Effexor Activists Tribe's topics - tribe.net

viagra as treatment for antidepressant side effects and surprisingly enough not just the sexual problems

2009-11-11T07:43:47Z

Viagra to treat antidepressant damage besides sexual disfuction- used for pph –one of the stated problems for babies whos mothers took antidepressants while pregnant….

When I was still taking effexor I was sick the last couple years on it at one point was told I had chronic obstructive lung disease is what t I didn't think that was my problem but maybe. ....now I am thinking there are others with lung problems same as me makes sense it is fromt eh drugs as so much else was I am speculating here.. I felt I was drowning especially when they made me lay down at hosp I had to get up immediately felt I was drowning and told them so. Some day they may prove me right we will see.

http://www.ems1.com/medical-clinical/articles/601939-Sildenafil-Drug-Whys/

Sildenafil: Drug Whys
By Mike McEvoy
Generic Name: Sildenafil (no generic available – U.S. patent expires in 2012)
Common Brand Name: Viagra (Pfizer – U.S.)
Popularity: 37th most commonly prescribed drug between 2002 and 2008 (U.S.)
Class: Erectile dysfunction agent, phosphodiesterase inhibitor – type 5 specific.
Treatment Uses — Primary erectile dysfunction, or erectile dysfunction secondary to atherosclerosis, depression, diabetes, dialysis, drug effects, Parkinson's disease, prostatectomy, radiation therapy, or spinal cord injury. Treatment and prevention of rebound pulmonary hypertension following nitric oxide withdrawal. Treatment of Primary Pulmonary Hypertension (PPH) in adults and children (superior to inhaled nitric oxide). Treatment of sexual dysfunction (usually delayed ejaculation) associated with antidepressant drug therapy (requires high dose sildenafil). Used for treatment and prevention of high altitude pulmonary hypertension and high altitude pulmonary edema (HAPE) in mountain climbers. Improves microcirculation in Raynaud's phenomenon resistant to vasodilator therapy. Studied with conflicting results in treatment of female sexual arousal disorder as well as (male) premature ejaculation. May be useful for improving in vitro fertilization (IVF) results in certain women by improving uterine artery blood flow.
Dosing and Administration — Orally, 50 milligrams taken as needed, about 1 hour before sexual activity. Normally effective when taken anywhere from 30 minutes to 4 hours before sexual activity. Dose may be increased to a maximum of 100 milligrams or decreased to 25 milligrams based on effectiveness and tolerance. Use of sildenafil is not recommended more than once per day. Tachyphylaxis, a phenomenon where increasingly higher doses of a drug are needed to obtain similar effects, has been known to occur with sildenafil. For sildenafil, loss of effectiveness seems to occur at an average of 11 months, regardless of frequency of use, and typically requires doubling the dose to regain effect. A note for those unfamiliar with tachyphylaxis: patient susceptibility to drug side effects and toxicity remains unaffected despite requirements for progressively higher doses.
For treatment of pulmonary hypertension in adults (to improve exercise capacity), the recommended dose is 20 milligrams three times daily with spacing of at least 4 to 6 hours between doses. Doses above 20 milligrams have not been shown to offer any greater effectiveness.
A starting dose of 25 milligrams should be used in geriatric (over 65-year-old) patients and patients with kidney failure or impaired liver function. Poor clearance of sildenafil is observed in these populations, necessitating lowered dosing. Caution should be exercised in patients with impaired renal function (as opposed to renal failure) although dose adjustments are not typically needed. Sildenafil is well tolerated in patients following renal transplant and does not appear to affect transplanted kidney function or interact with immunosuppressive drugs.
Pediatric doses used for treatment of PPH follow several different formulas, but tend to approximate 0.3 mg per kilogram per dose given at 4 to 8 hour intervals and titrated to effect.
Healthy volunteers given up to 800 milligrams of sildenafil had side effects similar to those seen with recommended doses, but these side effects happened more frequently and were more significant. In overdoses, hemodialysis is unlikely to accelerate clearance of sildenafil because the drug is highly bound to plasma proteins and not eliminated in the urine.
Pharmacology/Pharmacokinetics/Stability — Following oral administration, sildenafil is rapidly absorbed, reaching peak bloodstream concentrations between 30 and 120 minutes on an empty stomach, and between 90 and 180 minutes with or immediately after meals. While food slows absorption, it does not significantly reduce the total amount of drug absorbed. The average half-life (time needed for half the active drug to be eliminated from the body) of sildenafil is 4 hours. This coincides with the effects of the drug in allowing for adequate erections up to 4 hours after ingestion. Keep in mind that sildenafil does not produce erections; it only improves ability to initiate and sustain adequate erections with sexual stimulation.
The liver processes sildenafil producing byproducts from this metabolism that actually account for some of the drug's effects. Most of the drug (80 percent) is eliminated in feces. The kidneys excrete 13 percent of the drug and small amounts are eliminated in semen. It is unknown whether sildenafil is excreted in breast milk.
Erections require release of nitric oxide (NO) into the penis during sexual stimulation. NO produces a series of reactions leading to penile smooth muscle relaxation that allows inflow of blood. Sildenafil works to enhance the effect of NO by inhibiting phosphodiesterase type 5 (PDE5) which degrades the reaction necessary for smooth muscle relaxation.
Sildenafil tablets are blue, film-coated, rounded diamond shaped and come in 25, 50, and 100 milligram strengths. They should be stored at room temperature (77 F) but remain stable when briefly kept at extremes between 59-86 F. For children, a compounding pharmacy can prepare an oral suspension of 2.5 milligrams per milliliter which is stable for 91 days in an amber plastic bottle either refrigerated or at room temperature.
Cautions and Warnings — Sildenafil and nitrates are a dangerous mixture and not recommended within 24 hours of each other. The large and sudden drops in blood pressure resulting from this combination prompted the Food and Drug Administration (FDA) to warn emergency physicians they should inquire about sildenafil use before administering nitrates.
While the literature is rife with warnings about deaths resulting from sildenafil nitrate combinations, a careful literature search failed to produce any case reports of deaths directly related to the mixture. Multiple studies have been conducted in an attempt to determine how soon nitrates can be given following sildenafil. It appears that men with stable angina can safely take nitrates 8 hours after using sildenafil and healthy men can safely take nitrates 4 hours after sildenafil.
Oddly, few EMT textbooks mention this contraindication when instructing on assisted medications. Before giving a patient nitroglycerine or isosorbide, (or other PDE5 inhibitor) use within the previous 24inquire about Viagra hours. "Poppers" or nitrates inhaled for recreational use have similar hypotensive effects when combined with sildenafil. Don't rule out the possibility that your female patients might also be using sildenafil.
Following the hype about precipitous drops in blood pressure, several recent, well-designed studies found no adverse cardiovascular or hemodynamic effects from sildenafil on either healthy or unhealthy patients. On average, a single dose of 25, 50, or 100 milligrams of sildenafil given to healthy volunteers produced a maximal reduction in sitting systolic and diastolic blood pressure by 8.3/5.3 mmHg at 1 to 2 hours after dosing.

Cervical level spinal cord injury (SCI) patients can develop significant hypotension with sildenafil. Multiple studies evaluating the risk of myocardial infarction (MI) with sildenafil found no greater risk of MI with sildenafil than with sexual intercourse (without use of sildenafil). Timing of MI and strokes has also not correlated with use of sildenafil.
Important Side Effects and Interactions — Facial flushing (10 percent) and headache (16 percent) are the most commonly reported side effects of sildenafil. Other side effects include dizziness (2 percent), diarrhea (4 percent), indigestion (5 percent), and skin rash (2 percent). Nasal congestion and visual disturbances (blue haze with increased brightness) are frequently mentioned.
Nasal congestion is a result of vasodilator drug action. All of the aforementioned side effects are typically mild-to-moderate, and of short duration. Sudden loss of vision (some permanent) resulting from non-arteritic ischemic optic neuropathy (NAION) has occurred in a small number of patients taking sildenafil and other PDE5 inhibitors.
It is not known whether the drug caused vision loss or contributed to it in patients with underlying risk factors. NAION results from blood flow blockage to the optic nerve and usually occurs in patients with vascular risk factors. Rare cases of priapism (painful, persistent erections exceeding 6 hours duration) have been reported. Most have occurred in patients already predisposed to priapism including those with sickle cell anemia, multiple myelomas, or leukemia. Any erection lasting longer than 4 hours requires immediate medical attention to avert tissue damage and permanent impotence.
There are 38 drugs reported to interact with sildenafil, most importantly the previously mentioned nitrate family. Patients taking alpha-blocker agents often prescribed for treatment of Benign Prostatic Hyperplasia (BPH) may develop hypotension from more than 25 mg of sildenafil within 4 hours of taking the alpha-blocker. Certain antiretroviral agents considerably prolong the half-life of sildenafil, necessitating not only lower dosing, but longer intervals between doses as well. Grapefruit juice does funny things to the absorption and blood concentrations of sildenafil and although not dangerous, makes response rather unpredictable. The combination should be avoided.
Average Costs — U.S.
• 50 mg tablet (brand name Viagra)
Patient cost: $18.82 each
Large Hospital cost: $14.20 each
References:
1. MICROMEDEX® Healthcare Series: Thomson Micromedex, Greenwood Village, Colorado (accessed October, 2009).
2. Albany Medical Center Pharmacy, Albany, New York.

________________________________________
Mike McEvoy, PhD, REMT-P, RN, CCRN, is the EMS coordinator for Saratoga County and the EMS director on the Board of the New York State Association of Fire Chiefs. Formerly a forensic psychologist, he is a clinical specialist in cardiac surgery and teaches critical care medicine at Albany Medical College, where he also co-chairs the Resuscitation Committee and serves on the Formulary Committee. Mike is a paramedic for Clifton Park-Halfmoon Ambulance, chief medical officer for West Crescent Fire Department, and past chair and current member of the New York State EMS Council.

Mike is the Fire-EMS technical editor for Fire Engineering magazine and has authored numerous publications including the book, "Straight Talk About Stress for Emergency Responders." He is also a popular speaker at fire, EMS and medical conferences and is an avid hiker and winter mountain climber in his free time. Contact Mike at mike.mcevoy@ems1.com.

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Posted by marjorum on Tuesday, November 10, 2009 06:25 PM Pacific Report Abuse

You left out some things.

For treatment of PPH, sildenafil citrate 20mg is marketed under the trade name
Revatio. It is a small, round, white tablet with Pfizer embossed on one side and RVT 20 on the other (the lettering is so small a magnifying glass is required to read it). All the side effects, interactions, cautions and warnings apply to this dose of sildenafil, the same as Viagra.

Page 1

posted in Effexor Activists Tribe - 0 replies

Venlafaxine also causes more frequent features of the serotonin syndrome.

2009-10-27T07:27:31Z

Summary
Clinical Toxicology
2004, Vol. 42, No. 1, Pages 67-71

Comparative Toxicity of Citalopram and the Newer Antidepressants After Overdose
C. A. Kelly‌, N. Dhaun‌, W. J. Laing‌, F. E. Strachan‌, A. M. Good‌ and D. N. Bateman‌
Scottish Poisons Information Bureau, Royal Infirmary, Little France Crescent, Edinburgh, Scotland, UK

Objective: To compare the toxicity of citalopram, venlafaxine, mirtazapine, and nefazadone after overdose. Methods: Two‐year retrospective review of consecutive patients admitted to the toxicology unit of Edinburgh Royal Infirmary. Outcome measure included physiological variables, ECG recordings, peak creatine kinase, development of arrhythmias, seizure, tremor or agitation, and the need for admission to a critical care facility. Results: A total of 225 patients were studied. Venlafaxine was associated with a significantly higher pulse rate (p < 0.0001) and tremor (p = 0.007) than other antidepressants. Citalopram was associated with a significantly longer QT interval on ECG recording (p < 0.0001) but mean QTc durations were not significantly different between all drugs studied. No arrhythmias were recorded. Only venlafaxine and citalopram caused seizures and were associated with the need for admission to Intensive Care, but there was no significant difference between them. Conclusions: Mirtazapine and nefazadone appear safe in overdose and were associated with minimal features of neurological or cardiovascular toxicity. Citalopram is more likely to cause QT prolongation but other features of cardiovascular toxicity were uncommon. Both citalopram and venlafaxine are proconvulsants. Venlafaxine also causes more frequent features of the serotonin syndrome.

http://www.informahealthcare.com/doi/abs/10.1081/CLT-120028747

posted in Effexor Activists Tribe - 1 reply

Reduced to blubbering

2009-10-27T07:24:10Z

I was taking Effexor 150mg for almost 2 years. Then all of a sudden it just stopped working for me. So, my doctor and I developed a plan to get me off of this so we can figure out what to do next. The plan was to reduce the dose to 75mg for a couple of weeks then 37.5mg for a couple of weeks. Damn, so as I did the first reduction the withdrawl symptoms started. I've always been a very strong person so I bucked up and stuck to it.. Now I've been off of it it completely for 3 days and I now know what hell is. Besides the nervousnes, queasiness, adjitation, sleeplessness and the other stuff associated with withdrawls for no clear reason, at the oddest times I start blubbering like a baby. Last night I almost jumped out of my wife's car as we passed over a bridge. What the HELL is going on here? I feel brain damaged. If I can get just one person to not take this crap I can let go in peace.

posted in Effexor Activists Tribe - 3 replies

Assistance getting off Efexor.

2009-10-27T07:11:44Z

Hi,

I have been on this drug since July this year, started on 37.5mg for two weeks then on 75mg for 2 weeks and now I'm on 112.5mg since the last two weeks. I have missed my dose this AM thats about 14 hous ago, and I happened to be looking this up on the web when I came across this site. And I'm horrorfied to say the least... I have absolutly no intention in taking any more of these tablets at all.
I was given these by my doctor as I was feeling very lethargic and had lost intrest in my business... about the size of it.

So, I would like to know if I going to be safe / well etc now for stopping or will I suffer these hidious withdrawals I'm reading about??

Thanking you for your help and guidance,

Tim.

posted in Effexor Activists Tribe - 5 replies

Pfizer pleads guilty to felony crime for fraudulent marketing

2009-10-27T06:44:30Z

http://www.naturalnews.com/026963_Pfizer_Bextra_health.html

(NaturalNews) For the last several years, I've referred to drug companies as "criminal" operations. They have engaged in price fixing, marketing fraud, science fraud and many other criminal activities that we've written about here on NaturalNews. And yet, until today, they always managed to avoid the criminal charges by settling with the government for a few million dollars in payouts. This was their racket: Violate the law, then when you get caught, just settle with some cash. (And there's always some spare cash to go around since fraudulent science and fraudulent marketing is very, very lucrative.)

But all that changed today with the announcement of a Dept. of Justice criminal case that has resulted in Pfizer pleading guilty to a felony crime. Which crime? "...for misbranding Bextra with the intent to defraud or mislead." You can read the DOJ documents describing the settlement here: http://www.usdoj.gov/opa/pr/2009/Se...

Essentially, Pfizer asked the FDA to approve Bextra for a variety of diseases and conditions, and when the FDA refused those approvals, Pfizer decided to go ahead and market the drugs for those diseases and conditions anyway (off-label marketing).

But that's not all. In the DOJ statement, you'll read the following:

Pfizer has agreed to pay $1 billion to resolve allegations under the civil False Claims Act that the company illegally promoted four drugs -- Bextra; Geodon, an anti-psychotic drug; Zyvox, an antibiotic; and Lyrica, an anti-epileptic drug -- and caused false claims to be submitted to government health care programs for uses that were not medically accepted indications and therefore not covered by those programs. The civil settlement also resolves allegations that Pfizer paid kickbacks to health care providers to induce them to prescribe these, as well as other, drugs. The federal share of the civil settlement is $668,514,830 and the state Medicaid share of the civil settlement is $331,485,170. This is the largest civil fraud settlement in history against a pharmaceutical company.

False claims, kickbacks, felony crimes and civil fraud... it seems that the truth about pharmaceutical companies like Pfizer is finally starting to emerge.

And here's the best part: Pfizer's own whistleblowers will cash in! "Six whistleblowers will receive payments totaling more than $102 million from the federal share of the civil recovery," says the DOJ.

$2.3 billion in fines

Along with this admission of guilt for committing a felony crime, Pfizer is paying well over $1 billion in criminal fines, plus another $1 billion or so to resolve civil allegations against its fraudulent marketing practices. In all, the multi-billion dollar settlement is the largest in the history of the DOJ.

All I can say is: Good work! I've often stated that the pharmaceutical industry should be subjected to our nation's laws, and yet it has operated in a largely lawless fashion for decades. The FTC, for example, which should be investigating the drug industry monopolies that rip off American consumers and limit consumer choice, has all but ignored the monopolistic (and highly illegal) practices of the pharmaceutical industry. But the Dept. of Justice has now apparently decided that enough is enough -- it's going to investigate and prosecute serious criminal fraud being committed by drug companies.

posted in Effexor Activists Tribe - 2 replies

Dr Grace E Jackson on Neuroleptic Induced Deficit Syndrome

2009-09-02T15:26:44Z

I knew this lady was a winner and she just keeps coming through.
Dr Grace E Jackson on Neuroleptic Induced Deficit Syndrome

here's the link:
http://74.125.113.132/search?q=cache:bwjknC-g-DcJ:psychrights.org/Drugs/DrJacksonUCELecture(UK)09.06.04.pdf+dr+grace+e+jackson&cd=1&hl=en&ct=clnk&gl=ca

and a teaser:

For those who aren’t familiar with anti-psychotic medications, three of the short-term effects includeParkinsonian symptoms; a sometimes lethal condition called Neuroleptic Malignant Syndrome; andthe third is called NIDS (Neuroleptic Induced Deficit Syndrome). I don’t imagine many people haveheard about this last one. Does anybody know what that is (some response from crowd)? Great,there are some well-informed people here. NIDS was never a part of my training, so that’s great

posted in Effexor Activists Tribe - 0 replies

Please help me, I'm in my 20's and feel my life is over because of effexor!

