Dr. Ann Blake Tracy's commentary on the David Ragsdale case:
Combine simple math and common sense (which is far from common any longer!) and you have the answer that Grosser, Peterson, Paulson and Yau were unwilling to venture a guess as to whether David Ragsdale's medications could have caused him to kill his wife.
1. Recent research shows that antidepressants are of no more benefit than a sugar pill yet have page after page of adverse reactions along with reports of terrible withdrawal.
2. Look at package warnings for antidepressants and you find the most commonly prescribed antidepressant currently, Effexor, has the warning of "homicidal ideation" - obsessive thoughts of killing and how to kill.
Significant to note is that the company kept the data hidden for over 10 years before adding this to the drug information, leading one to ask just how many other manufacturers of antidepressants with different brand names, yet with similar action in the brain, are still hiding that information about their drugs?
(Next our society must ask ourselves, "Since when has homicide become an acceptable side effect to a medication?!!")
3. In August Dr. Thomas Insel, head of the National Institute of Mental Health admitted that antidepressants produce the same effect as Ketamine, a sister drug to PCP, and a dissociative anesthetic, yet they take a little longer to produce that effect. PCP and Ketamine are now known to produce psychosis coupled with incredible violence although they were initially thought to have "a large margin of safety in humans."
4. There is case history: Turn to the Donald Schell case in 2001 in WY. After consuming only two pills of one antidepressant, Paxil, which David Ragsdale was taking, this mild mannered loving husband and father shot his wife, daughter, infant granddaughter and then himself. After hearing all the evidence (the most damaging coming from the Paxil manufacturer's own expert) the jury ruled that the consumption of two Paxil pills was the main cause of this tragedy and awarded $6.4 Million to what was left of this family.
5. We have absolutely no idea what two drugs mixed together will do because they are never tested together, only individually. And we certainly have NO IDEA what taking 7 medications can do when mixed in a human body or brain!
6. Simple math: As Scott Peterson was candid enough to admit one drug taken with another can multiply the response, as well as side effects, by 10 times - exactly what Paxil and Doxepin do taken together. Multiply any of the possible side effects listed for either Paxil or Doxepin by 10 times and you see the extreme likelihood of medication-induced psychosis, mania, amnesia, seizure, etc.
Nurse Tamara Ragsdale, David's sister, listed the adverse effects produced by these drugs as "manic reaction, suicide, homicidal tendencies, hallucinations, delusions, psychosis, amnesia, panic and seizures." All one needs do is pull up the product information on each of these drugs and find those listed for most of the 7 mind altering medications David was taking.
One last point brought up by Dr. Grosser is that cases like David Ragsdale's are being trumpeted "as a demonstration of how dangerous these drugs are." I will agree that these case reports are exactly what gets any drug pulled from the market. And just as it was the missing arms and legs of the babies born to moms taking Thalidomide that kept that drug off the market in the US, it will be the Utah murder cases of David Ragsdale, Sergi Babarin, Sharon Al-Shimmary, Gloria Clements, Margaret Kastanis, JC Gardner, Debbie Loiselle, Ronald Cunningham, Mark Ott, Lenny Gall, Carl Lindeman, Christopher Jessop, Mitchell Sawaya, Brian Christopher Sullivan, Darrell Kinyon, Scott Ellison, Claudio Martinez, Art Henderson, etc., etc., etc. (www.drugawareness.org), not to mention the cases nationwide and worldwide, that will pull these deadly drugs from the market.
But beyond the homicides, another factor for their withdrawal will be all the suicides and the all too often fatal birth defects related to the heart and lung damage in the offspring born to moms who take these drugs.
[WARNING: The FDA has warned that any abrupt change in dose of an antidepressant can produce suicide, hostility or psychosis!]
Ann Blake-Tracy, PhD, Executive Director,
International Coalition for Drug Awareness
www.drugawareness.org & author of Prozac:
Panacea or Pandora? - Our Serotonin Nightmare
Thursday, April 17, 2008
Sarina's Voice supports the Health Ranger!
When you search the internet and start to see the myriad of information available about Big Pharma; the FDA; the Legislature; mandatory drug screening; horror stories from victims; the direct to consumer advertising dangers; the dangers of SSRI anti-depressants and other prescription drugs in general, there are a few people that really stand out as being well educated, informed and generally concerned about society. Mike Adams, the Health Ranger, is one of those people. Sarina's Voice would like to support and thank Mike for all of his hard work!
Here is a letter he wrote recently to NaturalNews:
Dear NaturalNews / NewsTarget readers,
Due to widespread misreporting of the Illinois shooting incident by the mainstream media (MSM), I'm issuing a weekend e-mail alert that tells the truth about the link between psychiatric drugs and every school shooting that has taken place in the United States in the last decade. Here's the first section from the article posted today:
(NaturalNews) It comes as no surprise to anyone who's been following school shootings all the way back to the Colombine High massacre in Colorado: Every young, male shooter that has gone on a killing spree in the United States also has a history of treatment with psychotropic drugs -- typically SSRI antidepressants. These shootings have three things in common: 1) The shooters are young males. 2) The shooters exhibit a mind-numbed disconnect with reality. 3) The shooters have a history of taking psychiatric drugs.
