9/1/2003 • A Systematic Chart Review of the Nature of Psychiatric Adverse Events in

9/1/2003 • A Systematic Chart Review of the Nature of Psychiatric Adverse Events in Children and Adolescents Treated with Selective Serotonin Reuptake Inhibitors

Timothy E. Wilens MD ; Joseph Biederman MD ; Anne Kwon MS ; Rhea Chase BA ; Laura Greenberg BA ; Eric Mick ScD ; Thomas J. Spencer MD

Journal of Child and Adolescent Psychopharmacology Volume: 13 Number: 2 Page: 143 — 152

Conclusion: Based on the retrospective review of medical charts, youth receiving SSRI appear to be at risk for treatment emergent PAE and recurrence with re-exposure to an SSRI. Prospective longer term studies evaluating the course and prognosis of youths manifesting PAE to SSRI are necessary.

A Systematic Chart Review of the Nature of Psychiatric Adverse Events in Children and Adolescents Treated with Selective Serotonin Reuptake Inhibitors

Timothy E. Wilens MD ; Joseph Biederman MD ; Anne Kwon MS ; Rhea Chase BA ; Laura Greenberg BA ; Eric Mick ScD ; Thomas J. Spencer MD

Journal of Child and Adolescent Psychopharmacology Volume: 13 Number: 2 Page: 143 — 152

Conclusion: Based on the retrospective review of medical charts, youth receiving SSRI appear to be at risk for treatment emergent PAE and recurrence with re-exposure to an SSRI. Prospective longer term studies evaluating the course and prognosis of youths manifesting PAE to SSRI are necessary.

A report in the Journal of Child and Adolescent Psychopharmacology (abstract below) Dr. Timothy Wilens, Dr. Joseph Biederman, et al, child psychiatrists at Harvard’s teaching hospital, Massachusetts General, found that 22% of children and adolescents who had been prescribed any one of the selective serotonin reuptake inhibitor (SSRI) antidepressants suffered drug-induced psychiatric adverse effects within three months. Furthermore, the authors, who have long advocated prescribing psychotropic drugs for children, reported: “Overall, 74% if children and adolescents experienced [i.e., suffered] an adverse event to an SSRI over the course of their treatment.”

The SSRI drugs prescribed for these children were: Prozac, Paxil (Seroxat), Zoloft, Luvox and Celexa. Proof that the adverse effects were drug-induced is borne out by the fact that after the drugs were withdrawn and the children were re-exposed to an SSRI, 44% suffered another psychiatric adverse effect.

This report validates what critics—who are not receiving financial support from drug companies—have been pointing out for some time: Antidepression drugs are not the solution for troubled children. The documented evidence consistently shows that the drugs are causing children mental distress that can only aggravate their problems.

Of particular concern: According to the authors, the most frequent adverse effects induced by SSRI drugs are sleep disturbance (35%) and agitation. That combination is a prescription for violent outbursts—such as, self injury, suicide attempts, and / or violent outbursts toward others.

It is scandalous that the National Institute of Mental Health has remained absolutely silent about mounting evidence that these drugs pose hazards for children’s health and lives. NIMH officials disregard the evidence of suicidal acts by children in clinical trials. The same evidence led the medical authorities in Great Britain to ban the use of an SSRI in children under 18. See documents at: http://www.ahrp.org/index.html

Despite evidence of harm, NIMH continues to promote the use of SSRIs and sponsors clinical trials that expose little children and adolescents to the hazards of these drugs. See: http://www.nimh.nih.gov/ncdeu/abstracts2002/ncdeu2062.cfm http://www.nimh.nih.gov/ncdeu/abstracts2002/ncdeu2061.cfm http://www.nimh.nih.gov/ncdeu/abstracts2002/ncdeu3016.cfm

For additional documentation about the harm being done to children who are inappropriately and indiscriminately prescribed psychotropic drugs, visit the AHRP website at: www.ahrp.org

Abstract: Objective: Despite a rapidly growing literature on the efficacy of the selective serotonin reuptake inhibitors (SSRI) in the treatment of juvenile psychiatric disorders, relatively little is described about emotional, behavioral, and cognitive adverse effects associated with their use. To this end we completed a retrospective analysis of medical charts to determine the incidence, nature, and clinical correlates of treatment emergent adverse effects in the behavioral, cognitive, and emotional domains.

Methods: We systematically evaluated the medical charts of children treated with SSRI for depressive or obsessive-compulsive disorders for a mean (±SD) of 26.9 ± 20.8 months to determine the incidence, nature, and clinical correlates of treatment emergent psychiatric adverse events (PAE). Charts were reviewed for diagnoses, type and dose of SSRI and adjunct medication, specific type of PAE, and time to onset and offset of PAE.