2009-08-11T06:09:41Z

Ok, this is such a very long story,
I was in an accident once upon a time ago many moons back we're going over 6 years now. I had smashed my head on the pavement because of being hit by a bike, required 10 staples to close my bleeding head. They said I was Bipolar after getting real nervous and "weird" at work. About 4 years ago, they started me on wellbutrin & Clonazepam, this really helped me at the time & I felt it to be a godsend. Then it wore off so I spent about another while trying different antidepressants including Zyprexa , Paxil, Risperal, none hepled then came...Effexor xr.
I was started on a low dosage it helped not only my feelings, I got so much energy & I lost weight too. This was about 4 years ago. Since these past 4 yrs being on this drug they kept increasing my doses. This past year & a half has been the worst. I've been admitted to the hospital for trying to kill myself & put in the pysc ward on a safety hold as a danger to myself! I had tried to take my bottle of 150mgs effexor pills and took a handful in an attempt to OD. My parents called 911 which saved my life. I don't remember being able to control myself as my anger issues had been getting worse for a while, finally I snapped. I do remember reading in the course of these past 4 yrs that HOMICIDAL IDEOLOGY has been added as a warning for this drug! I wasn't ever warned of anything like that. So simple enough, stop taking it right? I can't, I really honestly can not. My brain shakes, I get really dizzy and have a strange out of body feeling..Then I start crying non stop and become truly delusional I MUST end my life somehow. I feel stuck forever...The past 1and half yrs I've become a Cutter, I've sat around becoming interested in true crime stuff (unlike me). I know I wouldn't hurt another person, strictly my heart would DIE , but its me whos at danger here please help? Oh & I don't trust drs anymore they try to push more on me, it's disgusting, I should be on 300mg a day I'm taking 150. My weight has become a problem I'm gaining and can't stop help?

posted in Effexor Activists Tribe - 4 replies

Generation Rx and other interests

2009-07-26T06:03:26Z

Generation Rx Trailer
http://www.youtube.com/watch?v=xehHwkPpevk

Canadian Documentary
http://www.youtube.com/watch?v=XgngMWe1_Bs

Generation Rx part 1
http://www.youtube.com/watch?v=wviiFzzPiro
parts 2 and 3 are listed if you are interested.

http://www.youtube.com/watch?v=oSk7IP_Yljw
Suing to get drugs advertised in Canada

posted in Effexor Activists Tribe - 0 replies

Grace E Jackson M.D. we got a winner here

2009-07-12T05:50:00Z

--------------------------------------------------------------------------------
Open Letter to the Federal Coordinating Council for Comparative Effectiveness Research
by Grace E. Jackson, M.D.

April 12, 2009

Dear Federal Coordinating Council:

This statement is written with respect to the allocation of money (1.1 billion dollars) from the 2009 Recovery Act fund for the purpose of achieving Comparative Effectiveness Research.

Recommendation #1 Prioritize the End of Corporate Fraud

PS
You may want to do a google search on this firecracker she is on the up and up not sure if she is enough but it sure is great to have her step up.

She has a couple of books I would like to read as well as some interesting med files online.

Research into the comparative effectiveness of medical treatments is a laudable goal, but only if it does not repeat the same errors of the past. When, in the early 1990s, medical journals, medical schools, residency and postgraduate training curricula, and health care facilities came under the influence of Evidenced Based Medicine (or EBM), the favored treatments in American medicine came to reflect the following values and priorities:

1) symptom suppression (rather than elimination of root cause of illness)
2) short-term studies (e.g., Randomized, Placebo Controlled Trials)
3) fraudulent research designs (e.g., placebo washout/lead-in)
4) concealment of data unfavorable to the interests of the drug industry
5) academic censorship (e.g., non-disclosure and confidentiality agreements)
6) distortions in the medical literature (ghostwriting, file drawer effect)
7) treatment by consensus (rather than treatment based upon science)

Each of these developments contributed to the hegemony of sham standards of care.
Effectiveness Research will be meaningless if it repeats these errors of the past.

Recommendation #2 Focus Upon Basic Science and Biology

The current system for approving new medications and medical devices emphasizes proof of efficacy in principle, rather than proof of effectiveness in fact. This system has given rise to the introduction and widespread use of one, after another, copycat therapies based upon dubious definitions of benefit (e.g., checklists of subjective symptoms in psychiatry; measurements of "risk factors" and surrogate endpoints as substitutes for real progress in ameliorating the symptoms of chronic disease). Most critically, the past 20 years of American medicine have diverted attention away from the study of basic physiology and the mechanisms of disease.

Unless and until the treatment paradigm in American medicine returns to an emphasis upon root causes of illness and disease, and upon the eradication or amelioration of those causes, the system of healthcare will continue to reflect interventions which are largely futile for patients.

What might be done:

1) identify environmental sources of illness and map the epidemiology of risk factors and diseases related to same [e.g., the U.S.A. needs a national equivalent of Green Cross International]

2) re-evaluate national healthcare policy with respect to HPDP [Health Promotion / Disease Prevention]
-- verify or refute high cholesterol as the necessary and sufficient cause of heart disease
-- verify or refute the existence of cumulative safety thresholds for diagnostic radiology
-- verify or refute the long-term harmfulness of the current immunization schedule (particularly, with respect to autoimmune dysfunction, diabetes, asthma, obesity, and neurobehavioral syndromes)
-- verify or refute the long-term harmfulness of fetal ultrasound
-- verify or refute the long-term hazards of fluoridation
-- verify or refute the validity of Gallo's work, positing HIV as the cause of AIDS
[see Nortin Hadler's books: The Last Well Person and Worried Sick]

Recommendation #3 Prevent and Mitigate Iatrogenic Harm

The allopathic model of medicine is failing America because authorities will not acknowledge the unnecessary harmfulness of synthetic chemicals. All of the existing training programs, textbooks, Board Certifications, and treatment algorithms emphasize the use of pharmaceuticals that are based upon short-term drug trials, and short-term studies in lab animals. Yet, human subjects (at least, in the U.S.A.) are increasingly encouraged to consume multiple medications for life. This philosophy of lifetime, prescription drug dependence ignores the scientific realities of what happens to patients under the influence of chronic medication.

Unless and until health care providers, policy makers, and regulators recognize the problems of allostatic load (the body's adaptations to therapy which ultimately result in diminishing benefits or worsening disease) and prioritize the avoidance, amelioration, and/or reversal of target organ toxicity, no amount of "effectiveness research" will be meaningful.

What might be done:

1) effectiveness research must involve considerations of treatment UTILITY ( Benefits and Hazards)
2) effectiveness research must include considerations of Target Organ Toxicity [e.g., how various treatments harm the diseased organ] and allostatic load [e.g., how various treatments induce changes in gene expression which may result in delayed but potentially long-lasting effects]
3) effectiveness research must include considerations of treatment effects upon the environment (e.g., xenobiotic diffusion via sewage; air pollution from hospital incinerators) and environmental effects upon treatment (proximity of treatment facilities and patients to radon, radioactive waste, Superfund or other toxic waste sites, petrochemicals, etc)

Recommendation #4 Recruit the Best Treatments from Around the World

The federal government gives lip service to the importance of research in the areas of complementary and alternative systems of health care. However, the U.S.A. has become a pharmaceutical oligarchy which permits no challenge or rival to allopathic medicine. No amount of effectiveness research will be meaningful unless and until the yoke of pharmaceutical authoritarianism is broken. Ideally, effectiveness research will incorporate the "best treatments" (herbs, diet and lifestyle modification, environmental modification) from around the world.

Recommendation #5 Protect the Privacy of Patients and Physicians

Given the pervasiveness of corporate fraud and the denigration of integrity within the American health care system -- particularly, as these have progressed in the era of Evidence Based Medicine -- patients and physicians require protection from harmful practices. Treatment facilities, insurance companies, and State Medical Boards mandate compliance with a corporately shaped, corporately biased Group Think. Clinicians have lost the right to practice medicine by using their best clinical judgment, informed by an understanding of basic science, direct observation, and the consideration of the unique circumstances of each and every patient.

It is extremely unlikely that America's pharmaceutical oligarchy will ever be displaced or transformed into the kind of system which serves mankind, rather than profit and power. This being so, the results of effectiveness research must not be allowed to infringe or violate the privacy of patients, nor the rights of clinicians who desire the freedom to honor the ethical principles of patient autonomy, physician beneficence, and physician non-maleficence.

What might be done:

1) patients and providers must be allowed to opt out of electronic medical records system, health care registries, and other databases where biological and social information can -- and most likely will -- be used to ration health care, restrict employment or travel, or reduce entitlements

2) patients must be protected from medical tyranny (i.e., medical blackmail --- the allocation of therapies or benefits based upon compliance with dubious and potentially harmful treatments)

3) health care providers must be protected from medical tyranny (i.e., medical blackmail in the form of Pay-for-Performance programs, "Consensus" Statements, Sham Peer Review/Disruptive Physician proceedings, etc).

Summary

Effectiveness research is a laudable goal, but only if it is conducted in a way which avoids the tragic errors of the past (i.e., the corporate medical fraud which has gained traction under the influence of EBM, the Daubert decision of 1993, the Prescription Drug User Fee Act, the Bayh-Dole Act, Direct-to-Consumer Advertising, etc), and only if it anticipates new challenges of the future.

Particularly in the context of emerging technologies (brain mapping, gene mapping, high-speed information exchange), there will be ever more opportunities for the leaders of allopathic medicine -- and for the leaders in government -- to enslave, rather than to serve, the providers and consumers of health care.

Ultimately, effective health care must also be ethical health care. This will require a return of integrity in the conduct of American medical research. It will also require a health care system which prioritizes the delivery of services that are consistent with fundamental human rights, and with the human species' duty to protect (rather than to plunder) the planet's biosphere.

Thank you for the opportunity to contribute these ideas and opinions.

Respectfully,

Grace E. Jackson, MD
Wilmington NC 28405

posted in Effexor Activists Tribe - 2 replies

drug free but still have sypmtoms of withdrawal

2009-07-03T22:48:29Z

After taking Effexor over the last 10 yrs, I have tapered off Effexor completely, but 13 days later, I'm still experiencing discomfort. It feels like bugs crawling/zapping me.. everywhere! My hair started falling out as soon as I began to taper off the drug. I'm hypersensitive to sounds, have headaches, can't remember things like I used to, and I'm extremely irritable; to the point of being nasty and aggressive. My doctor said that my system should be cleared of the drug, and that she has never had an Effexor patient experience such strange effects. Then she alluded to my age and hormones as the cause for my discomfort, but I didn't have a problem while still on Effexor except for the fatigue. How long is this going to go on? What can I do to ease the creepy skin feeling? Am I loosing my mind or what?

posted in Effexor Activists Tribe - 8 replies

What if psychiatrist tells employer he thinks I sould stay on Effexor?

2009-07-03T22:15:07Z

Hi, I am new to this discussion, but have been reading alot on the Effexor Activist Site.
I have been taking Effexor for 4 years, and its been a nightmare. I am a zombie on it and I get dizzy to the point of non-stop vommitting when I try to get off it. None of the original symptoms of depression have been an issue, but new cognitive and other physical symptoms, such as restless legs, inability to concentrate which is bad on the drug, worse going off, etc have been plaguing me the whole time.

To make things worse, I do a safety critical job with federal guidlines that requires that my employer has medical records on me. I have been trying to get off these drugs for years, and have had to go to a psychiatrist that believes I should stay on them. I have told him allready that the side effects are bad, and the withdrawal symtoms- (a tight head, zapping, dizzy, naseus) are unbearable.

I had to go on stress leave because I had to renovate my house by the end of December in order to get it rented out and save losing it.
My employer said I had to get a report from this Psychiatrist before I got back to work. He wouldn't see me at first.

I live in a small town, with only one Psychiatrist. My family doctor convinced him to see me and do the Back to Work report. I just came from there. I would have had to get on a longer waiting list to see a different doctor.

I was apologetic about not following his advise, but I told him the side effects were bad, and I needed help to go off them. He refused to help, told me to talk to my family doctor.

Oh yeah, I live in Canada, although the rules for safety critical are similar in the States I believe. When the family doctor did my report to the employer he put down depression as the cause, with "numerous occassions" as my past record, which is untrue, it is the symptoms of the Effexor that is the problem, and I took the stress leave to meet a legal deadline- which WAS STRESSFULL! (worked 14 hour days 7 days a week for 2 months.

This doctor is my ticket to continued employment. I feel as it I should have lied to him.
Can anyone think of a way I could get around this drug pushing doctor and have it accepted by my employee health services that I could be a more alert and productive employee OFF the drug?

posted in Effexor Activists Tribe - 16 replies

ViLift ????

2009-07-03T20:33:13Z

http://www.viliftplus.com/?gclid=CNPg6OauupsCFRxNagodgShIAw

If any one here has tried ViLift Please let us know how it worked for you

WARNING WARNING WARNING WARNING WARNING WARNING WARNING WARNING
Do not use this formula with any SSRI or SSNRI antidepressant.

ViLift Ingredients: St. Johns Wort (Hypericum perforatum - 300mg), SKULLCAP (Scutellaria Lateriflora - 100mg), 5-HTP (Griffonia simplicifolia),
Korean Ginseng (Panax Quinguefolius L. - 33.3mg), Vitamin B Complex - 5mg

posted in Effexor Activists Tribe - 0 replies

antidepressants and aids drugs have something in common? for those with some time on there hands interesting read

2009-07-01T06:07:12Z

http://exlibhollywood.blogspot.com/2...v-mystery.html

After listening to Karri’s story and comparing notes with other reports, I noted similarities between Karri’s symptoms and known withdrawal syndromes, including those of antidepressants. I also found reports that HIV drugs were being crushed and smoked by addicts in Africa:.......

While being studied as a possible treatment for tuberculosis in 1952, this antibacterial agent was discovered to have psychoactive properties. “Terminally ill patients who were given this drug became cheerful, more optimistic, and more physically active.” Iproniazid and similar compounds slowed the breakdown of norepinephrine, serotonin, and dopamine “via inhibition of the mitochondrial enzyme monoamine oxidase.” These neurochemicals affect the same receptors as cocaine, heroin, methamphetamines, cannabis, and other more commonly known addictive drugs. These antibacterial agents have since become known as monoamine oxidase inhibitors (MAOIs), which are now used as antidepressants (SSRIs) under the names of Prozac, Paxil, Lexapro, Zoloft, and Effexor. Iproniazid withdrawal symptoms were similar to those Karri described

The link to this post does not get interesting until you get to this reply which I am working on.

Reply:
Sorry for introducing a lot of chemistry, but your hypothesis is very interesting.

Indeed, the depleting of iodide by sustiva is not difficult to explain.
The formation of thyroxine is made by oxidization of iodide anion (which exist in sea, food, but cannot give itself the thyroidal hormones.

This oxidization occurs in the "iodine trap", and requires hydrogen peroxide.

This process leads to an electrophilic iodine (the cation iodine I+), which reacts very quickly with the activated aromatics rings of the precursors of thyroxine.

But, if you oppose to I+ another nucleophilic compound, which reacts more quickly, the thyroxine cannot be made.

Sustiva contains an alkyne function (a triple bond between two carbons), which reacts very quickly - in a reaction named "electrophilic addition" - with the electrophilic halides Cl+, Br+ and I+.

Finally, Sustiva appears as an "electrophilic" iodine trap.

These article :

http://www.sciencedirect.com/ sci...bb9524b5ec5eca9

shows that carbamates and propargylic compound have antidepressant activities. And Sustiva is indeed a real carbamate, and propargylic compound (the carbon-carbon triple bond is bound with a C-O structure).

The scientific community says that the mechanism of action of these compounds is not clear and requires further elucidation.

But, as sustiva is an electrophilic trap, it can too trap the nitrosative oxidants, such the peroxynitrites, which appears to be intimately linked with the hiv phenomenon, which is, as David Rasnick says it, only a tentacle of aids.
jean umber

Thinking it has more to do with iodine but not sure will get back to you on this.

posted in Effexor Activists Tribe - 0 replies

antidepressant induced mitochondrial disorders

2009-07-01T05:59:36Z

Although effexor is not on the list I am posting this here as I for one have taken more than one antidrpessant and there are many other drugs on the list including statins and antibiotics. FYI to date drug companies are not required to report that a drug can cause mitochondrial damage. The authors of this article suggest testing of new meds for mitochondrial damaging effects could save a lot of greif.