This latest shooting by 27-year-old Stephen Kazmierczak shares the same three factors. Stephen was considered a "normal, undistressed person," according to press reports. He was considered "an outstanding student" and even received a Dean's Award for outstanding work in sociology. So what happened to Stephen's brain that caused him to snap and open fire on students in a college classroom?
Psych meds make good people do bad things
Psychiatric drugs, of course, are well known to cause extremely violent thoughts and behavior in young males. This is actually acknowledged by the FDA and is found in the black-box warnings printed on the packaging for such drugs. In Europe, the prescribing of many such drugs to children and teens is actually illegal. But in the United States, where psychiatric medications have become the "new medicine" for American youth, nobody seems to pay attention to the simple fact that every school shooting we've seen in the last decade has been committed by a young male with a history of treatment with these dangerous mind-altering chemicals...
Click here to continue reading this article at NaturalNews
Regards,
- Mike Adams, the Health Ranger
Here is a letter he wrote recently to NaturalNews:
Dear NaturalNews / NewsTarget readers,
Due to widespread misreporting of the Illinois shooting incident by the mainstream media (MSM), I'm issuing a weekend e-mail alert that tells the truth about the link between psychiatric drugs and every school shooting that has taken place in the United States in the last decade. Here's the first section from the article posted today:
(NaturalNews) It comes as no surprise to anyone who's been following school shootings all the way back to the Colombine High massacre in Colorado: Every young, male shooter that has gone on a killing spree in the United States also has a history of treatment with psychotropic drugs -- typically SSRI antidepressants. These shootings have three things in common: 1) The shooters are young males. 2) The shooters exhibit a mind-numbed disconnect with reality. 3) The shooters have a history of taking psychiatric drugs.
This latest shooting by 27-year-old Stephen Kazmierczak shares the same three factors. Stephen was considered a "normal, undistressed person," according to press reports. He was considered "an outstanding student" and even received a Dean's Award for outstanding work in sociology. So what happened to Stephen's brain that caused him to snap and open fire on students in a college classroom?
Psych meds make good people do bad things
Psychiatric drugs, of course, are well known to cause extremely violent thoughts and behavior in young males. This is actually acknowledged by the FDA and is found in the black-box warnings printed on the packaging for such drugs. In Europe, the prescribing of many such drugs to children and teens is actually illegal. But in the United States, where psychiatric medications have become the "new medicine" for American youth, nobody seems to pay attention to the simple fact that every school shooting we've seen in the last decade has been committed by a young male with a history of treatment with these dangerous mind-altering chemicals...
Click here to continue reading this article at NaturalNews
Regards,
- Mike Adams, the Health Ranger
Friday, April 4, 2008
SEROXAT SUFFERERS - STAND UP AND BE COUNTED
SSRI’s like Paxil (Seroxat) are extremely dangerous , Bob Fiddaman is a Seroxat patient campaigner and he has been blogging about the Seroxat scandal for some years. Recently GSK (manufacturers of Seroxat – GlaxoSmithKline) have used threatening and intimidating tactics to try and suppress his voice.
I am calling all mental health campaigners to highlight this on their blogs if they can.
http://fiddaman.blogspot.com/2008/03/gsk-lawyers-target-seroxat-campaigner.html
I am calling all mental health campaigners to highlight this on their blogs if they can.
http://fiddaman.blogspot.com/2008/03/gsk-lawyers-target-seroxat-campaigner.html
Wednesday, March 26, 2008
Texting Mental Disorder - What's Next?
Yet another push to inundate the world with psychotropic drugs. This petition's author put it this way:
'We, the citizens of the United States who are sick and tired of your bogus, dangerous and self serving fraudulent enterprise;
Do hereby tell the American Psychiatric Association and the blood thirsty, money sucking psych drug manufacturers:
Texting is not a Mental 'disorder'. Take Your Mental Disorders and Your Psych Drugs and Your Unscientific Diagnostic & Statistical Manual and Shove Them!'
And we agree.
The doctor who invented this 'Texting Mental Disorder' stands to profit more than normal as he holds a patent that can be used to restrict computer access.
We're all for 'Free Enterprise,' we just don't want to harm or even kill people in the process. I guess we're the crazy ones.
Please sign this petition and pass it on.
Update on Ridiculous New 'Texting Mental Disorder'
Sign the Brand New Petition - - Texting is not a Mental Disorder. Take Your Mental Disorders and Your Psych Drugs and Your Unscientific Diagnostic & Statistical Manual and Shove Them! Sign here:
http://www.petitiononline.com/textmess/petition.html
--------------------------------------------------------------------------------
26,299 Signatures Against TeenScreen:
http://www.petitiononline.com/TScreen/petition.html
Video:
http://www.youtube.com/watch?v=RfU9puZQKBY
'We, the citizens of the United States who are sick and tired of your bogus, dangerous and self serving fraudulent enterprise;
Do hereby tell the American Psychiatric Association and the blood thirsty, money sucking psych drug manufacturers:
Texting is not a Mental 'disorder'. Take Your Mental Disorders and Your Psych Drugs and Your Unscientific Diagnostic & Statistical Manual and Shove Them!'
And we agree.
