being carted off to the hospital by police when they call the PPD hotline. I hope you will alert your reporters to this news item which pertains to a federal bill introduced by your State's Senator in the US Senate, Robert Menendez:
For those of you considering who to vote for in the upcoming presidential election you need to know that the co-sponsor of this bill, The Mother's Act, is no other than Barak Obama. And no, this is NOT saying that Hillary is any better. She is on the committee voting on this bill and is all for "government health programs" so it remains to be seen where she stands on this issue.
[Note from Dr. Tracy: I will take bets she stands right beside Obama on this one!!!! The only candidate that knows what is up with the FDA, big Pharma and all this drugging and is willing to do something about it is Dr. Ron Paul.]
For those of you who have read my book you have seen the study in the beginning section which declares that science has known for decades that most mental illness is caused by blood sugar imbalances. This should not surprise us much because initially what was done to "cure" mental illness was to throw the patient into insulin shock. These drugs we are now told "cure" mental illness are designed to do basically the same thing with a pill, thus the high diabetic rate produced by them all.
Since so many women go into gestational diabetes we need to stop and think how many more must be going into the beginning stages of pancreatic malfunction which is manifested in symptoms of hypoglycemia or low blood sugar. Depression is generally one of the first symptoms we see with low blood sugar. Therefore it should be clear that the majority of the cases of Post Partum stem from exhaustion and hypoglycemia brought on by the stress of the pregnancy and/or labor and delivery.
There is great concern over Post Partum Psychosis as the blood sugar becomes even more disrupted as it is ignored as a cause, yet with the addition of antidepressants which interfere even more with the blood sugar balance, the chances of suffering Post Partum Psychosis jumps by TEN FOLD (Read the package insert)!
The drugs they are planning to give all these young mothers who are screened and show signs of depression during and/or after pregnancy are the same drugs that Melanie Stokes (the mother the Mother's Act was named after) was taking when she jumped to her death. Her death was one of four suicides by young mothers in the Chicago area in a very short time period. Of the four three were taking antidepressants which we know at least double the rate of suicide. (Data was not available for the fourth mother.)
These so called antidepressant medications also produce miscarriage and serious birth defects for which the manufacturers are facing close to a couple of hundred lawsuits currently that I am familiar with.
This law is nothing more than additional intrusion into the lives of Americans and an attempt by the drug industry to drum up more customers. Clearly they are targeting the unborn in an attempt to get them hooked on their drugs before they ever get a chance to take their first breath! They can never seem to get enough money!
Far fetched? Not at all. Look how many mothers were prescribed amphetamines in the late 60's early 70's to make sure these mothers did not gain too much weight during pregnancy. Although that is shocking to us now to hear, it happened. And now those babies are living in a world where meth=amphetamine has been of America's worst illegal drug problems.
I had a neighbor who became addicted to amphetamines in the womb in this way who has suffered from this addiction his entire life. How many more were and who has bothered to investigate? I believe that this medical practice of drugging these mothers was a huge contributor to this meth problem that has cost this country so much, not only in finances, but in lost lives and lost productive lives. Are we ready to relive that history with these antidepressants that work so similarly to LSD or PCP?
Go to "www.drugawareness.org" to learn more about the dangers of these drugs. And find below some additional information from Amy Philo who is working hard to get more information out on the impact of this bill. Then we ask that you please rush to the following link to sign the petition against implementing this act into law. The Senate is meeting on this very soon:
"http://www.thepetitionsite.com/1/stop-the-dangerous-and-invasive-mothers-act"
Ann Blake Tracy, Ph.D., Executive Director,
International Coalition For Drug Awareness
Website: "www.drugawareness.org" &
"www.ssristories.com"
Author: Prozac: Panacea or Pandora? - Our Serotonin Nightmare
& CD or audio tape on safe withdrawal: "Help! I Can't Get
Off My Antidepressant!"
Order Number: 800-280-0730
FROM AMY:
The Mother's Act is the new Teen Screen program but this time for new
mothers instead of teens. I found this on the ICSPP website "http://www.icspp.org/" with regard to Teen Screen. It says that 90% of Teen Screen Subjects walked out with a prescription. Now multiply that by the millions with all the new moms we have each year. CAN YOU IMAGINE WHAT IS GOING TO HAPPEN NEXT IF THE MOTHER'S ACT IS SIGNED INTO LAW?!!! Teen Screen is not even GOVERNMENT MANDATED...THE MOTHER'S ACT WOULD BE. CAN YOU IMAGINE WHAT WILL HAPPEN IF THE MOTHERS ACT GOES THROUGH????????? GOD HELP US ALL!!!
To a New Jersey newspaper where the Mother's Act is already in place:
I am aware that the mental health screening program in your state has been an utter disaster with moms being carted off to the hospital by police when they call the PPD hotline. I hope you will alert your reporters to this news item which pertains to a federal bill introduced by your State's Senator in the US Senate, Robert Menendez:
For those of you considering who to vote for in the upcoming presidential election you need to know that the co-sponsor of this bill, The Mother's Act, is no other than Barak Obama. And no, this is NOT saying that Hillary is any better. She is on the committee voting on this bill and is all for "government health programs" so it remains to be seen where she stands on this issue.
[Note from Dr. Tracy: I will take bets she stands right beside Obama on this one!!!! The only candidate that knows what is up with the FDA, big Pharma and all this drugging and is willing to do something about it is Dr. Ron Paul.]
Tuesday, February 19, 2008
Since we know this to be true and Researchers know this to be true, Why is it still allowed to happen?
OH MY GOSH JAY!!!! THANK YOU FOR THIS!!! HOW DID I MISS IT BEFORE? I WATCH FOR ANYTHING EVER PUBLISHED ON RBD. WITH WHAT YOUR OWN SON WENT THROUGH IN TAKING A GUN TO SCHOOL AFTER BEING DROPPED ABRUPTLY FROM PAXIL & PUT ON EFFEXOR IT IS NO WONDER YOU WOULD NOTICE THIS STUDY BECAUSE THIS IS EXACTLY WHAT HAPPENED TO SOMEONE IN YOUR OWN FAMILY. YOU SHOULD BE IN FLORIDA ANSWERING REPORTER'S QUESTIONS FOR MR. KAZMIERCZAK UNTIL HE CAN HANDLE IT ON HIS OWN! AFTER LOSING HIS WIFE LAST YEAR AND NOW THIS? POOR MAN!!
KIM, THIS IS EXACTLY WHAT HAPPENED TO DAVID WHEN HE TOOK THE LIVES OF TESS AND SAM AFTER DROPPING OFF PAXIL AND STARTING ON PROZAC.
AND RUSTY, YOU ALREADY KNOW THAT THIS IS WHAT HAPPENED TO ANDREA AFTER HAVING THE DOSE OF BOTH EFFEXOR AND REMERON ADJUSTED DRASTICALLY JUST TWO DAYS BEFORE SHE DROWNED YOUR CHILDREN.
AS I HAVE ALWAYS MAINTAINED, NONE OF YOUR LOVED ONES WERE CONSCIOUS WHEN THEY DID WHAT THEY DID ON THESE DRUGS OR IN WITHDRAWAL FROM THEM. THIS SLEEPWALK STATE IS NOT A CONSCIOUS STATE AS EVIDENCED BY THE BRAIN WAVE PATTERNS IN MY BOOK.
THIS STUDY IS VERY, VERY SIGNIFICANT AND IT SOUNDS AS IF THESE RESEARCHERS REALLY UNDERSTAND THE SIGNIFICANCE OF THIS POTENTIAL OF ANTIDEPRESSANTS TO PRODUCE THIS RBD EFFECT IN PATIENTS!!! FINALLY, IT APPEARS SOMEONE IS WAKING UP TO THE EXTREME SIGNIFICANCE OF THIS ISSUE AS A PUBLIC SAFETY ISSUE - LIKE THE SHOOTING AT THE UNIVERSITY THURSDAY DID NOT HELP US TO SEE THAT?? (Although the charts did not come through when copied and pasted, you may pull up the file that is attached to see those.)
DR. TRACY
_________________________________________________________
Conclusions: Subjects taking serotonergic antidepressants had more
EMG activity in the submental lead during REM sleep than did controls.
This correlated with measures of REM suppression and age. Individuals
taking such medications may be at increased risk of developing REM
sleep behavior disorder, particularly with increasing age.
. . . there are substantial potential public health implications
of REM sleep abnormalities in individuals taking serotonergic
antidepressants. Nearly 10 million people in the United States are taking
these medications on a routine basis. Increased awareness of RBD
among physicians who see individuals with sleep disorders, and among
those who prescribe serotonergic antidepressants, will allow for an accurate
estimate of sleep-related behavioral abnormalities observed as a
result of serotonergic antidepressants.
"http://www.journalsleep.org/Articles/270219.pdf"
SLEEP, Vol. 27, No. 2, 2004 317 Serotonergic Antidepressants and REM Sleep—Winkelman and James
Serotonergic Antidepressants are Associated with REM Sleep Without Atonia
PARASOMNIAS
John W. Winkelman, MD, PhD1; Lynette James2
1Divisions of Psychiatry and Sleep Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass 02459, USA; 2School of
Biomedical and Molecular Sciences, University of Surrey, Guildford, Surrey, GU2 7XH, UK
Study Objectives: Rapid eye movement (REM) sleep behavior disorder
(RBD) is generally observed in older men and in individuals with specific
neurologic diseases. There are case reports of RBD in individuals taking
serotonergic antidepressants. Our objective was to assess electromyogram
(EMG) activity during REM sleep in individuals taking serotonergic
antidepressants and in a matched control group not on such medication.
Design: Chart review of clinical and polysomnographic data.
Setting: Sleep laboratory affiliated with a general hospital.
Participants: 15 subjects taking a serotonergic antidepressant and 15
age-matched individuals not on such medication.
Measurements: Submental and anterior tibialis tonic and phasic EMG
activity during REM sleep, REM latency, time in REM, apnea-hypopnea
index, periodic leg movements of sleep index, and sleep-architecture
measures.
Results: Tonic, but not phasic, submental EMG activity during REM sleep
was significantly more common in the antidepressant-treated group than
in the control group (P < .02). Tonic REM submental EMG activity correlated
with REM latency (r =.42, P = .02) and inversely with REM time (r =
-.36, P = .05). Subject age correlated with tonic REM submental EMG
activity (r = .58, P = .02) in the antidepressant group There were also
trends for more phasic activity in the anterior tibialis (P = .09) and submental
(P = .07) EMG in REM sleep in the antidepressant group than in
the control group.
Conclusions: Subjects taking serotonergic antidepressants had more
EMG activity in the submental lead during REM sleep than did controls.
This correlated with measures of REM suppression and age. Individuals
taking such medications may be at increased risk of developing REM
sleep behavior disorder, particularly with increasing age.
Key Words: REM sleep, antidepressants, serotonergic, REM sleep
behavior disorder, EMG activity
Citation: Winkelman JW; James L. Serotonergic antidepressants are
associated with REM sleep without atonia. SLEEP 2004;27(2):317-21.
Disclosure Statement
No significant financial interest/other relationship to disclose.
Submitted for publication October 2003
Accepted for publication December 2003
Address correspondence to: John W. Winkelman, MD, PhD, Brigham and
Women’s Hospital, Sleep Health Center, 1400 Centre Street, Suite 109,
Newton Center, MA 02459; Tel: 617 527 2227; Fax: 617 527 2098;
E-mail: jwinkelman@sleephealth.com
INTRODUCTION
ATONIA OF SKELETAL MUSCLES IS ONE OF THE CARDINAL
FEATURES OF RAPID EYE MOVEMENT (REM) SLEEP.
Superimposed on this atonia is intermittent activity in both axial and
limb muscles. REM sleep behavior disorder (RBD) is characterized by
excessive motor activity during REM sleep with acting out of dreams.1
The diagnosis of RBD is made by the appearance of elevated submental
electromyogram (EMG) tone during REM and/or excessive phasic submental
or anterior tibialis EMG activity, combined with polysomnographic
documentation or a history of frank movements during REM
sleep.2 RBD is more common in elderly men, and at least half of those
followed for 10 years develop Parkinson disease.3
Muscle-tone abnormalities in REM sleep may consist along a spectrum,
with maintenance of full atonia at one end and full RBD at the
other end. REM sleep without atonia has been described as an intermediate
condition, in which REM sleep atonia is reduced on polysomnography,
in the absence of reports of abnormal behaviors by the patient or
bed partner. This polysomnographic finding has also been called “subclinical”
RBD. Eisensehr’s recent report4 demonstrating that those
patients with subclinical RBD have an intermediate reduction of striatal
dopamine transporters, roughly halfway between normal individuals and
those with RBD, establishes the potential importance of this disorder.
Antidepressants have substantial effects on REM sleep. Many studies
show that they prolong REM sleep latency and suppress REM sleep
time.5 They are also associated with reports of “vivid” dreams.6 In addition,
case reports dating back 30 years show that antidepressants can
induce RBD7 or reduce REM sleep atonia.8 In fact, medications with a
wide variety of mechanisms of action have been implicated in producing
loss of REM sleep atonia, including serotonergic reuptake blockers
such as fluoxetine,9 monoamine oxidase inhibitors,10 β-adrenergic
receptor blockers,11 the noradrenergic and 5-HT1A-mediated serotonergic
enhancer mirtazapine,12 and the tricyclic antidepressants.13 However,
no study has systematically assessed EMG tone during REM sleep in
individuals chronically taking antidepressants. Given the number of
individuals taking these medications, this issue is potentially of substantial
public health importance.
The objective of this study was to compare tonic and phasic EMG
during REM sleep in individuals without a complaint of abnormal
behavior during sleep who were taking serotonergic antidepressants with
the REM characteristics of matched controls not taking such medications.
We hypothesize that serotonergic antidepressants will increase
tonic and phasic submentalis and anterior tibialis EMG activity during
REM sleep compared to the control population not taking such medications.
METHODS
Subjects were recruited from the polysomnography database of Sleep
Health Centers, Newton Center, Mass. All sleep studies between June
2001 and August 2003 were reviewed and excluded if any of the following
features were present: apnea-hypopnea index > 15 per hour;
REM-related apnea-hypopnea index > 10; continuous positive airway
pressure use during the sleep study; complaint of abnormal behavior
during sleep or abnormal behavior on polysomnogram; duration of REM
sleep < 20 minutes; active neurologic disease (other than migraine); or
benzodiazepine, antipsychotic, or anticonvulsant use.
All subjects who met these criteria and were taking a serotonergic
antidepressant were included as the antidepressant group (n = 15). Five
subjects were taking fluoxetine (20-50 mg per day), 3 were taking
paroxetine (15-40 mg per day), 3 were taking citalopram (20-40 mg per
day), 3 were taking sertraline (100-225 mg per day), and 1 was taking
venlafaxine (400 mg per day). Two subjects in the antidepressant group
were taking bupropion (200 mg) in the morning in addition to their sero-
tonergic antidepressant. Duration of antidepressant treatment was
unknown, though subjects had been taking such medications for at least
2 weeks (based upon questionnaire data). Four of the 15 subjects in the
antidepressant group reported a history of depression only, and 4
described a history of an anxiety disorder only; 7 described a history of
both an anxiety and a depressive disorder. Fluoxetine equivalents were
calculated for antidepressant doses of all subjects by the following equation14:
fluoxetine = 5; sertraline = 1.2; paroxetine = 5; citalopram = 3.33;
venlafaxine = 1.
An age- and sex-matched sample fulfilling the inclusion and exclusion
criteria and not taking an antidepressant or any other centrally acting
agent was identified as the control group. No subjects in the control
group reported a history of either depressive or anxiety disorders. Fiftythree
percent (8/15) of subjects in the control group and 40% (6/15) in
the serotonergic antidepressant group were women. All subjects were
referred to rule-out obstructive sleep apnea. Data from an extensive
sleep, psychiatric, and medical history questionnaire were entered into a
database for all subjects.
All polysomnograms were performed in the same laboratory using
Alice 3 and 4 digitizing software (Respironics, Murrysville, Penn)
according to the following standard methods: left and right central and
occipital electroencephalogram (EEG) leads referenced to the opposite
ear; bilateral electrooculogram, submental EMG, bilateral anterior tibialis
EMG, and cardiorespiratory recordings consisting of nasal pressure
monitoring, nasal-oral thermistors, abdominal and chest effort, pulse
oximetry from the digit, and electrocardiogram.
Sleep staging was performed according to standard criteria,15 though
scoring of REM sleep was modified according to the method of Lapierre
and Montplaisir.16 In this modification, a REM epoch is terminated for
an EEG arousal but not as a result of increased EMG submental tone.
Each REM period for each subject was assessed for both tonic and phasic
EMG activity. REM epochs in which an EEG arousal (scored according
to standard guidelines), snore artifact in the submental EMG, periodic
leg movement (in a group of 4, with a stable intermovement interval),
or a hypopnea was present were eliminated from all further analyses.