Medication documented to induce mitochondrial damage

http://74.125.113.132/search?q=cache:qiqNqGbokh0J:psychrights.org/research/Digest/NLPs/DrugsCauseMitochondrialDamage.pdf+medication+on+mitochondrial+dysfunction&cd=3&hl=en&ct=clnk

Table 5. Medications documented to induce mitochondrial damage [10, 35, 63–90]
Drug class
Drugs
Alcoholism medications
Disulfiram (Antabusem)
Analgesic (for pain) and anti-inflammatory Aspirin, acetaminophen (Tylenol), diclofenac (Voltarenm, Voltarolm, Diclonm, Dicloflexm
Difen and Cataflamm), fenoprofen (Nalfonm), indomethacin (Indocinm, Indocidm, Indochron
E-Rm Indocin-SRm), Naproxen (Alevem, Naprosynm)
Anesthetics
Bupivacaine, lidocaine, propofol
Angina medications
Perhexiline, amiodarone (Cordaronem), Diethylaminoethoxyhexesterol (DEAEH)
Antiarrhythmic (regulates heartbeat)
Amiodarone (Cordarone)
Antibiotics
Tetracycline, antimycin A
Antidepressants
Amitriptyline (Lentizol), amoxapine (Asendis), citalopram (Cipramil), fluoxetine (Prozac,
Symbyax, Sarafem, Fontex, Foxetin, Ladose, Fluctin, Prodep, Fludac, Oxetin, Seronil,
Lovan)
Antipsychotics
Chlorpromazine, fluphenazine, haloperidol, risperidone, quetiapine, clozapine, olanza-
pine
Anxiety medications
Alprazolam (Xanaxm), diazepam (valium, diastat)
Barbiturates
Amobarbital (Amytalm), aprobarbital, butabarbital, butalbital (Fiorinalm, hexobarbital
(Sombulexm), methylphenobarbital (Mebaralm), pentobarbital (Nembutalm), phenobarbital
(Luminalm), primidone, propofol, secobarbital (Seconalm), Talbutalm), thiobarbital
Cholesterol medications
Statins – atorvastatin (Lipitorm, Torvastm), fluvastatin (Lescolm), lovastatin (Mevacorm,
Altocorm), pitavastatin (Livalom, Pitavam), pravastatin (Pravacholm, Selektinem, Lipostatm),
rosuvastatin (Crestorm), simvastatin (Zocorm, Lipexm) bile acids – cholestyramine (Ques-
tranm), clofibrate (Atromid-Sm), ciprofibrate (Modalimm), colestipol (Colestidm), colesevelam
(Welcholm)
Cancer (chemotherapy) medications
Mitomycin C, profiromycin, adriamycin (also called doxorubicin and hydroxydaunorubicin
and included in the following chemotherapeutic regimens – ABVD, CHOP, and FAC)
Dementia
Tacrine (Cognexm),Galantamine (Reminylm)
Diabetes medications
Metformin (Fortametm, Glucophagem, Glucophage XR, Riomet
1
), troglitazone, rosiglita-
zone, buformin
HIV/AIDS medications
AtriplaÔ, Combivirm, Emtrivam, Epivirm (abacavir sulfate), EpzicomÔ, Hividm (ddC, zalcita-
bine), Retrovirm (AZT, ZDV, zidovudine), Trizivirm, Truvadam, Videxm (ddI, didanosine),
Videxm EC, Vireadm, Zeritm (d4T, stavudine), Ziagenm, Racivirm
Epilepsy/Seizure medications
Valproic acid (Depaconm, Depakenem, Depakene syrup, Depakotem, depakote ER,
depakote sprinkle, divalproex sodium)
Mood stabilizers
Lithium
Parkinson's disease medications
Tolcapone (Tasmarm, Entacapone (COMTanm, also in the combination drug Stalevom)

posted in Effexor Activists Tribe - 0 replies

effexor

2009-07-01T05:47:11Z

what has happened to the petition on effexor

posted in Effexor Activists Tribe - 2 replies

protracted withdrawal or panes

2009-07-01T05:30:33Z

I quit effexor cold turkey nov 18 2007 I was extremely ill while the last few years taking effexor and have improved in some respects. Other issues however remain. I have been frequenting paxilprogress.org and have found others on that site which are experiencing the same issues as I am from quitting effexor. I wonder if this is a protracted withdrawal or damage done by the drug that does not heal. The main idea on pp is that the damage will reverse if given enough time. I am doubting that perhaps the damage done by paxil heals and that from effexor does not. Protracted withdrawal is a very active topic on paxil progress and I am thinking effexor may have the same withdrawal issues they sure seem very close. I am hoping in a few years it may pass but have heard from some that are still dealing with it 3 years later.
I checked a site today that was referred by the effexor activist which as a good site called "coming off psychiatric meds" I have to say that it states withdrawal should end a few wks after the drug is stopped. This has not been my experience and so I would not recommend this site. I find I am still dealing with withdrawal and I am sure many others are too. For me it is debilitating. The lack of information and support by the medical comunity is disgraceful. The idea these drugs are still on the market to me is criminal.
I would like to hear back from others that feel they are in protracted withdrawal from effexor.

posted in Effexor Activists Tribe - 7 replies

Beware of Prestiq

2009-06-13T22:45:43Z

http://clinpsyc.blogspot.com/2007/03/more-on-pristiq.html

Thursday, March 01, 2007

More on Pristiq

Marissa Miller has a fine post about desvenlafaxine (Pristiq), Wyeth's attempt to cover up for their bestseller Effexor coming off patent in the near future. Coverup? Considering that desvenlafaxine is a clear knockoff of Effexor (venlafaxine), yes, I'm sticking with that descriptor. Why do research to develop an innovative medication when you can just sell one that is quite highly similar to the one that is already a sales blockbuster?

The idea is not new – make a drug that very closely resembles your existing product, then get it FDA-approved slightly before the old one goes off patent. Lexapro-Celexa, Invega-Risperdal, and now Effexor-Pristiq. The new drug offers no advantage over the drug that is about to go generic, and why would it – if you have a red 1975 Ford Pinto or a green 1975 Pinto, you still have the same crappy car.

Aren’t patents supposed to protect inventions that possess the potential to benefit people? Aren’t patents supposed to reward creativity? There is no creativity here – we’re talking a slight manipulation of a molecule to create a new compound that is no better than the first one.

But the blame does not just lie with the patent process. Why are physicians prone to fall for this game? Why do so many physicians prescribe Lexapro (escitalopram), which is pert-near a clone of Celexa (citalopram), when Lexapro is much more pricey? In fact according to Walgreens, 90 pills of 10mg generic citalopram will run $127.59, whereas the same supply of Lexapro costs $210.79. The marketing miracle that constitutes the heart and soul of modern psychiatry is damn good at convincing physicians that newer equals better.

Perhaps if physicians received adequate training in research methods and statistics during medical school, they could actually learn to critically review clinical trial data to discover that the ploy of near-clone medicines usually does nothing but increase costs. Then doctors could also laugh their way through continuing medical education or, better yet, insist that CME start to resemble education rather than advertising.

posted in Effexor Activists Tribe - 3 replies

prestiq nearly killed my self and children

2009-05-17T19:12:05Z

They need to take Prestiq off the market as well. I was on this stuff for about three months before I finally realized what it was doing to me. It took running in to the side of an 18 wheeler, hitting a curb and busting two tires one time, hitting another curb another time, nearly running off the road numerous times, nearly rear ending cars at lights several times and losing my job before I realized what it was doing to me. I didn't realize this because my mental awareness was also effected by this drug and it wasn't until I lost my job and my boss made a comment that I realized it was Prestiq. Within a few days of not taking it I was myself again. I shiver when I think about how many close calls I had and stupid I was not to realize it sooner. I am furious with Wyeth and my doctor for prescribing this stuff to me. My doctor just happen to have samples and knowing that I was having a hard time financially gave it to me. At least that is how I feel. I hope that they put together a class action lawsuit against Prestiq as well if they haven't already and get this stuff off of the market!!!

posted in Effexor Activists Tribe - 1 reply

Pneumonia...

2009-05-11T17:15:38Z

Anyone suffer this side effect as the result of withdrawals?

posted in Effexor Activists Tribe - 5 replies

effexor damage

2009-05-09T14:06:53Z

it has been 10 months since i last took effexor. i ttok it for about 4 months its now apr 09. had to stop taking it because my vision would vibrate since then i am left emotionless, have no desire to do anything. cant seem to get the words oout to talk, or i stutter.confusion, memory problems, cant drive, blurry vision. i used to have really bad anxiety, and depression. now i have nothing. are there any tests or can the damage be reversed. PLEASE HELP

posted in Effexor Activists Tribe - 4 replies

How can doctors be so ignorant?

2009-04-24T03:37:49Z

Nancy asked How can doctors be so ignorant?
It is because doctors are being deliberately trained to be ignorant. Most have no idea of how corrupt the industry and the FDA are.

I have found that the best way to learn how the industry works and how your doctor gets information, is the documentary "Money Talks"

Watch a clip from the educational documentary, "Money Talks", by the maker of "Side Effects" It is well worth buying the full movie.
http://www.moneytalksthemovie.com/film.html

There are also several excellent books on the subject.

The Truth About Drug Companies: How They Deceive Us and What to Do About It By Marcia Angell M.D.
http://www.amazon.com/gp/product/037550 ... 1?n=283155

Overdosed America : The Broken Promise of American Medicine
by John Abramson M.D.
http://www.amazon.com/gp/product/006056 ... 9744/sr=2-

On the Take: How Big Business Is Corrupting American Medicine
By Jerome Kassirer, M.D.
http://www.amazon.com/gp/product/019517 ... e&n=283155

The Big Fix: How the Pharmaceutical Industry Rips Off American Consumers by Katharine Greider,
http://www.amazon.com/Big-Fix-Pharmaceu ... 1586481851

Selling Sickness: How the World's Biggest Pharmaceutical Companies Are Turning Us All into Patients by Ray Moynihan, Alan Cassels
http://www.amazon.com/gp/product/156025 ... e&n=283155

Generation Rx : How Prescription Drugs Are Altering American Lives, Minds, and Bodies by Greg Critser
http://www.amazon.com/gp/product/061839 ... e&n=283155

Innocent Casualties : The FDA's War Against Humanity by Elaine Feuer
http://www.amazon.com/gp/product/080593 ... e&n=283155

posted in Effexor Activists Tribe - 6 replies

If you received the following message from the effexor activist

2009-04-06T08:57:15Z

If you received the following message from the effexor activist -

("You have been permanently banned from this board.
Please contact the Board Administrator for more information.
A ban has been issued on your username. ")

You were not really banned. We all got the same message. It was just a glitch at the site.

It should be working fine now.

Sorry for any inconvenience.

posted in Effexor Activists Tribe - 0 replies

My old shrink...

2009-04-06T07:45:14Z

... is takin' his sweet time getting some info to me. I asked him about my my history of Effexxor prescription dosages while under his care. Just seems weird, like he doesn't want me to know that info.

posted in Effexor Activists Tribe - 1 reply

POSSIBLE EFFEXOR HELP

2009-03-25T02:32:09Z

I was on effexor for 10 years and got off it two years ago. Up until 8 months ago, I still had withdrawl symptoms that never went away (Heavy head, brain zaps, dizziness, nausea, slow thinking etc.). It got a little better after the first 5 months of going off effexor and switched to 150mg Zoloft, but I still had these persistant symptoms that never went away. I tried EVERYTHING to fix this - I had MRIs to try to find a cause, detox therapys, acupunture, went to neurologist and had a EEC, - you name it, I have probably tried it. I would go to bed crying every night because I felt so helpless and could do nothing to stop the agony. I finally discovered a PAXIL discussion group that delt with withdrawl symptoms and SSI drugs. Someone mentioned in the post that the drug can be held in fatty tissue. It was a long shot, but I was so desperate that I would try ANYTHING. So, even though it was the MOST PAINFUL thing I have ever done in my life, I started walking on a treadmill every day and cut my calories. It was hard because walking was the worst thing I could do because it made me the dizziest. My logic for doing this was that if it was still stored in my fatty tissue, if I could get rid of it then maybe, just maybe, I could start to feel some relief. I was skeptical at first because it was sooooo hard to get myself to walk everyday. Not only that but at that point I didn't even know if it would work or not. To be honest, I was doubtful. But I was so desperate for relief that I was willing to just suffer for it. Well, I was 5'0 and 160 pounds, so I was already overweight. The weight came off slowly as I was only able to do a little each day and I could only walk and not run. I did not feel anything at all for a while, but when I had lost about 10 pounds, I could tell a noticeable difference. The symptoms were still far from gone, but they were definately better. This encouraged me to keep on exercising and dieting. Also, the walking got easier. After 25 pounds I stopped thinking constantly about my symptoms, as they were not very noticeable anymore. After 30 lbs I did not have ANY SYMPTOMS!!!!! I am SOOOOOOOO happy and glad to be free of this evil drug... It has been 2 months since I stopped having symptoms and I have happy to feel normal again. I am still on Zoloft and Trileptil (I'm bipolar). I thought I should mention this after reading your post in case it might work for you and anyone else. Last month I told a classmate who also happened to be going through the long-term withdrawls of this drug.She was skinny and did not really have much weight to lose, but she ended up trying it and it helped! I am not saying that this is a cure-all, but if it helped two people get over their symptoms, who knows? I hope it helps... If anyone does end up trying it please post so we can see if this might help other people or not. Thanks and good luck!

posted in Effexor Activists Tribe - 2 replies

WHAT LONG-TERM EFFECTS DO YOU HAVE?

2009-03-22T16:49:33Z

Link to PANES (Persistent Advers Neurological Effects of SSRI) on theeffexoractivist web site, for your reference:

http://theeffexoractivist.org/forum/viewforum.php?f=52

WHAT LONG-TERM EFFECTS DO YOU HAVE?

I took Effexor XR 75mg for one year, involuntarily, in exchange for desperately needed hormonal therapy from a physician who refused to help me unless I complied. I was essentially blackmailed into it.

He offered me three antidepressants. I asked him which one had the fewest side effects and he chose Effexor for me. I should have known better than to trust a doctor who blackmails patients into treatment. Of the three, Effexor is the newest and he just wanted to experiment on me with a new toy.

I expressed my sincere misgivings and I reported my side effects... namely, visual and auditory noise, severe fatigue, severe loss of stamina, rapid heart beat, loss of depth perception, feeling of being stoned... and was ignored.

Upon withdrawal I cut the dose down to 37.5mg and immediately (within 2 days) developed severe torticollis, which went into remission upon resuming the larger dose. My doctor wanted to switch me to Prozac, telling me I needed a "serotonin stabilizer". This last deception was the final straw that broke the patient's back. Then I fired my doctor, bought The Antidepressant Fact Book and began opening my capsules, using graph paper and a credit card to spread the caplets out like a line of cocaine along the graticule, measuring out precise titrations.

I tapered the dose by 10% per week. I felt like a drug addict, complete with paraphernalia and ritual.

I developed severe uncontrolled twitching and convulsive spasms 70% of the way into withdrawal. I felt sick as a dog with nausea and dizziness. I developed zaps and swooshing sounds when I moved my eyes. I saw snow in the dark and rain on the ceiling. I continued withdrawing anyway, wanting to get the poison out of my system as soon as possible. As it was, I took Effexor for a total of 16 months. That was 16 months too long.

I had other side effects and withdrawal symptoms too, but they mostly went away over the course of a year. I only mentioned the side effects and withdrawal symptoms that I still have, five years later. Yes they abated somewhat, but yes some of them never went away and the rest, well they also keep coming back. I feel them before falling asleep and upon waking. I notice them more when I am physically exhausted, in severe pain, cold, hot, emotionally distressed, hungry, sick, off my diet, recovering from a late-night bender... in short, under any form of stress at all.

The one that has been with me from the first month of treatment until today without ever letting up is the severe loss of stamina. To this day I pant and my heart races when I climb stairs. Mountain climbing is a thing of the past. I have not been able to do it for five years. I can barely ride a bicycle on flat pavement. I think my heart was damaged. My resting heart rate used to be 65. Now it is 90.

I have read the other cases of PANES here and on other sites, and mine seems to be the worst case I know of. It developed on a low dose, it developed quite early in the treatment, it got so much worse in withdrawal, and it has so many profound effects.

Unfortunately I also know of three other individuals who experienced similar persistent problems on Paxil and Prozac -- and I did not even look too hard for examples. They live right in my neighborhood. I suspect that there is a small army of brain-damaged disillusioned victims walking around out there.

Serotonin nerves are the most numerous in the body. Shutting off the serotonin re-uptake mechanism is like plugging the biggest bathtub in sight with the largest fire hose filling it, and letting it overflow while blithely dancing in the puddles. The damaging effects are pervasive. I know of no other highly-populated and widely distributed classes of drugs that have such great potential to cause sudden death as serotonin-boosting drugs do if taken in the wrong combination.

Even short of outright fatality, it is already known that these drugs can cause neuronal death in some areas and neuronal proliferation in others, re-wiring the brain seemingly at random. It also makes sense that the neurons would fight back by down-regulating the serotonin secretion sites and proliferating the re-uptake sites, and there is research to support this hypothesis. The end result is a brain that bears little resemblance to its former configuration, at the neuronal level. No wonder I see and hear non-existent things now.

I suppose that my movement disorder could be the result of over-excited neuronal firing, but I think of it in terms more similar to detuned electrical negative feedback between my joint position sensors and my motor cortex (sorry, yes I am a enganeer). With the right amount of pathological phase delay, perhaps from burned-out nerves firing at a reduced rate in longer, back-up pathways that replaced the now-defunct formerly healthy circuits, by the time the position signal (feedback) arrives, the motor neurons (forward path) have already overshot the mark, just like a new driver jerks on the accelerator and brake pedals while veering from side to side with the wheel when learning how to lightly steer, accelerate, and brake when driving a modern automobile .

Such damage would make sense given the widespread nature of serotonin neurons and the many interconnections they have with nearly every other type of neuron in the system.

So, too, the recovery, coming slowly, never complete, seems like recovering from a stroke, as burned-out pathways partially regenerate or are bypassed.

One has to wonder, if so many people are experiencing what is most likely a severe and permanent post-treatment down-regulation of serotonin activity, coupled with deleterious serotonin-induced burn-out, sensitization, or proliferation style changes in the neural network downstream from serotonin nerves that could potentially induce permanent personality changes (as I have experienced), yet have NO KNOWN LONG-TERM RISK OF SEVERE, PERMANENT DEPRESSION as a result of this severe loss or corruption of serotonin function, then...

what possible connection could there be between serotonin and depression?

Yes, I know that we victims of this fraud do have less joy than we used to. After all, our brains are burned out. But are we sitting around crying hysterically and threatening to slit our own throats forever afterward? No. We are sitting around dizzy, with zaps and white noise in eyes and ears, hoping for recovery, disillusioned, and angry.

Fraud, that is what it is. In my opinion serotonin has nothing to do with 'depression' that is any different than the relationship between any other neurotransmitter and depression. Just a scam. Patient gets dumped on by life, patient can no longer slave away for the benefit of the plutocracy, give patient stimulants, sedatives, anything to keep patient quiet and nose to the grindstone so that we do not have to ever fix the real problems. That is my understanding.