The doctor who invented this 'Texting Mental Disorder' stands to profit more than normal as he holds a patent that can be used to restrict computer access.
We're all for 'Free Enterprise,' we just don't want to harm or even kill people in the process. I guess we're the crazy ones.
Please sign this petition and pass it on.
Update on Ridiculous New 'Texting Mental Disorder'
Sign the Brand New Petition - - Texting is not a Mental Disorder. Take Your Mental Disorders and Your Psych Drugs and Your Unscientific Diagnostic & Statistical Manual and Shove Them! Sign here:
http://www.petitiononline.com/textmess/petition.html
--------------------------------------------------------------------------------
26,299 Signatures Against TeenScreen:
http://www.petitiononline.com/TScreen/petition.html
Video:
http://www.youtube.com/watch?v=RfU9puZQKBY
Labels:
Big Pharma,
mental disorder,
psychotropic drugs
Sunday, March 23, 2008
It is a SICK WORLD
It is a sick world.
To most of us that means many people can be cruel, heartless and greedy no matter the effect on our fellow human beings or on other living things. To Big Pharma, and their cronies, it means we should all take drugs! Their drugs! The legal kind that aren't dangerous. OH WAIT! In the U.S. alone, more people die each year from unintentional deaths due to antidepressants, sleeping pills, and tranquilizers than all cocaine and heroin deaths combined. Not to mention all the lives ruined by the violent outbursts and irrational behavior that is spurred from mind altering drugs. The effects ripple through all society with such deadly and disastrous results that it makes second-hand smoke seem like a blast of fresh air straight from a rain forest. SSRI Anti-depressants and the like are forever making the world that much sicker.
Thanks to Justice Lover for this latest thing that is considered a "Mental Illness".
Sarina's Voice
http://10thoutlawpsychiatry.blogspot.com/
BEWARE : A NEW "MENTAL ILLNESS" INVENTED BY THE SHRINKS. HAS BIG PHARMA THE "MEDICATIONS" FOR IT ? WOULD THEY BE "ANTIPSYCHOTICS" OR "ANTIDEPRESSANTS" ?
by Justice Lover
Let us leave aside the internet for now , although it is apparently a major headache for the rulers (BIG BUSINESS) as it keeps spreading the truth and exposing their crimes against humanity, including those of psychiatry itself !
What about the excessive nonstop lies by the rulers and by their stooges (like the shrinks, for example) ?
What about the excessive nonstop lies by the rulers' trusted zionist allies who cannot survive without their horrendous lies ?
What about the excessive greed and obsession with power of all those crooks, and their ambitions to rule the entire world at any cost, even if it means the destruction of life on our planet ?
Surely, if merely surfing and communicating via the internet is a "mental illness", then the rulers and their allies and stooges are all psychotics who should be locked up in loony bins immediately TO SAVE HUMANITY, as their greed and obsessions are infinitely more dangerous ?
The following is the official news from the bosses' media :
http://www.news.com.au/story/0,23599,23414957-2,00.html
To most of us that means many people can be cruel, heartless and greedy no matter the effect on our fellow human beings or on other living things. To Big Pharma, and their cronies, it means we should all take drugs! Their drugs! The legal kind that aren't dangerous. OH WAIT! In the U.S. alone, more people die each year from unintentional deaths due to antidepressants, sleeping pills, and tranquilizers than all cocaine and heroin deaths combined. Not to mention all the lives ruined by the violent outbursts and irrational behavior that is spurred from mind altering drugs. The effects ripple through all society with such deadly and disastrous results that it makes second-hand smoke seem like a blast of fresh air straight from a rain forest. SSRI Anti-depressants and the like are forever making the world that much sicker.
Thanks to Justice Lover for this latest thing that is considered a "Mental Illness".
Sarina's Voice
http://10thoutlawpsychiatry.blogspot.com/
BEWARE : A NEW "MENTAL ILLNESS" INVENTED BY THE SHRINKS. HAS BIG PHARMA THE "MEDICATIONS" FOR IT ? WOULD THEY BE "ANTIPSYCHOTICS" OR "ANTIDEPRESSANTS" ?
by Justice Lover
Let us leave aside the internet for now , although it is apparently a major headache for the rulers (BIG BUSINESS) as it keeps spreading the truth and exposing their crimes against humanity, including those of psychiatry itself !
What about the excessive nonstop lies by the rulers and by their stooges (like the shrinks, for example) ?
What about the excessive nonstop lies by the rulers' trusted zionist allies who cannot survive without their horrendous lies ?
What about the excessive greed and obsession with power of all those crooks, and their ambitions to rule the entire world at any cost, even if it means the destruction of life on our planet ?
Surely, if merely surfing and communicating via the internet is a "mental illness", then the rulers and their allies and stooges are all psychotics who should be locked up in loony bins immediately TO SAVE HUMANITY, as their greed and obsessions are infinitely more dangerous ?