Results: In total, 82 charts of children and adolescents (mean age 12.2 ± 3.2 years) were examined. PAE occurred in 22% of children and were most commonly related to disturbances in mood. PAE were not associated with psychiatric diagnosis(es), age, sex, concurrent medications, doses or specific serotonin reuptake inhibitors. The onset of PAE was observed typically 3 months after SSRI exposure (median = 91 days). Although PAE diminished with SSRI discontinuation, those that emerged early in treatment diminished significantly more rapidly than those that emerged later (median offset was 10 and 49 days, respectively). Re-exposure to an SSRI resulted in another PAE in 44% (n = 18) of the group.

Copyright © by Mary Ann Liebert, Inc. 2003 Reference Links: 17 (View Links)

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8/21/2003 • Research challenges role of antidepressants

8/21/2003 • Research challenges role of antidepressants

Professor Joe Collier, editor of DTB

Drug and Therapeutics Bulletin (DTB)

The DTB said that most patients with mild depression fell below the threshold of severity used in clinical trials for antidepressants.
Research challenges role of antidepressants

http://www.societyguardian.co.uk

Professor Joe Collier, editor of DTB

Drug and Therapeutics Bulletin (DTB)

The DTB said that most patients with mild depression fell below the threshold of severity used in clinical trials for antidepressants.

People with mild depression are being prescribed antidepressants despite a lack of proof that it is the best treatment for them, according to a report published today.

Antidepressant prescriptions issued by family doctors doubled between 1975 and 1998 to 23.4m per year, research by the Drug and Therapeutics Bulletin (DTB) found.

Yet few clinical trials have studied the effectiveness of the drugs with regards to GP patients, with the vast majority focusing on severely ill patients in hospital. The DTB investigation questioned whether prescribing antidepressants was the best way to treat mild depression when other therapies were available and preferred by patients.

Professor Joe Collier, editor of DTB, said: “Serious questions must be asked as to whether there is any real benefit from the routine early use of antidepressant drugs in patients with the sort of mild depression seen in UK general practice.”

Ike Icheanacho, deputy editor of DTB, published by the Consumers’ Association, said: “Most of the trials of antidepressants have been done in hospital settings rather than general practice.

“This calls into question whether people should be rushing to prescribe antidepressants in so-called mild cases of depression.”

The DTB said that most patients with mild depression fell below the threshold of severity used in clinical trials for antidepressants.

The study noted that surveys suggested many patients would prefer psychological therapies such as counselling instead of medication.

But Mr Icheanacho said there were complex reasons behind a GP’s decision to prescribe antidepressants.

He said there was increased awareness of depression among both doctors and patients, leading to greater use of antidepressants.

The pharmaceutical industry had also intensively promoted new antidepressants.

Mr. Icheanacho said: “There has also been increased pushing of antidepressants by the pharmaceutical industry.

“They are very heavily marketed as a good treatment for depression.”

“The level of prescribing might be appropriate but we haven’t got the evidence that to say conclusively.

“That makes us question if that is the right thing for patients to have immediately when there are sometimes alternatives available.”

But Mr. Icheanacho said that in many areas, services such as counselling were not available or had long waiting lists so GPs were unable to offer patients an alternative to medication.

The report said it was not necessarily wrong for GPs to prescribe antidepressants, but questioned whether they should be given as a routine treatment for mild depression.

It stated: “For many patients with depressive symptoms seen in general practice, a supportive ‘watchful waiting’ approach is reasonable.

“An immediate prescription for anti-depressant medication is not usually justified.”

The report added that GPs needed to look out for any major depressive illness that might need more urgent treatment and those with milder symptoms would need to be followed to ensure they did not deteriorate.

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11/11/2002 • Genes play a part, but violence may be viral

11/11/2002 • Genes play a part, but violence may be viral

By TOM SIEGFRIED
The Dallas Morning News
ORLANDO, Fla.

Harvard Medical School

This interesting article states: “Those genes are found in nerve cells (or neurons) that produce the brain chemicals dopamine and serotonin. When active, the genes tell the neurons to pump more of the chemicals into the fly’s nervous system. When the genes are turned off, dopamine and serotonin production falls off”.

“Some flies are genetically engineered with a “gene switch” that depends on temperature. Turn up the heat, and you turn off the genes. In this case, Harvard researcher Selby Chen and collaborators engineered flies who fight away when the temperature is a pleasant 77 degrees Fahrenheit. But when the scientists heat up the lab to a toasty 86, the flies equipped with a genetic switch in the dopamine and serotonin neurons throw in the towel. (Ordinary flies are happy to keep on fighting in the heat.) The apparent implication is that dopamine and serotonin genes play an important role in aggressive violence”.