Tonic EMG activity for each 30-second REM epoch was scored as
present (or put another way, was scored as absence of atonia) if greater
than 50% of the epoch had submental EMG activity greater than 4 times
the lowest level in that REM period. The percentage of epochs without
atonia was computed for each REM period and averaged for each subject.
Phasic EMG was scored in 2-second bins separately for the submental
and bilateral anterior tibialis leads according to the method of
Lapierre and Montplaisir.16 Each 2-second bin containing EMG activity
lasting 0.1 to 5.0 seconds, which exceed 4 times the lowest EMG activity
in that epoch, was counted as a bin with phasic activity. The percentage
of bins with phasic activity in the anterior tibialis and submental
leads was computed for each REM period and then averaged for each
subject. Phasic activity was also scored by the method of Eisensehr,4 in
which “long” EMG phasic activity was quantified. EMG bursts were
defined as “long” when they exceeded 0.5 seconds. A 10-second epoch
of REM was considered to have “long” EMG activity when the total of
such long bursts exceeded 1.0 seconds (eg, either at least 2 bursts lasting
0.5 seconds or 1 burst exceeding 1.0 seconds). The percentage of such
10-second epochs was determined for each subject for each REM period
and then averaged for each subject.
Statistical analyses were performed with the Student t test in normally
distributed data. The rank-sum test was used for variables that were
not normally distributed.
RESULTS
The 2 study groups did not differ in age, sex, body mass index, or
complaint that initiated the sleep study (see Table 1). On polysomnography,
subjects taking antidepressants had less REM time, longer REM
latency, greater sleep latency, a higher percentage of stage 2 sleep, and a
higher periodic limb movements of sleep index (see Table 1). No statistically
significant differences in apnea-hypopnea index (total or REMrelated)
or arousal index were noted between groups.
Subjects taking antidepressants had significantly more 30-second
REM epochs without submental atonia (with submental tone) than control
subjects (P = 0.02) (Table 2). There were significant correlations
between the submental EMG tone during REM and the degree of REM
suppression in the total sample, such that REM latency was positively
correlated with submental EMG tone (r = .42, P = .02) (see Figure 1),
and REM time was negatively correlated with submental EMG tone (r =
-.36, P = .05). There was a significant correlation between age and submental
EMG tone during REM in the antidepressant group (r = .58, P =
.02) (see Figure 2). This association was not significant in the control
group. There was no correlation between submental EMG tone during
REM and antidepressant dose (in fluoxetine equivalents).
There were trends for the subjects taking antidepressants to have more
2-second epochs in REM with phasic EMG activity in both the submental
(P = .07) and anterior tibialis (P = .09) leads than the control group
(see Table 2). There was a negative correlation between such phasic
activity in the anterior tibialis and REM time (r = -0.42, P = .02). There
was no correlation between either phasic submental or anterior tibialis
EMG activity in REM and medication dose (in fluoxetine equivalents).
SLEEP, Vol. 27, No. 2, 2004 318 Serotonergic Antidepressants and REM Sleep—Winkelman and James
Table 1—Demographic and Polysomnographic Features of
Antidepressant and Control Groups
Demographic or Control Serotonergic P value
Polysomnographic Feature Antidepressant
No. 15 15
Age (range), y 42.0 ± 14.1 (18-63) 45.5 ± 10.8 (26-60)
Men, no. (%) 8 (53) 6 (40)
BMI, kg/m2 25.0 ± 3.4 27.1 ± 5.5
Arousal index, arousals/h 15.3 ± 4.8 18.9 ± 9.7
Sleep efficiency, % 84.9 ± 11.9 81.7 ± 9.3
Sleep latency, min 13.0 ± 12.7 24.7 ± 14.4 .03
REM latency, min 68.8 ± 20.1 185.7 ± 73.7 < .001
PLM index, PLM/h 3.6 ± 6.3 18.8 ± 19.8 .08
Sleep stage, %
1 8.3 ± 5.9 9.05 ± 5.4
2 62.6 ± 6.8 69.6 ± 9.5 .03
3 6.1 ± 4.0 5.3 ± 3.7
4 7.2 ± 7.8 4.9 ± 7.4
REM 21.0 ± 4.8 14.4 ± 5.3 .001
REM time, min 79.1 ± 26.5 49.4 ± 21.3 .002
AHI, events/h 4.0 ± 2.5 4.7 ± 2.7
AHI during REM, events/h 5.6 ± 4.4 7.1 ± 5.4
Data are presented as mean ± SD, unless otherwise noted. All P values are not significant
unless otherwise noted.
BMI refers to body mass index; REM, rapid eye movement; PLM, periodic leg movement,
AHI, apnea-hypopnea index.
Table 2—Submental and Anterior-Tibialis Characteristics in
Antidepressant and Control Groups
Epochs, % Control Serotonergic P value
(n = 15) Antidepressant
(n = 15)
30-second with
submental EMG tone* 2.36 ± 3.88 9.54 ± 9.06 .02
2-second with phasic EMG†
Submental 5.63 ± 5.31 10.74 ± 9.16 .07
Anterior tibialis 9.72 ± 8.64 16.82 ± 14.69 .09
10-second with long EMG‡
Submental 6.71 ± 6.06 13.39 ± 11.62 .03
Anterior tibialis 2.98 ± 2.63 8.94 ± 12.59 .06
Data are presented as mean ± SD, unless otherwise noted.
*Electromyogram (EMG) tone considered present if more than 50% of the epoch had submental
EMG activity greater than 4 times the lowest level in that rapid eye movement
(REM) period.
†Phasic EMG considered present if EMG activity lasted 0.1 to 5.0 seconds and exceeded 4
times the lowest EMG activity in that epoch.
‡EMG considered present if the total of “long” bursts ( > 0.5 seconds) exceeded 1.0
seconds.
The antidepressant group had significantly more 10-second REM
epochs with “long” phasic activity than the control group in both the
submental (P = .03) and anterior tibialis (P = .06) leads. REM latency
correlated with submental “long” EMG activity for the entire sample (r
= .52, P = .003).
\The REM-period number (ie, 1 vs 2 vs 3) did not influence the degree
of EMG tone during REM in the submental lead or the extent of phasic
activity in the anterior tibialis or submental recordings.
DISCUSSION
Our results demonstrate that serotonergic antidepressants are associated
with a statistically significant and persistent reduction in REMsleep
atonia, even in individuals without overt clinical features of RBD.
We have also demonstrated that the degree of REM sleep without atonia
is correlated with other evidence of antidepressant effects on REM sleep
(suppression of REM time and prolongation of REM latency). Previous
case reports have described RBD in individuals taking antidepressants
for depression,17-18 narcolepsy,19 or Parkinson disease.12 Two previous
reports describe absence of atonia in REM sleep with the use of the tricyclic
antidepressant clomipramine.20-21 Guilleminault20 reported that
EMG atonia was “generally absent” in his narcoleptic subjects taking
clomipramine. Niyama21 identified this sleep stage as 1-REM in his normal
control subjects given single doses of 25 to 50 mg of clomipramine.
This is a retrospective study, and future studies of EMG tone after
medication treatments should address issues that we were unable to,
given this design. For instance, data on length of antidepressant treatment
and details regarding dream emotional quality and motor activity
would be of great interest. Further, increased numbers of subjects,
preferably in an age range that might be more vulnerable to REM sleep
without atonia (over 60 years), would also increase the power of such
studies. In addition, prospective studies of EMG tone before and after
chronic administration of a single serotonergic antidepressant are recommended
to confirm our findings and to better establish the precise
nature of this relationship.
A number of limitations of our data exist, which should be considered.
We did not evaluate the sleep of individuals prior to medication administration
and, thus, cannot definitely conclude that the serotonergic
antidepressants were responsible for the elevation in EMG activity during
REM sleep. Three of the subjects in the antidepressant group were
taking medication with effects beyond the serotonergic system: 2 were
taking bupropion, which enhances dopaminergic neurotransmission, and
1 was taking venlafaxine, which, in addition to its serotonergic properties,
produces noradrenergic reuptake blockade. It is possible that some
of our results may be a consequence of these other biologic effects. It is
also possible that depression or anxiety disorders themselves produced
these findings. It should be noted, however, that these findings have been
demonstrated acutely in normal volunteers.21 Similarly, these findings
were observed in our subjects treated for both depression and anxiety
disorders. Our subjects were not a random sample of individuals taking
serotonergic antidepressants but were recruited from individuals referred
for sleep study. To minimize this referral bias, we excluded individuals
with a description of behavioral abnormalities during sleep. All of our
subjects were referred to rule-out sleep apnea. Finally, we excluded subjects
taking medications such as benzodiazepines and anticonvulsants to
eliminate the potential effects of these medications on the polysomnogram
and to avoid a potential referral bias, as these medications may
have been used to treat sleep disruption resulting from the use of antidepressants.
This restriction may thus in fact have reduced the observed
prevalence of REM sleep abnormalities.
For a diagnosis of RBD, the International Classification of Sleep
Disorders2 requires both (1) abnormal behavior and (2) “excessive” submental
EMG tone or “excessive” phasic submental or limb twitching
during polysomnography. Although the behavioral markers for RBD
may be relatively clear,22 the polysomnographic criteria for what constitutes
“excessive” submental or anterior tibialis EMG tone during REM
sleep have not been established. Gagnon et al23 suggested that absence
of atonia (requiring 50% of the epoch with elevated tone) in greater than
20% of REM epochs is abnormal. In their study, 19 of 33 (57%) subjects
with Parkinson disease exceeded this degree of REM sleep without atonia,
whereas only 1 of 16 (6%) normal subjects exceeded this threshold.
By comparison, 2 of our 15 (13.3%) subjects taking antidepressants
exceed this criterion, whereas none of our control subjects did.
Eisensehr4 defined the upper limit of normal motor activity during
REM sleep as 15% of 10-second REM epochs containing at least 1 second
of elevated submental EMG activity (counting only “long” EMG
bursts, as described above). No unselected normative data were cited to
support the validity of this figure. Nevertheless, 8 of our 15 subjects taking
antidepressants (53%) exceeded this threshold in either the anterior
tibialis or submental lead, compared to only 1 of our 15 controls (7%).
Gagnon et al23 recently demonstrated the increased sensitivity of submental
EMG tone compared to anterior tibialis EMG tone in distinguishing
patients with Parkinson disease with RBD from both patients
with Parkinson disease without RBD and controls. In our data as well,
submental EMG tone over 30-second REM epochs was more sensitive
than either submental or anterior tibialis leads over shorter REM epoch
durations in distinguishing antidepressant from control groups. When 2-
second REM epochs were used, submental and anterior tibialis phasic
EMG were roughly equivalent in distinguishing subjects taking antidepressants
from the control subjects.
Figure 2—Correlation between submental electroencephalogram (EMG) tone and age in
the group taking antidepressants (r = 0.58; P = .02).
Figure 1—Correlation between submental electroencephalogram (EMG) tone and rapid eye
movement (REM) sleep latency (r = 0.42; P = .02).
Integrity of motor atonia during REM sleep is maintained by a number
of neuronal systems and, thus, may be disrupted by lesions or biochemical
interventions at a variety of sites.24 In fact, based on animal
experiments, separate systems, potentially colocalized at some points,
have been postulated to control the atonia and phasic locomotor aspects
of REM.25 Gilman et al’s26 recent demonstration of anatomic distinctions
between areas subserving atonia and those underlying phasic motor activation
in REM in subjects with RBD associated with multiple system
atrophy is further evidence of this. Our data demonstrating an effect of
serotonergic antidepressants on submental motor tone, in the absence of
robust effects on phasic activity, are consistent with other clinical reports
indicating a similar dissociation.7 The absence of reported abnormal
nocturnal behaviors in the majority of individuals taking serotonergic
antidepressants (including our subjects) may thus be due to the fact that
serotonergic antidepressants primarily disrupt tonic rather than phasic
components of motor activity during REM sleep.
The pathophysiology of RBD and REM sleep without atonia, as suggested
above, are likely complex. Dopaminergic mechanisms have
recently been suggested by imaging studies in patients with RBD and
Parkinson disease or multiple system atrophy.4,26-27 On the other hand,
basic research on motor control during REM sleep implicates glycinergic,
GABAergic, noradrenergic, and serotonergic transmitter systems.28-
30 In an animal model of RBD, Trulson et al28 found that raphe neurons,
which are usually quiet in REM, became tonically active. Similarly,
Lai’s30 recent finding that electrical or acetylcholine stimulation of the
pontine inhibitory area produces both motor-tone suppression and reductions
in serotonergic (and noradrenergic) activity further emphasizes the
importance of serotonergic inputs on spinal motor units in REM sleep.
Serotonergic antidepressants could thus influence motor tone during
REM sleep indirectly at brainstem levels (pedunculopontine nucleus or
pontine inhibitory area), or directly at spinal levels, producing REM
sleep without atonia.
The clinical status of REM sleep without atonia is ambiguous.
Although it is not listed in the International Classification of Sleep
Disorders nosology, it appears to be common in populations vulnerable
to RBD. In a recent study, 58% of patients with Parkinson disease
demonstrated atonia in REM sleep on polysomnography, 42% of whom
had no history of behavioral manifestations.31 In our series of consecutive
subjects without RBD taking antidepressants, 15% to 53% had evidence
of REM sleep without atonia, depending upon the definition.
REM sleep without atonia may be a “sentinel” finding on polysomnography,
expressing a vulnerability to overt RBD.31 From this perspective,
it may be a form fruste of early or evolving RBD. The evolution of RBD
into Parkinson disease in a high percentage of patients suggests that
EMG activity during REM sleep may be a sensitive indicator of early
central nervous system dysfunction. Finally, the distinction between
REM sleep without atonia and RBD may be blurred, as some individuals
with the former may in fact have behavioral manifestations of RBD
that are missed or ignored by patients and their bed partners and/or are
not present on a single night of polysomnography. In summary, it is
unclear whether elevated REM tone is just a polysomnographic finding
or whether it represents an important clinical prognostic finding.
Longitudinal studies of patients with Parkinson disease probably represent
the best opportunity to address this question scientifically.
If REM sleep without atonia is an early stage of RBD, it will be
important to understand the mediators of this response to antidepressants.
Our data suggests that age, in agreement with the increase in idiopathic
RBD in the elderly,1 is one such potential mediator. Older subjects
taking serotonergic antidepressants were more vulnerable to antidepressant-
related disinhibition of submental EMG tone in REM sleep. It is
unclear whether age is a surrogate for other factors that mediate this relationship
(central nervous system damage, antidepressant-receptor binding
or metabolism, etc.). However, we are aware of no other data that
demonstrate an influence of age on antidepressant effects on sleep.
Serotonergic antidepressant suppression of REM sleep (increased
REM latency and decreased REM time) was also a marker of the degree
of REM sleep without atonia in our subjects. Although no such correlations
have been demonstrated for patients with idiopathic (or Parkinsonrelated)
RBD, percentage of REM time is no different between those
with idiopathic RBD and normal controls.16 This may suggest that the
mechanisms producing abnormalities in EMG tone in REM sleep are
different in patients with idiopathic RBD and those given serotonergic
antidepressants. In both RBD and “idiopathic” REM sleep without atonia
(subclinical RBD), there are striatal presynaptic dopamine-transporter
deficits.4 On the other hand, serotonergic agonism may be more
relevant to REM suppression and increased EMG tone in our antidepressant
group.32-34\
Other potential vulnerability markers were not of value in predicting
REM sleep without atonia. For instance, male sex is an important risk
factor for idiopathic RBD.1 We did not find an increased vulnerability to
REM sleep atonia with male sex in our antidepressant group. Similarly,
we did not find a relationship between antidepressant dose (in fluoxetine
equivalents) and inhibition of REM sleep atonia. The relationship
between REM latency and antidepressant serum level has only been documented
for discontinuation of fluoxetine after subchronic use.35
Whether this is true at steady state after chronic dosing is unclear. One
important mediator on which we did not have data was length of treatment.
It is not clear whether length of time on an antidepressant may predispose
the individual to developing REM sleep without atonia. Future
studies of antidepressant effects on sleep should address this issue.
Although the clinical significance of REM sleep without atonia has
not been established, there are substantial potential public health implications
of REM sleep abnormalities in individuals taking serotonergic
antidepressants. Nearly 10 million people in the United States are taking
these medications on a routine basis. Increased awareness of RBD
among physicians who see individuals with sleep disorders, and among
those who prescribe serotonergic antidepressants, will allow for an accurate
estimate of sleep-related behavioral abnormalities observed as a
result of serotonergic antidepressants.
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15. Rechtschaffen A, Kales A. A Manual of Standardized Terminology, Techniques, and
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30. Lai YY, Kodama T, Siegel JM. Changes in monoamine release in the ventral horn and
hypoglossal nucleus linked to pontine inhibition of muscle tone: an in vivo microdialysis
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31. Gagnon JF, Bedard MA, Fantini ML, et al. REM sleep behavior disorder and REM sleep
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32. Rush AJ, Armitage R, Gillin JC, et al. Comparative effects of nefazodone and fluoxetine
on sleep in outpatients with major depressive disorder. Biol Psychiatry 1998;44:3-14.