The following is the official news from the bosses' media :
http://www.news.com.au/story/0,23599,23414957-2,00.html
Friday, March 14, 2008
CHAADA / UNITE / COPES FOUNDATION / ICFDA OPPOSITION TO THE MOTHERS ACT, S. 1375 / H.R. 20
THERE IS NO ESCAPING THE DANGEROUS REALITY OF THIS BILL
March 3, 2008
Contacts:
Amy Philo
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
Ann Tracy, 801-209-1800 direct, 801-335-4727 fax
Camille Milke
505-269-2286 direct or 505-213-0999 fax
www.copesfoundation.com
www.drugawareness.org
The supporters of The MOTHERS Act have been engaging for the past few years in an aggressive attempt to pass an incredibly broad federal law which will transform the U.S. market for “antidepressant” or “antipsychotic” drugs from a voluntary pool of patients who are encouraged by commercials to seek help from their doctors, to a government-sponsored screening program to select patients who are deemed to need “antidepressant” or “antipsychotic” drugs from among the female childbearing-age population. These promoters of the bill have had vast resources and ample time to obtain support and backing from the legislators they have influenced. The bill has passed the U.S. House, and needs approval from the Senate, final agreement from the House if any changes are made, and a signature from President Bush. This could happen in a matter of days or weeks.
The timing of the impending vote on this bill in the U.S. Senate is highly ironic in light of the tremendous amount of negative news we have seen on antidepressants and antipsychotics over the past several months. It is especially shocking to see it being promoted at a time when our society is being terrified by frequent shootings and murder-suicides which have been preceded by the perpetrator’s use and sometimes improper discontinuation of antidepressant drugs, and in the wake of several notable celebrities’ deaths which were the result of prescription drug toxicity. The evidence against these drugs is frightening, and the reality is that, if The MOTHERS Act is passed, those who are the most innocent and vulnerable and in need of protection FROM these drugs will instead be put ON these drugs, and placed in serious danger from all of the negative drug effects - including spontaneous abortion, a tenfold increased risk of psychosis for postpartum women, birth defects, suicide, and homicide (YES, THIS IS A LISTED ANTIDEPRESSANT SIDE EFFECT).
The bill creates funding for development of new drugs at taxpayers’ expense. Doctors will be under greater pressure to prescribe drugs to pregnant and postpartum women due to federal law which would ensure the promotion of earlier “detection” and “treatment.” Despite the fact that the law admits that the causes of depression or psychosis can vary between many life situations and social realities, and perhaps some unknown biological factors, and the manufacturers’ own research (kept hidden for years but recently revealed) shows that antidepressants have no more benefit than a sugar pill, the bill endorses drugs and hospitalization as essential and necessary treatment options. Many women who seek treatment or reach out for help under this proposed legislation would be under the watchful eyes of the government rather than simply under the care and guidance of their doctors or counselors. The potential for creating violence, death, and destroying families through the administration of drugs combined with possible involvement of police, CPS, and the courts, as well as the invasions of privacy and individual freedoms that this bill would ensure, must not be accepted.
Since we first issued our press release opposing S. 1375, The MOTHERS Act on February 11, thousands of people have been made aware of this bill, which at one time flew way under the public radar. Many people have come forward for the first time with sad stories of personal harm caused by the drugs, while a few others have, unfortunately, gone on to continue their support for a bill that threatens to bring about a dire and dangerous situation, sacrificing life, family, children, motherhood, freedom, and our future.
Some people pushing for the bill have taken notice of our efforts, and in response simply told the public and the media that The MOTHERS Act is mainly about “education.” That sounds so innocuous and harmless that it’s nearly impossible for most people to disagree with the bill if they have not read its contents. But even if that were the true purpose, or if the Senate were to rewrite the bill and remove most of the negative wording, leaving ONLY education as its goal, let us consider this idea for a moment - what is the impact of an education or awareness campaign promoting certain psychiatric labels?
In a 1996 study cited by Dr. Grace Jackson in her book, Rethinking Psychiatric Drugs, researchers discovered that an awareness campaign in the UK called “Defeat Depression” resulted in a significant increase in prescriptions for antidepressants, a change in physician practices of increased willingness to prescribe, and a large increase in agreement from the public that antidepressant drugs are effective and should be given to patients. Furthermore, to summarize from a follow-up study in 2001, researchers concluded that since there were still so many people who favored alternative treatments such as yoga, meditation and natural remedies over antidepressants, “further efforts to improve public knowledge about pharmacotherapy of mental disorders [were] needed.”
Would passing The MOTHERS Act in effect counter the ideas of those who have wised up to the drug companies, by creating a sense of legitimacy through governmental drug endorsements? By promoting earlier detection and treatment of postpartum depression or psychosis, or depression in pregnancy, it makes sense that we would see the numbers of prescriptions for antidepressants and antipsychotic drugs significantly increase in pregnant and postpartum women. This would be a boon to the drug industry, which has had to deal with the potential for decreasing sales since the FDA issued black box warnings on SSRIs for doubling the risk of suicide in 2004, and black box warnings on “antipsychotic” drugs for doubling suicides just a few weeks ago. Eli Lilly received a “Not Approvable” letter for their new injectable Zyprexa application several days ago. Also, a recent analysis of all studies submitted to the FDA prior to approval of many antidepressant drugs showed that the drugs overall were no more effective than placebo, but that most of the studies in which antidepressants did worse than placebo were never made public, or the results were misreported.