Anyway, why I posted this... What dose did you take, how long did you take it, how fast did you withdraw, what symptoms did you have, when did they appear, how well have you recovered, how long did it take, and what other drugs (prescription or recreational) were co-administered?

Although I acknowledge that abrupt withdrawal is potentially torturous and life-threatening, I have this hypothesis that it makes little difference how fast someone withdraws, for the long-term outcome. I am curious if we can detect a trend, since many have told me that I withdrew too fast and that is why I got sick. I am skeptical of this claim, as I am of other claims. I suspect that it is the dose, length of treatment, individual susceptibility, and interactions with other drugs that determine the long-term outcome... not how fast one withdraws.

OK, prove me wrong, people? :lol:

posted in Effexor Activists Tribe - 9 replies

Serotonin Enhancing Psychotropic Pharmaceuticals

2009-03-22T06:03:17Z

In the 1930s, physicians approached the mental illness of depression a bit differently that we do today. While acknowledging typically the etiology for their patients is likely due to some great misfortune in their individual lives, the physician focused on what was known as a complex.
A complex is the disturbances of ideas and impulses that are the cause of consistent habitual patterns of thought, feelings, and behavior.
An example of this state of mind of one who is depressed is one who experiences an exaggerated or obsessive concern or fear. And the etiology for this mental disorder was often undefined. People react differently to life stressors in their life, so depression cannot be empirically determined.
Also in the 1930s, at times, behavioral or cognitive therapy was recommended for treating the depressed patient, and not pharmacological treatment, overall. Also considered for the depressed patient was positive lifestyle changes that may lessen the pain that the depression was causing them.
Try and be grateful, they would tell their patient, as well as thankful and appreciative for whatever good may be in their life, and normally the depressed patient would eventually recover.
Times have changed since then.
Presently, serotonin-enhancing drugs are the therapeutic regimens for those who are suspect of having a depressed state or mood disorder. Patients believing they have such cognitive issues often ask for such medications. The drugs are known as SSRIs, or SRNIs.
What is remarkable is that the mood disorders which will be discussed are subject to debate that progresses in its intensity as the more of these certain types of drugs are used in others
Such disorders, presuming they exist at all, have been brought to the attention to so many others through disease awareness campaigns by the makers of these classes of drugs. So mental flaws claimed to be relieved by SSRI drugs may not be entirely accurate. Disease mongering takes many forms- including front groups wearing a mask.
With depression, the most severe cognitive and behavioral malfunctions are expressed in what is called a major depressive disorder, as well as clinical depression or major depression. Depression is thought to affect twice as many women than men.
Symptoms of this type of depression, which is the most concerning to health care providers in particular due to its severity, include decreased or flat affect, decreased interest in activities once enjoyable, self perceptions of worthiness, guilt, regret, helplessness, and hopeless by the sufferer, to name a few of the diagnostic features that may be present with one who has such a major depressive disorder.
The disease has a vexing insistence on staying with the victim for a lengthy period of time- often continuing to progress symptomatically in severity and discomfort. This disease is very disabling, and cannot be lifted by one’s will, so all health care professionals likely agree that depression is a potentially serious condition with their patients. Suicidal ideation and attempts are associated with major depression. Treatment, it appears, is reasonable and necessary for the depressed patient.
These SSRI drugs mentioned earlier are known by some health care providers as third generation anti-depressants. Such drugs, drugs that affect the mind, are called psychotropic medications.
SSRIs also include a few drugs in this class that include the addition of a norepinephrine uptake inhibitor added to the SSRI in one capsule, and these drugs are referred to as SNRI medications. The combination of two different drugs has made them the top class of prescriptions for those suspected of psychological misalignment.
There are several available SSRIs presently, and a few SRNIs. Both classes of medications are prescribed for similar mental conditions.
Some consider these classes of meds, the serotonin enhancers in these medications, to be the next generation mood enhancers- after the benzodiazepine hype decades ago, which was followed by what were called trycyclic drugs for depression for some time as well, it is believed.
Furthermore, regarding SNRIs, adding the additional agent of norepinepherine is presumed to increase the effectiveness of SSRIs by some, yet not everyone claims relief from these types of drugs included in the SRNI class.
Some Definitions:
Serotonin is a neurotransmitter thought to be associated with mood. The hypothesis was first suggested in the mid 1960s that this neurotransmitter may play a role in moods and emotions in humans. Yet to this day, the serotonin correlation with such behavioral and mental conditions is only theoretical.
In fact, the psychiatrist’s bible, which is known as the DSM, states that the definite etiology of depression remains a mystery and remains unknown with complete certainty. So a chemical imbalance in the brain is not proven to be the cause of mood disorders, it is only suspected as a result of limited scientific evidence.
Diagnosing mental diseases such as depression is based on subjective assessment only, as interpreted by the prescriber, so one can examine the accuracy of such diagnoses.
Norepinepherine is a stress hormone, which many believe help those who have such mood disorders as depression. Basically, with the theory that by adding this hormone, the SSRI will be more efficacious for a patient prescribed such a med, as suggested earlier.
And the depressive state of a patient certainly can be aggravated by another mood disorder at the same time with some patients. Anxiety usually exists with one who has a major depressive disorder. An objective diagnosis of such a mental condition is rather impossible to assess objectively. Therefore any diagnosis made for a mental abnormality lacks complete accuracy and assurance.
So such speculated mental illnesses can only be assessed conceptually. As a result, the diagnosis or impression concluded by the patient’s health care provider is dependent on subjective criteria expressed by the suspected patient that is presumed to be not mentally sound.
At times, there have been screening programs that have been used for identifying depressed patients have proven to be largely ineffective.
A social patient history is uncertain and tricky as well, some have said, yet is obtained often from such patients. There is no objective diagnostic testing for any mental malfunction to validate as to whether or not such a disease is present- just the perception of the health care provider, and survey questions related to a particular mental disorder.
A health care provider has to assess as to whether certain non-verbal or vocalized features are present with a patient in order to conclude confidently that one may have in fact some degree or level of depression or any other mental disorder.
To assess a suspected depressed patient is further complicated by the fact that the exact cause of major depression is unknown. Research says that there is a strong genetic component to this illness, however.
The diagnosis of depression as well as mood disorders that may exist within patients has increased quite a bit over the past few decades. Some have asked themselves, as well as others- actually how many people are really and actually depressed, or affected by any other mental disorder?
What is believed is that if one determined to be cognitively impaired from a mental paradigm, then this may be in fact major depression. If this mental disorder is determined by a health care provider, it is possible that pharmacological therapy may be considered reasonable and necessary, as well as psychotherapy either suggested to be performed with or in place of medicinal therapy.
Studies show that both therapies working together may be of most benefit for the depressive patient, yet it is not a guaranteed protocol for treatment in this way.
It has been reported that around 10 percent of the U.S. population will at some point be affected by an episode of what may be a major depressive disorder. This is much greater in number than just a few decades ago.
Perhaps media sources are to blame to some degree for the progressive increase in diagnosing mental disorders by suggesting to the public that they may have such disorders. So the diagnosis and medicinal treatment have clearly increased in a relatively short period of time in the United States.
Of course, the expansion of those claimed and determined to be depressed does not sadden the makers of these drugs used to treat this mental disorder one bit, it is safe to say.
Some have said that so many more people seek treatment now for what they believe is a major depressive disorder they are experiencing, when in fact it may be possibly intense sadness, perhaps, due to a loss of some sort in their lives. There is a difference, and health care providers should have the appropriate tools and knowledge to discriminate between the two states of mental conditions.
Sadness is not a medical problem. Symptoms associated with an unfavorable mental state need to be excessive and chronic to be considered to have in fact the medical problem of a major depressive disorder, as stated by others.
In Time magazine’s June 16th 2008 cover story, it was reported that the military personnel in the Iraq war are pounding down SSRIs often. Every time there is a new war, there is a new drug, it seems. Yet the story may illustrate the frequent usage of these types of medications in a variety of different areas for different reasons.
Some reasons may be valid and appropriate, yet others perhaps may not be reasonable for such medicinal therapy. However, as illustrated in this situation, they appear to be accepted as a treatment option without reservation.
In regards to those pharmaceutical companies who make and market such psychotropic drugs in the manner that their manufacturers do is largely unknown to others, such as with screenings performed essentially by front groups, and so forth.
However, what is known is that the psychiatry specialty, as they often treats and manages depressed patients, is the one specialty that receives the most monetary funding that is paid to them by these certain pharmaceutical companies for ultimately what they hope will be continued and additional support of the psychotropic meds that they currently promote to these doctors.
Needless to say, the desire and the aspect of the pharmaceutical industry clearly is primarily concerned with encouraging as much use out of their products as possible- with both doctors and patients being the route of that increased use they desperately hope will occur.
Regardless, SSRIs and SRNIs are the preferred treatment methods if depression or other mood disorders that are suspected and determined by the health care providers who treat such patients. Yet these drugs discussed clearly are not the only treatments, medicinally or otherwise, for depression and other related and suspected mental disease states, moods, or disorders.
Patients should be aware of this fact as well as caregivers. And they may not be aware of the options available to them.
For example, tens of millions of prescriptions are written by health care providers for these types of medications for their patients.
These drugs are not inexpensive, either, as it is not unusual for a patient to pay greater than one hundred dollars to have their prescription filled for only a month’s worth of these particular drugs.

Presently, there are about ten different SSRI/SRNI meds available, many of which are now generic, yet essentially, they appear to be similar in regards to their efficacy and adverse events.
The newest one, a SNRI called Pristiq, was approved in 2008, and is believed to be launched as a treatment for menopause.
The first one of these SSRI meds was Prozac, which was available in 1988, and the drug was greatly praised for its ability to transform the lives of those who consumed this medication in the years that followed. Some termed Prozac, ‘the happy pill’.
In addition, as the years went by and more drugs in this class became available, Prozac was the one of preference for many doctors for children. A favorable book was published specifically regarding this medication soon after it became so popular with others.
Furthermore, these meds have received upon request of their makers to the FDA to have additional indications besides depression for these types of drugs they produce and market, and the indications they have received are for some really questionable conditions, such as social phobia and premenstrual syndrome.
Also included with indications that now exist with these types of medications are the quite devastating conditions of what may be mild anxiety and shyness, yet the makers of these drugs consider such patients as having chronic anxiety with severe anxiety disorder, which others have said is rather obsurd.
And it gets worse with the indications received for these types of drugs, which now include Obsessive-Compulsive Disorder, Panic Disorder, Agoraphobia, Post Traumatic Stress Disorder, Bulimia, and any form of stress disorders in general. I understand they are seeking indications for pain management as well with these SSRI or SRNI pharmaceuticals.
Likely, they will get the indication for their drugs to treat such creative cognitive states apparently others have in great numbers.
With some of these indications for these classes of drugs, I question as to whether or not they are actual and treatable disease states or medical problems. Yet with additional indications for particular drugs in these classes of medications, one can be assured that the market for these drugs will continue to grow- as more are prescribed to those patients who are progressively asking for them specifically for relief they anticipate they will receive from taking these drugs.
What such patients are not aware of is that studies have shown that this class of medications is only effective in roughly half of those who take them. And some of the indications granted to drugs in these classes of medications may be considered disease mongering tacitly performed by the makers and marketers of these drugs to again grow the market share for particular drugs of this type.
This is combined with drug companies who make these types of meds either forming or creating front groups in order to have more diagnosed with various medical problems that may not exist so their medication can be utilized more.
And as mentioned earlier, such pharmaceutical companies have been known to either create or support front groups to ultimately encourage who may be normal people to get evaluated for the diseases indicated with these medications. Of course, such tactics implemented by such pharmaceutical companies are deceptive, inappropriate, unreasonable, unnecessary, and potentially if not actually dangerous to others.
Perhaps of greater concern and danger with these particular psychotropic medications involve the adverse effects associated with these types of drugs, which include suicidal thoughts and actions, violence- including acts of homicide, and aggression- and this is only to name a few. Such events are devastating and have been demonstrated by those who have or are taking these types of drugs.
It has been reported that the makers of such drugs are suspected to have known about these toxic and dangerous effects of their drugs and did not share them with the public in a timely and critical manner until forced to do so.
While most SSRIs and SNRIs are approved for use in adults only, prescribing these meds to children and adolescents has drawn the most attention and debate with others for understandable reasons, which have included those in the medical profession as well as citizen watchdog groups.
The reasons for this attention are due to the potential off-label use of these meds in this population of children, yet what may be most shocking is the fact that some of the makers of these meds did not release clinical study information about the risks of suicide as well as the other adverse events related to such populations, combined with the true decreased efficacy of SSRIs in general, which is believed to be only less than 10 percent more effective than a placebo.
The makers of Paxil caught the attention of the government regarding this issue of data suppression some time ago, this hiding of such important information- Elliot Spitzer specifically was the catalyst for this awareness, as I recall.
Furthermore, that drug is in the spotlight once again years later. Some believe the drug maker knew about possible risk to the youth as early as 1991. Yet did not disclose such danger associated with their drug to the public or the FDA, and this was done with intent.
And there are very serious questions about the use of SSRIs in children and adolescents regarding the possible damaging effects of these meds on them as they get older- these children and teenagers who are prescribed these drugs. Others are asking if this is really necessary- and are these drugs doing more harm than good for their children.
For example, do the SSRIs correct or create brain states considered not within normal limits, which in effect would possibly cause harm rather than benefit a patient on such a drug? Are adolescents really depressed, or just experiencing what was once considered normal teenage angst?

Do SSRIs have an effect on the brain development and their self identity of such young people? Do adolescents in particular become dangerous or bizarre due to SSRIs interfering with the myelination occurring within their still developing brains?
No one seems to know the correct answer to such questions, yet the danger associated with the use of SSRIs does in fact exist, as demonstrated by others. It is observed in some who take such drugs, but not all who take these drugs.
Yet health care providers possibly should be much more aware of these possibilities, possibly, along with the black box warning now on SSRI prescribing information for the youth that has existed since 1994. There are other medications health care providers could prescribe for such patients that have no less benefit for them then the serotonin drugs discussed.
Finally, if SSRIs or SNRIs are discontinued by a patient rapidly, abruptly, and without medical supervision, withdrawals experienced by many of these patients are believed to be quite brutal that follow soon after this drug is not taken anymore by a former patient. This in itself may be a catalyst for one to consider or attempt suicide, others have suggested.
Many are aware and understand that discontinuing these SSRIs and SSNIs leaves the brain in a state of neurochemical instability for some great length of time as the neurons need to recalibrate after existing in a brain over-saturated with serotonin and neuron alteration.
This occurs to some degree with any psychotropic medication, yet the withdrawals can reach a state of danger for the victim in some classes of meds such as SSRIs and SNRIs, it is believed. And this seems to concern many, yet does not inhibit health care providers for continuing to select such therapy with these drugs for their patients.
SSRIs and SRNIs have been claimed by doctors as well as patients to be extremely beneficial for the patient’s well -being regarding their apparent mental issues that resolve in time. Yet overall, the factors associated with this class of medications may outweigh any perceived benefit for the patient taking such a drug that can harm themselves and others.
Before these medications mentioned were developed, doctors praised trycyclics, another class of anti-depressants mentioned earlier, in a similar manner since their advent in the 1950.
Considering the lack of efficacy that has been demonstrated objectively with these new serotonin specific psychotropics, along with the deadly adverse events with these SSRI and SSNI meds only recently brought to the attention of others, other pharmacological and non- pharmacological treatment options should probably be considered, but that is up to the discretion of the prescriber.
And the perception of the benefits derived by these types of drugs may be flawed, as there has been no decrease in incidences of suicide or remission of depression since these drugs have been available, many have concluded.

Yet antidepressants in general have been considered by others to create amotivational syndrome, which is a lack of interest in various activities, as well as creating a state of flat affect of users of antidepressants.
Furthermore, recent studies have suggested that the supplement, St. John’s Wart, has shown to be as effective as medicine for major depression. Deficiencies in vitamins B12 and Folate have been suggested as a cause for depression as well. One study showed that a small jog performed by a depressed patient offered similar if not greater relief than a SSRI drug.
It is my hope that such a prescriber rules out possible other etiologies for their patients’ mental conditions before they conclude that such a patient is suffering from true mental illness requiring the medications mentioned earlier, such as asking their patients about life stressors and other medications these patients have taken or are presently taking. Because at times, a doctor can in fact do harm without intent.
“I use to care, but now I take a pill for that.” ---
Author unknown*
www.nmha.org
www.nami.org
Dan Abshear

posted in Effexor Activists Tribe - 2 replies

Fucked for life?