Genes play a part, but violence may be viral

http://www.dallasnews.com/health/columnists/tsiegfried/stories/111102dnlivtomcol.13af7.html

By TOM SIEGFRIED
The Dallas Morning News
ORLANDO, Fla.

Harvard Medical School

This interesting article states: “Those genes are found in nerve cells (or neurons) that produce the brain chemicals dopamine and serotonin. When active, the genes tell the neurons to pump more of the chemicals into the fly’s nervous system. When the genes are turned off, dopamine and serotonin production falls off”.

“Some flies are genetically engineered with a “gene switch” that depends on temperature. Turn up the heat, and you turn off the genes. In this case, Harvard researcher Selby Chen and collaborators engineered flies who fight away when the temperature is a pleasant 77 degrees Fahrenheit. But when the scientists heat up the lab to a toasty 86, the flies equipped with a genetic switch in the dopamine and serotonin neurons throw in the towel. (Ordinary flies are happy to keep on fighting in the heat.) The apparent implication is that dopamine and serotonin genes play an important role in aggressive violence”.

It’s not exactly something you’d try to market for Pay-Per-View, but fruit flies sometimes stage some pretty fierce fights. Put two males in a laboratory ring and, under the right conditions, they’ll battle it out for the flyweight championship.

The scientists who serve as the fans at such fights aren’t interested in seeing flies bash their brains out, but rather are trying to understand something about brains in general.

It’s the brain, after all, that controls behavior, whether fighting or fleeing, speaking or thinking. Figuring out what goes on in a brain that tells it to fight might help reduce the risk of unnecessary violence in the world.

In the case of the flies, new research shows, violent aggression involves brain chemicals produced by specific genes. Turning off those genes induces the flies to stop throwing punches and return to their corners, Harvard Medical School scientists reported in Orlando, Fla., last week at the annual meeting of the Society for Neuroscience.

Those genes are found in nerve cells (or neurons) that produce the brain chemicals dopamine and serotonin. When active, the genes tell the neurons to pump more of the chemicals into the fly’s nervous system. When the genes are turned off, dopamine and serotonin production falls off.

Usually there’s not much you can do to manipulate genes quickly enough to stop a fight in mid-round. But fruit fly researchers have developed a neat trick for immediate gene control with a system that’s as simple as adjusting a thermostat. Some flies are genetically engineered with a “gene switch” that depends on temperature. Turn up the heat, and you turn off the genes.

In this case, Harvard researcher Selby Chen and collaborators engineered flies who fight away when the temperature is a pleasant 77 degrees Fahrenheit. But when the scientists heat up the lab to a toasty 86, the flies equipped with a genetic switch in the dopamine and serotonin neurons throw in the towel. (Ordinary flies are happy to keep on fighting in the heat.)

The apparent implication is that dopamine and serotonin genes play an important role in aggressive violence. But genes cannot be the whole story of violence in the animal kingdom.

Consider baboons, for instance. In the wild they are normally peaceful and live in harmony with their fellow primates. But after associating with humans for a while, baboons turn nasty. They attack each other rather viciously, in fact, sinking their fangs into the most sensitive of body regions. Females try to bite the tails off of other females.

“They just rip into each other,” says Timothy Smock of the University of Colorado at Boulder. “You wonder if they had guns, would they blow each other away. I’m quite convinced that they would.”

Dr. Smock and collaborator David Langoi, a veterinarian at the Institute for Primate Research in Nairobi, Kenya, have studied the brains of both peaceful and violent baboons. In the violent ones, a brain region called the superior temporal gyrus seems enlarged on the left side. In peaceful baboons that region seemed larger on the right side of the brain. For some reason, the violent baboons’ brains become modified in a way that promotes aggression.

Dr. Smock, who presented the findings at last week’s neuroscience meeting, does not know what causes the brain differences. But he has a suggestion that might be worth exploring. Maybe, he says, the aggression is the result of a virus. Perhaps there’s a virus for violence that somehow the baboons acquire from people.

“It’s total speculation,” Dr. Smock said in an interview. “But I’m hoping it’s a virus, because if we can find a virus that causes excessive violence, think about the implications for the type of insanity we’ve seen in the last 50 years. … The implications could be immense. ”

For one thing, a viral cause of violence would open a whole new avenue of understanding aggressive behavior. Much current research tries to draw conclusions about violence from studies of rats or mice. But such aggression, Dr. Smock points out, is typically not as senseless as the common human variety, but rather is directed toward specific goals involving territory or mates.

“We could possibly have a model for violence in people that’s different from simple aggression seen in rodents,” he said.

So far, though, there is no real evidence for the virus idea (although baboons do appear to acquire other diseases from humans, such as tuberculosis). And the preliminary findings are based on studies of only 10 baboon brains (five violent, five peaceful).