With the truth stacked against the drugs and against this bill, we have no option other than to campaign vigorously against the passage of The MOTHERS Act. There are many steps you can take right now to help ensure its defeat and safeguard our women, unborn babies, and the innocent bystanders whose paths sometimes cross people who commit crimes during altered states while under the influence of prescription drugs.
First, sign our petition against the MOTHERS Act
http://www.thepetitionsite.com/1/stop-the-dangerous-and-invasive-mothers-act
Next, contact the U.S. Senate and demand that they consider the truth and stop this bill dead in its tracks. For phone and fax numbers for the Senate please go to
http://uniteforlife.org/senatecontactlist.htm
Please share this information with everyone you possibly can and urge them to act now.
Please also read the addendum to this press release, especially the excerpts which follow the links, and feel free to forward this entire information packet.
Sincerely,
Amy Philo
Founder, www.uniteforlife.org
Co-Founder, www.chaada.org
Survivor of Zoloft-induced homicidality, suicidality, and psychosis during the postpartum period
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
Blog and YouTube channel for Julie, whose son, Manie, was born with a life-threatening Paxil heart defect (Julie has 5 kids, 4 of whom are healthy, but she took Paxil during her pregnancy with Manie, her 4th child)
http://www.bigpharmavictim.blogspot.com
http://www.youtube.com/jledgi
Moms in NJ (which has a similar law to the proposed MOTHERS Act) were treated like criminals for seeking help for PPD
http://www.uniteforlife.org/ppdcriminals.htm
Our original press release with an addendum, which includes references to medical studies on dangers, including pregnancy dangers and suicide / homicide dangers, toxicity dangers, and articles on PPD alternatives, actual safely treatable causes, and prevention:
http://www.uniteforlife.org/MOTHERpress.htm
A lack of sufficient data to support the alleged safety of breastfeeding while using psychiatric drugs
http://www.uniteforlife.org/breastfeeding.html
A decline in suicides since the FDA Black Box Warning
http://www.uniteforlife.org/decline%20in%20sucicides.html
Lowest level of suicides in 30 years as prescriptions for antidepressants drop by half (England, Wales)
http://www.uniteforlife.org/englandwales.htm
A Swedish study revealing that psychiatric drug use preceded about 80% of all adult suicides
http://ahrp.blogspot.com/2008/03/antidepressants-linked-to-52-of.html
Antipsychotic drugs get slapped with black box warning for doubling suicides
http://www.uniteforlife.org/socalledmoodstabilizersdoublesuicide.htm
Adrenal exhaustion as a cause of PPD (including information about thyroid conditions and the fact that antidepressants exacerbate adrenal problems):
http://www.uniteforlife.org/adrenalppd.htm
Media coverage of the NEJM analysis revealing the data suppression and ineffectiveness of antidepressants
http://www.uniteforlife.org/suppresseddata.htm
Flyer to use for massive advertising against the bill and to solicit petition signatures
http://www.uniteforlife.org/flyermom.htm
An outreach letter that can be used for emails asking for support and endorsements of our efforts against this bill
http://www.uniteforlife.org/requestforhelp.htm
Amy Philo’s YouTube Videos including her personal story of Zoloft-induced psychosis and homicidal and suicidal urges during the postpartum period:
http://www.youtube.com/watch?v=LQW23XCmOCw
http://www.youtube.com/watch?v=W4B8I_8wz6I
==================
Please read some of these excerpts from emails and blogs that we have found or received in the past few weeks:
================
“I was on very low dose Desyrel for depression during pregnancy. But when I got tired of being tired, I took myself off. A year later they put me on Prozac. I felt better, but began behaviors that distressed me. They told me that I needed it. I switched to Zoloft. Later to Paxil. Each time I tried to get off of it, I had what I later learned was withdrawal effects, but they told me it was proof I needed it. Later, when I heard someone tell my story about the withdrawal effects, I took myself off cold turkey, knowing that I would get through it. And I did. During these years on SSRI's, I was diagnosed with Type II Bipolar Disorder (mild mania). When I got off of SSRI's those symptoms disappeared. My relationship with my son was permanently damaged by my behavior, and horrible 'legal' things happened to me as the result of my drug induced behavior. The psychiatric community denies this is why, but recently, my doctor was looking for something for my panic attacks and some depression and said that she wouldn't put me back on SSRI's because of the manic symptoms they induced... this is the doctor, one of them, who denied the SSRI's were causing my problems! I still have panic attacks, but never had them before these medications. I had depression, but not these panic attacks...which now may be something I'm going to have to deal with ongoing.
I can't believe what incredible suffering some supposedly "human" beings can perpetrate on other human beings...FOR PROFIT!!! It's a disgusting legacy of a culture of greed and indifference, and is the cause of U.S. interference and imperialism...greed, power, profit. They have no conscience, no shame...no humanity!!
The damage to my life was great...particularly to my relationship with my son, who has only known me with my behavior on those drugs...so, though we are close, and the relationship was loving and protective, I did behave badly at times. He has a lot of pain to deal with because of it...and it affects our relationship. It's a source of great pain, sorrow and shame for me. I didn't get off these drugs until he was out of the house at 18. He left before he graduated from high school.