2009-03-22T05:54:49Z

Does *any*one have any success stories about getting off of this shit?!
All I read about is RLS, nausea, aches, pain, insomnia, depression, ad nauseum....
So, are we fucked for life?

posted in Effexor Activists Tribe - 4 replies

Antidepressant labels to carry new warning of life-threatening side effect

2009-02-13T01:06:32Z

http://latimesblogs.latimes.com/booster_shots/2009/02/antidepressant.html
Antidepressant labels to carry new warning of life-threatening side effect
1:12 PM, February 5, 2009
The FDA has ordered a wide range of antidepressants to carry new warnings of an unusual but potentially deadly side effect seen most often in the first few weeks of treatment or when a patient increases dosages. The labels of two classes of new-generation medications for depression -- selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) must now notify patients that malignant neuroleptic syndrome has been linked to the use of these drugs.
Among the drug companies ordered to revise their labels to alert patients of the danger were those making Celexa, Cymbalta, Effexor, Lexapro, Paxil, Pexeva, Pristiq, Prozac, Venlafaxine and Zoloft. The orders were dated Feb. 4, but disseminated this morning in a public notice of FDA actions.
In malignant neuroleptic syndrome, patients experience muscle rigidity, extreme variations in body temperature and wild fluctuations of heart rate and blood pressure -- all signs of malfunction in the body's autonomic nervous system, which regulates involuntary body functions. Malignant neuroleptic syndrome has been associated with older antipsychotic medication such as haloperidol, lithium salts and risperidone. But the widespread use of SSRI and SNRI antidepressants has made this syndrome a more common and visible affliction.
With one in 10 Americans taking prescription antidepressants, medicines such as Zoloft, Prozac and Effexor are currently the most commonly prescribed class of drugs in the United States, just ahead of high-blood pressure medicine, according to the Centers for Disease Control. And SSRIs and SNRIs have become by far the most common types of antidepressant dispensed by pharmacies, driving a tripling of prescriptions since 1988.
Malignant neuroleptic syndrome is a rare but extremely dangerous condition that results in death in, by some estimates, 10% to 20% of cases. Until recently, it was so uncommon it was unlikely to be recognized in many emergency departments. But the widespread use of SSRIs and SNRI antidepressants had made this bizarre syndrome a more common affliction seen in emergency departments.
A Food and Drug Administration spokeswoman said this afternoon that she had not been notified of the labeling change and was unaware of what lead to it.

eMedicine Specialties > Psychiatry > Emergency
Neuroleptic Malignant Syndrome
Joseph Tonkonogy, MD, PhD, Clinical Professor of Psychiatry and Neurology, University of Massachusetts Medical School; Consulting Staff, Departments of Psychiatry and Neurology, University of Massachusetts Medical Center
Darius P Sholevar, MD, Fellow, Cardiovascular Disease, Albert Einstein Medical Center; Ellen H Sholevar, MD, Director of Child and Adolescent Psychiatry, Associate Professor, Department of Psychiatry, Temple University School of Medicine
Contributor Information and Disclosures

Introduction

Neuroleptic malignant syndrome (NMS) refers to the combination of hyperthermia, rigidity, and autonomic dysregulation that can occur as a serious complication of the use of antipsychotic drugs. Delay first used the term in 1960, after observing patients treated with high-potency antipsychotics.
Even the newer atypical antipsychotics, which are not classified accurately as neuroleptics, can cause NMS. Over the past 30 years, the syndrome has been associated with a variety of drugs that lead to decreased dopamine receptor activation.
While some clear risk factors for NMS are present, the low incidence of this syndrome and the consequent difficulty in studying it in a controlled, prospective manner make clinical features, predisposing conditions, treatment, and prognosis difficult to define.
Pathophysiology
The most widely accepted mechanism by which antipsychotics cause NMS is that of dopamine D2 receptor antagonism. In this widely accepted model, central D2 receptor blockade in the hypothalamus, nigrostriatal pathways, and spinal cord leads to increased muscle rigidity and tremor via extrapyramidal pathways. Hypothalamic D2 receptor blockade results in an elevated temperature set point and impairment of heat-dissipating mechanisms. Peripherally, antipsychotics lead to increased calcium release from the sarcoplasmic reticulum, resulting in increased contractility, which can contribute to hyperthermia, rigidity, and muscle cell breakdown.
Beyond these direct effects, D2 receptor blockade might cause NMS by removing tonic inhibition from the sympathetic nervous system. The resulting sympathoadrenal hyperactivity and dysregulation leads to autonomic dysfunction. This model suggests that patients with baseline high levels of sympathoadrenal activity might be at increased risk. While this has not been proven in controlled studies, several such states have been proposed as risk factors for NMS.
Direct muscle toxicity also has been proposed as a mechanism of NMS.
Frequency
United States
NMS is associated with the use of various antipsychotic medicines, most frequently the older antipsychotics, termed neuroleptics. Development of NMS appears to be independent of the conditions that these medicines treat.
The syndrome can occur after any duration of treatment, although two thirds of cases occur within the first week. The frequency has been variably reported as 0.07–2.2% of patients taking neuroleptics. Data largely come from case control studies rather than prospective randomized trials.
International
The frequency of NMS internationally parallels the use of antipsychotics, especially neuroleptics, in a given region. No data suggest geographic or racial variation. The one large randomized trial conducted in China showed an incidence of 0.12% in patients taking neuroleptics. A retrospective study conducted in India showed an incidence of 0.14% (Chopra, 1999).
Mortality/Morbidity
Mortality from NMS is very difficult to quantify due both to the case report designs of most of the literature and to the inconsistency of the diagnostic parameters used.
• In some series, mortality rates as high as 76% have been reported. Most series suggest, however, that the mortality rate is 10-20%. When reporting bias is factored in, the true rate of mortality from NMS might be much lower.
• Studies have also found that the mortality rate has been decreasing over the past 2 decades. Mortality is generally higher in patients who develop severe muscle necrosis and resulting rhabdomyolysis.
Race
No data suggest geographic or racial variation.
Sex
Incidence is higher in males.
Age
• Incidence is higher in persons younger than 40 years. Differential incidence simply might reflect a population that has a high rate of antipsychotic usage.
• Some small case series looking at NMS in elderly patients suggest that onset might occur after a longer duration of antipsychotic use.
• Studies in children suggest that clinical presentation might be somewhat different.
Clinical
History
• Criteria for the diagnosis of NMS are based on clinical features. Cardinal features are the development of severe muscular rigidity, hyperthermia, autonomic instability, and changes in the level of consciousness associated with the use of an antipsychotic medication, most often a neuroleptic.
• In addition to hyperthermia and rigidity, at least 2 other clinical features of NMS, including leukocytosis and laboratory evidence of muscle injury, should be present.
• The key to diagnosis is that symptoms occur only after exposure to antipsychotics. Symptoms should improve after the antipsychotic is stopped. No new focal neurological deficits should develop, although cases of neurological sequelae have been reported rarely.
• A summary of the clinical features of NMS includes the following:
o Diaphoresis
o Dysphagia
o Tremor
o Incontinence
o Delirium, mutism progressing to lethargy, stupor, coma
• Labile blood pressure
• Pallor
• Dyspnea
• Psychomotor agitation
• Rigidity
• Hyperthermia
• Tachycardia
• Shuffling gait
• For accurate diagnosis, rule out reaction to another medication or medical condition that might be a more likely cause of the symptoms than use of an antipsychotic.
• Various other medications cause conditions that are indistinguishable from NMS and likely involve similar chemical structure and the same pathophysiology. All of these agents, including metoclopramide, prochlorperazine, promethazine, and droperidol, cause decreased dopamine receptor activation.
• A similar syndrome also has been associated with the rapid removal of medications with dopaminergic properties (eg, in patients treated for Parkinson disease). Medications in these classes often are used to treat Parkinson disease and include levodopa, bromocriptine, and amantadine. Dopaminergic drugs should be started as soon as possible to prevent rhabdomyolysis and renal failure.
• Lethal catatonia (LC) is a similar condition that might be confused with NMS. LC occurs in people with schizophrenia or during manic episodes. Neuroleptics might either improve or worsen the symptoms of LC. Distinguishing LC from NMS can be difficult, although a detailed history might reveal episodes of catatonia while a patient is not taking neuroleptics. LC also tends to have a prodrome of excitement and agitation prior to the onset of rigidity, while NMS tends to begin with rigidity.
• Antipsychotics can cause a variety of reactions that can be confused with NMS. These reactions often occur with increasing medication dosages. Neuroleptic-induced acute dystonia is an abnormal contraction or spasm of a group of skeletal muscles, often involving the head or neck. Neuroleptic-induced acute akathisia is motor restlessness, particularly involving the legs. Neuroleptic-induced tardive dyskinesia involves involuntary, rhythmic movements starting with mouth movements. Neuroleptic-induced parkinsonism, or pseudoparkinsonism, presents with the classic triad of tremor, muscular rigidity, and akinesia. Despite the term neuroleptic-induced, these conditions also can be caused, although less frequently, by many of the newer, nontraditional antipsychotic medications as well. In future editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM), the terminology might be changed to include nonneuroleptic antipsychotics.
• The serotonin syndrome is very similar to NMS. The triad of (1) altered mental status, (2) autonomic dysfunction, and (3) neuromuscular abnormalities that occurs on exposure to serotonergic agents characterizes the serotonin syndrome. Selective serotonin reuptake inhibitors (SSRIs) are the most frequently used medications in this class. The proposed mechanism is excessive 5-hydroxytryptamine (5-HT or serotonin) stimulation. Given the increasing use of the SSRIs, the serotonin syndrome might become increasingly prevalent. The serotonin syndrome can be distinguished from NMS in most cases by a detailed history of medication use with particular attention to recent dosage changes and the absence of severe rigidity. Treatment of this condition includes removal of the offending drug and supportive management, though 5-HT1A antagonists might have a role in the future.
• Medication-induced movement disorders not otherwise specified can be very similar to NMS but occur on exposure to other psychotropic medications. Malignant hyperthermia (MH) occurs after administration of halogenated inhalational anesthetics, such as halothane, and depolarizing muscle relaxants, such as succinylcholine, to genetically susceptible individuals. An underlying defect is an autosomal dominant mutation in the ryanodine receptor, which leads to excessive calcium release from the sarcoplasmic reticulum in skeletal muscle when one of the above agents is administered. A multifactorial pattern of inheritance also has been postulated. MH can be distinguished readily by history. Treatment is based on supportive care, use of dantrolene to decrease calcium release, and avoidance of precipitating medications. No evidence shows that NMS occurs more frequently in patients susceptible to MH.
• Heat stroke can cause a similar picture, but patients have dry skin and flaccidity in addition to hyperthermia and hypotension.
• General medical conditions that might mimic NMS include central nervous system infections, status epilepticus, stroke, brain trauma, neoplasms, acute intermittent porphyria, and tetanus.
• Laboratory abnormalities observed in NMS have broad differential diagnoses and only specific points are presented in this chapter (see Lab Studies). Elevated creatinine kinase (CK) can be observed with intramuscular injections and the use of restraints. Leukocytosis occurs with central nervous system infections.
Physical
NMS tends to start with muscular rigidity and progress to hyperthermia with autonomic instability and a fluctuating level of consciousness. Compared to disease in adults, NMS in children and adolescents tends to present with more dystonia and less tremor.
• Symptoms of autonomic dysregulation include high fever, diaphoresis, tachypnea, tachycardia, and increased or labile blood pressure. In rare cases, a reversible cardiomyopathy mimicking cardiac infarction may develop the autonomic involvement in the course of NMS.
• Extrapyramidal symptoms include so-called lead pipe rigidity; dysphagia; a short, shuffling gait; resting tremor; dystonia; and dyskinesia.
• Tremor and excessive or purposeless motor activity can reflect psychomotor agitation.
• Delirium, mutism, incontinence, lethargy, stupor, or coma can reflect changes in the level of consciousness.
• Other features include pallor, rash, and dyspnea.
Causes
All classes of antipsychotics have been associated with NMS, including low-potency neuroleptics, high-potency neuroleptics, and the newer (or atypical) antipsychotics. NMS has been reported most frequently in patients taking haloperidol and chlorpromazine.
• The clearest risk factors relate to the time course of therapy. Strongly associated factors are the use of high doses of antipsychotics (particularly the high-potency neuroleptics), rapid antipsychotic dosage increases, and the use of depot, the long-acting injectable forms of antipsychotics. In the United States, only 2 long-acting forms are available at present—fluphenazine decanoate or enanthate and haloperidol decanoate.
• Other factors related to a patient's pharmacotherapy might be relevant, although their role has not been proven in controlled studies. Inconsistent use of neuroleptics and the use of other psychotropic medications, particularly lithium, have been suggested as risk factors. Prior treatment with electroconvulsive therapy (ECT) also has been proposed to have a role.
• Environmental and psychological factors that might predispose to NMS are hot and humid conditions, agitation, dehydration, and exhaustion.
• A number of demographic features have been implicated, many of which simply might reflect populations that have a high rate of neuroleptic usage. These include male sex and age younger than 40 years. NMS has been reported in postpartum women.
• Genetic factors also might play a role. Case reports have been published on NMS occurring in identical twins as well as in a mother and 2 of her daughters.
• Patients who have experienced episodes of NMS previously are at risk for recurrences. The risk of recurrence is strongly related to the elapsed time between an episode of NMS and restarting antipsychotics.
o If patients are rechallenged with antipsychotics within 2 weeks of an episode of NMS, 63% will have a recurrence. If more than 2 weeks have elapsed, only 30% will have a recurrence.
o Eighty-seven percent of patients who develop NMS will be able to tolerate an antipsychotic at some point in the future. Given the present understanding of this syndrome, on reintroducing an antipsychotic, switch to a different antipsychotic class and, if possible, use an atypical antipsychotic because these might be less likely than traditional neuroleptics to cause NMS.
• A summary of medications that may induce movement disorders includes the following:
o MAOIs
o MAOIs combined with tricyclic antidepressants
o MAOIs combined with serotonergic agents
o MAOIs combined with meperidine
o Lithium at toxic levels
o Anticholinergics
o Amphetamines
o Fenfluramine
o Cocaine
o Phencyclidine
o 3,4-Methylenedioxymethamphetamine (MDMA; ecstasy, XTC)
o Methylphenidate
• A summary of the well supported risk factors for NMS includes the following:
o High-potency neuroleptic use
o High-dose neuroleptic use
o Rapid increase in neuroleptic dose
o Depot injectable neuroleptic use
o Prior episodes of NMS
o Age younger than 40 years
o Male sex
• A summary of the potential risk factors for NMS includes the following:
• Dehydration
• Agitation
• Exhaustion
• Malnutrition
• Organic brain syndromes
• Nonschizophrenic mental illness
• Lithium use
• Past history of ECT
• Warm and humid environments
• Inconsistent use of neuroleptics
• Postpartum period

They can now add antidepressants to this list. I feel I have had this as I had all the symptoms but even tho I went to three or four different emergency rooms in different citys I could not get a diagnosis the only thing that saved me was cold turkey withdrawal.

posted in Effexor Activists Tribe - 1 reply

My experience coming off of Effexor

2009-02-08T23:56:38Z

Hello -

I have been taking 300mg/day of Effexor (not XR or XL) for over 6 years. Approximately 3 years ago, I switched to the generic. Over the past two months, I started decreasing my dosage incrementally. About two weeks ago, I took my last dose. My physician has advised me of the tough time I may have coming off this medication - and I have been following discussions online with similar prediction.

I can confirm my withdrawal experience from Effexor has been, and continues to be fierce. Mentally, I feel superb and better than I've felt in a very long time. Physically, however, my body is having a tough time adapting. I've read a lot of posts about "brain shivers" - I experience something similar, almost like my brain is about a half-second behind the rest of my body when I'm moving my head in a visually stimulating environment such as driving, watching TV, reading, etc. I've experimented by moving my head with my eyes open, and with my eyes closed. I do not experience the "shivers" when my eyes are closed, however I do when they're open. I can extrapolate a connection between visual stimulus and the movement of my head ... I can't explain it ... but it's there. The only recent change in my life and environment is the removal of Effexor - so the experiences I'm having must have to do with coming off the medication.

My body, in general, aches like I've been running a marathon. It's similar to what I feel when noticing that I'm beginning to get the flu. I often feel nauseous, and I've vomited several times - not from the usual stomach kinds of ailment, but rather from what I think might be a form of motion sickness. If I weren't aware of the withdrawal symptoms before actually coming off Effexor, I could easily see slipping back into depression simply from these crazy physical symptoms.

As I mentioned, however, mentally I feel exceptional. I have had no further symptoms of depression that I can point to at this juncture. A near immediate and very positive affect of stopping Effexor, for me, has been the return to normal sexual function. It's amazing to me what a "depressing" affect Effexor had on my sexual health. Before, I was rarely in the mood for sex, and it often took a tremendous amount of effort to reach orgasm - and I'm a guy!!! Although I'm now 40, I feel like I'm 18 again. This, for me, is truly amazing, and I will be asking myself, in future, whether the side effects of any drug are worth the benefit.

Considering the very negative side effects, and conversely the very positive side effects of removing the drug from my system, I can surmise that Effexor was not a good drug choice for me. My experiences with the side effects run the extreme - very extreme. There's not been a middle ground for me. It's both good and bad that I had to stop taking Effexor to realize these things.

My advice to anyone attempting to come off of Effexor - hang in there. I am not a medical professional, but in my opinion, the best thing you can do for yourself is to get Effexor out of your system. Keep close connection with your health professional and be sure to report renewed feelings of depression or loss of hope. There are lots of anti-depression drugs available - ones that may work better for you than Effexor.

posted in Effexor Activists Tribe - 0 replies

3-18 months after antidepressants this is what to expect.....and what not to do now.

2009-01-29T16:17:04Z

http://web.archive.org/web/20071010132124/www.antidepressantsfacts.com/reaction.htm

This is a bout a reaction which seems the same to me as what happen when you quit taking the meds.

By Charly Groenendijk
The Netherlands
Sept 9, 2000

You experienced a negative reaction to an (SSRI/SNRI) AntiDepressant, what (not) to do Now?

"Who does Not Know the Truth, is simply a Fool...
Yet who Knows the Truth and Calls it a Lie, is a Criminal."
- In "Galileo Galilei" by Berthold Brecht (1898-1956)
Go to General Side-Effects SSRI/SNRI/SSNRI Antidepressants: cases, reviews, articles & studies
Go to Tapering Off Anti-depressants
Go to Introduction
Take notice that also non SSRI anti-depressants (and even Ritalin) may interact (primary or secondary) with the serotonergic (or serotoninergic) system in the brain.

After your reaction to an (SSRI/SSNRI) Anti-Depressant
The first 3-18 months
One of the long term side-effects after experiencing a reaction to an (SSRI) antidepressant, is an extreme hyper-sensitivity of the nervous system to light, sound, supplements, herbs and fabricated synthetic vitamins. Furthermore physical symptoms such as muscle tightness, electrical shocks through the brain and the body, feelings of burning on the surface or inside of the skin (deregulation of pain perception), visual and/or auditory hallucinations, as well as emotional and psychological problems. For a more detailed discussion regarding above mentioned side-effects click here.

We do not recommend to expose your body to synthetic chemicals whilst experiencing more or less severe hypersensitivity of the nervous system. We rather recommend to get your essential elements from preferably organic low acid food. Low acidic foods have a high pH value which is ALKALINE or BASIC! You need to 'alkalinize' your system (body) above a pH value of '7' !