33. Seifritz E, Stahl SM, Gillin JC. Human sleep EEG following the 5-HT1A antagonist pindolol:
possible disinhibition of raphe neuron activity. Brain Res 1997;759:84-91.
34. Landolt HP, Kelsoe JR, Rapaport MH, Gillin JC. Rapid tryptophan depletion reverses
phenelzine-induced suppression of REM sleep. J Sleep Res 2003;12:13-8.
35. Feige B, Voderholzer U, Riemann D, Dittmann R, Hohagen F, Berger M. Fluoxetine and
sleep EEG: effects of a single dose, subchronic treatment, and discontinuation in healthy
subjects. Neuropsychopharmacology 2002;26:246-58.
SLEEP, Vol. 27, No. 2, 2004 321 Serotonergic Antidepressants and REM Sleep—Winkelman and James
KIM, THIS IS EXACTLY WHAT HAPPENED TO DAVID WHEN HE TOOK THE LIVES OF TESS AND SAM AFTER DROPPING OFF PAXIL AND STARTING ON PROZAC.
AND RUSTY, YOU ALREADY KNOW THAT THIS IS WHAT HAPPENED TO ANDREA AFTER HAVING THE DOSE OF BOTH EFFEXOR AND REMERON ADJUSTED DRASTICALLY JUST TWO DAYS BEFORE SHE DROWNED YOUR CHILDREN.
AS I HAVE ALWAYS MAINTAINED, NONE OF YOUR LOVED ONES WERE CONSCIOUS WHEN THEY DID WHAT THEY DID ON THESE DRUGS OR IN WITHDRAWAL FROM THEM. THIS SLEEPWALK STATE IS NOT A CONSCIOUS STATE AS EVIDENCED BY THE BRAIN WAVE PATTERNS IN MY BOOK.
THIS STUDY IS VERY, VERY SIGNIFICANT AND IT SOUNDS AS IF THESE RESEARCHERS REALLY UNDERSTAND THE SIGNIFICANCE OF THIS POTENTIAL OF ANTIDEPRESSANTS TO PRODUCE THIS RBD EFFECT IN PATIENTS!!! FINALLY, IT APPEARS SOMEONE IS WAKING UP TO THE EXTREME SIGNIFICANCE OF THIS ISSUE AS A PUBLIC SAFETY ISSUE - LIKE THE SHOOTING AT THE UNIVERSITY THURSDAY DID NOT HELP US TO SEE THAT?? (Although the charts did not come through when copied and pasted, you may pull up the file that is attached to see those.)
DR. TRACY
_________________________________________________________
Conclusions: Subjects taking serotonergic antidepressants had more
EMG activity in the submental lead during REM sleep than did controls.
This correlated with measures of REM suppression and age. Individuals
taking such medications may be at increased risk of developing REM
sleep behavior disorder, particularly with increasing age.
. . . there are substantial potential public health implications
of REM sleep abnormalities in individuals taking serotonergic
antidepressants. Nearly 10 million people in the United States are taking
these medications on a routine basis. Increased awareness of RBD
among physicians who see individuals with sleep disorders, and among
those who prescribe serotonergic antidepressants, will allow for an accurate
estimate of sleep-related behavioral abnormalities observed as a
result of serotonergic antidepressants.
"http://www.journalsleep.org/Articles/270219.pdf"
SLEEP, Vol. 27, No. 2, 2004 317 Serotonergic Antidepressants and REM Sleep—Winkelman and James
Serotonergic Antidepressants are Associated with REM Sleep Without Atonia
PARASOMNIAS
John W. Winkelman, MD, PhD1; Lynette James2
1Divisions of Psychiatry and Sleep Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass 02459, USA; 2School of
Biomedical and Molecular Sciences, University of Surrey, Guildford, Surrey, GU2 7XH, UK
Study Objectives: Rapid eye movement (REM) sleep behavior disorder
(RBD) is generally observed in older men and in individuals with specific
neurologic diseases. There are case reports of RBD in individuals taking
serotonergic antidepressants. Our objective was to assess electromyogram
(EMG) activity during REM sleep in individuals taking serotonergic
antidepressants and in a matched control group not on such medication.
Design: Chart review of clinical and polysomnographic data.
Setting: Sleep laboratory affiliated with a general hospital.
Participants: 15 subjects taking a serotonergic antidepressant and 15
age-matched individuals not on such medication.
Measurements: Submental and anterior tibialis tonic and phasic EMG
activity during REM sleep, REM latency, time in REM, apnea-hypopnea
index, periodic leg movements of sleep index, and sleep-architecture
measures.
Results: Tonic, but not phasic, submental EMG activity during REM sleep
was significantly more common in the antidepressant-treated group than
in the control group (P < .02). Tonic REM submental EMG activity correlated
with REM latency (r =.42, P = .02) and inversely with REM time (r =
-.36, P = .05). Subject age correlated with tonic REM submental EMG
activity (r = .58, P = .02) in the antidepressant group There were also
trends for more phasic activity in the anterior tibialis (P = .09) and submental
(P = .07) EMG in REM sleep in the antidepressant group than in
the control group.
Conclusions: Subjects taking serotonergic antidepressants had more
EMG activity in the submental lead during REM sleep than did controls.
This correlated with measures of REM suppression and age. Individuals
taking such medications may be at increased risk of developing REM
sleep behavior disorder, particularly with increasing age.
Key Words: REM sleep, antidepressants, serotonergic, REM sleep
behavior disorder, EMG activity
Citation: Winkelman JW; James L. Serotonergic antidepressants are
associated with REM sleep without atonia. SLEEP 2004;27(2):317-21.
Disclosure Statement
No significant financial interest/other relationship to disclose.
Submitted for publication October 2003
Accepted for publication December 2003
Address correspondence to: John W. Winkelman, MD, PhD, Brigham and
Women’s Hospital, Sleep Health Center, 1400 Centre Street, Suite 109,
Newton Center, MA 02459; Tel: 617 527 2227; Fax: 617 527 2098;
E-mail: jwinkelman@sleephealth.com
INTRODUCTION
ATONIA OF SKELETAL MUSCLES IS ONE OF THE CARDINAL
FEATURES OF RAPID EYE MOVEMENT (REM) SLEEP.
Superimposed on this atonia is intermittent activity in both axial and
limb muscles. REM sleep behavior disorder (RBD) is characterized by
excessive motor activity during REM sleep with acting out of dreams.1
The diagnosis of RBD is made by the appearance of elevated submental
electromyogram (EMG) tone during REM and/or excessive phasic submental
or anterior tibialis EMG activity, combined with polysomnographic
documentation or a history of frank movements during REM
sleep.2 RBD is more common in elderly men, and at least half of those
followed for 10 years develop Parkinson disease.3
Muscle-tone abnormalities in REM sleep may consist along a spectrum,
with maintenance of full atonia at one end and full RBD at the
other end. REM sleep without atonia has been described as an intermediate
condition, in which REM sleep atonia is reduced on polysomnography,
in the absence of reports of abnormal behaviors by the patient or
bed partner. This polysomnographic finding has also been called “subclinical”
RBD. Eisensehr’s recent report4 demonstrating that those
patients with subclinical RBD have an intermediate reduction of striatal
dopamine transporters, roughly halfway between normal individuals and
those with RBD, establishes the potential importance of this disorder.
Antidepressants have substantial effects on REM sleep. Many studies
show that they prolong REM sleep latency and suppress REM sleep
time.5 They are also associated with reports of “vivid” dreams.6 In addition,
case reports dating back 30 years show that antidepressants can
induce RBD7 or reduce REM sleep atonia.8 In fact, medications with a
wide variety of mechanisms of action have been implicated in producing
loss of REM sleep atonia, including serotonergic reuptake blockers
such as fluoxetine,9 monoamine oxidase inhibitors,10 β-adrenergic
receptor blockers,11 the noradrenergic and 5-HT1A-mediated serotonergic
enhancer mirtazapine,12 and the tricyclic antidepressants.13 However,
no study has systematically assessed EMG tone during REM sleep in
individuals chronically taking antidepressants. Given the number of
individuals taking these medications, this issue is potentially of substantial
public health importance.
The objective of this study was to compare tonic and phasic EMG
during REM sleep in individuals without a complaint of abnormal
behavior during sleep who were taking serotonergic antidepressants with
the REM characteristics of matched controls not taking such medications.
We hypothesize that serotonergic antidepressants will increase
tonic and phasic submentalis and anterior tibialis EMG activity during
REM sleep compared to the control population not taking such medications.
METHODS
Subjects were recruited from the polysomnography database of Sleep
Health Centers, Newton Center, Mass. All sleep studies between June
2001 and August 2003 were reviewed and excluded if any of the following
features were present: apnea-hypopnea index > 15 per hour;
REM-related apnea-hypopnea index > 10; continuous positive airway
pressure use during the sleep study; complaint of abnormal behavior
during sleep or abnormal behavior on polysomnogram; duration of REM
sleep < 20 minutes; active neurologic disease (other than migraine); or
benzodiazepine, antipsychotic, or anticonvulsant use.
All subjects who met these criteria and were taking a serotonergic
antidepressant were included as the antidepressant group (n = 15). Five
subjects were taking fluoxetine (20-50 mg per day), 3 were taking
paroxetine (15-40 mg per day), 3 were taking citalopram (20-40 mg per
day), 3 were taking sertraline (100-225 mg per day), and 1 was taking
venlafaxine (400 mg per day). Two subjects in the antidepressant group
were taking bupropion (200 mg) in the morning in addition to their sero-
tonergic antidepressant. Duration of antidepressant treatment was
unknown, though subjects had been taking such medications for at least
2 weeks (based upon questionnaire data). Four of the 15 subjects in the
antidepressant group reported a history of depression only, and 4
described a history of an anxiety disorder only; 7 described a history of
both an anxiety and a depressive disorder. Fluoxetine equivalents were
calculated for antidepressant doses of all subjects by the following equation14:
fluoxetine = 5; sertraline = 1.2; paroxetine = 5; citalopram = 3.33;
venlafaxine = 1.
An age- and sex-matched sample fulfilling the inclusion and exclusion
criteria and not taking an antidepressant or any other centrally acting
agent was identified as the control group. No subjects in the control
group reported a history of either depressive or anxiety disorders. Fiftythree
percent (8/15) of subjects in the control group and 40% (6/15) in
the serotonergic antidepressant group were women. All subjects were
referred to rule-out obstructive sleep apnea. Data from an extensive
sleep, psychiatric, and medical history questionnaire were entered into a
database for all subjects.
All polysomnograms were performed in the same laboratory using
Alice 3 and 4 digitizing software (Respironics, Murrysville, Penn)
according to the following standard methods: left and right central and
occipital electroencephalogram (EEG) leads referenced to the opposite
ear; bilateral electrooculogram, submental EMG, bilateral anterior tibialis
EMG, and cardiorespiratory recordings consisting of nasal pressure
monitoring, nasal-oral thermistors, abdominal and chest effort, pulse
oximetry from the digit, and electrocardiogram.
Sleep staging was performed according to standard criteria,15 though
scoring of REM sleep was modified according to the method of Lapierre
and Montplaisir.16 In this modification, a REM epoch is terminated for
an EEG arousal but not as a result of increased EMG submental tone.
Each REM period for each subject was assessed for both tonic and phasic
EMG activity. REM epochs in which an EEG arousal (scored according
to standard guidelines), snore artifact in the submental EMG, periodic
leg movement (in a group of 4, with a stable intermovement interval),
or a hypopnea was present were eliminated from all further analyses.
Tonic EMG activity for each 30-second REM epoch was scored as
present (or put another way, was scored as absence of atonia) if greater
than 50% of the epoch had submental EMG activity greater than 4 times
the lowest level in that REM period. The percentage of epochs without
atonia was computed for each REM period and averaged for each subject.
Phasic EMG was scored in 2-second bins separately for the submental
and bilateral anterior tibialis leads according to the method of
Lapierre and Montplaisir.16 Each 2-second bin containing EMG activity
lasting 0.1 to 5.0 seconds, which exceed 4 times the lowest EMG activity
in that epoch, was counted as a bin with phasic activity. The percentage
of bins with phasic activity in the anterior tibialis and submental
leads was computed for each REM period and then averaged for each
subject. Phasic activity was also scored by the method of Eisensehr,4 in
which “long” EMG phasic activity was quantified. EMG bursts were
defined as “long” when they exceeded 0.5 seconds. A 10-second epoch
of REM was considered to have “long” EMG activity when the total of
such long bursts exceeded 1.0 seconds (eg, either at least 2 bursts lasting
0.5 seconds or 1 burst exceeding 1.0 seconds). The percentage of such
10-second epochs was determined for each subject for each REM period
and then averaged for each subject.
Statistical analyses were performed with the Student t test in normally
distributed data. The rank-sum test was used for variables that were
not normally distributed.
RESULTS
The 2 study groups did not differ in age, sex, body mass index, or
complaint that initiated the sleep study (see Table 1). On polysomnography,
subjects taking antidepressants had less REM time, longer REM
latency, greater sleep latency, a higher percentage of stage 2 sleep, and a
higher periodic limb movements of sleep index (see Table 1). No statistically
significant differences in apnea-hypopnea index (total or REMrelated)
or arousal index were noted between groups.
Subjects taking antidepressants had significantly more 30-second
REM epochs without submental atonia (with submental tone) than control
subjects (P = 0.02) (Table 2). There were significant correlations
between the submental EMG tone during REM and the degree of REM
suppression in the total sample, such that REM latency was positively
correlated with submental EMG tone (r = .42, P = .02) (see Figure 1),
and REM time was negatively correlated with submental EMG tone (r =
-.36, P = .05). There was a significant correlation between age and submental
EMG tone during REM in the antidepressant group (r = .58, P =
.02) (see Figure 2). This association was not significant in the control
group. There was no correlation between submental EMG tone during
REM and antidepressant dose (in fluoxetine equivalents).
There were trends for the subjects taking antidepressants to have more
2-second epochs in REM with phasic EMG activity in both the submental
(P = .07) and anterior tibialis (P = .09) leads than the control group
(see Table 2). There was a negative correlation between such phasic
activity in the anterior tibialis and REM time (r = -0.42, P = .02). There
was no correlation between either phasic submental or anterior tibialis
EMG activity in REM and medication dose (in fluoxetine equivalents).
SLEEP, Vol. 27, No. 2, 2004 318 Serotonergic Antidepressants and REM Sleep—Winkelman and James
Table 1—Demographic and Polysomnographic Features of
Antidepressant and Control Groups
Demographic or Control Serotonergic P value
Polysomnographic Feature Antidepressant
No. 15 15
Age (range), y 42.0 ± 14.1 (18-63) 45.5 ± 10.8 (26-60)
Men, no. (%) 8 (53) 6 (40)
BMI, kg/m2 25.0 ± 3.4 27.1 ± 5.5
Arousal index, arousals/h 15.3 ± 4.8 18.9 ± 9.7
Sleep efficiency, % 84.9 ± 11.9 81.7 ± 9.3
Sleep latency, min 13.0 ± 12.7 24.7 ± 14.4 .03
REM latency, min 68.8 ± 20.1 185.7 ± 73.7 < .001
PLM index, PLM/h 3.6 ± 6.3 18.8 ± 19.8 .08
Sleep stage, %
1 8.3 ± 5.9 9.05 ± 5.4
2 62.6 ± 6.8 69.6 ± 9.5 .03
3 6.1 ± 4.0 5.3 ± 3.7
4 7.2 ± 7.8 4.9 ± 7.4
REM 21.0 ± 4.8 14.4 ± 5.3 .001
REM time, min 79.1 ± 26.5 49.4 ± 21.3 .002
AHI, events/h 4.0 ± 2.5 4.7 ± 2.7
AHI during REM, events/h 5.6 ± 4.4 7.1 ± 5.4
Data are presented as mean ± SD, unless otherwise noted. All P values are not significant
unless otherwise noted.
BMI refers to body mass index; REM, rapid eye movement; PLM, periodic leg movement,
AHI, apnea-hypopnea index.
Table 2—Submental and Anterior-Tibialis Characteristics in
Antidepressant and Control Groups
Epochs, % Control Serotonergic P value
(n = 15) Antidepressant
(n = 15)
30-second with
submental EMG tone* 2.36 ± 3.88 9.54 ± 9.06 .02
2-second with phasic EMG†
Submental 5.63 ± 5.31 10.74 ± 9.16 .07
Anterior tibialis 9.72 ± 8.64 16.82 ± 14.69 .09
10-second with long EMG‡
Submental 6.71 ± 6.06 13.39 ± 11.62 .03
Anterior tibialis 2.98 ± 2.63 8.94 ± 12.59 .06
Data are presented as mean ± SD, unless otherwise noted.
*Electromyogram (EMG) tone considered present if more than 50% of the epoch had submental
EMG activity greater than 4 times the lowest level in that rapid eye movement
(REM) period.