I worked with a young woman going through a crisis, brand new mom... she was 3 months post partum... something horrible happened and they arrested her, took her away from her child... she never got her back. She already had mental problems, but what they did to her made it worse.
Doctors and law enforcement are lazy and indifferent...really jaded... and they have stopped caring. They rely on what they think they know and what is expedient. So laws like this will make it worse.”
– Lucy
=================
Excerpts from The Star-Ledger (Newark, New Jersey)
December 9, 2007 Sunday
“Promised lifeline for new moms falls short
Postpartum depression law called a disappointment so far
BYLINE: SUSAN K. LIVIO, STAR-LEDGER STAFF
…A `HORRIBLE' RESPONSE
Maxine Garcia of Sayreville says that when she asked for help she got a response that left her stunned. Police officers and rescue squad workers arrived unannounced at her home last year, an hour after she called the hotline to say she was six months pregnant and "depressed out of my mind." According to the police report, Garcia threatened to hurt herself, but she denies it. She and her two children were forced to go to the emergency room. "I felt like I had no rights," Garcia said. "I really just needed someone to talk to."
Yolanda Iyube of Franklin in Somerset County says she confided to her gynecologist two years ago she was consumed with scary thoughts about her baby dying violently. Before she left the office, a police-escorted social worker took her to the emergency room. "They brought me in a police car to the hospital. It was horrible - everyone was looking at me like I had committed a crime."
Venis said such responses can discourage women with postpartum depression from seeking help.
...When the law took effect, there was an initial reluctance from physicians treating new mothers - a fear that "we won't be able to discharge anyone from the hospital," said Edward Wolf, vice chairman of the Department of Obstetrics and Gynecology at Saint Barnabas Medical Center in Livingston.
Wolf said the law added responsibilities for obstetricians already vulnerable to malpractice lawsuits. He said there was a fear of "I am going to get this thrown on my lap without help."”
===================
Excerpts from Julie’s blog
http://www.bigpharmavictim.blogspot.com/
“Manie is 3 years old.
Was born with Transposition of the Great Arteries.
Had a balloon procedure shortly after birth to keep him alive.
Had open heart surgery at 1 week old.
Had 3 cardiac caths to correct problems with collaterals.
Has had several coils put in his collaterals.
Has a leak in his valve.
Manie has to take medicine for high blood pressure.
Manie has also suffered from acid reflux
Manie was on an adult dose of meds for acid reflux for six months.
Because of the acid reflux Manie has bad teeth. His baby teeth are ruined.
When Manie goes to the dentist he has to have dental work done with out Novocaine or nitrous oxide.
The reason why Manie was born with a congenital heart defect was because of my ingestion of an antidepressant while I was pregnant. I took Paxil within the first three months that I was pregnant with Manie. At the time that I was pregnant with Manie Paxil was a class C drug. Now Paxil is a class D drug.
What is a category D: Definite fetal risk, maybe given in spite of risk if needed in life-threatening conditions. What could be so important to risk a unborn baby's life? If something is life-threatening I would think a person should be under supervision as not to hurt them self or their unborn child. In Mosbys Drug Reference Paxil is a category B drug in 2003. Now I ask when did Glaxo know about paxil causing birth defects???????? Now that is a good question isn't it.
This is what I have to say to any one who is pregnant or could become pregnant. If you are depressed get help indeed. However please think about this... Wouldn't it be better to seek some other kind of help for your depression? I have been through having a child with a birth defect and I will always be going through it. I can never turn back the hands of time and not take that pill. Unlike you I did not know. I did not have a clue. Until recently I did not know why Manie was born with a heart defect. I looked and looked for a reason why and always came up with nothing. Until one day I found out that it was because I took paxil. The guilt I feel will never go away even though it was not my fault. If you think that you are depressed now wait until your life is flipped upside down when your baby is born with a horrible birth defect like Manie was.
==========
Manie has three sisters and one brother. Manie is number four out of five kids. Manie loves to hunt frogs and go fishing. Manie loves being outside in the summer time. I had a normal pregnancy with Manie. I even had a couple of ultrasounds done while I was pregnant with Manie. There were no clues that Manie had a rare heart defect. I had already 3 perfectly healthy kids and did not expect for Manie to be any different.
As soon as Manie was born he began to turn blue. The more he cried the more he turned blue. Our doctor did not know what was wrong with Manie. The doctor thought that it might be his heart or his lungs.
Manie was flown to a hospital an hour and a half away from where we live. I had to stay at the hospital where I had Manie. The doctors called me when Manie arrived and told me Manie had transposition of the great arteries.
I was told that Manie had to have a procedure done to save his life. The doctors went through the artery on the inside of Manie's right leg. The doctors snaked a balloon all the way through the artery to Manie's heart. Once the doctors were in Manie's heart they blew the balloon up and ripped a hole in Manie's heart.
In the days following the surgery Manie's leg and foot started to turn a dark purple. The doctors told us that Manie may have to have his leg amputated because the procedure damaged the artery in Manie's leg.
Right before Manie's open heart surgery the doctors put Manie on blood thinners. Shortly after putting Manie on blood thinners they were able to detect a pulse in Manie's foot. Manie kept his leg.