Eat enough fruit and vegetables in a variable alkalinizing balanced diet, and drink lots of water. For instance tomatoes, bananas, kiwi's, broccoli, aloe vera, carrots, cabbage, beans, cucumbers, etc., are a very rich source of essential minerals, vitamins and amino acids. Do not take 5-HTP to create more serotonin in your brain. By simply leaving your serotonergic neural system alone, you will assist it the most to find it's own natural balance again. Unfortunately this will take some time.

Do not charge your nervous system like you always did before your reaction to an (SSRI) antidepressant. If you charge your nervous system too much, like too much stress, a surgery, unhealthy eating patterns, etc., you actually delay your recovery. You will have to learn to listen to your body, what means that you know when to withdraw and when to get active.

When you suffered a reaction to an (SSRI) antidepressant your nervous system becomes hyper-sensitive to ALL stimuli. What are stimuli? It is everything that acts on your nervous system (directly or indirectly) like light, sound, but also violence on TV, stressors, certain supplements or fabricated vitamins, etc. All these things act as stimulants to your nervous system. Actually the effects of a psychoactive drug and watching a horror movie are very much comparative to each other...that is: they BOTH act on your nervous system!

The key solution to recovery is NOT to stimulate your nervous system, but, to sedate your nervous system. Every time when you stimulate a nervous system that in fact needs to be sedated to recover, you delay the process of healing. We know it will be impossible to lock your self up in a dark, silent room and this is definitely not what we are trying to say. You just have to learn when to withdraw yourself (and thus your nervous system) from stimuli and when to come out.

Consider sweat baths (sauna baths). This is a very healthy habit. Sweat baths are extremely sedating to the nervous system. When you take a sweat bath on a regular base this will strengthen your cardiovascular system and improve the blood circulation. Next to this, go out in nature, trees, green, oxygen, gentle walking, etc..

About taking supplements
We learned that everyone who is experiencing (SSRI) antidepressant side-effects, is looking for the quick relief. People are experimenting with whatever supplement or fabricated synthetic vitamin they can get their hands on. Simply avoid this if that is possible.

As previously mentioned above, we do not recommend to expose your body to synthetic chemicals whilst experiencing more or less severe hypersensitivity of the nervous system. We rather recommend to get your essential elements from preferably organic low acid food in a variable balanced diet.

Two to three simple bananas and kiwi's, an egg-sandwich, 2-3 glasses of milk, a few tomatoes and an avocado a day provides many of the essential vitamins, (trace)minerals & amino acids you need on a daily base. Vegetables especially rich in essential elements are: Peas, Potatoes, Broccoli, Squash (Summer), Spinach, Lima Beans & Kale. The taste of nature is nice and it saves you money on unnecessary supplements too!

However we also understand that getting your essentials from a variable diet requires some skills in preparation and cooking of your daily meal. Not everyone is able or willing to do that. In that case you need to add your essential elements otherwise. We understand if you feel the need to take a daily multi-vitamin complex. There are many different multi-vitamin complex products, unfortunately a lot of rubbish amongst them. Most of them contain extra added synthetic chemicals which you must avoid. If you are going to take a multi-vitamin complex you need to be aware of the following:

make sure that it doesn't contain Vitamin K. Vitamin K plays a role in the manufacture of blood clotting. Too much of this vitamin might interact with plasma serotonin which is also known to make blood form cloths (see article, "2.a. Serotonergic functioning"). Although there is more research needed regarding this matter, the anecdotal reports of (former) (SSRI) antidepressant users imply fabricated vitamin K as a cause for the worsening of their already exisiting symptoms.
make sure that ALL B-vitamins are low(never above the daily recommended standard). It is important to note that most B-vitamins work as stimulants to the nervous system. You need to avoid that.
make sure that the B3 compound is as niacinamide and NEVER as niacine (this will give a flush which could make you re-live all of your symptoms again).
Depending on the severeness of the reaction you experienced to an (SSRI) antidepressant we also recommend that if you decide to take your essential elements otherwise, to take calcium/magnesium/zinc in a vegetarian formula. Never exceed the daily dose of Calcium 1000mg, Magnesium 400mg and Zinc 15mg. Although calcium/magnesium/zinc are not known to act as stimulants, caution is needed. Always start with small amounts (1/6 of the daily dose), gradually build up and keep monitoring yourself.
In these first 3-18 months the cycles or the emotional rollercoasters (the tricks your brain is playing on you) can be extremely frightening. And it will seem like it never ends, especially when you find a bit of hope in the evening to be back at square one in the morning. Be firm! We all understand its the most frustrating experience right now for you. It's serotonin related and that's why you are experiencing delayed (withdrawal) side effects and flashbacks, but gradually it will get better. Evaluate your recovery by weeks and months, not days.

You are going to experience minutes, hours and days that you will start to feel better. The cycles will get longer in duration and eventually you will have more good then bad days. Though, it is most important you also treat your nervous system with care during these better days. Don't think when the better days arrive that you can charge your nervous system like you always did before. It will give you a major set-back! Stick to the list we provide you below, on how to assist your recovery during this period.

Friends and Family
These times are very tough to experience. Your friends and family cannot even imagine the powerful influence these drugs have on your mind and your sub-consciousness. They simply cannot believe that these drugs can have such a powerful effect on someone's brain. You might loose your trust in them after this. Try to accept and understand their ignorant and frustrating reactions. Avoid them for a while, if that's possible.

How can I assist my recovery during this period?

Avoid any psycho-stimulants such as medications, herbs, but especially: violence on TV. Why? Because right now your nervous system has become hyper-sensitive and extremely susceptible to every input from your surroundings, not only light and sound! You must also protect your sub-consciousness until you reach a level of emotional stability.
Ingest low acid foods and try to minimize the ingestion of high acidic foods with a low pH-grade! REMEMBER: You need to 'alkalinize' your system (body) above a pH value of '7' !
Avoid Grapefruit Juice. Grapefruit juice is an inhibitor of the cytochrome P-450 enzymes. These enzymes are known to metabolise (break down) (SSRI) antidepressants in the liver. Drinking grapefruit juice whilst you are taking an (SSRI) antidepressant can create a serious toxic reaction, because the (SSRI) antidepressant will build to toxic levels in the bloodstream! For more information click here.
No caffeine. Drink lots of chamomile tea, sweetened with honey.
No alcohol.
Don't take Saint John's Worth. St. John's Worth works more or less as a natural SSRI (on post synaptic receptors), also interacting with your serotonergic neural system
Don't take Ma-Huang (Ephedra) because it's a powerful adrenalin (epinephrine) stimulant, triggering adrenalin rushes.
Don't take Kava Kava, it can intensify (SSRI) antidepressant (withdrawal) side-effects or give flashbacks to previous side-effects you experienced.
Eat neutral alkaloids, vegetables, etc..
Consider fasting for 1 to 10 days. Fasting detoxifies your body, but be careful and monitor your bloodsugar levels daily.
Don't do any intensive exercise like jogging or aerobics, but instead try meditation, gentle stretching, gentle walking.
Go out in Nature, or go to a Sauna, or whatever environment where you may find a little peace of mind and body.
Listen to light Classic music or New Age music, watch cartoons (or anything else without violence), go walking, take hot or cold showers, anything that might work for you, anything to "manage" the "twilight zone" of suicidal and offensive thoughts and dissociated emotions.
Focus on memories of events in your past (like childhood memories) which will recall positive emotions. Hang on to them!
Learn during this period, which thought or view will give you any positive emotional response and write this down into the form of an affirmation! Read these affirmations for yourself every morning when you wake up! In this way you will slightly re-program your brain to tune into positive emotions.
Time and Nature will be your best friends in your healing process. In this battle you don't fight to win because you can't. You simply will survive it. Focus on the thought to survive this, and you will, just as other individuals did. Don't force yourself to become the person again that you were before this, but make a statement to yourself that you will come out of this "trip." Make this statement to your self everyday, every hour.
Whilst You are Recovering...
We strongly persist not to take any supplements, herbs and/or synthetic vitamins until your nervous system has strengthened over time. Continue to ingest proper food, vegetables and fruit during this period. Treat your nervous system with care. As mentioned above: don't think when the better days arrive that you can charge your nervous system like you always did before. It will give you a major set-back! Be careful and monitor your body closely whilst you are ingesting a supplement or herb.

posted in Effexor Activists Tribe - 5 replies

toxic buildup of chemicals from dying muscle cells, and liver cell death

2009-01-10T06:41:40Z

EFFEXOR: COURT CASES

Antidepressant Effexor Poses Fatal Overdose Risk

Effexor, the world’s most lucrative antidepressant has been found to pose a risk of overdose and even death in patients taking the drug. Effexor is for the treatment of major depressive disorder, and is most frequently prescribed for patients with symptoms of depression, generalized anxiety disorder or social anxiety disorder.

In October 2006, the U.S. Food and Drug Administration warned doctors to prescribe Effexor in the smallest possible quantities, to reduce the risk of overdose. In a letter to health-care providers, Wyeth, the maker of Effexor (venlafaxine HCI), stated that death had been reported from overdose of the drug. The letter was posted on the FDA Web site, and requested that doctors prescribe low doses “consistent with good patient management.”

Wyeth's warning letter did not disclose how many Effexor overdose cases had been reported. The most commonly reported Effexor overdose effects include fast heart rate, changes in consciousness (ranging from sleepiness to coma), seizures, vomiting, and eye pupil dilation.

The letter also notes that death, electrocardiogram (EKG) changes, slow heart rhythms, low blood pressure, vertigo, toxic buildup of chemicals from dying muscle cells, and liver cell death have also been reported with Effexor overdoses.
http://www.neurosoup.com/effexorcourtcases.htm

The label revision was also made to the extended-release version of Effexor, known as Effexor XR. The new label notes published studies showing that Effexor's risk of fatal overdoses may be higher than the class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs). The label also notes that the fatal-overdose risk is lower than that of older depression drugs called tricyclic antidepressants. SSRIs include Prozac, Paxil, Celexa, and Zoloft. Tricyclic antidepressants include Elavil and Norpramin.

Register your Effexor Case:

If you or a loved one has been the victim of violent, destructive,or irrational behavior induced by the use of Effexor, you may qualify for damages or remedies that may be awarded in a possible Effexor class action lawsuit.

posted in Effexor Activists Tribe - 12 replies

Sexual Side Effects

2009-01-05T07:09:20Z

I am frustrated with the complete lack of information out there on sexual side effects of SSRI's for women! I have been on Effexor for many years and am now working on weaning myself off of it (with the help of my doctor, based on Sweettooth's article on the Effexor Activist site). I came to realize that my lack of sex drive and thereby, complete lack of interest in a life relationship have made me more depressed over the years, have lessened my motivation, and my artistic inspiration all because of this void in my life.
Any information on help for this side effect seems to deal with erectile dysfunction or immediately suggests options like Viagra without even acknowledging that this symptom may be a problem for women. What's more is that women are statistically more apt to seek treatment for depression than are men!
I have decided to try natural ways of dealing with my depression (lifestyle changes, supplements) rather than remain in this desert of Effexor. Why look for relief of depression in a drug that simply replaces it with a different form of depression?

posted in Effexor Activists Tribe - 14 replies

FIBROMYALGIA as PANES

2008-12-31T20:02:50Z

I have a sneaking suspicion that fibromyalgia may be PANES masquerading as an inflammatory disorder.

I am highly suspicious, because I took Effexor and my chronic pain level doubled post-withdrawal... but never got any less when the drug was introduced.

Everyone I know who was ever diagnosed with fibromyalgia had previously taken an SSRI or an SNRI, either for chronic pain or depression.

Re-introducing a potent SSRI/SNRI such as Cymbalta might actually be treating brain damage and neurotransmitter deficit from prior exposure to serotonin/norepinephrine poisoning.

posted in Effexor Activists Tribe - 3 replies

New Tribe- Public Assistance CA

2008-12-30T02:17:11Z

New Tribe- Public Assistance CA

http://tribes.tribe.net/publicassistanceca

For anyone trying to deal with the endless red tape of public assistance.

posted in Effexor Activists Tribe - 0 replies

Effexor withdrawal symptoms - 1-1/2 years later??

2008-12-30T02:01:54Z

Hello. Can Effexor still be impacting my life a year and a half after withdrawal?

From July 2006 to December 2006 I went through a slow and difficult withdrawal from Effexor 37.5, after being on Effexor for about 10 years or so. I used the program and supplements from theroadback.org faithfully, to help with the withdrawal, and my doctor was aware of the program (He is an alternative MD and is well aware of the hazards of anti-depressants). I had symptoms I called "wooziness" all during that time. I always had such symptoms when I missed a dose by even a couple hours, so I knew it was going to be difficult. But I was determined to stick it out.

I woke up on the morning of November 11, 2006, during the withdrawal period, with a very odd feeling in my head, more dramatic than just "wooziness". I thought I had slept wrong, and blamed it on doing headstands during yoga the night before. I thought I had messed up my neck. I saw neurologists, physical therapists, a dizziness specialist (althought it's not really Dizziness and I don't have nystagmus), chiropractors, a neurologist-chiropractor, eye doctor, and even a reflux doc based on the possibiity that reflux was getting up into my ear canal. No relief from anything I've tried. A recent acupuncture treatment (1 time) seemed to make it worse.

I continued with the Effexor withdrawal through 2006, thinking if it WAS effexor-related, the best thing I could do would be to finally get OFF the stuff. But...

Over 1-1/2 years later (I finished withdrawal December 2006) I still have the symptoms I woke up with that day. It's there when I wake up, when I go to sleep, and if I get up during hte night. It is though I have two weights attached to both sides of my head, and when I move, the weights swing and throw me off balance. Head movement seems to be the main trigger. Walking/hiking is bad. When I turn my head, it feels llike my brain hasn't caught up. Sometimes it's accompanied by what feels like an intense tension headache. The symptoms are never gone, although they may vary. I thought for sure it couldn't be Effexor after all this time...

Is it possible I could still be having Effexor-related symptoms? If so, what the heck do I do now? Should I try to take a low dose for a few days and see if it goes away? If so, at least my question is answered (and not knowing WHAT THIS IS is almost the worst of it). But I'm afraid to swallow Effexor again. But the symptoms are having, and have been having, a serious impact on my quality of life. I struggle through each day. This has been going on since 2006 and I am SO tired of feeling bad.

Any ideas? Help. This is crazy. Thanks.

Wendy

posted in Effexor Activists Tribe - 20 replies

Parkinson's Disease~ New Tribe

2008-12-22T03:59:23Z

I searched, but couldn't find a Parkinsonian tribe, so I just started one:

tribes.tribe.net/parkinsons

Can't write much today, up to my eyeballz in pea soup thick brain fog %^(

posted in Effexor Activists Tribe - 8 replies

permanent damage to your health what is that sex? other things?????? anybody know?

2008-12-21T21:27:00Z

Quote from Leslies post titled if you are in withdrawal :

"Quitting “cold turkey can cause psychosis or."

Thing I am wondering do they know what permanent damage it does cause to your body is there a list some place and is part of this damage sexual dysfunction that does not heal.

As I was force into cold turkey by severe health issues I need to know where can I find that information. Perhaps it is worse than no sex maybe not either way I have a right to this information so I can care for myself in an informed manner.

If anybody has this info please post it I do however suspect it is just this kind of infor that is being withheld. Referred to only in passing in many article I have read never any details or sources. What is with that?

posted in Effexor Activists Tribe - 0 replies

Must see video

2008-12-10T09:29:00Z

http://www.youtube.com/watch?v=gaq54C2R-GY&feature=PlayList&p=8F76BCB2763008C9&index=2

posted in Effexor Activists Tribe - 2 replies

another must see video

2008-12-04T06:10:02Z

http://fiddaman.blogspot.com/2008/11/making-killing.html
This video is in 10 parts so take your time with it. Worth seeing for sure.

posted in Effexor Activists Tribe - 0 replies

Getting better 1year off effexor.

2008-11-27T18:02:53Z

Hi I am a year off effexor and feeling better. Many of the syptoms of withdrawal are gone such as night sweats - zaps- ear ringing-vomitting bile-I no longer need gerd meds- high blood pressure meds or cholesterol meds- I still have pain in the upper right quadrant ( the liver area) the liver cysts have cleared my liver on last ultra sound was still slightly fatty. There are so many symptoms that it is difficult to think of them all if they are not actually present I would say I still am not thinking like I should and my memory is not back to normal. There is an improvement I am hoping for more. I have lost a lot the last few years and think about how to start my life over at 49 with no money job home it is a terrible place to be no doubt but at least I can take extremely ill off the list...now I consider myself recovering.
I am not advocating anything but there are a few things I did that may or may not have helped. Just after the nuerologist ordered the mri of my brain to check for ms I went to a health food store and asked if there were any suppliments for ms...I was given fish oil and have taken it faithfully since for two years. Fish oil supposedly gives your body the essentials to rebuild damaged cells general idea is structual rebuilding needs high hpa functional rebuilding is high epa I am not positive and there are many confilicting reports on this issue I use both high epa high hpa...I think it has helped. There are claims fish oil helps with depression. 7-8 months into withdrawal I experienced the most extreme fatigue back at the health food store I bought a liquid B vitamin high in B12. I took a multivitamin for about 6 months of withdrawal not sure of the benefit of that.
I am not completely out of the woods but physically I am healing.

posted in Effexor Activists Tribe - 2 replies

How long will this take?

2008-11-26T05:08:50Z

This is the question we hear the most at The effexor activists.

I wish we had an answer that fits all. But the fact is, each person responds to withdrawal differently.