†Phasic EMG considered present if EMG activity lasted 0.1 to 5.0 seconds and exceeded 4
times the lowest EMG activity in that epoch.
‡EMG considered present if the total of “long” bursts ( > 0.5 seconds) exceeded 1.0
seconds.
The antidepressant group had significantly more 10-second REM
epochs with “long” phasic activity than the control group in both the
submental (P = .03) and anterior tibialis (P = .06) leads. REM latency
correlated with submental “long” EMG activity for the entire sample (r
= .52, P = .003).
\The REM-period number (ie, 1 vs 2 vs 3) did not influence the degree
of EMG tone during REM in the submental lead or the extent of phasic
activity in the anterior tibialis or submental recordings.
DISCUSSION
Our results demonstrate that serotonergic antidepressants are associated
with a statistically significant and persistent reduction in REMsleep
atonia, even in individuals without overt clinical features of RBD.
We have also demonstrated that the degree of REM sleep without atonia
is correlated with other evidence of antidepressant effects on REM sleep
(suppression of REM time and prolongation of REM latency). Previous
case reports have described RBD in individuals taking antidepressants
for depression,17-18 narcolepsy,19 or Parkinson disease.12 Two previous
reports describe absence of atonia in REM sleep with the use of the tricyclic
antidepressant clomipramine.20-21 Guilleminault20 reported that
EMG atonia was “generally absent” in his narcoleptic subjects taking
clomipramine. Niyama21 identified this sleep stage as 1-REM in his normal
control subjects given single doses of 25 to 50 mg of clomipramine.
This is a retrospective study, and future studies of EMG tone after
medication treatments should address issues that we were unable to,
given this design. For instance, data on length of antidepressant treatment
and details regarding dream emotional quality and motor activity
would be of great interest. Further, increased numbers of subjects,
preferably in an age range that might be more vulnerable to REM sleep
without atonia (over 60 years), would also increase the power of such
studies. In addition, prospective studies of EMG tone before and after
chronic administration of a single serotonergic antidepressant are recommended
to confirm our findings and to better establish the precise
nature of this relationship.
A number of limitations of our data exist, which should be considered.
We did not evaluate the sleep of individuals prior to medication administration
and, thus, cannot definitely conclude that the serotonergic
antidepressants were responsible for the elevation in EMG activity during
REM sleep. Three of the subjects in the antidepressant group were
taking medication with effects beyond the serotonergic system: 2 were
taking bupropion, which enhances dopaminergic neurotransmission, and
1 was taking venlafaxine, which, in addition to its serotonergic properties,
produces noradrenergic reuptake blockade. It is possible that some
of our results may be a consequence of these other biologic effects. It is
also possible that depression or anxiety disorders themselves produced
these findings. It should be noted, however, that these findings have been
demonstrated acutely in normal volunteers.21 Similarly, these findings
were observed in our subjects treated for both depression and anxiety
disorders. Our subjects were not a random sample of individuals taking
serotonergic antidepressants but were recruited from individuals referred
for sleep study. To minimize this referral bias, we excluded individuals
with a description of behavioral abnormalities during sleep. All of our
subjects were referred to rule-out sleep apnea. Finally, we excluded subjects
taking medications such as benzodiazepines and anticonvulsants to
eliminate the potential effects of these medications on the polysomnogram
and to avoid a potential referral bias, as these medications may
have been used to treat sleep disruption resulting from the use of antidepressants.
This restriction may thus in fact have reduced the observed
prevalence of REM sleep abnormalities.
For a diagnosis of RBD, the International Classification of Sleep
Disorders2 requires both (1) abnormal behavior and (2) “excessive” submental
EMG tone or “excessive” phasic submental or limb twitching
during polysomnography. Although the behavioral markers for RBD
may be relatively clear,22 the polysomnographic criteria for what constitutes
“excessive” submental or anterior tibialis EMG tone during REM
sleep have not been established. Gagnon et al23 suggested that absence
of atonia (requiring 50% of the epoch with elevated tone) in greater than
20% of REM epochs is abnormal. In their study, 19 of 33 (57%) subjects
with Parkinson disease exceeded this degree of REM sleep without atonia,
whereas only 1 of 16 (6%) normal subjects exceeded this threshold.
By comparison, 2 of our 15 (13.3%) subjects taking antidepressants
exceed this criterion, whereas none of our control subjects did.
Eisensehr4 defined the upper limit of normal motor activity during
REM sleep as 15% of 10-second REM epochs containing at least 1 second
of elevated submental EMG activity (counting only “long” EMG
bursts, as described above). No unselected normative data were cited to
support the validity of this figure. Nevertheless, 8 of our 15 subjects taking
antidepressants (53%) exceeded this threshold in either the anterior
tibialis or submental lead, compared to only 1 of our 15 controls (7%).
Gagnon et al23 recently demonstrated the increased sensitivity of submental
EMG tone compared to anterior tibialis EMG tone in distinguishing
patients with Parkinson disease with RBD from both patients
with Parkinson disease without RBD and controls. In our data as well,
submental EMG tone over 30-second REM epochs was more sensitive
than either submental or anterior tibialis leads over shorter REM epoch
durations in distinguishing antidepressant from control groups. When 2-
second REM epochs were used, submental and anterior tibialis phasic
EMG were roughly equivalent in distinguishing subjects taking antidepressants
from the control subjects.
Figure 2—Correlation between submental electroencephalogram (EMG) tone and age in
the group taking antidepressants (r = 0.58; P = .02).
Figure 1—Correlation between submental electroencephalogram (EMG) tone and rapid eye
movement (REM) sleep latency (r = 0.42; P = .02).
Integrity of motor atonia during REM sleep is maintained by a number
of neuronal systems and, thus, may be disrupted by lesions or biochemical
interventions at a variety of sites.24 In fact, based on animal
experiments, separate systems, potentially colocalized at some points,
have been postulated to control the atonia and phasic locomotor aspects
of REM.25 Gilman et al’s26 recent demonstration of anatomic distinctions
between areas subserving atonia and those underlying phasic motor activation
in REM in subjects with RBD associated with multiple system
atrophy is further evidence of this. Our data demonstrating an effect of
serotonergic antidepressants on submental motor tone, in the absence of
robust effects on phasic activity, are consistent with other clinical reports
indicating a similar dissociation.7 The absence of reported abnormal
nocturnal behaviors in the majority of individuals taking serotonergic
antidepressants (including our subjects) may thus be due to the fact that
serotonergic antidepressants primarily disrupt tonic rather than phasic
components of motor activity during REM sleep.
The pathophysiology of RBD and REM sleep without atonia, as suggested
above, are likely complex. Dopaminergic mechanisms have
recently been suggested by imaging studies in patients with RBD and
Parkinson disease or multiple system atrophy.4,26-27 On the other hand,
basic research on motor control during REM sleep implicates glycinergic,
GABAergic, noradrenergic, and serotonergic transmitter systems.28-
30 In an animal model of RBD, Trulson et al28 found that raphe neurons,
which are usually quiet in REM, became tonically active. Similarly,
Lai’s30 recent finding that electrical or acetylcholine stimulation of the
pontine inhibitory area produces both motor-tone suppression and reductions
in serotonergic (and noradrenergic) activity further emphasizes the
importance of serotonergic inputs on spinal motor units in REM sleep.
Serotonergic antidepressants could thus influence motor tone during
REM sleep indirectly at brainstem levels (pedunculopontine nucleus or
pontine inhibitory area), or directly at spinal levels, producing REM
sleep without atonia.
The clinical status of REM sleep without atonia is ambiguous.
Although it is not listed in the International Classification of Sleep
Disorders nosology, it appears to be common in populations vulnerable
to RBD. In a recent study, 58% of patients with Parkinson disease
demonstrated atonia in REM sleep on polysomnography, 42% of whom
had no history of behavioral manifestations.31 In our series of consecutive
subjects without RBD taking antidepressants, 15% to 53% had evidence
of REM sleep without atonia, depending upon the definition.
REM sleep without atonia may be a “sentinel” finding on polysomnography,
expressing a vulnerability to overt RBD.31 From this perspective,
it may be a form fruste of early or evolving RBD. The evolution of RBD
into Parkinson disease in a high percentage of patients suggests that
EMG activity during REM sleep may be a sensitive indicator of early
central nervous system dysfunction. Finally, the distinction between
REM sleep without atonia and RBD may be blurred, as some individuals
with the former may in fact have behavioral manifestations of RBD
that are missed or ignored by patients and their bed partners and/or are
not present on a single night of polysomnography. In summary, it is
unclear whether elevated REM tone is just a polysomnographic finding
or whether it represents an important clinical prognostic finding.
Longitudinal studies of patients with Parkinson disease probably represent
the best opportunity to address this question scientifically.
If REM sleep without atonia is an early stage of RBD, it will be
important to understand the mediators of this response to antidepressants.
Our data suggests that age, in agreement with the increase in idiopathic
RBD in the elderly,1 is one such potential mediator. Older subjects
taking serotonergic antidepressants were more vulnerable to antidepressant-
related disinhibition of submental EMG tone in REM sleep. It is
unclear whether age is a surrogate for other factors that mediate this relationship
(central nervous system damage, antidepressant-receptor binding
or metabolism, etc.). However, we are aware of no other data that
demonstrate an influence of age on antidepressant effects on sleep.
Serotonergic antidepressant suppression of REM sleep (increased
REM latency and decreased REM time) was also a marker of the degree
of REM sleep without atonia in our subjects. Although no such correlations
have been demonstrated for patients with idiopathic (or Parkinsonrelated)
RBD, percentage of REM time is no different between those
with idiopathic RBD and normal controls.16 This may suggest that the
mechanisms producing abnormalities in EMG tone in REM sleep are
different in patients with idiopathic RBD and those given serotonergic
antidepressants. In both RBD and “idiopathic” REM sleep without atonia
(subclinical RBD), there are striatal presynaptic dopamine-transporter
deficits.4 On the other hand, serotonergic agonism may be more
relevant to REM suppression and increased EMG tone in our antidepressant
group.32-34\
Other potential vulnerability markers were not of value in predicting
REM sleep without atonia. For instance, male sex is an important risk
factor for idiopathic RBD.1 We did not find an increased vulnerability to
REM sleep atonia with male sex in our antidepressant group. Similarly,
we did not find a relationship between antidepressant dose (in fluoxetine
equivalents) and inhibition of REM sleep atonia. The relationship
between REM latency and antidepressant serum level has only been documented
for discontinuation of fluoxetine after subchronic use.35
Whether this is true at steady state after chronic dosing is unclear. One
important mediator on which we did not have data was length of treatment.
It is not clear whether length of time on an antidepressant may predispose
the individual to developing REM sleep without atonia. Future
studies of antidepressant effects on sleep should address this issue.
Although the clinical significance of REM sleep without atonia has
not been established, there are substantial potential public health implications
of REM sleep abnormalities in individuals taking serotonergic
antidepressants. Nearly 10 million people in the United States are taking
these medications on a routine basis. Increased awareness of RBD
among physicians who see individuals with sleep disorders, and among
those who prescribe serotonergic antidepressants, will allow for an accurate
estimate of sleep-related behavioral abnormalities observed as a
result of serotonergic antidepressants.
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SLEEP, Vol. 27, No. 2, 2004 321 Serotonergic Antidepressants and REM Sleep—Winkelman and James
Friday, February 15, 2008
ALL who witness these crimes and do nothing are GUILTY!
Shame on the FDA, Bush, and all who witnessed the harms of the drugs and did
nothing. Every "so called protective agency (Texas DHS, Texas O.I.G., Texas
MEFU, CMS, APS, the Attorney ADLitem in Hood County guardianship case, 3 nursing
home doctors, lazy nurses who just want all patients drugged into perpetual
objects, all saw the harms of the Texas Medication Algorithm Projet (TMAPS - read more "HERE")drugs to Mom, they all ignored and even
tried to cover-up. You may also add much of the media for not reporting to
inform and warn citizens.
Yes, I'd love to go before the FDA. But, the big picture is that the
pharmaceutical companies, doctors, corrupt over-sight agencies, and G.W. Bush
should be prosecuted for the harms and killings of the atypical antipsychotic
drugs which are mandated by Bush's TMAPS for-profit scheme.
There have been far more deaths to nursing home residents and children due to
the side effects of the drugs, than there have been due to suicide, and caring
family members who did research and tried to stop the prescribing of the drugs
being forced upon our loved ones, only got retaliated against.
There are plenty of listed side effects of the drugs, even without those that
were hidden, and though suicide is a high concern, patients and family members
should not continue to take side effects lightly.
G.W. Bush and all those involved should be prosecuted for all the harms and
killings (not just suicides). With criminal charges that the pharmaceutical
companies are facing due to TMAPS, why leave the other criminals out. If you
want change, justice, care, and accountability, the mission should be to impeach
and prosecute to send a strong message to the industries and the politicians who
have put their love of blood money above delivering care, justice, and
accountability.
Tell Congress, it's not too late to impeach and prosecute Bush for all the
reported harms, killings, and frauds.
Brenda A. Durant
nothing. Every "so called protective agency (Texas DHS, Texas O.I.G., Texas
MEFU, CMS, APS, the Attorney ADLitem in Hood County guardianship case, 3 nursing
home doctors, lazy nurses who just want all patients drugged into perpetual
objects, all saw the harms of the Texas Medication Algorithm Projet (TMAPS - read more "HERE")drugs to Mom, they all ignored and even
tried to cover-up. You may also add much of the media for not reporting to
inform and warn citizens.
Yes, I'd love to go before the FDA. But, the big picture is that the
pharmaceutical companies, doctors, corrupt over-sight agencies, and G.W. Bush
should be prosecuted for the harms and killings of the atypical antipsychotic
drugs which are mandated by Bush's TMAPS for-profit scheme.
There have been far more deaths to nursing home residents and children due to
the side effects of the drugs, than there have been due to suicide, and caring
family members who did research and tried to stop the prescribing of the drugs
being forced upon our loved ones, only got retaliated against.
There are plenty of listed side effects of the drugs, even without those that
were hidden, and though suicide is a high concern, patients and family members
should not continue to take side effects lightly.
G.W. Bush and all those involved should be prosecuted for all the harms and
killings (not just suicides). With criminal charges that the pharmaceutical
companies are facing due to TMAPS, why leave the other criminals out. If you
want change, justice, care, and accountability, the mission should be to impeach
and prosecute to send a strong message to the industries and the politicians who
have put their love of blood money above delivering care, justice, and
accountability.
Tell Congress, it's not too late to impeach and prosecute Bush for all the
reported harms, killings, and frauds.
Brenda A. Durant
Thursday, February 14, 2008
Dr Ann Tracy's post in USA Today on the prescription drug use
Yes they have taken the bait again and fallen hook line and sinker, but this time the cost will be FAR GREATER!!! The death toll at this point is beyond belief with "properly prescribed" prescription drugs killing as many every week as we lost at 9/11. (That is according to a study done by pharmacists - www.drugawareness.org) And who has gone to war over this type of terrorism? The whole country should be up in arms yet we continue to sleep through it all wondering what is wrong with our world!
Do the drug companies care like they tell us they do on TV? Why should they? They are much too busy making trips to the bank - the biggest industry of death and destruction on the planet. Wish everyone could see how many deaths I see every day as a result of this mass drugging. If they would just drop dead that would be one thing, but on antidepressants and other serotonergic meds (pain killers & atypical antipsychotics) they generally take their families out before taking their own lives.
They tried giving us LSD and PCP as prescription drugs in the late 50's and they were pulled from the market, but now we have them as the most popular prescription drugs on the market with all new names. And they did it without us even noticing why they called this the Decade of the Brain in our Orwellian nightmare society. WAKE UP AMERICA!!!
Dr. Ann Blake Tracy, Executive Director,
International Coalition for Drug Awareness
www.drugawareness.org & www.ssristories.com
Do the drug companies care like they tell us they do on TV? Why should they? They are much too busy making trips to the bank - the biggest industry of death and destruction on the planet. Wish everyone could see how many deaths I see every day as a result of this mass drugging. If they would just drop dead that would be one thing, but on antidepressants and other serotonergic meds (pain killers & atypical antipsychotics) they generally take their families out before taking their own lives.
They tried giving us LSD and PCP as prescription drugs in the late 50's and they were pulled from the market, but now we have them as the most popular prescription drugs on the market with all new names. And they did it without us even noticing why they called this the Decade of the Brain in our Orwellian nightmare society. WAKE UP AMERICA!!!
Dr. Ann Blake Tracy, Executive Director,
International Coalition for Drug Awareness
www.drugawareness.org & www.ssristories.com
Wednesday, February 13, 2008
SM 9 Passed! Study Anti-Depressants and Suicide.
Sarina's Voice "will" be heard, Sarina's life "will" be celebrated, Sarina's death "will not" be in vain,
As Sarina's mother, I "will" do everything in my power to Abolish Suicide-Causing Anti-Depressants!!!