“We need to do a lot more work,” Dr. Smock acknowledged. For one thing, more intricate examination of the baboon brains is needed to determine whether some underlying defect is causing the enlarged regions seen on the surface.

Nevertheless, the idea of a violence virus is intriguing. Violent aggression may just turn out not to be only a societal sickness, but a medical one as well.

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11/5/2002 • Adolescent Drug Use Creates Long-Term Imbalance

11/5/2002 • Adolescent Drug Use Creates Long-Term Imbalance
Even commonly prescribed amphetamines may lead to addictive behavior.

By Ross Grant
Health ScoutNews Reporter

Thomas Jefferson University
Philadelphia

Here is more evidence that there is significant brain alteration within brain cells in response to synthetic chemicals that change brain function in many unknown ways. Could these abnormal proteins that form in response to foreign chemicals that cross the blood brain barrier, be part of the mysterious amyloid deposits that are markers for Alzheimers Disease? An educated guess, from some observers who have noted a relationship between Alzheimer’s and people who have taken a lot of brain-altering drugs during their lifetimes, says yes. Has anybody else noticed such a connection? Until we have a long term study on that very question, the drug companies have to be up front and say that they don’t know if their particular synthetic chemical can cause Alzheimers or not. In the meantime, we should avoid taking their drugs until they can prove that they don’t have such long term adverse effects.

Adolescent Drug Use Creates Long-Term Imbalance
Even commonly prescribed amphetamines may lead to addictive behavior.

http://www.healthscout.com/template.asp?ap=43&page=newsDetail&id=510032

By Ross Grant
Health ScoutNews Reporter

Thomas Jefferson University
Philadelphia

Here is more evidence that there is significant brain alteration within brain cells in response to synthetic chemicals that change brain function in many unknown ways. Could these abnormal proteins that form in response to foreign chemicals that cross the blood brain barrier, be part of the mysterious amyloid deposits that are markers for Alzheimers Disease? An educated guess, from some observers who have noted a relationship between Alzheimer’s and people who have taken a lot of brain-altering drugs during their lifetimes, says yes. Has anybody else noticed such a connection? Until we have a long term study on that very question, the drug companies have to be up front and say that they don’t know if their particular synthetic chemical can cause Alzheimers or not. In the meantime, we should avoid taking their drugs until they can prove that they don’t have such long term adverse effects.

Drug use during adolescence, including such commonly prescribed drugs as Ritalin, may upset brain chemistry more than any other time in a person’s life, new research says.

The findings should help scientists better understand why addictions generally begin during adolescence, and what the long-term risks result.

“This is a major public health question,” says the lead researcher, Dr. Michelle Ehrlich, a neurology professor at Thomas Jefferson University in Philadelphia. “The adolescent brain appears to be more sensitive to certain effects of these psycho-stimulant drugs. We need to see whether this sensitivity leads to permanent brain changes and behavior changes.”

In the study, which just appeared in the Journal of Neuroscience, the researcher gave cocaine and amphetamine to groups of adult, adolescent and baby mice every day for a week. Then they compared the chemistry in two sections of the mice brains against that of a control group. Because mice have many of the same brain functions as humans, scientists believe the results should shed light on our brains, Ehrlich says. After taking the drugs, all the mice had elevated levels of an addiction-marking protein in the part of the brain that controls movement and hyperactivity. But adolescent mice also had high levels of the protein in the part of the brain that controls the “reward” mechanism.

Because of that chemical imbalance, adolescents may depend on drugs to stimulate their reward mechanism, leading to addictive behavior, Ehrlich says. Meanwhile, other studies have shown that the protein, called DeltaFosB, stimulates other chemical responses in the brain months after drug use has stopped, which may contribute to drug cravings.

“The implications are that there is an increased adaptation in the younger brain than in the older brain to these psycho-stimulants,” Ehrlich says. But Ehrlich isn’t worried only about the effects of illegal drugs. The same long-term changes in brain chemistry may also occur after adolescents take prescribed amphetamine.

“Amphetamine is one of the most commonly used drugs for attention deficit disorder. Ritalin is one of the most well-known ones,” Ehrlich says. “I prescribe these drugs. I work with children on these drugs. I’m not saying we shouldn’t use them, but we should know about their long-term effects.”

In some cases, the risks of prescribing amphetamine drugs are worthwhile, says Dr. Eric Nestler, chairman of the psychiatry department at the University of Texas Southwestern Medical Center. But Nestler, who was one of the first researchers to discover Delta FosB, says such drugs are prescribed too often, when the risks aren’t worthwhile.