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(TGA means the aorta and pulmonary arteries in the heart are switched. When a child is born with TGA there is very little oxygen in the blood. The aorta receives the oxygen-poor blood from the right ventricle, but it's carried back to the body without receiving more oxygen. The pulmonary artery receives the oxygen-rich blood from the left ventricle but carries it back to the lungs.)
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Manie loves to go to a lake by our house and hunt frogs and go fishing. Manie also likes to go to the park. Manie really likes to go to the mall and play video games. Manie also loves to dance especially to 80s music.
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When he first started going to the dentist at about a year old because his teeth were going bad and this was before we knew that he had been suffering with acid reflux I was blamed for it then too. I was told his teeth were bad because I was still nursing him and I needed to stop. So I have learned that they are just looking for someone to blame. I take care of my kids teeth. If I did not then why does Manie's older brother have perfect teeth and never had any cavities at all? I just took Manie's older brother and one of his older sisters to the dentist two weeks ago. Guess what no cavities and no problems. Hmmm what does that tell ya? So it looks like Manie is going back to the dentist in four months and at that time the student said "they will talk to me about putting him under to have all his teeth done at once." I am not going to worry about that right now I guess. I will keep on brushing and praying that his teeth will be fine. Manie made it through another dental appointment and he is such a brave little boy. I am so proud of him. This was just a small insite into what Manie has to go through. I wish I could take it all away and make it better for him, but all I can do is be there to love him.
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…I do not care if it is 1% or a 100% of women who take antidepressants that have children born with birth defects the suffering these babies have to go through is too much. What woman would want to be that 1%? No one would, but they are saying take the chance if you need too. GSK PLEASE stop funding these studies and misleading woman. Have you not done enough already. Except the fact that you did wrong instead of trying to belittle what my son and others have gone through with these studies that say the risk is so small. You are just trying to take some of the heat off. GSK it seems to me you have just made a big ass out of your self again. I for one am not fooled by your attempts to lessen what you have done. I only hope that other women listen to the whole story instead of just the headlines and realize that antidepressants do cause birth defects.
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Big Pharma has been abusing people for profits. This problem has been going on since the begining of Big pharma. We need to let "them" know that we are not going to tolerate this any longer. We need to let the government know that we demand something be done. Why is Big Pharma allowed to hurt people and get away with it. You have seen the pictures of Manie when he was born and you have heard me talk about the torture he has to deal with, if someone is responsible for his pain then why are they not punished? Do not think for a minute that something like this could not happen to you. Do something about it before it does. Write to your Senators let them know how you feel about what big pharma has done in the past. Encourage them to do something about this. It is clear that big pharma does not care about anyone. If they are willing to hurt babies their is nothing that is going to stop them. I say do some research on big pharma. Type big pharma into a search engine and see what comes up. Find out for yourself what has been going on that you do not know about. Be aware of what is going on take care of yourself because no one is looking out for you, but you.
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What does this mean for the future of our family minivacation tradition? It looks like Manie will be stuck riding the Infant Ocean for the rest of his life or sitting and watching as everyone else has fun on the rides. It might be that the family will just have to find a new family tradition. What happens when Manie becomes a teenager and wants to go with his friends? Will he ride the rides anyways and risk it all just to find out what it feels like to ride the Mixer or the Dragon.
========
T
his vacation has left me thinking what else is there that Manie can't do because of his heart problems? I want to be able to tell Manie that he can do anything he wants and to never let his heart problems stop him, but in this case I can't say that because there are just somethings he will not be aloud to do. I hate using the word can't when it comes to any of my children. I always want my children to know they can do anything if they want it bad enough. I guess GSK has taken that away from Manie too.
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I could not believe what I was reading this morning on seroxatsecrets blog. You have to be kidding me I thought. Apparently GSK has bought Reliant a pharmaceutical company that makes HEART MEDS! Is it me or does something smell a little fishy here. Go to
http://seroxatsecrets.wordpress.com/2007/11/21/oh-the-irony-of-it-glaxo-buys-reliant-pharma-for-165billion/ to read the post. Lets examine this situation. My son and others like him were born with HEART DEFECTS because of Paxil which came from GSK. Now these kids that are growing up with HEART CONDITIONS are going to need HEART MEDS probably for the rest of there life. Now GSK has bought a pharmaceutical company that makes HEART MEDS. Isn't there a law against profiting off of the tragedy that you have caused? Does anyone know? If you do please contact me and inform me. If there is not a law against this there should be. I am disgusted about this. I am disgusted because the same company that caused my son so much pain is now going to probably profit from what they have done.