I will spend the remainder of my days fighting the use of Psychotropic Drugs, I will fight for the rest of my life to educate about the link between SSRI's and Suicide, I will make it my personal battle to bring Prescription Drug Awareness to the general public and I will do this with the help of my army behind me; all of you that have supported me, my cause, my crusade and my daughter. Thank you -
Thank you for the collaboration it took from everyone to get this Memorial Act passed; All the Letters of Support, the emails, blogs and website postings truly made the difference.
I am honored to have all of you on my side and to call you all friends and family.
Here is the link to the New Mexico Legislature Website to check out SM9.
"http://legis.state.nm.us/lcs/_session.asp?year=08&chamber=S&number=9&type=M&w=com"
My work I do for Sarina and all the others out there who are, have been and could be innocent victims to these killer drugs.
There is no need for this to be in our society. The truth needs to be told so we do not lose any more people to this tragic death. These Anti-Depressant drugs have caused too much havoc for far too long and if not stopped now will continue to wreak more and more suicides, murder/suicides, school shootings and murder.
This Multi-Billion Dollar Industry has proof that over 63,000 suicides are directly related to these drugs. There is entirely too much human suffering caused by SSRI's..
200,000 people die each year from prescription drugs, yet only 20,000 die as a result from illegal drug use.
More people have been killed by SSRI's than were killed by Terrorists in 9/11, who are the real Terrorists??
My next battle is to challenge the FDA, please email me as someone who wants to support me, join me, make a difference and save lives. I need hundreds of people with me to go face to face with the FDA.
Who's in???
Email me your full name, email address, city and state if you are in on my "Going face-to-face with the FDA Challenge", We will add a button to our website with your names and links to your personal letters or testimonials that you want beside your name, so include them too.
Please forward this letter to "everyone" in your address book, as usual, ask them to forward it to everyone in their address book and so on and so on, Post this on any and all forums, blogs and websites you can.
WE WILL NOT BACK DOWN!!!
My Mission is for the World to hear Sarinas Voice; for she is no longer with me to speak.
But she will be heard, through me, her Mother.
For I live with her inside me and I will live out loud, her voice will be heard.
My Crusade is to Abolish Suicide Causing AntiDepressants. There is strength in numbers,
I need the support of those who hold this issue close to their hearts; to assure that other parents and their children live a happy life without pain and without suicide.
My Campaign is to pass a Bill which will ultimately become Sarina's Law.
Camille Milke, Eternal "Mommy" of Sarina Angel
Yesterday, Today, Tomorrow and Forever........
My Beautiful Baby Girl, 1/26/86 - 10/28/07, 21 years 9 months 3 days
COPES Foundation (Coalition Of Parents Enduring Suicide)
Founder and President, Main - 505-269-2286, Fax - 505-213-0999
"SarinasVoice@aol.com"
"www.COPESFoundation.com"
"www.ILoveYouSarina21.last-memories.com"
NM Director of the International Coalition for Drug Awareness
"www.DrugAwareness.org"
As Sarina's mother, I "will" do everything in my power to Abolish Suicide-Causing Anti-Depressants!!!
I will spend the remainder of my days fighting the use of Psychotropic Drugs, I will fight for the rest of my life to educate about the link between SSRI's and Suicide, I will make it my personal battle to bring Prescription Drug Awareness to the general public and I will do this with the help of my army behind me; all of you that have supported me, my cause, my crusade and my daughter. Thank you -
Thank you for the collaboration it took from everyone to get this Memorial Act passed; All the Letters of Support, the emails, blogs and website postings truly made the difference.
I am honored to have all of you on my side and to call you all friends and family.
Here is the link to the New Mexico Legislature Website to check out SM9.
"http://legis.state.nm.us/lcs/_session.asp?year=08&chamber=S&number=9&type=M&w=com"
My work I do for Sarina and all the others out there who are, have been and could be innocent victims to these killer drugs.
There is no need for this to be in our society. The truth needs to be told so we do not lose any more people to this tragic death. These Anti-Depressant drugs have caused too much havoc for far too long and if not stopped now will continue to wreak more and more suicides, murder/suicides, school shootings and murder.
This Multi-Billion Dollar Industry has proof that over 63,000 suicides are directly related to these drugs. There is entirely too much human suffering caused by SSRI's..
200,000 people die each year from prescription drugs, yet only 20,000 die as a result from illegal drug use.
More people have been killed by SSRI's than were killed by Terrorists in 9/11, who are the real Terrorists??
My next battle is to challenge the FDA, please email me as someone who wants to support me, join me, make a difference and save lives. I need hundreds of people with me to go face to face with the FDA.
Who's in???
Email me your full name, email address, city and state if you are in on my "Going face-to-face with the FDA Challenge", We will add a button to our website with your names and links to your personal letters or testimonials that you want beside your name, so include them too.
Please forward this letter to "everyone" in your address book, as usual, ask them to forward it to everyone in their address book and so on and so on, Post this on any and all forums, blogs and websites you can.
WE WILL NOT BACK DOWN!!!
My Mission is for the World to hear Sarinas Voice; for she is no longer with me to speak.
But she will be heard, through me, her Mother.
For I live with her inside me and I will live out loud, her voice will be heard.
My Crusade is to Abolish Suicide Causing AntiDepressants. There is strength in numbers,
I need the support of those who hold this issue close to their hearts; to assure that other parents and their children live a happy life without pain and without suicide.
My Campaign is to pass a Bill which will ultimately become Sarina's Law.
Camille Milke, Eternal "Mommy" of Sarina Angel
Yesterday, Today, Tomorrow and Forever........
My Beautiful Baby Girl, 1/26/86 - 10/28/07, 21 years 9 months 3 days
COPES Foundation (Coalition Of Parents Enduring Suicide)
Founder and President, Main - 505-269-2286, Fax - 505-213-0999
"SarinasVoice@aol.com"
"www.COPESFoundation.com"
"www.ILoveYouSarina21.last-memories.com"
NM Director of the International Coalition for Drug Awareness
"www.DrugAwareness.org"
Tuesday, February 12, 2008
MOTHERS ACT WOULD SUBJECT PREGNANT MOTHERS TO DRUGS CAUSING SPONSTANEOUS ABORTION AND BIRTH DEFECTS
A bill which has passed the House of Representatives is about to be voted on
by the key Senate Committee in charge of this legislation — it is called "The
Mother's Act" (S. 1375)
WE DON'T WANT THIS BILL TO PASS. SCREENING PREGNANT WOMEN FOR DEPRESSION WILL
OPEN THE DOOR TO FALSE LABELS AND DRUGGING.
Contact your Representatives and Senators and tell them to stop the Mother’s Act (H.R. 20 / S. 1375).
CALLS, OR FAXES, ARE NEEDED TODAY TO THE LIST OF SENATE COMMITTEE MEMBERS
BELOW.
This easy to do:
1) Call the numbers below and when the receptionist answers say, "I would like
to leave a message for the Senator."
2) The receptionist will take your message.
3) TELL THEM YOU ARE OPPOSED TO "THE MOTHER'S ACT" (S.1375) because of the
damage that will be done to mothers and infants due to the treatment that
will result from the legislation. Mothers need understanding and
compassionate medical care, not unscientific labels and mind altering
drugs. (Use your own words...keep it brief, mention the bill number)
4) Pass this on to others....THANKS!!!!!
Sen. Michael B. Enzi (WY)
Tele 202 224-3424
Fax: 202 228-0359
Sen. Judd Gregg (NH)
Tele 202 224-3324
Fax 202 224-4952
Sen. Lamar Alexander (TN)
Tele 202 224-4944
Fax 202 228-3398
Sen. Richard Burr (NC)
Tele 202 224-3154
Fax 202 228-2981
Sen. Johnny Isakson (GA)
Tele 202 224-3643
Fax 202 228-0724
Sen. Lisa Murkowski (AK)
Tele 202 224-6665
Fax 202 224-5301
Sen. Orrin G. Hatch (UT)
Tele 202 224-5251
Fax 202 224-6331
Sen. Pat Roberts (KS)
Tele 202 224-4774
Fax 202 224-3514
Sen. Wayne Allard (CO)
Tele 202 224-5941
Fax 202 224-6471
Sen. Tom Coburn (OK)
Tele 202 224-5754
Fax 202 224-6008
Current legislation moving through Congress called the “Mother’s Act” (H.R. 20 in the House and S 1375 in the Senate) seeks to "educate," “screen” and "treat" new mothers for postpartum depression. This sounds like a good idea, until you hear the specifics of what is planned.
The bill defines postpartum depression as “a devastating mood disorder which strikes many women during and after pregnancy." The idea is to first screen as many pregnant women and new mothers as possible for depression using a 10-question survey, and “treat” those who they deem have depression or postpartum depression with antidepressants.
Despite numerous studies showing a link between Selective Serotonin Reuptake Inhibitor (SSRI) antidepressant use by pregnant women and spontaneous abortion or birth defects in newborns, the primary treatments that will be recommended are these newer SSRI antidepressants!
SSRIs Have Been Linked to Spontaneous Abortion
and Birth Defects in Newborns
Here is just a sampling of studies that point this out:
May 1993: A study published in the Journal of The American Medical Association reported that of 117 pregnancies where the mother took Prozac during the first trimester, the risk of miscarriage was 14.8% compared to 7.8% in mothers not exposed to Prozac or other antidepressants.[1]
November 1993: The Journal of the American Medical Association reported in a study that the risk of spontaneous abortion in women taking the SSRI antidepressant Prozac was as high as 15.9% and 3.4% perinatal (around the birth) malformations.[2]
August 2003: The Australian Therapeutic Goods Administration reported that the use of SSRIs during or after pregnancy could result in newborn babies experiencing withdrawal effects and could also experience a toxic effect from ingestion of an SSRI in breast-milk. Withdrawal effects the baby experienced included agitation, jitteriness, poor feeding, sleepiness/lethargy, gastrointestinal symptoms and hypotania (deficient tone or tension).[3] (The Physicians Desk Reference also warns that Paxil can be secreted through breast milk).
September 2005: Studies conducted by Danish and U.S. researchers determined that the use of SSRIs in the first three months of pregnancy was linked to a 40% increased risk of birth defects such as cleft palate and cardiac defects appeared to be 60% more likely when women used SSRIs.[4]
February 9, 2006: The New England Journal of Medicine found that mothers who took SSRIs in the second half of their pregnancies were 6 times more likely to give birth to infants with a lung disorder called persistent pulmonary hypertension (PPHN). Between 10% and 20% of infants with PPHN will end up dying even if they receive treatment.[5]
July 2006: The FDA warned of the risk of a fatal lung condition in newborns whose mothers took SSRIs during pregnancy.[6]
October 2006: The journal Epidemiology, reported that babies born to women who took SSRI's during the second or third month of pregnancy had nearly 2 times the risk of having congenital malformations, with the most common being cardiovascular in 29%, muscle and bone malformations in 31% and 14% had digestive malformations.
May 2007: A study published in the Journal of The American Medical Association reported that of 117 pregnancies where the mother took Prozac during the first trimester, the risk of miscarriage was 14.8% compared to 7.8% in mothers not exposed to Prozac or tricyclic antidepressants.[7]
The U.S. government should not be funding research and treatment of expectant mothers that will result in spontaneous abortion or birth defects to their young!
STUDIES AND DRUG REGULATORY AGENCY WARNINGS AGAINST PSYCHIATRIC DRUG USE DURING PREGNANCY
EXECUTIVE SUMMARY
Any legislation that provides for further funding of research into “post partum depression” opens the door to creating an even greater risk to pregnant women. Such research ultimately recommends biological (drug) treatments, which never cure, but potentially damage and place newborns at risk of serious physical problems, withdrawal and even death. Dozens of studies already show that these drugs are hazardous to pregnant women and infants.
"These babies are bathed in serotonin [from Prozac-like antidepressants] during a key period of their development and we really don't know what it's doing to them or what the long-term effects might be. It could be that they go ‘cold turkey' when they are born or the serotonin could be having an effect on their brains, or it could be a bit of both."
Philip Zeskind, a professor of pediatrics,
The American Journal of Pediatrics 2004
BIRTH DEFECTS AND OTHER ADVERSE EFFECTS SUFFERED BY INFANTS WHOSE MOTHERS WERE PRESCRIBED ANTIDEPRESSANTS DURING PREGNANCY
Abnormal crying
Agitation
Bluish skin color from lack of oxygen
Breathing problems
Congenital anomaly (abnormality)
Convulsions
Feeding difficulties
Heart defects
Low birth rate
Jitteriness
Lethargy
Miscarriage
Neurological problems (symptoms include irritability, constant crying, convulsions)
Omphalocele (abnormality in which the infant's intestine or other abdominal organs protrude from the navel)
Premature birth
Rapid breathing
Respiratory difficulties
Restlessness
Rigidity
Seizures
Small intestine defects
Spontaneous abortions
Suction problems
Tremors
Withdrawal effects, including convulsions, agitation (symptoms could begin on the first day after birth and persist for 10 days even though levels of the antidepressant were undetectable on day 6)
These adverse reactions were reported in: Archives of Pediatrics and Adolescent Medicine, New England Journal of Medicine, World Health Organization, Epidemiology, The Archives of General Psychiatry, Harvard, The American Journal of Pediatrics, Science, American Journal of Obstetrics and Gynecology, Archives of Pediatrics and Adolescent Medicine, Journal of The American Medical Association, the FDA, Australian Therapeutics Goods Association.
According to one of the world's leading experts on SSRI (Prozac-like) antidepressants, Dr David Healy, a professor at the University of Wales College of Medicine, "There is quite a movement at the moment to say all pregnant women are depressed." However, "There is no good reason to prescribe antidepressants, because only 1 out of 10 people are likely to respond to the drugs rather than to attention and support." "So in essence," he notes, "nine out of 10 pregnant women will be subject to the risks of the SSRIs….”
Experts critical of antidepressant use during pregnancy all agree that in the absence of any proven effectiveness of treatment with SSRIs, potential harm to the fetus cannot be justified.
____________________________________________________________________
____________________________________________________________________
WHY H.R. 20/S. 1375, THE “MOTHER’S ACT” IS OPEN TO ABUSE
The “Mother’s Act” (H.R. 20/S.1375) has a reported purpose to ensure that new mothers and their families are educated about postpartum depression, screened for symptoms, and provided with essential services, and to increase research at the National Institutes of Health on postpartum depression. There are numerous problems with this bill:
Despite the fact that the National Institute of Mental Health (NIMH) has already spent nearly $19 million during the last 10 years on postpartum depression, with no effective treatments found, the Mother’s Act calls for an unspecified amount of money over the next two years for even more research.
The bill does not acknowledge that there is diverse medical opinion about “postpartum depression” and whether it exists as a mental disability or as a physical condition that can be treated by normal medical or alternative means, already available.
Of great concern, the National Center for Complementary and Alternative Medicine lists no research grants for postpartum depression on its website for the last 3 years, and the bill provides no indication that alternatives that would be safer to both mother and child are available.
The only treatment for put forth in the bill for women either during pregnancy or after childbirth is biological agents (antidepressants or other psychotropic drugs), when naturopaths, chiropractors and others in the alternative health field confirm there are natural ways of treating so-called post partum depression.
The bill fails to address the fact that studies show that antidepressants prescribed to pregnant women can cause miscarriage, premature birth, and in babies born to pregnant women taking these drugs, congenital heart birth defects, life-threatening lung disease, neurological symptoms, and withdrawal symptoms.
This treatment modality forwarded by the bill could lead to thousands of lawsuits, as hundreds have already been filed concerning the effects of antidepressant use during pregnancy. Children have been born with club foot, cleft pallet, and some have required several surgeries to correct the condition alleged to have been caused by psychiatric drug use during pregnancy.
Mental health screening, whether for postpartum depression or otherwise, is not the same as medical testing that show a tangible result. Rather it relies upon subjective questionnaires that are then evaluated based solely on opinion.
This bill makes no provision to protect women from this, to protect the fetus and infants from harmful psychotropic drugs most commonly prescribed for “post partum depression” and opens the door to massive increases in healthcare costs arising from treatment of iatrogenic-caused conditions through drug prescriptions.