“There has to be a concern,” he says. “Kids with attention deficit disorder are really impaired. A drug like Ritalin works well with those conditions, and to deny it to a kid who really need it is a disservice. The problem comes when the diagnosis of attention deficit disorder is made too frequently.”

So far, though, no one has studied whether Ritalin and other prescribed drugs raise the level of Delta FosB like cocaine and amphetamine, Nestler says. “That would be an interesting study,” he says.

Nestler says he is surprised that Erlich’s team didn’t see higher Delta FosB levels in both parts of the adult mouse brain. In his research, he found that both adolescent and adult mice have elevated levels, although he thinks he used a more sensitive method of detecting Delta FosB.

Still, if Ehrlich’s research shows that adolescents have a higher level of Delta FosB than do adults, it reveals key evidence about the addiction process, he says.

“This is the first finding to suggest that the adolescent brain is more sensitive. That is very interesting,” Nestler says. What To Do

To learn more about these drugs, visit this site at the California State University at San Marcos. Or for more information about how amphetamine is prescribed to treat attention deficit/hyperactivity disorder, try the National Center for Birth Defects and Developmental Disabilities. Copyright © 2002 ScoutNews, LLC. All rights reserved. Last updated 11/5/2002

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10/31/2002 • Ethyl-Eicosapentaenoate Could Be Effective In Persistent Depression

10/31/2002 • Ethyl-Eicosapentaenoate Could Be Effective In Persistent Depression

By Elda Hauschildt

Archives of General Psychiatry, 2002; 59: 913-919

Ethyl-eicosapentaenoate at a dose of 1 gram per day could be effective in treating depression in patients with persistent illness after standard antidepressant therapy.
Ethyl-Eicosapentaenoate Could Be Effective In Persistent Depression

http://www.docguide.com/news/content.nsf/news/8525697700573E1885256C5B005A901A

By Elda Hauschildt

Archives of General Psychiatry, 2002; 59: 913-919

Ethyl-eicosapentaenoate at a dose of 1 gram per day could be effective in treating depression in patients with persistent illness after standard antidepressant therapy.

“Ethyl-eicosapentaenoate offers an approach to depression that is radically different from that of existing drugs,” say British researchers who conducted a double-blind trial of the drug. They suggest the drug’s position in the treatment spectrum needs to be established by further trials.

The investigators, from Swallownest Court Hospital in Sheffield, England and Laxdale Research in Stirling, Scotland, randomised 70 patients with persistent depression despite ongoing therapy with an adequate dose of standard antidepressant.

Patients received either placebo or ethyl-eicosapentaenoate at one of three dosages: 1 g/d, 2 g/d or 4 g/d. Therapy lasted 12 weeks and was in addition to background medication, which remained unchanged.

Of 52 patients in ethyl-eicosapentaenoate group, 46 (88 percent) completed therapy, as did 14 of 18 patients (78 percent) receiving placebo. No adverse events were observed.

Participants in the 1-g/d ethyl-eicosapentaenoate group showed significantly better outcomes than placebo participants on three assessment scales: the 17-item Hamilton Depression Rating Scale, the Montgomery-Asberg Depression Rating Scale and the Beck Depression Inventory.

In the intention-to-treat group, nine of 17 patients (53 percent) in the 1-g/d ethyl-eicosapentaenoate group achieved a 50 percent reduction in the Hamilton Depression Rating Scale score. This compared with five of 17 patients (29 percent) in the placebo group.

The researchers observed improvements on all individual items in the three assessment scales with the 1-g/d ethyl-eicosapentaenoate dosage compared with placebo. They say there were beneficial effects on items rating depression, anxiety, sleep, lassitude, libido and suicidality.

There was little evidence of efficacy in 2-g/d ethyl-eicosapentaenoate participants, and 4-g/d ethyl-eicosapentaenoate participants displayed non-significant trends toward improvement.

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5/1/2002 • Timing of New Black Box Warnings and Withdrawals for Prescription Medications

5/1/2002 • Timing of New Black Box Warnings and Withdrawals for Prescription Medications

Karen E. Lasser, MD, MPH; Paul D. Allen, MD, MPH; Steffie J. Woolhandler, MD, MPH; David U. Himmelstein, MD; Sidney M. Wolfe, MD; David H. Bor, MD

Journal of the American Medical Association
JAMA. 2002;287:2215-2220

Serious ADRs commonly emerge after Food and Drug Administration approval. The safety of new agents cannot be known with certainty until a drug has been on the market for many years.

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4/10/2002 • Effect of Hypericum perforatum (St John's Wort) in Major Depressive Disorder

4/10/2002 • Effect of Hypericum perforatum (St John’s Wort) in Major Depressive Disorder

David J. Kupfer, MD, Department of Psychiatry, University of Pittsburgh Medical School, Western Psychiatric Institute and Clinic, 3811 O’Hara St, Pittsburgh, PA 15213 (e-mail: kupferdj@msx.upmc.edu).