For most people it seems to be between 2 weeks to three months depending on How long you were on the drug and how slowly you wean off the drug. As well as your own metabolism.

posted in Effexor Activists Tribe - 5 replies

Health Canada Warns of Venlafaxine Overdosage

2008-11-02T03:17:33Z

Health Canada Warns of Venlafaxine Overdosage, Increased Risk of Fatal Outcome

http://www.docguide.com/news/content.nsf/news/852571020057CCF6852574F20057E6F2

OTTOWA, Ontario -- October 30, 2008 -- Health Canada, along with the manufacturers of extended release (XR) venlafaxine capsules, are informing healthcare professionals of an association between venlafaxine XR overdosage and the increased risk of fatal outcome compared with that observed with selective serotonin reuptake inhibitor (SSRI) antidepressants, but lower than that of tricyclic antidepressants.

Although the extent to which the finding of an increased risk of fatal outcomes can be attributed to the toxicity of venlafaxine in overdosage, as opposed to some characteristics of venlafaxine-treated patients, is not clear, post-market reports of fatal acute overdoses have been received for venlafaxine alone at doses as low as approximately 1 gram.
∑ Prescriptions for venlafaxine XR should be written for the smallest quantity of drug consistent with good patient management, in order to reduce the risk of overdose, particularly in patients who have more severe illness or risk factors for suicidal behaviour.
∑ The potential for suicide attempt in seriously depressed patients is inherent to the illness, and may persist until significant remission occurs. Clinical monitoring for suicidal ideation and/or other indicators of suicidal behaviour is recommended for all depressed patients.
∑ Increased risk of behavioural and emotional changes, including self-harm, has been seen with treatment with venlafaxine, as with other antidepressant drugs, and health care providers, patients, family members and/or caregivers should be vigilant for such changes.

Manufacturers of all extended release venlafaxine products are working with Health Canada to include this safety information in the Overdosage section in all Canadian Product Monographs for venlafaxine extended release capsules.

Any case of overdose or other serious or unexpected adverse reactions in patients receiving venlafaxine XR should be reported to the manufacturer or Health Canada. The manufacturers of venlafaxine XR include Cobalt Pharmaceuticals Inc., Genpharm, Laboratoire Riva Inc., Novopharm Limited, Pharmascience Inc., ratiopharm, Sandoz Canada Inc., and Wyeth Canada.

For a complete list of the manufacturer's addresses and phone numbers, please see: http://www.hc-sc.gc.ca/dhp-mps/alt_formats/hpfb-dgpsa/pdf/medeff/venlaflaxine_hpc-cps-eng.pdf

SOURCE: Health Canada

posted in Effexor Activists Tribe - 1 reply

Salmon, blueberries, spinach among best foods to lift your mood

2008-11-02T03:14:43Z

Salmon, blueberries, spinach among best foods to lift your mood
http://www.ajc.com/services/content/printedition/2008/10/29/feelgood.html?cxntlid=inform_artr

By Julie Deardorff
McClatchy Tribune
Wednesday, October 29, 2008
Chocolate cake is a popular home remedy for depression, but it comes with some unwelcome side effects. Sweet treats don’t just pack on the pounds; they give us a sugar high that’s inevitably followed by a demoralizing crash.

Still, there’s growing recognition in the medical community that the right food choices can improve your mood. Though drugs are often considered the first line of treatment for depression, a dietary change might be all you need, says James Gordon, a psychiatrist who advocates nondrug approaches to depression.

Gordon, a clinical professor at the Georgetown University School of Medicine, believes what we eat affects how we think and feel. “It’s a wake-up call to let us know our body is out of balance.”

Food can help restore that equilibrium, Gordon wrote in his new book, “Unstuck” (The Penguin Press, $25.95). The trick is knowing which key nutrients to include, and which foods to avoid.

Nutritional changes aren’t a magic bullet; they’re subtle pieces of a treatment plan that might also include therapy, exercise —- one of the most effective depression busters —- and stress-reduction techniques.

But “diet can help with virtually any chronic condition” including depression, said registered dietitian Wendy Bazilian, who holds a doctorate in public health. Just remember that major depression might require an integrative approach that uses food in conjunction with other therapies, including medication and counseling. And never abruptly stop taking medication even if you’re experiencing side effects such as weight gain and sexual dysfunction; talk to your doctor about tapering down.

EAT MORE …

> Salmon. Fatty, cold-water fish such as salmon contain omega-3 fatty acids, which keep cell membranes pliable and flexible, said neurosurgeon Larry McCleary, founder of a research group that looks at natural ways to treat health issues. It’s also in tuna, anchovies and sardines, but since fish fat is also a good place to store heavy metals, pesticides and polychlorinated biphenyls (PCB), consider plant-based sources, including walnuts, flax seeds, pumpkin seeds and green, leafy vegetables.

> Oatmeal, soy milk and two scrambled eggs. This meal will give you 500 milligrams of tryptophan, an amino acid that’s a precursor for the neurotransmitter serotonin, the brain’s feel-good hormone. Many antidepressants are designed to prolong the activity of serotonin in our cells, but you can actually increase the levels by eating carbohydrates (with the exception of fructose, the sugar in fruit), said Judith Wurtman, author of “The Serotonin Power Diet” (Rodale, $24.95).

> Spinach: Low levels of the B vitamin folate, found in spinach, peas, navy beans, orange juice, wheat germ or avocado, may play a role in depression in some patients, said Brent Bauer, director of the Mayo Clinic’s Complementary and Integrative Medicine Program.

> Vitamin D supplement. Vitamin D has been shown to help with seasonal affective disorder, said Bruce Hollis, professor of pediatrics at the Medical University of South Carolina. It may also have an anti-inflammatory effect and increase the flexibility of cell membranes, making the brain’s neurotransmitters work better. While primarily generated after the skin soaks up the sun’s ultraviolet B rays, Vitamin D can be obtained from oily fish and supplemented products like cow or soy milk and orange juice.

But Hollis says the recommended daily allowance —- 200 to 400 international units per day —- is far too low. Instead, supplement with 2,000 IUs or higher, especially between October and April. At these levels, though, food isn’t a good option, since you’d have to drink a gallon of milk a day and no one needs those calories, Hollis said.

> Broccoli and blueberries: When combined with protein in fish, chicken and turkey, high-fiber, nonstarchy vegetables help stabilize blood sugar levels, said Jack Challem, author of “The Food-Mood Solution” (Wiley, $24.95). “Our moods usually track with blood sugar levels,” Challem said. “When our blood sugar is on the rise right after we eat, most people feel pretty contented. If it goes up too high, people feel sleepy because high blood sugar turns off orexins, a family of neuropeptides involved in feeling alert.” Superfruits such as blueberries are high in antioxidants, which are substances that absorb the free radicals produced by stress. Too many free radicals cause wear and tear on the body. Challem recommends green leafy vegetables, broccoli, cauliflower, raspberries, blueberries, blackberries and kiwifruit.

> Quinoa. Whole grains, a good source of B vitamins, break down and release sugar slowly, so you don’t get high levels of insulin and the ups and down of blood sugar, said Gordon. Quinoa, a seed that is classified as a grain, is considered one of the best sources of protein in the vegetable kingdom. Also try oats, brown rice or whole wheat bread or pasta.

EAT LESS …

> Red meat. As you increase omega-3s, try to cut down on the other type of fatty acid, omega-6, which is found in beef. Though essential for brain health, omega-6s are associated with promoting inflammation. Omega-6s are also found in corn and vegetable oils.

> Fried foods. Fat is a very important part of a cell’s membranes. But trans fats and saturated fats make the membranes rigid; then the neurotransmitters don’t work as well. Fried foods, hamburgers, french fries, butter, cheesecake, whole milk and beef are high in saturated fat. A product has trans fats if the ingredients list “partially hydrogenated oils.” Food manufacturers are allowed to list amounts of trans fat with less than 0.5 gram as 0 on the Nutrition Facts panel. To avoid it, read labels.

> Gas station food. Processed foods contain refined flour and give you high doses of sugar but lack critical nutrients, said Gordon. “You’ll often experience a feeling of well-being from the sugar when levels are high, but when it’s low you experience a letdown or fatigue.” Refined sugars include white table sugar, white flour, high-fructose corn syrup.

> Alcohol and caffeine. Though alcohol is a stimulant in low doses, it also depletes the brain’s mood elevator, serotonin. Caffeine blocks the soothing effects of the brain’s “feel-good” messenger called GABA (gamma-amino butyric acid) that can calm mood and the digestive tract, said Molly Siple, author of “Eating for Recovery” (Lifelong, $17.95). “Refined foods and caffeine tend to raise the blood glucose,” she said. “The drop is a route into depression.”

posted in Effexor Activists Tribe - 0 replies

doctors who acknowledge effexor as dangerous and treat the fallout??????

2008-11-02T03:10:44Z

ARE THERE ANY??? If you know of any doctor who acknowledges the dangers and knows how treat the fallout of from effexor could we please start a list because I cannot find one and am so tired of being unheard and untreated. I am sure they are out there someplace but I cannot find one.
I am sure I am not the only one trying to find help with this. I am sure a lot of doctors know but will not acknowledge or treat for whatever reasons that I do not give a crap about. I just want a doctor who is knowledgable and effective to treat me.
I have been off effexor for 5 months and I am concerned about permanent damage.

posted in Effexor Activists Tribe - 8 replies

Wyeth scraps Pristiq (child of Efexor) in Europe October

2008-10-24T00:19:38Z

http://www.network54.com/Forum/281849/

Read carefully

Wyeth scraps Pristiq (child of Efexor) in Europe October 15 2008

http://phx.corporate-ir.net/phoenix.zhtml?c=78193&p=irol-newsArticle&ID=1209892&highlight=

Wyeth Provides Regulatory Update Regarding Desvenlafaxine for the Treatment of Major Depressive Disorder

Company Underscores Commitment to Availability in Worldwide Markets

COLLEGEVILLE, Pa., Oct. 15 /PRNewswire-FirstCall/ -- Wyeth Pharmaceuticals, a division of Wyeth (NYSE: WYE), today provided an update on its global strategy for desvenlafaxine for the treatment of major depressive disorder (MDD) in adults.

Desvenlafaxine has already been approved for the treatment of MDD in adults in the United States, Australia and Brazil, and applications are currently pending in 22 markets. As part of its global regulatory strategy, and in consultation with the Committee for Medicinal Products for Human Use of the European Medicines Agency, the Company has chosen not to pursue its central European Marketing Authorisation Application at this time. Wyeth remains committed to making desvenlafaxine available to patients with MDD around the world, including in Europe. It is available in the United States under the name PRISTIQ.

"We are considering a number of options to support depressed patients and their families," says Gary L. Stiles, M.D., Executive Vice President and Chief Medical Officer. "There are millions of patients with depression, and clearly more treatments are necessary."

Wyeth has a long history of innovation in neuroscience. In 1993, the Company introduced the first serotonin-norepinephrine reuptake inhibitor, which has been prescribed to millions of people worldwide. Building on this research platform, desvenlafaxine represents Wyeth's newest antidepressant therapy.

About Wyeth Pharmaceuticals

Wyeth is one of the world's largest research-driven pharmaceutical and health care products companies. It is a leader in the discovery, development, manufacturing and marketing of pharmaceuticals, vaccines, biotechnology products and non-prescription medicines that improve the quality of life for people worldwide. The Company's major divisions include Wyeth Pharmaceuticals, Wyeth Consumer Healthcare and Fort Dodge Animal Health.

The statements in this press release that are not historical facts are forward-looking statements that are subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statements. These risks and uncertainties include, without limitation, the inherent uncertainty of the timing and success of, and expense associated with, research, development, regulatory approval and commercialization of our products and pipeline products (including future regulatory action regarding our pending applications in other countries for desvenlafaxine for the treatment of major depressive disorder and the treatment of vasomotor symptoms, as to which no assurance can be given); government cost-containment initiatives; restrictions on third-party payments for our products; substantial competition in our industry, including from branded and generic products; emerging data on our products and pipeline products; the importance of strong performance from our principal products and our anticipated new product introductions; the highly regulated nature of our business; product liability, intellectual property and other litigation risks and environmental liabilities; uncertainty regarding our intellectual property rights and those of others; difficulties associated with, and regulatory compliance with respect to, manufacturing of our products; risks associated with our strategic relationships; economic conditions including interest and currency exchange rate fluctuations; changes in generally accepted accounting principles; trade buying patterns; the impact of legislation and regulatory compliance; risks and uncertainties associated with global operations and sales; and other risks and uncertainties, including those detailed from time to time in our periodic reports filed with the Securities and Exchange Commission, including our current reports on Form 8-K, quarterly reports on Form 10-Q and annual report on Form 10-K, particularly the discussion under the caption "Item 1A, RISK FACTORS" in our Annual Report on Form 10-K for the year ended December 31, 2007, which was filed with the Securities and Exchange Commission on February 29, 2008. The forward-looking statements in this press release are qualified by these risk factors. We assume no obligation to publicly update any forward-looking statements, whether as a result of new information, future developments or otherwise.

SOURCE Wyeth Pharmaceuticals

posted in Effexor Activists Tribe - 0 replies

If not Effexxor, then what instead?

2008-10-15T21:09:43Z

I have been suffering from depression for 35+ years. Trazodone did nothing. Lexapro made me nauseous and gave me nightmares. Effexor definitely helped. I don't remember the withdrawal symptoms the 1st time I went off it. In 2005, I was extremely depressed and resumed the medication. It helped the depression. I'm not saying everything was totally hunky-dory, but things started to get better. Now with a Parkinson's diagnosis at hand along with now living on disability and no health insurance, I decided to wean myself off of it again. It took me 8 months to go from 300 mgs/day to 0 mgs/day. At first I just slowly reduced the amount I was taking, going up and down between 300/225, then 225/150, 150/75, 75/37.5. After that, I started skipping days. I was experiencing a lot of unpleasant symptoms that I had attributed to the Parkinson's and possibly Fibromyalgia. It's been about 4 months since last I did any.

Anyhow, I am definitely noticing that I am falling into another episode of depression. So if not Effexxor, then what instead?

posted in Effexor Activists Tribe - 11 replies

I want to stop taking Effexor but....

2008-09-15T09:04:11Z

I was given Effexor about 3-4 years ago when I started early menopause. I didn't want to go on standard Hormone Replacement Theraphy because I had read that they caused cancer of cervix and other issues. I tried other forms of natural HRT's prior to Effexor, but I was still feeling irrated, fatiqued, and my doctor said I should probably go on anti depressants for a while to see if I feel better. I started feeling better for awhile, but then my joints started hurting...ie... hands, hips, back. Also had vision problems and weight gain.
I gradually started taking myself off the Effexor. I went from 37.5 to 1/2 that and then started skipping a day. I COULDN'T DO IT. I tried twice now and I'm not successful. My eyes start twitching, my body aches and my brain feels like it's not connected. Almost like someone unplugged my cord. Each time I just go back on it because I can't afford to be unplugged at work. I need to be aware and alive since I'm responsible for about 15 other people, and make major decisions that impact money for my company.
DOES ANYONE KNOW OF A BETTER WAY THAT CAN HELP ME GET OFF THIS DRUG?

posted in Effexor Activists Tribe - 8 replies

What is a me to drug?

2008-08-31T05:54:05Z

http://stanmed.stanford.edu/2005summer/drugs-metoo.html

Me-too drugs
Sometimes they're just the same old, same old

By ROSANNE SPECTOR

It’s expensive to produce an innovative drug. On average, the bill runs to more than $400 million. So drug companies often take a less costly route to create a new product. They chemically rejigger an oldie but goodie, craft a new name, mount a massive advertising campaign and sell the retread as the latest innovative breakthrough.

This strategy has shown great success for turning profits. Nexium, a “me-too” drug for stomach acid, has earned $3.9 billion for its maker, AstraZeneca, since it went on the market in 2001. The U.S. Food and Drug Administration classified three-fourths of the 119 drugs it approved last year as similar to existing ones in chemical makeup or therapeutic value.

Though there are hints that consumers are more aware of drug marketing ploys, many fall for the sales hype, despite an absence of evidence that the new drug is better than the tried-and-true remedy. In 2003, the industry spent $25.3 billion marketing drugs, according to the industry trade group Pharmaceutical Researchers and Manufacurers of America.

Nexium illustrates the drug makers’ strategy. Many chemicals come in two versions, each a mirror image of the other: an L-isomer and an R-isomer. (The “L” is for left, the “R” is for right.) Nexium’s predecessor Prilosec is a mixture of both isomers. When Prilosec’s patent expired in 2001, the drug maker was ready with Nexium, which contains only the L-isomer.

Is Nexium better? So far, there’s no convincing evidence that it is, says Stanford drug industry watcher Randall Stafford, MD, PhD.

“Newer isn’t always better, when it comes to drugs,” says Stafford, associate professor of medicine with the Stanford Prevention Research Center.

“The FDA approves drugs on the basis of their superiority to placebo, not their superiority to existing drugs,” Stafford says. “I think people misunderstand the nature of FDA approval and the criteria used to allow drugs to enter the market.”

The findings of an annual survey on direct-to-consumer advertising released in April suggest consumers are becoming less gullible. The national Rodale survey, which polled 1,504 adults from Dec. 28 to Jan. 12, found that among those who asked their doctors about an advertised drug, the portion asking directly for the drug fell to 21 percent — 5 percentage points lower than last year. The poll’s analysts interpret this drop as evidence that consumers are paying less attention to the likely benefits of advertised drugs and more to the potential risks.

Experts also believe consumers are beginning to take steps to weed through the marketing mumbo jumbo and find the most effective drug at the best price. The new drug information Web site — www.CRBestBuyDrugs.org — launched in December by Consumers Union racks up between 2,000 and 5,000 visits a day, according to Gail Shearer, the program’s project director.

The site compares the effectiveness and cost of drugs for prevalent health problems including high blood pressure, high cholesterol, pain and depression. The underlying source of analysis for the site is the Drug Effectiveness Review Project, a highly-regarded, evidence-based review of clinical effectiveness carried out by Oregon Health and Science University. Twelve states use this same data to choose which drugs to make available in their markets.