______________________________________________________________________
______________________________________________________________________
SAMPLE STUDIES SHOWING PSYCHOTROPIC DRUG USE DURING PREGNANCY IS DANGEROUS, PLACING THE FETUS, MOTHER AND INFANTS AT RISK
May 1993: A study published in the Journal of The American Medical Association reported that of 117 pregnancies where the mother took Prozac during the first trimester, the risk of miscarriage was 14.8% compared to 7.8% in mothers not exposed to Prozac or other antidepressants.[1]
August 1993: Between 1988 and August 1993, the FDA Adverse Drug Reaction reports for listed incidents of 17 babies being born with a congenital anomaly to mothers who had taken Prozac prior to or during pregnancy.[2]
November 1993: Eli Lilly, manufacturer of Prozac, admitted that the risk of spontaneous abortion in women taking Prozac was as high as 15.9% and 3.4% perinatal (around the birth) malformations.[3]
1996: The New England Journal of Medicine reported a study that showed higher rates of premature delivery, low birth weight, admissions to intensive care units, including respiratory and feeding difficulties, and jitteriness, in children born to women who took Prozac during pregnancy. [4]
March 2003: A Harvard study showed that infants exposed in the womb to valproate (Depakote, Depakene or Epivil) prescribed for mood disorders, had twice as many birth defects as previously thought—8.8% had serious abnormalities compared to previously reported rate of 4%.[5]
July 2003: A Finnish study published in The Archives of General Psychiatry found that infants whose mothers took antidepressants during pregnancy could suffer neurological problems during their first week of life. The symptoms included tremors, restlessness and rigidity. Previous studies had shown that pregnant women taking SSRIs during the third trimester of pregnancy could experience neurological symptoms such as irritability, constant crying, convulsions and eating and sleeping disorders.[6]
August 2003: The Australian Therapeutic Goods Administration reported that the use of SSRIs during or after pregnancy could result in newborn babies experiencing withdrawal effects and could also experience a toxic effect from ingestion of an SSRI in breast-milk. withdrawal effects the baby experienced included agitation, jitteriness, poor feeding, sleepiness/lethargy, gastrointestinal symptoms and hypotania (deficient tone or tension).[7]
2004: The FDA revised SSRI labels to warn that some infants had developed problems requiring prolonged hospitalization, respiratory support, and tube feeding. [8]
February 2004: The American Journal of Pediatrics found direct evidence of a link between fetal exposure to SSRIs and disrupted neurological development. "Researchers linked abnormal sleeping patterns, heart rhythms and levels of alertness” to SSRIs.[9]
June 2004: A study published in Prescrire International found that newborns exposed to SSRIs toward the end of pregnancy showed signs of agitation, altered muscle tone, and breathing and suction problems, with an estimated 20% to 30% of the infants in the study affected. [10]
June 2004: The FDA also recorded 19 adverse events in pregnant women who took Effexor, an antidepressant closely related to SSRIs, including seizures, jitteriness, and jaundice. [11]
July 2004: The adverse event reports prompted the FDA to change the labeling for all SSRIs, warning that newborns exposed to SSRIs have developed problems requiring prolonged hospitalizations, respiratory support, and tube feeding. [12]
October 2004: Researchers from Columbia University published a study in the journal, Science, suggesting that exposure to Prozac in the womb and in early childhood may permanently alter the brain's circuitry and disrupt neural development, leading to serious emotional disorders later in life. [13]
2005: Researchers in France published a paper suggesting that serotonin exerts an impact on developmental processes of the embryo much earlier than previously believed. According to psychiatrist, Dr Grace Jackson, author of Rethinking Psychiatric Drugs: A Guide for Informed Consent, prescribing SSRIs as a preventative measure during pregnancy is a terrible idea. The major reason why preventive use is so dangerous, she says, is the research suggesting that the SSRIs exert a direct effect upon the early embryo.[14]
February 2005: Researchers from the University of La Laguna in Spain reported the use of antidepressants was associated with newborn withdrawal syndrome, in the British medical journal, Lancet—symptoms include convulsions, irritability, abnormal crying and tremor. [15]
September 2005: The Journal of Psychopharmacology published a study in which researchers discussed whether the symptoms found with infants at birth represented Paxil (paroxetine) toxicity or a withdrawal syndrome. The infant's symptoms began on the first day after birth and persisted for 10 days even though levels of paroxetine were undetectable on day 6. [16]
September 2005: GlaxoSmithKline (GSK) advised health care professionals of a Paxil label change that, according to data obtained from the National Birth Defects Prevention Study of infants, women who took an SSRIs were more likely to have an infant with omphalocele (abnormality in which the infant's intestine or other abdominal organs protrude from the navel). The study above also found an association of exposure to SSRIs and giving birth to an infant with craniosynostosis (a congenital defect-present at birth. The connections between sutures-skull bones prematurely close during the first year of life, which causes an abnormally shaped skull.) [17]
September 2005: Studies conducted by Danish and U.S. researchers determined that the use of SSRIs in the first three months of pregnancy was linked to a 40% increased risk of birth defects such as cleft palate and cardiac defects appeared to be 60% more likely when women used SSRIs.[18]
September 2005: The Australian Therapeutic Goods Administration warned health professionals warning that SSRI use—especially Paxil—in early pregnancy could cause congenital heart abnormalities in newborns.[19]
September 2005: The FDA and GSK issued a warning that pregnant women taking Paxil or other antidepressants during their first trimester of pregnancy experienced an increased risk of major congenital (birth defect) and cardiovascular malformations at birth; also premature births in pregnant women exposed to SSRIs.[20]
February 2006: An analysis of World Health Organization medical records found that infants whose mothers took antidepressants while pregnant may suffer withdrawal effects. A study conducted by researchers at the University of British Columbia and published in the British Lancet. [21] Researchers determined that about one out of three newborns exposed to SSRIs in the womb showed signs of neonatal (newborn) drug withdrawal. About 30% exhibited signs of withdrawal in the hours after birth. None of the infants who were not exposed to SSRIs had symptoms. [22]
February 2006: The Archives of Pediatrics and Adolescent Medicine reported that nearly one-third of newborn infants whose mothers took SSRI antidepressants during pregnancy experienced withdrawal symptoms. Previous studies had identified other symptoms such as rapid breathing, bluish skin color from lack of oxygen, feeding difficulties, low blood sugar and jitteriness.[23]
February 9, 2006: The New England Journal of Medicine found that mothers who took SSRIs in the second half of their pregnancies were 6 times more likely to give birth to infants with a lung disorder called persistent pulmonary hypertension (PPHN). The condition occurs when a newborn's circulation system does not adapt to breathing outside the womb and causes high pressure in the blood vessels of the lungs making them unable to get enough oxygen into their bloodstream and can be fatal. Between 10% and 20% of infants with PPHN will end up dying even if they receive treatment.[24]
February 2006: In a related study involving 73 infants who were exposed to an SSRI right up until delivery, and 101 infants who were only exposed during the first trimester of pregnancy, researchers found that babies exposed throughout the entire pregnancy had significantly increased complications like hypotonia [having less than normal muscular tone or tension], respiratory problems and jitteriness compared to the other infants. [25]
March 2006: Health Canada issued a warning that SSRIs and other newer antidepressants when taken by pregnant women placed newborns at risk of developing a rare lung and heart condition.[26]
April 2006: American Journal of Obstetrics and Gynecology reported that taking SSRIs doubled the mother's risk of delivering a stillborn infant and increased the risk of premature delivery, underweight babies, and seizures. [27]
April 7, 2006: A Canadian study from the University of Ottawa, found those who used SSRIs were more likely to have premature and low birth weight babies. Almost 20% of women who used SSRIs gave birth prematurely, compared to 12% of mothers who did not use the drugs. Infants born to women using SSRIs were also found to be more likely to have seizures. [28]
July 2006: The FDA warned of the risk of a fatal lung condition in newborns whose mothers took SSRIs during pregnancy.[29]
November 2006: The journal Epidemiology published by researchers from Aarhus University in Denmark who found that pregnant women who take the newer type of antidepressants are more likely to have babies with birth defects than mothers who don’t take these drugs.[30]
December 29: A new Canadian study published in Birth Defects Research Part B: Developmental and Reproductive Toxicology, examined in greater detail the association between first trimester exposure to paroxetine (Paxil and Paxil CR) and the occurrence of major congenital malformation, especially major cardiac malformations. Paroxetine was significantly associated with a “two-fold increase in the risk of major congenital anomalies, and more specifically with a three-fold increase in the risk of major cardiac anomalies.”[31]
May 8, 2007: The German Drug Regulatory Agency (BfArM) warned of increased risk of cardiac malformation in newborns when the mother took Paxil during pregnancy.
May 2007: A study published in the Journal of The American Medical Association reported that of 117 pregnancies where the mother took Prozac during the first trimester, the risk of miscarriage was 14.8% compared to 7.8% in mothers not exposed to fluoxetine or tricyclic antidepressants.[32]
by the key Senate Committee in charge of this legislation — it is called "The
Mother's Act" (S. 1375)
WE DON'T WANT THIS BILL TO PASS. SCREENING PREGNANT WOMEN FOR DEPRESSION WILL
OPEN THE DOOR TO FALSE LABELS AND DRUGGING.
Contact your Representatives and Senators and tell them to stop the Mother’s Act (H.R. 20 / S. 1375).
CALLS, OR FAXES, ARE NEEDED TODAY TO THE LIST OF SENATE COMMITTEE MEMBERS
BELOW.
This easy to do:
1) Call the numbers below and when the receptionist answers say, "I would like
to leave a message for the Senator."
2) The receptionist will take your message.
3) TELL THEM YOU ARE OPPOSED TO "THE MOTHER'S ACT" (S.1375) because of the
damage that will be done to mothers and infants due to the treatment that
will result from the legislation. Mothers need understanding and
compassionate medical care, not unscientific labels and mind altering
drugs. (Use your own words...keep it brief, mention the bill number)
4) Pass this on to others....THANKS!!!!!
Sen. Michael B. Enzi (WY)
Tele 202 224-3424
Fax: 202 228-0359
Sen. Judd Gregg (NH)
Tele 202 224-3324
Fax 202 224-4952
Sen. Lamar Alexander (TN)
Tele 202 224-4944
Fax 202 228-3398
Sen. Richard Burr (NC)
Tele 202 224-3154
Fax 202 228-2981
Sen. Johnny Isakson (GA)
Tele 202 224-3643
Fax 202 228-0724
Sen. Lisa Murkowski (AK)
Tele 202 224-6665
Fax 202 224-5301
Sen. Orrin G. Hatch (UT)
Tele 202 224-5251
Fax 202 224-6331
Sen. Pat Roberts (KS)
Tele 202 224-4774
Fax 202 224-3514
Sen. Wayne Allard (CO)
Tele 202 224-5941
Fax 202 224-6471
Sen. Tom Coburn (OK)
Tele 202 224-5754
Fax 202 224-6008
Current legislation moving through Congress called the “Mother’s Act” (H.R. 20 in the House and S 1375 in the Senate) seeks to "educate," “screen” and "treat" new mothers for postpartum depression. This sounds like a good idea, until you hear the specifics of what is planned.
The bill defines postpartum depression as “a devastating mood disorder which strikes many women during and after pregnancy." The idea is to first screen as many pregnant women and new mothers as possible for depression using a 10-question survey, and “treat” those who they deem have depression or postpartum depression with antidepressants.
Despite numerous studies showing a link between Selective Serotonin Reuptake Inhibitor (SSRI) antidepressant use by pregnant women and spontaneous abortion or birth defects in newborns, the primary treatments that will be recommended are these newer SSRI antidepressants!
SSRIs Have Been Linked to Spontaneous Abortion
and Birth Defects in Newborns
Here is just a sampling of studies that point this out:
May 1993: A study published in the Journal of The American Medical Association reported that of 117 pregnancies where the mother took Prozac during the first trimester, the risk of miscarriage was 14.8% compared to 7.8% in mothers not exposed to Prozac or other antidepressants.[1]
November 1993: The Journal of the American Medical Association reported in a study that the risk of spontaneous abortion in women taking the SSRI antidepressant Prozac was as high as 15.9% and 3.4% perinatal (around the birth) malformations.[2]
August 2003: The Australian Therapeutic Goods Administration reported that the use of SSRIs during or after pregnancy could result in newborn babies experiencing withdrawal effects and could also experience a toxic effect from ingestion of an SSRI in breast-milk. Withdrawal effects the baby experienced included agitation, jitteriness, poor feeding, sleepiness/lethargy, gastrointestinal symptoms and hypotania (deficient tone or tension).[3] (The Physicians Desk Reference also warns that Paxil can be secreted through breast milk).
September 2005: Studies conducted by Danish and U.S. researchers determined that the use of SSRIs in the first three months of pregnancy was linked to a 40% increased risk of birth defects such as cleft palate and cardiac defects appeared to be 60% more likely when women used SSRIs.[4]
February 9, 2006: The New England Journal of Medicine found that mothers who took SSRIs in the second half of their pregnancies were 6 times more likely to give birth to infants with a lung disorder called persistent pulmonary hypertension (PPHN). Between 10% and 20% of infants with PPHN will end up dying even if they receive treatment.[5]
July 2006: The FDA warned of the risk of a fatal lung condition in newborns whose mothers took SSRIs during pregnancy.[6]
October 2006: The journal Epidemiology, reported that babies born to women who took SSRI's during the second or third month of pregnancy had nearly 2 times the risk of having congenital malformations, with the most common being cardiovascular in 29%, muscle and bone malformations in 31% and 14% had digestive malformations.
May 2007: A study published in the Journal of The American Medical Association reported that of 117 pregnancies where the mother took Prozac during the first trimester, the risk of miscarriage was 14.8% compared to 7.8% in mothers not exposed to Prozac or tricyclic antidepressants.[7]
The U.S. government should not be funding research and treatment of expectant mothers that will result in spontaneous abortion or birth defects to their young!
STUDIES AND DRUG REGULATORY AGENCY WARNINGS AGAINST PSYCHIATRIC DRUG USE DURING PREGNANCY
EXECUTIVE SUMMARY
Any legislation that provides for further funding of research into “post partum depression” opens the door to creating an even greater risk to pregnant women. Such research ultimately recommends biological (drug) treatments, which never cure, but potentially damage and place newborns at risk of serious physical problems, withdrawal and even death. Dozens of studies already show that these drugs are hazardous to pregnant women and infants.
"These babies are bathed in serotonin [from Prozac-like antidepressants] during a key period of their development and we really don't know what it's doing to them or what the long-term effects might be. It could be that they go ‘cold turkey' when they are born or the serotonin could be having an effect on their brains, or it could be a bit of both."
Philip Zeskind, a professor of pediatrics,
The American Journal of Pediatrics 2004
BIRTH DEFECTS AND OTHER ADVERSE EFFECTS SUFFERED BY INFANTS WHOSE MOTHERS WERE PRESCRIBED ANTIDEPRESSANTS DURING PREGNANCY
Abnormal crying
Agitation
Bluish skin color from lack of oxygen
Breathing problems
Congenital anomaly (abnormality)
Convulsions
Feeding difficulties
Heart defects
Low birth rate
Jitteriness
Lethargy
Miscarriage
Neurological problems (symptoms include irritability, constant crying, convulsions)
Omphalocele (abnormality in which the infant's intestine or other abdominal organs protrude from the navel)
Premature birth
Rapid breathing
Respiratory difficulties
Restlessness
Rigidity
Seizures
Small intestine defects
Spontaneous abortions
Suction problems
Tremors
Withdrawal effects, including convulsions, agitation (symptoms could begin on the first day after birth and persist for 10 days even though levels of the antidepressant were undetectable on day 6)
These adverse reactions were reported in: Archives of Pediatrics and Adolescent Medicine, New England Journal of Medicine, World Health Organization, Epidemiology, The Archives of General Psychiatry, Harvard, The American Journal of Pediatrics, Science, American Journal of Obstetrics and Gynecology, Archives of Pediatrics and Adolescent Medicine, Journal of The American Medical Association, the FDA, Australian Therapeutics Goods Association.
According to one of the world's leading experts on SSRI (Prozac-like) antidepressants, Dr David Healy, a professor at the University of Wales College of Medicine, "There is quite a movement at the moment to say all pregnant women are depressed." However, "There is no good reason to prescribe antidepressants, because only 1 out of 10 people are likely to respond to the drugs rather than to attention and support." "So in essence," he notes, "nine out of 10 pregnant women will be subject to the risks of the SSRIs….”
Experts critical of antidepressant use during pregnancy all agree that in the absence of any proven effectiveness of treatment with SSRIs, potential harm to the fetus cannot be justified.
____________________________________________________________________
____________________________________________________________________
WHY H.R. 20/S. 1375, THE “MOTHER’S ACT” IS OPEN TO ABUSE
The “Mother’s Act” (H.R. 20/S.1375) has a reported purpose to ensure that new mothers and their families are educated about postpartum depression, screened for symptoms, and provided with essential services, and to increase research at the National Institutes of Health on postpartum depression. There are numerous problems with this bill:
Despite the fact that the National Institute of Mental Health (NIMH) has already spent nearly $19 million during the last 10 years on postpartum depression, with no effective treatments found, the Mother’s Act calls for an unspecified amount of money over the next two years for even more research.
The bill does not acknowledge that there is diverse medical opinion about “postpartum depression” and whether it exists as a mental disability or as a physical condition that can be treated by normal medical or alternative means, already available.
Of great concern, the National Center for Complementary and Alternative Medicine lists no research grants for postpartum depression on its website for the last 3 years, and the bill provides no indication that alternatives that would be safer to both mother and child are available.
The only treatment for put forth in the bill for women either during pregnancy or after childbirth is biological agents (antidepressants or other psychotropic drugs), when naturopaths, chiropractors and others in the alternative health field confirm there are natural ways of treating so-called post partum depression.