JAMA Vol. 287 No. 14

This study fails to support the efficacy of H perforatum in moderately severe major depression. The result may be due to low assay sensitivity of the trial, but the complete absence of trends suggestive of efficacy for H perforatum is noteworthy.

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4/9/2002 • Sugar pills offer more relief than St. John’s wort, Zoloft

4/9/2002 • Sugar pills offer more relief than St. John’s wort, Zoloft

Robert Bazell

NBC News

Even in severely depressed patients, the antidepressant drug, Zoloft, was no better than placebo.

Sugar pills offer more relief than St. John’s wort, Zoloft

http://www.msnbc.com/news/736379.asp?0si=

Robert Bazell

NBC News

Even in severely depressed patients, the antidepressant drug, Zoloft, was no better than placebo.

Although promoted as an alternative therapy for depression, the herbal supplement St. John’s wort appears ineffective for people with moderate clinical depression, findings from a US study suggest. In the study of 340 patients diagnosed with moderate depression, St. John’s wort proved no more effective than inactive treatment with a placebo in alleviating symptoms. Active treatment with the antidepressant drug sertraline (Zoloft) worked somewhat better than placebo, according to findings published in the April 10th issue of The Journal of the American Medical Association (news – web sites).

A body of evidence suggests that St. John’s wort (Hypericum perforatum), used for more than 2,000 years to quell mood problems, does help symptoms of depression. In Germany, where many of the positive studies have been conducted, St. John’s wort is available as a prescription antidepressant.

But the quality of much of this research has been criticized—including the lack of studies using a placebo and a selective serotonin reuptake inhibitor (SSRI) like sertraline, according to the authors of the new study. SSRIs are a newer class of drugs commonly used to treat depression.

To address these concerns about earlier studies, researchers led by Dr. Jonathan R. T. Davidson of Duke University in Durham, North Carolina, randomly assigned patients to take St. John’s wort, sertraline or placebo for up to 26 weeks.

At the study’s end, the researchers found that neither the herb nor the drug was better than placebo in improving patients’ scores on a standard scale of depressive symptoms. Overall, nearly one third of placebo patients showed a full response to treatment, compared with roughly 24% in both the St. John’s wort and sertraline groups.

Patients on sertraline did, however, do better than placebo patients on a secondary test used to gauge a person’s daily functioning and levels of distress. The sertraline group also had a higher percentage of so-called “partial responders” to treatment than either the placebo or St. John’s wort groups.

Still, the findings do not indicate whether the herb can help people with mild depressive symptoms—a question additional research will have to address, Davidson told Reuters Health. St. John’s wort is marketed for the treatment of mild to moderate depression, but Davidson noted that it’s likely people with a range of depressive disorders try the herb.

“If someone is suffering from depression for weeks, they’re much better off going to a healthcare professional…than trying to self-treat,” he said.

And because St. John’s wort can interact with a range of drugs, including some used to treat cancer and HIV (news – web sites), people who do use the herb “should always tell their doctor they’re using it,” Davidson added.

As for the findings on sertraline, the researcher said that dosing “had a lot to do with” the lack of full response among patients on the drug. The study design permitted sertraline to be given only up to half of its highest recommended dose, and fewer patients on the drug had their doses “maximized,” compared with those on St. John’s wort or placebo.

Dosing “almost certainly contributed” to sertraline’s less-than-stellar performance in the study, according to an accompanying editorial by Drs. David J. Kupfer and Ellen Frank of the University of Pittsburgh Medical School in Pennsylvania.

They also stress that this study—along with a second one in the same journal issue documenting the rise of the “placebo effect” in recent research on depression drugs—highlight the importance of using a placebo and an active comparison drug in studies of unproven antidepressant agents.

The New York-based drug company Pfizer Inc. provided the sertraline for the study, and Lichtwer Pharma of Berlin, Germany, supplied the St. John’s wort product. Davidson holds stock in Pfizer, and has received speaker fees from both Pfizer and Lichtwer. Co-authors on the study have received funding from a number of pharmaceutical companies.

The study itself was funded by the US National Institutes of Health.

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3/26/2002 • Scientists find Prozac ‘link’ to brain tumours

3/26/2002 • Scientists find Prozac ‘link’ to brain tumours

Steve Connor
Science Editor

Independent

Scientists have discovered that Prozac, the antidepressant taken by millions of people around the world, may stimulate the growth of brain tumours by blocking the body’s natural ability to kill cancer cells.