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One Thing That Comes With the Territory
It amazes me how stupid some things just are. Like health insurance in America. Manie has government health insurance, called title 19. See here in America if you are poor enough for your child to get title 19 then you must stay poor to continue getting it. Manie's father and I are allowed $3,000.00 dollars in assets. How it works is we are allowed one car but if we have a second car they count it as an asset. We are allowed one house, which has to be the one we live in. The extra car, anything else of value, any income, and money in the bank can not ever exceed $3,000.00 or Manie will lose his health insurance. Manie is only allowed $2,000.00 in assets total. Now lets talk about health insurance. Manie can not go to the proper hospital because the health insurance in most cases will not cover out of state hospitals. When we have to take Manie to the hospital for heart checkup etc. we have to make sure we have an O.K. from our regular doctor first. Yeah like I am going to be just sitting around one day and think just for the hell of it I will go get my kid a cardiac cath. Manie's medication that he needs to keep him as healthy as he can be will not be covered by government insurance. Yet this same government insurance will cover a man to go on Viagra even if he has committed a sexual crime. Does this make any sense to anyone? What about private health insurance you might ask. Ha Manie had private health insurance through his fathers work when he was born. Can anyone say PREEXISTING CONDITION. Yep that's right just because he had the heart defect when he was born it is a preexisting condition and WA la they do not have to pay for anything. If it was not for government health insurance we would be screwed so I am grateful for what we have. I just don't understand why it works the way it does and why Manie can not get the proper care. If it seems like I am ungrateful for what we have I am not. I am very grateful, but I watch day after day as my son looks worse and worse and wonder if there is something wrong with him. See the hospital he goes to can not find anything wrong, besides the fact that he has a leak in his valve, which was caused by the open heart surgery. Last time I knew there was something wrong this same hospital told me Manie was fine and treated me like I was crazy. Months later they found the collateral's that had been growing off of Manie's heart. I had been right all along!(Not that I wanted to be, but a mother knows when there is something wrong) I think letting the collateral's go that long caused more problems then what they want me to know about. I just wanted to share a couple of issues that arise when having a child with a heart condition or any health problem. If there is anyone out there who thinks they are alone know that I am here and there are others out there who understand.
Labels:
Mothers act,
SSRI Antidepressants,
SSRI Suicide
Sunday, February 24, 2008
Death, Destruction, Lies, Deceit, Bribes, Corruption
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
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
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.]
Labels:
Anit-depressants,
depression,
Dr Ann Blake Tracy,
Mothers act
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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8. Guilleminault C, Raynal D, Takahashi S, et al. Evaluation of short-term and long-term
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Scand 1976;54:71-87.
9. Schenck CH, Mahowald MW, Kim SW, et al. Prominent eye movements during NREM
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10. Louden MB, Morehead MA, Schmidt HS. Activation by selegiline (Eldepryle) of REM
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12. Onofrj M, Luciano AL, Thomas A, et al. Mirtazapine induces REM sleep behavior disorder
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15. Rechtschaffen A, Kales A. A Manual of Standardized Terminology, Techniques, and
Scoring System for Sleep Stages of Human Subjects. Washington, DC: Public Health
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16. Lapierre O, Montplaisir J. Polysomnographic features of REM sleep behavior disorder:
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17. Schutte S, Doghramji K. REM behavior disorder seen with venlafaxine (Effexor). Sleep
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18. Nofzinger EA, Reynolds CF 3rd. REM sleep behavior disorder. JAMA 1994;27:820.
19. Bental E, Lavie P, Sharf B. Severe hypermotility during sleep in treatment of cataplexy
with clomipramine. Israel J Med Sci 1979;15:607-9.
20. Guilleminault C, Raynal D, Takahashi S, Carskadon M, Dement W. Evaluation of shortterm
and long-term treatment of the narcolepsy syndrome with clomipramine hydrochloride.
Acta Neurol Scand 1976;54:71-87.
21. Niiyama Y, Shimizu T, Abe M, Hishikawa Y. Cortical reactivity in REM sleep with tonic
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Electroencephalogr Clin Neurophysiol 1993;86:247-51.
22. Bologna, Genova, Parma and Pisa Universities group for the study of REM Sleep
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23. Gagnon J, Bedard MA, Fantini ML, et al. Comparison between submental and anterior
tibialis phasic EMG activity during REM sleep in Parkinson's disease with and without
REM sleep behavior disorder. Sleep 2003;26:A337.
24. Lai YY, Siegel JM. Medullary regions mediating atonia. J Neurosci 1988;8:4790-6.
25. Lai YY, Siegel JM. Muscle tone suppression and stepping produced by stimulation of
midbrain and rostral pontine reticular formation. J Neurosci 1990;10:2727-34.
26. Gilman S, Koeppe RA, Chervin RD, et al. REM sleep behavior disorder is related to striatal
monoaminergic deficit in MSA. Neurology 2003;61:29-34.
27. Eisensehr I, Linke R, Noachtar S, Schwarz J, Gildehaus Fj, Tatsch K. Reduced striatal
dopamine transporters in idiopathic rapid eye movement sleep behavior disorder.
Comparison with Parkinson's disease and controls. Brain 2000:123:1155-60.
28. Trulson ME, Jacobs BL, Morrison AR. Raphe unit activity during REM sleep in normal
cats and in pontine lesioned cats displaying REM sleep without atonia. Brain Res
1981;226:75-91.
29. Kubin L, Kimura H, Tojima H, Davies RO, Pack AI. Suppression of hypoglossal
motoneurons during the carbachol-induced atonia of REM sleep in not caused by fast
synaptic inhibition. Brain Res 1993;611:300-12.
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
study. J Neurosci 2001;21:7384-91.
31. Gagnon JF, Bedard MA, Fantini ML, et al. REM sleep behavior disorder and REM sleep
without atonia in Parkinson's disease. Neurology 2002;59:585-9.
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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