The bill fails to address the fact that studies show that antidepressants prescribed to pregnant women can cause miscarriage, premature birth, and in babies born to pregnant women taking these drugs, congenital heart birth defects, life-threatening lung disease, neurological symptoms, and withdrawal symptoms.
This treatment modality forwarded by the bill could lead to thousands of lawsuits, as hundreds have already been filed concerning the effects of antidepressant use during pregnancy. Children have been born with club foot, cleft pallet, and some have required several surgeries to correct the condition alleged to have been caused by psychiatric drug use during pregnancy.
Mental health screening, whether for postpartum depression or otherwise, is not the same as medical testing that show a tangible result. Rather it relies upon subjective questionnaires that are then evaluated based solely on opinion.
This bill makes no provision to protect women from this, to protect the fetus and infants from harmful psychotropic drugs most commonly prescribed for “post partum depression” and opens the door to massive increases in healthcare costs arising from treatment of iatrogenic-caused conditions through drug prescriptions.
______________________________________________________________________
______________________________________________________________________
SAMPLE STUDIES SHOWING PSYCHOTROPIC DRUG USE DURING PREGNANCY IS DANGEROUS, PLACING THE FETUS, MOTHER AND INFANTS AT RISK
May 1993: A study published in the Journal of The American Medical Association reported that of 117 pregnancies where the mother took Prozac during the first trimester, the risk of miscarriage was 14.8% compared to 7.8% in mothers not exposed to Prozac or other antidepressants.[1]
August 1993: Between 1988 and August 1993, the FDA Adverse Drug Reaction reports for listed incidents of 17 babies being born with a congenital anomaly to mothers who had taken Prozac prior to or during pregnancy.[2]
November 1993: Eli Lilly, manufacturer of Prozac, admitted that the risk of spontaneous abortion in women taking Prozac was as high as 15.9% and 3.4% perinatal (around the birth) malformations.[3]
1996: The New England Journal of Medicine reported a study that showed higher rates of premature delivery, low birth weight, admissions to intensive care units, including respiratory and feeding difficulties, and jitteriness, in children born to women who took Prozac during pregnancy. [4]
March 2003: A Harvard study showed that infants exposed in the womb to valproate (Depakote, Depakene or Epivil) prescribed for mood disorders, had twice as many birth defects as previously thought—8.8% had serious abnormalities compared to previously reported rate of 4%.[5]
July 2003: A Finnish study published in The Archives of General Psychiatry found that infants whose mothers took antidepressants during pregnancy could suffer neurological problems during their first week of life. The symptoms included tremors, restlessness and rigidity. Previous studies had shown that pregnant women taking SSRIs during the third trimester of pregnancy could experience neurological symptoms such as irritability, constant crying, convulsions and eating and sleeping disorders.[6]
August 2003: The Australian Therapeutic Goods Administration reported that the use of SSRIs during or after pregnancy could result in newborn babies experiencing withdrawal effects and could also experience a toxic effect from ingestion of an SSRI in breast-milk. withdrawal effects the baby experienced included agitation, jitteriness, poor feeding, sleepiness/lethargy, gastrointestinal symptoms and hypotania (deficient tone or tension).[7]
2004: The FDA revised SSRI labels to warn that some infants had developed problems requiring prolonged hospitalization, respiratory support, and tube feeding. [8]
February 2004: The American Journal of Pediatrics found direct evidence of a link between fetal exposure to SSRIs and disrupted neurological development. "Researchers linked abnormal sleeping patterns, heart rhythms and levels of alertness” to SSRIs.[9]
June 2004: A study published in Prescrire International found that newborns exposed to SSRIs toward the end of pregnancy showed signs of agitation, altered muscle tone, and breathing and suction problems, with an estimated 20% to 30% of the infants in the study affected. [10]
June 2004: The FDA also recorded 19 adverse events in pregnant women who took Effexor, an antidepressant closely related to SSRIs, including seizures, jitteriness, and jaundice. [11]
July 2004: The adverse event reports prompted the FDA to change the labeling for all SSRIs, warning that newborns exposed to SSRIs have developed problems requiring prolonged hospitalizations, respiratory support, and tube feeding. [12]
October 2004: Researchers from Columbia University published a study in the journal, Science, suggesting that exposure to Prozac in the womb and in early childhood may permanently alter the brain's circuitry and disrupt neural development, leading to serious emotional disorders later in life. [13]
2005: Researchers in France published a paper suggesting that serotonin exerts an impact on developmental processes of the embryo much earlier than previously believed. According to psychiatrist, Dr Grace Jackson, author of Rethinking Psychiatric Drugs: A Guide for Informed Consent, prescribing SSRIs as a preventative measure during pregnancy is a terrible idea. The major reason why preventive use is so dangerous, she says, is the research suggesting that the SSRIs exert a direct effect upon the early embryo.[14]
February 2005: Researchers from the University of La Laguna in Spain reported the use of antidepressants was associated with newborn withdrawal syndrome, in the British medical journal, Lancet—symptoms include convulsions, irritability, abnormal crying and tremor. [15]
September 2005: The Journal of Psychopharmacology published a study in which researchers discussed whether the symptoms found with infants at birth represented Paxil (paroxetine) toxicity or a withdrawal syndrome. The infant's symptoms began on the first day after birth and persisted for 10 days even though levels of paroxetine were undetectable on day 6. [16]
September 2005: GlaxoSmithKline (GSK) advised health care professionals of a Paxil label change that, according to data obtained from the National Birth Defects Prevention Study of infants, women who took an SSRIs were more likely to have an infant with omphalocele (abnormality in which the infant's intestine or other abdominal organs protrude from the navel). The study above also found an association of exposure to SSRIs and giving birth to an infant with craniosynostosis (a congenital defect-present at birth. The connections between sutures-skull bones prematurely close during the first year of life, which causes an abnormally shaped skull.) [17]
September 2005: Studies conducted by Danish and U.S. researchers determined that the use of SSRIs in the first three months of pregnancy was linked to a 40% increased risk of birth defects such as cleft palate and cardiac defects appeared to be 60% more likely when women used SSRIs.[18]
September 2005: The Australian Therapeutic Goods Administration warned health professionals warning that SSRI use—especially Paxil—in early pregnancy could cause congenital heart abnormalities in newborns.[19]
September 2005: The FDA and GSK issued a warning that pregnant women taking Paxil or other antidepressants during their first trimester of pregnancy experienced an increased risk of major congenital (birth defect) and cardiovascular malformations at birth; also premature births in pregnant women exposed to SSRIs.[20]
February 2006: An analysis of World Health Organization medical records found that infants whose mothers took antidepressants while pregnant may suffer withdrawal effects. A study conducted by researchers at the University of British Columbia and published in the British Lancet. [21] Researchers determined that about one out of three newborns exposed to SSRIs in the womb showed signs of neonatal (newborn) drug withdrawal. About 30% exhibited signs of withdrawal in the hours after birth. None of the infants who were not exposed to SSRIs had symptoms. [22]
February 2006: The Archives of Pediatrics and Adolescent Medicine reported that nearly one-third of newborn infants whose mothers took SSRI antidepressants during pregnancy experienced withdrawal symptoms. Previous studies had identified other symptoms such as rapid breathing, bluish skin color from lack of oxygen, feeding difficulties, low blood sugar and jitteriness.[23]
February 9, 2006: The New England Journal of Medicine found that mothers who took SSRIs in the second half of their pregnancies were 6 times more likely to give birth to infants with a lung disorder called persistent pulmonary hypertension (PPHN). The condition occurs when a newborn's circulation system does not adapt to breathing outside the womb and causes high pressure in the blood vessels of the lungs making them unable to get enough oxygen into their bloodstream and can be fatal. Between 10% and 20% of infants with PPHN will end up dying even if they receive treatment.[24]
February 2006: In a related study involving 73 infants who were exposed to an SSRI right up until delivery, and 101 infants who were only exposed during the first trimester of pregnancy, researchers found that babies exposed throughout the entire pregnancy had significantly increased complications like hypotonia [having less than normal muscular tone or tension], respiratory problems and jitteriness compared to the other infants. [25]
March 2006: Health Canada issued a warning that SSRIs and other newer antidepressants when taken by pregnant women placed newborns at risk of developing a rare lung and heart condition.[26]
April 2006: American Journal of Obstetrics and Gynecology reported that taking SSRIs doubled the mother's risk of delivering a stillborn infant and increased the risk of premature delivery, underweight babies, and seizures. [27]
April 7, 2006: A Canadian study from the University of Ottawa, found those who used SSRIs were more likely to have premature and low birth weight babies. Almost 20% of women who used SSRIs gave birth prematurely, compared to 12% of mothers who did not use the drugs. Infants born to women using SSRIs were also found to be more likely to have seizures. [28]
July 2006: The FDA warned of the risk of a fatal lung condition in newborns whose mothers took SSRIs during pregnancy.[29]
November 2006: The journal Epidemiology published by researchers from Aarhus University in Denmark who found that pregnant women who take the newer type of antidepressants are more likely to have babies with birth defects than mothers who don’t take these drugs.[30]
December 29: A new Canadian study published in Birth Defects Research Part B: Developmental and Reproductive Toxicology, examined in greater detail the association between first trimester exposure to paroxetine (Paxil and Paxil CR) and the occurrence of major congenital malformation, especially major cardiac malformations. Paroxetine was significantly associated with a “two-fold increase in the risk of major congenital anomalies, and more specifically with a three-fold increase in the risk of major cardiac anomalies.”[31]
May 8, 2007: The German Drug Regulatory Agency (BfArM) warned of increased risk of cardiac malformation in newborns when the mother took Paxil during pregnancy.
May 2007: A study published in the Journal of The American Medical Association reported that of 117 pregnancies where the mother took Prozac during the first trimester, the risk of miscarriage was 14.8% compared to 7.8% in mothers not exposed to fluoxetine or tricyclic antidepressants.[32]
Objection to the Proposed MOTHERS Act - Bill
FOR IMMEDIATE RELEASE
UNITE / CHAADA / ICFDA / COPES Foundation
Objection to the Proposed MOTHERS Act - Bill
before Senate Puts Young Children and
Mothers in Serious Danger
February 11, 2008
Contacts:
Amy Philo, mailto:amy@uniteforlife.org
214-705-0169 home, 817-793-8028 cell
"www.chaada.org" "www.uniteforlife.org"
Dr. Ann Blake Tracy, Executive Director of the ICFDA
"www.drugawareness.org"
mailto:atracyphd1@aol.com, 800-280-0730 direct
Camille Milke mailto:sarinasvoice@aol.com/
505-269-2286 direct or 505-213-0999 fax (USA numbers)
"www.copesfoundation.com","www.drugawareness.org"
To the HELP Committee of the United States Senate:
For years, the March of Dimes has warned not to use meds while pregnant. Why now encourage mothers to take drugs?
Please register this extreme objection to the proposed MOTHERS Act (S. 1375) which is now before you in committee. It is my earnest hope that you will immediately defeat this bill in committee. The bill has been brought to you under the guise of ensuring safety or support for new mothers- however, nothing could be further from the truth.
The bill was originally proposed in response to the death by suicide of Melanie Stokes, a pharmaceutical rep. who took her own life by leaping from a balcony several stories off of the ground. Contrary to popular understanding it was not post-partum depression that killed Melanie, but the numerous antidepressant drugs she was taking, which the FDA confirmed doubles the suicide risk.
Nobody is suggesting that new moms do not ever experience mood swings, depression, or even psychotic episodes. The more important issue is what the effect of this bill will be and why nobody is addressing potential methods of prevention. Everyone knows how many young moms experience gestational diabetes, but who is addressing the even higher rate of gestational hypoglycemia, which often initially manifests as depression? This is a physical condition that is treated with diet and is exacerbated by antidepressants (which list hypoglycemia as a side effect).
To simply screen women for post-partum mood disorders and ensure that they get "treatment," we would be setting families up for the expectation of tragedy and increasing the chances of that actually happening when we refer them to medical "professionals" who are oblivious to the negative mind-altering effects of psychiatric drugs. A popular opinion among medical caregivers these days is that "post-partum mood disorders" must be a sign of an underlying biochemical imbalance and would be corrected with drugs.
Current drugs used on post-partum women include SSRIs, atypical antidepressants, and even antipsychotic drugs. These pose a significant risk to the immediate safety and health of women as well as their children and families. SSRIs carry a black box warning for suicide and the most popular one, Effexor (the same med. Andrea Yates was taking when she drowned her 5 children), has the words “homicidal ideation” listed as a side effect. Nearly every recent case of infanticide which has made news can be clearly linked back to a psychiatric drug. These drugs endanger babies and mothers.
Additionally, the drugs can be extremely addictive and also pose a risk to nurslings or babies exposed in subsequent pregnancies. Some babies have died from SIDS linked to exposure from pregnancy or nursing; others have experienced coma, seizures, GI bleeding, heart defects, lung problems, and many babies died before reaching full term or soon after birth.
The bill does not address the fact that studies show that biological agents (antidepressants for example) cited in the bill and already prescribed to pregnant women can cause congenital heart birth defects where children have had to undergo open-heart surgeries to correct this. Also, some babies are being born with organs outside their bodies, requiring immediate surgery.
In closing I want to re-emphasize the total lack of any real answer to post-partum depression posed by this bill. If we can prevent post-partum depression or support moms through it, or offer proven SAFE and EFFECTIVE natural alternatives to dangerous drugs, then we should. However we should never, ever become party to a pharmaceutical campaign to push drugs on the public. We will set ourselves up for disaster if we allow an invasion into the privacy of every family in the country and suggest to our most vulnerable citizens that they might be mentally ill.
We must do everything in our power to protect innocent children, and giving their mothers addictive drugs which pose a significant risk of causing suicide and violence does not protect anyone. It does cause the child to become addicted while still in the womb and sets up drug dependence which can be lifelong.
We still have no idea what effect most drugs have on developing brains. It might take decades for the impact on the developing brain to become apparent.
For information on the research pertaining to the risks of antidepressants and other treatments for new moms and their babies, details about the Melanie Stokes case (or you can read the letter by Dr. Ann Blake Tracy at
"http://uniteforlife.org/MOTHERSact.htm#drtracymothersact", as well as information on prevention strategies and safe, effective treatments for post-partum mood disorders, please contact us.
Sincerely,
Amy Philo
Founder, "www.uniteforlife.org"
Co-Founder, "www.chaada.org"
Camille Milke
Founder, "www.copesfoundation.com",
New Mexico State Director of the ICFDA ("www.drugawareness.org")
Mother of a victim of psychiatric drug-induced suicide and grandmother to a now motherless child
Dr. Ann Blake Tracy
Executive Director of the ICFDA
("www.drugawareness.org")
Author of Prozac: Pancaea or Pandora? Our Serotonin Nightmare
Addendum(available online: "http://www.uniteforlife.org/MOTHERpress.htm")
Prevention and Alternatives Information from UNITE ("www.uniteforlife.org"):
I. Danger of drugs
A. Inducing suicide and homicide
"http://uniteforlife.org/SSRIs%20and%20Suicide.html"
"www.drugawareness.org"
"www.ssristories.com"
"www.breggin.com"
"www.healyprozac.com"
"http://www.fda.gov/cder/drug/antidepressants/default.htm"
"http://www.fda.gov/cder/warn/2007/Effexor_XRPromo.pdf"
"http://www.fda.gov/ohrms/dockets/dockets/04n0330/04N-0330-EC16.html"
"http://www.fda.gov/ohrms/dockets/ac/04/slides/2004-4065OPH1_04_Bostock_files/frame.htm#slide0012.htm",
B. Addiction, subsequent pregnancies threatened, nurslings threatened: "http://uniteforlife.org/breastfeeding.html"
"http://uniteforlife.org/antidepressants%20in%20pregnancy%20articles.html"
"http://uniteforlife.org/developing%20brains.htm"
"http://uniteforlife.org/health%20risks%20ssris.html"
"http://www.fda.gov/medwatch/SAFETY/2005/Paxil_DHCP%20Letter_Dec%202005.pdfhttp://www.fda.gov/medwaTCH/SAFETY/2002/Zoloft_USPI_rev4.pdf"
(See pages 17-18, Pregnancy paragraph - which states that an increase in stillbirths and newborn deaths occurred from pregnancy plus nursing exposure)
Note: despite claims of minimal exposure to nurslings by some health professionals, the data on safety of nursing a baby while taking SSRIs and antipsychotics is based on an extremely small sample (nevermind that serious adverse events have been observed even in the few studies actually done). For SSRIs the studies amount to a few dozen people, many of which were also supplementally feeding formula. The Zyprexa study purported to study only 7 nursing couples and only examined 6 children's blood. See "http://uniteforlife.org/zyprexa%20objection.htm" for more information on the risks of Zyprexa.
II. Prevention of Post-Partum Mood Disorders:
A. Avoid interventions in childbirth: HOME BIRTH or midwifery or otherwise natural childbirth statistically results in LESS PPD..