Scientists find Prozac ‘link’ to brain tumours

http://news.independent.co.uk/world/science_medical/story.jsp?story=278505

Steve Connor
Science Editor

Independent

Scientists have discovered that Prozac, the antidepressant taken by millions of people around the world, may stimulate the growth of brain tumours by blocking the body’s natural ability to kill cancer cells.

An international team of researchers led by John Gordon, professor of immunology at Birmingham University, found evidence to suggest cancer cells can be killed by “positive thinking”, which could be blocked when people take Prozac.

The study, to be published in the journal Blood next week, examined the effects of Prozac and other antidepressants on a group of tumour cells growing in a test tube. The researchers found that the drug prevented the cancer cells from committing “suicide”, thereby leading to a more vigorous growth of the tumours.

Although an increased risk of cancer has not so far been detected in Prozac patients, the latest findings could lead to a global re-evaluation of the drug’s long-term safety.

Prozac, a “happiness pill” that was first approved in the United States in 1987, is widely used for the treatment of depression, obsessive-compulsive disorder and bulimia nervosa. Doctors in Britain issue about three million prescriptions for it each year and worldwide sales reached £1.8bn in 1999.

Professor Gordon, whose study was jointly funded by Birmingham University and the Medical Research Council, emphasised that the results of his study cannot be taken as proof that Prozac stimulates the growth of tumours.

He said: “Although that extrapolation could be valid, there is no direct evidence from large-scale epidemiological studies currently to back it up. However, it’s important that we look again and again.”

The research work was designed to find new ways of treating lymphomas, a type of blood cancer, by investigating how the brain communicates with the immune system to induce “positive thinking” through a neuro-transmitter in the brain called serotonin.

“Serotonin is a natural chemical that regulates people’s moods, keeping them balanced. Too much serotonin affects appetite and sleep and too little affects the mood – often causing depression,” Professor Gordon said.

Prozac, along with other members of the class of antidepressants known as selective serotonin re-uptake inhibitors (SSRIs), works by preventing serotonin from being quickly reabsorbed by nerve cells in the brain.

The scientists tested other SSRIs such as Paxil and Celexa and found they, too, had the same effect in stimulating the growth of a type of tumour known as Burkitt’s lymphoma.

“An exciting property of serotonin is that it can tell some cells to self-destruct. We have found that serotonin can get inside the lymphoma cells and instruct them to commit suicide, thereby providing the potential for an effective therapy,” Professor Gordon said.

The researchers found that Prozac blocked the entry of serotonin into the test-tube tumour cells and therefore stopped them from committing suicide. That raised the question of whether Prozac can do the same in the brains of people taking the drug.

Professor Gordon said it was still premature to suggest that the drug was unsafe. “We must stress the effects shown for the SSRI on cancer cells is indirect and should cause no concern whatsoever to the many millions of people throughout the world who are prescribed this class of antidepressants,” he said.

Further work is underway to test Prozac further in this field. In particular, the scientists want to develop drugs that will mimic the cancer-destroying feature of serotonin which is blocked by Prozac.

A spokeswoman for Eli Lilly, the manufacturer of Prozac, said that the research is too new for the company to make a detailed response. “It’s not something we can directly comment on because we haven’t been involved in it,” she said.

NOTE FROM Ann Blake-Tracy

Over the past decade we have learned that there is a link to antidepressants and cancer. As I discussed the research of Dr. Loren Brandes out of Canada in my book Prozac: Panacea or Pandora? which demonstrated that antidepressants do trigger cancerous growth, the damage control patrol from the drug companies rushed into full swing discrediting Dr. Brandes’ work in any way they could.

Then a couple of years ago we got new research on the huge increase in breast cancer associated with these drugs. [You can find that article by searching our ICFDA archives.]

Now we learn about the possible increased chances of brain tumors being associated with the drugs. Are we supposed to be surprised?

Of course they tell us it all has to be researched and researched and re-researched before we REALLY know if this is true. Well, if they had researched the SSRIs that much to begin with none of this research would have been necessary! Why? Because we would know that these drugs are much too dangerous both physically and psychologically to even be on the market.

And keep in mind that it generally takes many years for tobacco to cause cancer, but the courts still found that it does cause cancer and the tobacco companies were held liable for it.

Note the standard line of misinformation about serotonin. Amazing how they can remain in denial for so long with 50 years of research staring them in the face which demonstrates that serotonin is a neurotoxin and has long been known to produce most of the common adverse effects we see listed for these drugs.

The research also indicates that, “An exciting property of serotonin is that it can tell some cells to self-destruct.”

REALLY?!! Did someone NOT notice that yet about serotonin?

I noticed long ago that serotonin does a GREAT job of telling ALL the cells to self-destruct! The message comes through so clearly that obviously this is why we see so many suicides and murder/suicides with these drugs.

This information on the serotonin message to self destruct may be even more important than the brain tumor link!

[An interesting side note: The spell check on my computer picks up the word “neurotoxin” and tells me to correct it by replacing it with the word “serotonin.” So you see, even my computer has seen enough evidence to know the truth about the effects of serotonin on the brain! 🙂 ]

Ann Blake-Tracy, Executive Director, International Coalition For Drug Awareness

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3/15/2002 • Rare Neurologic Syndrome Linked to Antidepressant

3/15/2002 • Rare Neurologic Syndrome Linked to Antidepressant

Jim Rosack

Psychiatric News March 15, 2002 Volume 37 Number 6, p. 31

Neurologists warn other clinicians that SSRIs could contribute to a potential increase in certain patients‚ risk of having a rare form of stroke.
Rare Neurologic Syndrome Linked to Antidepressant

http://www.neurology.org/cgi/content/abstract/58/1/130

Jim Rosack

Psychiatric News March 15, 2002 Volume 37 Number 6, p. 31

Neurologists warn other clinicians that SSRIs could contribute to a potential increase in certain patients‚ risk of having a rare form of stroke.

A new report from a group of neurologists warns that combinations of medications that modulate brain levels of serotonin, including SSRIs and other antidepressants, could lead to a relatively rare form of stroke due to marked vasoconstriction.

The report, which appeared in the January issue of Neurology, includes case studies of three patients who developed Call-Fleming syndrome, which is characterized by sudden-onset severe headache, focal neurological deficits, and seizures. Although rare, the syndrome is most commonly seen in women.

The first patient studied, a 46-year-old woman, developed a “worst ever” headache, nausea, and blurred vision, which were followed a few days later by escalating neurological symptoms. The woman‚s medications included sertraline and trazadone, and for two days prior to developing symptoms, she had taken an over-the-counter cold remedy that contained dextromethorphan. Diagnostic testing confirmed severe, diffuse, intracranial vasoconstriction, including a 70 percent constriction of the origin of the vertebral artery.

In addition, several areas of ischemic stroke were identified. Within a week of discontinuing both the sertraline and the cold remedy, the women was discharged in markedly improved condition.

The second case described a 45-year-old woman who developed a sudden, “explosive” headache, again with accompanying nausea. Four weeks earlier, she had been started on paroxetine 40 mg and clonazepam 0.25 mg for a recurrence of major depression. Shortly before the onset of the headache, she had taken a cold remedy with dextromethorphan and pseudoephedrine. Again, severe, bilateral vasoconstriction was demonstrated on cerebral angiography, and MRI demonstrated multiple areas of ischemic stroke. The patient‚s paroxetine was discontinued, and her symptoms subsided. Interestingly, four months later, this patient again had a worsening of her depression and was prescribed mirtazapine. Within two weeks she again developed headaches, which resolved when the mirtazapine was stopped.

The third patient was a 34-year-old male who developed an “explosive” headache with sensitivity to light, nausea, and extreme fatigue. His family history included migraine syndrome, and as a result, he was treated with sumatriptan, a common migraine medication known to be a serotonin receptor agonist that causes significant cerebral vasoconstriction. Following a second dose of that drug later the same day, the patient had a generalized seizure, and an MRI five days later showed multiple bilateral ischemic areas.

Although the patient denied any use of illicit drugs, recent cocaine use was suspected.

Aneesh Singhal, M.D., the primary author of the report, has seen about a dozen similar cases in his practice. Although he believes that Call-Fleming syndrome is rare, he told Psychiatric News that it includes a number of conditions that are often labeled in different ways, and thus the syndrome may be underrecognized.

“This is a preliminary observation; it needs confirmation,” he stressed. “It ‚s important to note that it is not the individual drugs, that by themselves might enhance the risk [of stroke from vasoconstriction], but rather the combination of drugs,” he told Psychiatric News.

“It is conceivable that someone who has a migraine syndrome, is trying to lose weight, and is depressed, which is not an uncommon situation, may take three or four agents, and thus have increased risk of vasoconstriction and end up with stroke.”

Singhal said that differential diagnosis needs to include the possibility of serotonin-induced vasoconstriction in any patient who has a sudden onset of severe headaches that are not explained by any of the accepted causes, most commonly a subarachnoid hemorrhage. “If the known causes are ruled out, you have to remember that there is one more cause, and that is vasoconstriction.”

Singhal said patients who are taking serotonin-modulating medications should be routinely asked about the presence of moderate to severe, persistent or recurrent headaches. He stressed that although headache is a common side effect of many of these medications, when the headache is recurrent or sustained and moderate or severe, medications should be at least temporarily suspended, and the cause of the headache investigated.

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