Mothers Can Avoid (Specifically):
1. Labor drugs, including pitocin which interferes with normal oxytocin stimulation of uterine contractions (oxytocin is the love hormone and sets off many chemicals in the brain associated with normal maternal bonding & protective behavior)
2. IVs with glucose water during labor which can lead to complications in the newborn like perceived excessive weight loss, hypoglycemia, thus creating "mommy guilt" from feeling as if she is unable to sustain her own baby's survival due to perceived inadequate milk supply and subsequent breastfeeding difficulty when baby is inevitably given supplemental feedings
3. Avoid epidural which can cause breastfeeding difficulties in the newborn and may be associated with mood problems (the anesthesia fentanyl in the epidural is derived from cocaine)
4. Avoid episiotomy which can lead to excessive blood loss and fatigue as well as significant pain leading to use of pain medications
5. Avoid restrictive dieting before / after childbirth which can cause preterm labor (not having enough calories and protein leads to low albumin and high blood pressure), low blood sugar and lack of energy
6. Avoid epinephrine, which is often necessary in labor because of fetal distress or maternal distress (trouble breathing, low blood pressure) which are side effects in both mom and baby from pitocin or other augmentation as well as epidurals. Epinephrine is synthetic adrenaline and has been linked to mental disturbances.
B. Post-partum period:
1. FOR MANY WEEKS MOMS WILL NEED: someone to help with meals, chores, child care, etc. Without that, women ARE FAR MORE LIKELY to feel symptoms of depression, anxiety, etc.
2. MOMS WILL NEED someone to help with breastfeeding if they are inexperienced or have problems. They can contact a La Leche League Leader or an IBCLC. Loss of breastfeeding is sometimes associated with PPD due to additional hormonal changes in moms, while breastfeeding itself is thought to ease PPD due to numerous factors.
3. MOMS (and families) WILL FEEL BETTER if they cosleep because they will be well-rested and breastfeeding will be easier. For safety tips on cosleeping moms can use common sense or write to mailto:amy@uniteforlife.org for more info. Contrary to campaigns by the Crib Manufacturers SIDS is actually more common in cribs.
III. Alternatives to Drugs:
1. Screen for underlying medical conditions such as Thyroid disorders, anemia, etc. and treat those as safely as is possible. Thyroid disorders such as hypothyroidism or hyperthyroidism (or both - postpartum thyroiditis) are quite common and can cause depression or anxiety.
2. Omega 3 Supplements (From Fish Oil, Flaxseed, etc.)
3. Exercise (although initially excessive exercise will not help a woman, after childbirth it is necessary to rest in order to recover, and not lose too much blood) "http://uniteforlife.org/exercise.html" Medication shown to cause relapse, exercise MORE effective than antidepressant drugs
4. Some people feel that counseling is effective
5. Some people find alternative treatments effective, for example: chiropractic, homeopathy (even for PSYCHOSIS), accupuncture, energy work, etc.
6. MOMS can FIND A SUPPORT GROUP or helpful PERSON but NOT one that will push them to use drugs.
IV. Alternative Ways to Support American Families:
If the government really wants to help moms, why not educate on these common sense strategies, push for better maternity leave allowances, improve obstetric cooperation with midwifery, or promote paternity leave or leave for grandparents who can help new mothers during their time of need?
V. The Bill Violates Basic American Principles and Rights:
Mothers want time in PEACE and PRIVACY to be with their new babies to bond. They DO NOT need to be dragged off to an invasive and dangerous screening for mental problems. The power of suggestion alone is enough to scare a significant amount of moms and this invasion of privacy goes far beyond anything EVER imposed on the U.S. Public.
Furthermore, similar programs like Teen Screen have been a total failure with an 84% or higher misdiagnosis rate. The vast majority of these misdiagnosed students were referred to mental health practitioners and put on drugs.
There is no language in the bill that protects thousands of mothers being erroneously screened and drugged with antidepressants that medical studies show cause birth defects and withdrawal symptoms, devastating families and driving up health care costs to treat these iatrogenic-caused conditions.
The bill seeks more appropriations to the National Institutes of Health to research postpartum depression but doesn't specify how the funds are to be used. For example, during the past 3 years, NIMH has already spent more than $10 million on 38 studies of PPD, yet the National Center for Complementary and Alternative Medicine lists no grants on its website for such research.
There is no language about the diverse medical opinion and studies about "post partum depression" and whether it exists as a mental disability or as a physical condition that can be treated by normal medical or alternative means.
While the bill promotes more research into the condition, it doesn't provide safeguards about this research and the effects of biological agents on the fetus--with studies suggesting that antidepressants may exert an impact on developmental processes of the embryo, and cause higher rates of premature delivery, low birth weight, admissions to intensive care units, and poor neonatal adaptation, including respiratory and feeding difficulties in infants.
The way in which the bill is currently worded could lead to thousands of suits as hundreds have already been filed concerning antidepressant use during pregnancy that has resulted in infants being born with a life-threatening lung disorder, PPHN and that between 10% and 20% of infants born with PPHN end up dying, even when they receive treatment.
UNITE / CHAADA / ICFDA / COPES Foundation
Objection to the Proposed MOTHERS Act - Bill
before Senate Puts Young Children and
Mothers in Serious Danger
February 11, 2008
Contacts:
Amy Philo, mailto:amy@uniteforlife.org
214-705-0169 home, 817-793-8028 cell
"www.chaada.org" "www.uniteforlife.org"
Dr. Ann Blake Tracy, Executive Director of the ICFDA
"www.drugawareness.org"
mailto:atracyphd1@aol.com, 800-280-0730 direct
Camille Milke mailto:sarinasvoice@aol.com/
505-269-2286 direct or 505-213-0999 fax (USA numbers)
"www.copesfoundation.com","www.drugawareness.org"
To the HELP Committee of the United States Senate:
For years, the March of Dimes has warned not to use meds while pregnant. Why now encourage mothers to take drugs?
Please register this extreme objection to the proposed MOTHERS Act (S. 1375) which is now before you in committee. It is my earnest hope that you will immediately defeat this bill in committee. The bill has been brought to you under the guise of ensuring safety or support for new mothers- however, nothing could be further from the truth.
The bill was originally proposed in response to the death by suicide of Melanie Stokes, a pharmaceutical rep. who took her own life by leaping from a balcony several stories off of the ground. Contrary to popular understanding it was not post-partum depression that killed Melanie, but the numerous antidepressant drugs she was taking, which the FDA confirmed doubles the suicide risk.
Nobody is suggesting that new moms do not ever experience mood swings, depression, or even psychotic episodes. The more important issue is what the effect of this bill will be and why nobody is addressing potential methods of prevention. Everyone knows how many young moms experience gestational diabetes, but who is addressing the even higher rate of gestational hypoglycemia, which often initially manifests as depression? This is a physical condition that is treated with diet and is exacerbated by antidepressants (which list hypoglycemia as a side effect).
To simply screen women for post-partum mood disorders and ensure that they get "treatment," we would be setting families up for the expectation of tragedy and increasing the chances of that actually happening when we refer them to medical "professionals" who are oblivious to the negative mind-altering effects of psychiatric drugs. A popular opinion among medical caregivers these days is that "post-partum mood disorders" must be a sign of an underlying biochemical imbalance and would be corrected with drugs.
Current drugs used on post-partum women include SSRIs, atypical antidepressants, and even antipsychotic drugs. These pose a significant risk to the immediate safety and health of women as well as their children and families. SSRIs carry a black box warning for suicide and the most popular one, Effexor (the same med. Andrea Yates was taking when she drowned her 5 children), has the words “homicidal ideation” listed as a side effect. Nearly every recent case of infanticide which has made news can be clearly linked back to a psychiatric drug. These drugs endanger babies and mothers.
Additionally, the drugs can be extremely addictive and also pose a risk to nurslings or babies exposed in subsequent pregnancies. Some babies have died from SIDS linked to exposure from pregnancy or nursing; others have experienced coma, seizures, GI bleeding, heart defects, lung problems, and many babies died before reaching full term or soon after birth.
The bill does not address the fact that studies show that biological agents (antidepressants for example) cited in the bill and already prescribed to pregnant women can cause congenital heart birth defects where children have had to undergo open-heart surgeries to correct this. Also, some babies are being born with organs outside their bodies, requiring immediate surgery.
In closing I want to re-emphasize the total lack of any real answer to post-partum depression posed by this bill. If we can prevent post-partum depression or support moms through it, or offer proven SAFE and EFFECTIVE natural alternatives to dangerous drugs, then we should. However we should never, ever become party to a pharmaceutical campaign to push drugs on the public. We will set ourselves up for disaster if we allow an invasion into the privacy of every family in the country and suggest to our most vulnerable citizens that they might be mentally ill.
We must do everything in our power to protect innocent children, and giving their mothers addictive drugs which pose a significant risk of causing suicide and violence does not protect anyone. It does cause the child to become addicted while still in the womb and sets up drug dependence which can be lifelong.
We still have no idea what effect most drugs have on developing brains. It might take decades for the impact on the developing brain to become apparent.
For information on the research pertaining to the risks of antidepressants and other treatments for new moms and their babies, details about the Melanie Stokes case (or you can read the letter by Dr. Ann Blake Tracy at
"http://uniteforlife.org/MOTHERSact.htm#drtracymothersact", as well as information on prevention strategies and safe, effective treatments for post-partum mood disorders, please contact us.
Sincerely,
Amy Philo
Founder, "www.uniteforlife.org"
Co-Founder, "www.chaada.org"
Camille Milke
Founder, "www.copesfoundation.com",
New Mexico State Director of the ICFDA ("www.drugawareness.org")
Mother of a victim of psychiatric drug-induced suicide and grandmother to a now motherless child
Dr. Ann Blake Tracy
Executive Director of the ICFDA
("www.drugawareness.org")
Author of Prozac: Pancaea or Pandora? Our Serotonin Nightmare
Addendum(available online: "http://www.uniteforlife.org/MOTHERpress.htm")
Prevention and Alternatives Information from UNITE ("www.uniteforlife.org"):
I. Danger of drugs
A. Inducing suicide and homicide
"http://uniteforlife.org/SSRIs%20and%20Suicide.html"
"www.drugawareness.org"
"www.ssristories.com"
"www.breggin.com"
"www.healyprozac.com"
"http://www.fda.gov/cder/drug/antidepressants/default.htm"
"http://www.fda.gov/cder/warn/2007/Effexor_XRPromo.pdf"
"http://www.fda.gov/ohrms/dockets/dockets/04n0330/04N-0330-EC16.html"
"http://www.fda.gov/ohrms/dockets/ac/04/slides/2004-4065OPH1_04_Bostock_files/frame.htm#slide0012.htm",
B. Addiction, subsequent pregnancies threatened, nurslings threatened: "http://uniteforlife.org/breastfeeding.html"
"http://uniteforlife.org/antidepressants%20in%20pregnancy%20articles.html"
"http://uniteforlife.org/developing%20brains.htm"
"http://uniteforlife.org/health%20risks%20ssris.html"
"http://www.fda.gov/medwatch/SAFETY/2005/Paxil_DHCP%20Letter_Dec%202005.pdfhttp://www.fda.gov/medwaTCH/SAFETY/2002/Zoloft_USPI_rev4.pdf"
(See pages 17-18, Pregnancy paragraph - which states that an increase in stillbirths and newborn deaths occurred from pregnancy plus nursing exposure)
Note: despite claims of minimal exposure to nurslings by some health professionals, the data on safety of nursing a baby while taking SSRIs and antipsychotics is based on an extremely small sample (nevermind that serious adverse events have been observed even in the few studies actually done). For SSRIs the studies amount to a few dozen people, many of which were also supplementally feeding formula. The Zyprexa study purported to study only 7 nursing couples and only examined 6 children's blood. See "http://uniteforlife.org/zyprexa%20objection.htm" for more information on the risks of Zyprexa.
II. Prevention of Post-Partum Mood Disorders:
A. Avoid interventions in childbirth: HOME BIRTH or midwifery or otherwise natural childbirth statistically results in LESS PPD..
Mothers Can Avoid (Specifically):
1. Labor drugs, including pitocin which interferes with normal oxytocin stimulation of uterine contractions (oxytocin is the love hormone and sets off many chemicals in the brain associated with normal maternal bonding & protective behavior)
2. IVs with glucose water during labor which can lead to complications in the newborn like perceived excessive weight loss, hypoglycemia, thus creating "mommy guilt" from feeling as if she is unable to sustain her own baby's survival due to perceived inadequate milk supply and subsequent breastfeeding difficulty when baby is inevitably given supplemental feedings
3. Avoid epidural which can cause breastfeeding difficulties in the newborn and may be associated with mood problems (the anesthesia fentanyl in the epidural is derived from cocaine)
4. Avoid episiotomy which can lead to excessive blood loss and fatigue as well as significant pain leading to use of pain medications
5. Avoid restrictive dieting before / after childbirth which can cause preterm labor (not having enough calories and protein leads to low albumin and high blood pressure), low blood sugar and lack of energy
6. Avoid epinephrine, which is often necessary in labor because of fetal distress or maternal distress (trouble breathing, low blood pressure) which are side effects in both mom and baby from pitocin or other augmentation as well as epidurals. Epinephrine is synthetic adrenaline and has been linked to mental disturbances.
B. Post-partum period:
1. FOR MANY WEEKS MOMS WILL NEED: someone to help with meals, chores, child care, etc. Without that, women ARE FAR MORE LIKELY to feel symptoms of depression, anxiety, etc.
2. MOMS WILL NEED someone to help with breastfeeding if they are inexperienced or have problems. They can contact a La Leche League Leader or an IBCLC. Loss of breastfeeding is sometimes associated with PPD due to additional hormonal changes in moms, while breastfeeding itself is thought to ease PPD due to numerous factors.
3. MOMS (and families) WILL FEEL BETTER if they cosleep because they will be well-rested and breastfeeding will be easier. For safety tips on cosleeping moms can use common sense or write to mailto:amy@uniteforlife.org for more info. Contrary to campaigns by the Crib Manufacturers SIDS is actually more common in cribs.
III. Alternatives to Drugs:
1. Screen for underlying medical conditions such as Thyroid disorders, anemia, etc. and treat those as safely as is possible. Thyroid disorders such as hypothyroidism or hyperthyroidism (or both - postpartum thyroiditis) are quite common and can cause depression or anxiety.
2. Omega 3 Supplements (From Fish Oil, Flaxseed, etc.)
3. Exercise (although initially excessive exercise will not help a woman, after childbirth it is necessary to rest in order to recover, and not lose too much blood) "http://uniteforlife.org/exercise.html" Medication shown to cause relapse, exercise MORE effective than antidepressant drugs
4. Some people feel that counseling is effective
5. Some people find alternative treatments effective, for example: chiropractic, homeopathy (even for PSYCHOSIS), accupuncture, energy work, etc.
6. MOMS can FIND A SUPPORT GROUP or helpful PERSON but NOT one that will push them to use drugs.
IV. Alternative Ways to Support American Families:
If the government really wants to help moms, why not educate on these common sense strategies, push for better maternity leave allowances, improve obstetric cooperation with midwifery, or promote paternity leave or leave for grandparents who can help new mothers during their time of need?
V. The Bill Violates Basic American Principles and Rights:
Mothers want time in PEACE and PRIVACY to be with their new babies to bond. They DO NOT need to be dragged off to an invasive and dangerous screening for mental problems. The power of suggestion alone is enough to scare a significant amount of moms and this invasion of privacy goes far beyond anything EVER imposed on the U.S. Public.
Furthermore, similar programs like Teen Screen have been a total failure with an 84% or higher misdiagnosis rate. The vast majority of these misdiagnosed students were referred to mental health practitioners and put on drugs.
There is no language in the bill that protects thousands of mothers being erroneously screened and drugged with antidepressants that medical studies show cause birth defects and withdrawal symptoms, devastating families and driving up health care costs to treat these iatrogenic-caused conditions.
The bill seeks more appropriations to the National Institutes of Health to research postpartum depression but doesn't specify how the funds are to be used. For example, during the past 3 years, NIMH has already spent more than $10 million on 38 studies of PPD, yet the National Center for Complementary and Alternative Medicine lists no grants on its website for such research.
There is no language about the diverse medical opinion and studies about "post partum depression" and whether it exists as a mental disability or as a physical condition that can be treated by normal medical or alternative means.
While the bill promotes more research into the condition, it doesn't provide safeguards about this research and the effects of biological agents on the fetus--with studies suggesting that antidepressants may exert an impact on developmental processes of the embryo, and cause higher rates of premature delivery, low birth weight, admissions to intensive care units, and poor neonatal adaptation, including respiratory and feeding difficulties in infants.
The way in which the bill is currently worded could lead to thousands of suits as hundreds have already been filed concerning antidepressant use during pregnancy that has resulted in infants being born with a life-threatening lung disorder, PPHN and that between 10% and 20% of infants born with PPHN end up dying, even when they receive treatment.
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