But in the end, the real question is about pharmaceutical innovation. While me-toos fill the development pipeline, the benefits flow largely to the haves of this world. Few resources go toward drugs targeting diseases that primarily affect developing nations. So, what about the rest of the world?

posted in Effexor Activists Tribe - 0 replies

Pristiq, Wyeths" "New" me-too anti-depressant

2008-08-31T05:50:53Z

You will find several articles here.

http://tribes.tribe.net/depressionhelp/thread/874d4ee5-b603-4d08-8b2c-365337861223

posted in Effexor Activists Tribe - 0 replies

MS don't know not a doc but

2008-08-27T20:32:24Z

http://www.paxilprogress.org/forums/showthread.php?t=35403&highlight=sclerosis

There is this web site called paxilprogress link above goes to the one mention of ms I could find there.
Although Paxil and Effexor are not the same drug you may find some helpfull information at this site.
From what I gleened so far the side effects and withdrawal symptoms of a drug are much alike.
They have a good explanation of what is going on in the brain during side effects and withdrawal along with a lot of scientific information.
Worth a look for sure if you are thinking of quitting effexor or any other neurotransmitter alteroing drug.
If you are not in a medical emergency quitting cold turkey is not recommended and of course talk with your doctor.
I gave me food for thought with many provocative threads...wellbeing...medical challenges...
protests...family support ....petitions....spirit... worth a look.

posted in Effexor Activists Tribe - 0 replies

effexor induced parkinsonism

2008-08-21T00:05:16Z

I have been doing research on all antidepressants and find they have a lot of the same
terrible side effects. I googled effexor induced parkinsonism and found plenty of sited however the information in most seemed to be messed with as they were not on topic or the information was missing. I found this one lone site that appears to be stable. Tho it does not give much info.

By Charly Groenendijk Back to Side-Effects
The Netherlands
2000 - 2004

SSRI & SSNRI Antidepressants Side-Effects

"Who does Not Know the Truth, is simply a Fool...
Yet who Knows the Truth and Calls it a Lie, is a Criminal."
- In "Galileo Galilei" by Berthold Brecht (1898-1956)

Take notice that also non SSRI antidepressants (and even Ritalin) may interact (primary or secondary) with the serotonergic (or serotoninergic) system in the brain. Every medication -especially SSRI antidepressants- boosting serotonin activity in the brain, has potential to induce the very dangerous and potentially fatal hyperserotonergic state of the Serotonin Syndrome.
--------------------------------------------------------------------------------
SSRI & SSNRI Antidepressants side-effects, neurological damage
Selective Serotonin / Nor-Epinehrine Re-Uptake Inhibitors
--------------------------------------------------------------------------------
Go to Introduction Antidepressants Negative personality, perception & physical changes
Go to Antidepressant Casualties in the Media Aggression, Homicide, Suicide & Self-Harm
Go to Recent Media Articles (SSRI) Antidepressants Pharmaceutical & FDA Fraud in 2004
--------------------------------------------------------------------------------
Tardive Dyskinesia/Dystonia, Parkinsonism & Akathisia
SSRI & SSNRI antidepressants induced side-effects (Iatrogenic Extrapyramidal Symptoms) are
recognized to be similar to Neuroleptic (anti-psychotic) induced side-effects. These side-effects are known as Tardive Dyskinesia/Dystonia (severe body movement disorder, mostly permanent), Parkinsonism (a sign of future Parkinson's disease) and Akathisia (a Neurological driven severe mania/agitation that can lead to suicidality, suicide attempts, self-harm & suicide). It is well documented in the medical literature that these neuroleptic induced side-effects refer to damage at dopaminergic neurons in the "motor system" of the
"Basal Ganglia", a structure deep in the "Limbic System" of the brain. 1, 2, 3, 4, http://www.emedicine.com/EMERG/topic338.htm (scroll down)
Serotonin Syndrome
The Serotonin Syndrome is a potentially lethal condition caused by excessive serotonergic activity. It is a very dangerous and a potentially fatal side effect of the serotonergic enhancing drugs such as SSRI & SSNRI antidepressants and is diagnosed by the presence of at least 3 of 10 symptoms: mental status changes (confusion, hypomania), agitation, myoclonus, hyperreflexia, diaphoresis, shivering, tremor, diarrhea, incoordination, and fever. This "hyperserotonergic" toxic condition requires heightened clinical awareness in order to prevent, recognize, and treat the condition promptly. Promptness is vital because, as we just mentioned, the serotonin syndrome can be fatal and death from this side effect can come very rapidly. The Serotonin syndrome is brought on by excessive levels of serotonin and is difficult to distinguish from the "Neuroleptic Malignant Syndrome" because the symptoms are so similar. The "Neuroleptic Malignant Syndrome" is a serious condition brought on by the use of neuroleptic drugs (anti-psychotics).
Source: Prozac: Panacea or Pandora? by Dr Ann Blake Tracy http://members.aol.com/atracyphd/syndrome.htm
Source: Journal of Clinical Psychiatry

Antidepressant induced neurological and/or physical toxicity (body and/or brain damage) either as a result of prolonged inhibition of P450-2D6 liver-enzymes, or as a result of impairing serotonin metabolism, can take on many forms as described below. A few examples are: Hyperserotonemia, such as the lifethreatening condition the Serotonin Syndrome, Epileptiform Discharges, Epileptic Seizures and/or Epilepsy, Hypoglycaemia/Hyperglycemia (Low/Elevated Blood Sugar Imbalance), Stroke/Hemorrhagic Syndromes, Frontal Lobe Syndrome, Tardive Dyskinesia/Dystonia, Parkinsonism, Akathisia, Mania, etc...

MEDICAL REPORTS OF SSRI/SSNRI ANTIDEPRESSANT INDUCED (IATROGENIC) SEVERE SYMPTOMS:

Go to: Newborn Babies (Neonatal) Neurological Damage & Withdrawal Side-Effects
Go to: General Physical & Mental Side-Effects
Go to: Body Movement Disorders (Dystonia) & Parkinsonism (future Parkinson's disease)
Go to: Akathisia, Mania, Restlessness & Restless Legs Syndrome
Go to: Serotonin Syndrome, Neuroleptic Malignant Syndrome
Go to: Blood/Organ Diseases, Stroke, Hemorrhage, TIA, Tumours & Bleedings
Go to: Hepato Toxicity (Liver Damage)
Go to: Cardiovascular Toxicity (Heart Damage) & Neurological Toxicity (Brain Damage)
Go to: Epileptiform Activity, Epilepsy, Seizures, REM Sleep/Memory/EEG Problems, Sleepwalking

Go to: Hypoglycemia (low blood sugar), Hyperglycemia (high blood sugar, Diabetes)
Go to: Urinary Incontinence, Dermatologic (Skin) Problems, Ocular (Eyes) Disturbances
Go to: Pain & Numbness, Swellings, Sexual (Organ) Problems, Hormonal Imbalances
Go to: Hyponatremia & Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
Go to: (Suicide Overdose)-Toxicity & Death
Go to: Suicide, Suicidality, Suicide Attempts & Self-Harm
Go to: Mental State, Perceptual, Emotional & Psychological Changes
Go to: Mental & Physical Side-Effects of Withdrawal/Discontinuation
Go to: Other Observations & Complications: Case Reports, Reviews & Studies

SSRI's & SSNRI's: NEWBORN BABIES (NEONATAL) NEUROLOGICAL DAMAGE & WITHDRAWAL SIDE EFFECTS
2004
09/00
Case/Study Neonatal toxicity: Fluoxetine concentrations in cord & maternal serum

2004
08/09
WARNING Health Canada: Potential Neurological Adverse Effects of SSRI's on Newborns

2004
08/00
Case/Study Using an SSRI during pregnancy has Damaging Teratogenic Effects on the Fetus

2004
06/00
Case/Review Baby SSRI (withdrawal) side-effects: agitation, breathing & suction problems

2004
02/00
Case/Study SSRI's during pregnancy: Foetal Brain Damage (Neurobehavioral Disruptions)

2003
11/00
Case/Review Neonatal (baby) Large Intraventricular Haemorrhage with maternal use of Paxil

2003
08/00
Case/Review Baby SSRI (withdrawal) effects: hypoglycaemia, bradycardia, tachycardia, jaundice

2003
07/00
Case/Review Increased risk for neonatal problems after exposure to SSRI's in late pregnancy

2003
07/14
Case/Review SSRI's During Pregnancy May Cause Neurologic Symptoms in Newborns

2003
07/12
Case/Review Withdrawal symptoms in New Born Baby after exposure to Effexor during pregnancy

2003
04/16
Case/Review Neonatal (baby) Convulsions & Subarachnoid Hemorrhage after exposure to Paxil

2001
09/00
Case/Review Neonatal Paxil withdrawal syndrome or actually serotonin syndrome?

2001
03/00
Case/Review New Born BABY SSRI withdrawal syndrome lasting up to one month after birth

2001
03/00
Case/Review New Born BABY Withdrawal Syndrome after exposure to SSRI's Celexa, Paxil, Prozac

2000
10/11
Case/Review Prozac Toxicity in preterm infant: marked motor automatism & skin manifestations

1999
11/00
Case/Study Breastfeeding while taking Prozac associated with reduced growth infants

1997
11/00
Case/Review SSRI's, Breast Milk and Withdrawal Symptoms in Newborn Babies

SSRI & SSNRI Antidepressants: GENERAL PHYSICAL & MENTAL SIDE-EFFECTS
2004
09/14
FDA US Antidepressant "BLACK BOX WARNING" On Suicidality Risk Recommended

2004
06/03
Health Canada Stronger warnings for SSRI's & other anti-depressants

2004
03/00
Case/Review Severe adverse drug reactions of (SSRI/SSNRI) antidepressants

2004
02/00
Case/Review Serotonin Syndrome and the use of SSRI's

2004
01/26
Case/Review Antidepressant Drugs and Suicidal/Aggressive Behaviors

2003
06/15
Case/Review Hyponatraemia with SSRI's

2003
05/00
Case/Review Antidepressant withdrawal-induced Mania in patients with mood disorders

2003
04/04
Case/Review Clinical Study Dr David Healy: Lines of evidence on risks of suicide with SSRI's

2003
03/31
Case/Review SSRI-induced Epileptic Seizures

2002
00/00
Case/Review Effects of antidepressant drugs on seizure threshold

2002
05/08
Case/Review Amotivational Syndrome (Frontal Lobe Syndrome) Link with SSRI Use in Youth

2002
03/15
Case/Review Rare Neurologic Syndrome (Call Fleming Syndrome) Linked to AntiDepressants

2002
03/07
Case/Review Antidepressants associated with increased risk of falling in elderly persons

2002
03/05
Case/Review Male Breast Neoplasia (cancer) in association with SSRI therapy: report of 3 cases

2002
02/00
Case/Review Hepatotoxicity (liver damage) associated with the new antidepressants

2002
01/00
Case/Review Cerebral Vasoconstriction and Stroke after use of Serotonergic Drugs

2001
06/00
Case/Review Amotivational (Frontal Lobe) Syndrome with SSRI's in children & adolescents

2001
01/20
Case/Review Selective serotonin uptake inhibitors and Pancreatitis

2000
12/00
Case/Review Serotonergic antidepressants and Urinary Incontinence

2000
10/24
Case/Review Post-SSRI LSD Flashbacks in Teenagers Related Link

2000
05/00
Case/Review Antidepressants can result in Toxicity and Death through serotonergic excess

2000
05/00
Case/Review SSRI Discontinuation Syndrome/Withdrawal: proposed diagnostic criteria

2000
05/17
Case/Review Antidepressant-Associated Mania & Psychosis Resulting in Psychiatric Admissions

2000
03/00
Case/Review Bleeding and selective serotonin reuptake inhibitors in childhood and adolescence

2000
02/00
Case/Review Hemorrhagic syndromes related to SSRI's. 7 case reports & review of literature

2000
02/00
Case/Review SSRI antidepressant drugs appear to Enhance Cocaine-induced Toxicity

1999
00/00
Case/Review Case Report: SSRI-induced Parkinsonism (future Parkinson's)

1999
00/00
Case/Review Antidepressants and seizure susceptibility: from in vitro data to clinical practice

1999
07/00
Case/Review Selective serotonin reuptake inhibitor Discontinuation/Withdrawal Symptoms

1999
03/00
Case/Review Antidepressant Exacerbation of Spasticity

1999
03/00
Case/Review Adverse Reactions of SSRI's: reports from a spontaneous reporting system

1998
00/00
Case/Review Antidepressant drugs: disturbing and potentially dangerous adverse effects

1998
00/00
Case/Review SSRI-induced Extrapyramidal side-effects & Akathisia: implications for treatment

1998
11/09
Case/Review Antidepressant Discontinuation-Related Mania also in Bipolar Depression

1996
10/00
Case/Review Movement Disorders associated with the serotonin selective reuptake inhibitors

1996
10/00
Case/Review SSRI Side-Effects: Akathisia, Dystonia, Parkinsonism & Tardive Dyskinesia

1996
10/00
Case/Review Serotonin reuptake inhibitor withdrawal

1996
09/01
Case/Review Hyponatremia & SIADH associated with SSRI's: a review of spontaneous reports

1991
12/00
Case/Review Serotonin reuptake inhibitors, Paranoia & the Ventral Basal Ganglia

Medical reports: BODY MOVEMENT DISORDERS (DYSTONIA) & PARKINSONISM (future Parkinson's disease)
2003
07/22
Case/Review Bupropion: Tremors, Agitation, Confusion, Insomnia & Rash

2002
00/00
Case/Review Fluoxetine-induced Torticollis, Bradykinesia & Cogwheel Rigidity in an adolescent

2002
12/00
Case/Review Acute dystonic reaction to paroxetine treatment in elderly patient

2002
05/00
Case/Review Case Report: Dystonia Induced by Mirtazapine (Remeron)

2002
05/08
Case/Review Fluoxetine-induced Exacerbation of Chorea in Huntington's Disease

2002
02/00
Case/Review Bupropion-induced Acute Dystonia

2001
08/00
Case/Review Myoclonus secondary to the concurrent use of trazodone and fluoxetine

2001
07/08
Case/Review Myoclonus during prolonged treatment with sertraline in an adolescent patient

2001
02/00
Case/Review Visual hallucination and tremor induced by sertraline and oxycodone

2001
04/00
Case/Review Parkinsonism and Parkinson's disease with long-term sertraline

2000
04/00
Case/Review Worsening of Parkinson's Disease

1999
00/00
Case/Review Case Report: SSRI-induced Parkinsonism (future Parkinson's)

1998
09/00
Case/Review Extrapyramidal Adverse Effects associated with Zoloft/Lustral

1998
07/00
Case/Review Involuntary Movement Disorders associated with Sertraline

1998
06/00
Case/Review Sertraline induced Parkinsonism. A case report and an in-vivo study

1998
06/27
Case/Review Severe Tardive Dyskinesia (permanent movement disorder) with Prozac & risperidone

1997
08/00
Case/Review Venlafaxine produces Sleep Disturbances & Abnormal Leg Movements

1996
10/00
Case/Review Movement Disorders associated with the serotonin selective reuptake inhibitors

1996
10/00
Case/Review SSRI Side-Effects: Akathisia, Dystonia, Parkinsonism & Tardive Dyskinesia

1996
09/00
Case/Review Tardive Dyskinesia (permanent body movement disorder) with Prozac/Sarafem

1996
07/13
Case/Review Zoloft/Lustral: Extrapyramidal Symptoms such as Rigidity and Tremors...

1996
05/00
Case/Review Complex Movement Disorders induced by fluoxetine

1995
10/00
Case/Review Parkinsonism associated with fluoxetine and cimetidine: a case report

1995
01/00
Case/Review Worsening Tremor & Problems with Word-Finding following fluoxetine treatment

1994
06/00
Case/Review Fluoxetine induced Dyskinesia

1994
05/00
Case/Review Reversible Intermittent Rhythmic Myoclonus with fluoxetine in pres. Pick's disease

1993
01/00
Case/Review Increase of Parkinson Disability after fluoxetine medication

1979
00/00
Case/Review Dystonic Reaction, Parkinsonian Rigidity & Increased Serum Prolactin levels

Medical reports, side-effects: AKATHISIA, MANIA, RESTLESSNESS & RESTLESS LEGS SYNDROME
2003
12/00
Case/Review Fluoxetine (Prozac) dose-increment related Akathisia in depression

2003
10/00
Case/Study Induction of mania in depression by Paxil/Seroxat (paroxetine)

2003
07/00
Case/Review Case report Zoloft (Lustral, sertraline)-induced Hypomania: a genuine side-effect

2003
06/00
Case/Review Mania associated with Effexor (Efexor, venlafaxine) discontinuation

2003
04/00
Case/Review Eroto-Mania induced by Effexor (venlafaxine): a case study

2002
12/00
Case/Review Restless Legs Syndrome induced by Remeron (mirtazapine)

2002
12/00
Case/Review Worsening of autosomal dominant Restless Legs Syndrome after use Mirtazapine

2002
11/00
Case/Review Dysphoric Mania with high-dose Mirtazapine: a case for Norepinephrine Syndrome?

2002
11/00
Case/Review Zoloft/Lustral-Induced Akathisia and Dystonia Misinterpreted as a Panic Attack

2002
07/08
Case/Review High-dose fluoxetine-induced Mania. Review and case report

2002
06/22
Case/Review Akathisia due to the higher dose of fluoxetine -scroll to case 3

2002
03/04
Case/Review Remeron (Remergil, mirtazapine)-induced acute Akathisia

2001
06/00
Case/Review Mania & Paranoid Ideation following Tramadol-Fluoxetine Combination

2000
01/12
Case/Review Antidepressant-Induced Mania in Bipolar Patients: Identification of Risk Factors

1999
03/02
Case/Review SSRI's induced Mania in obsessive compulsive disorder

1998
08/00
Case/Study Manic behaviors with Prozac (fluoxetine) in three 12- to 18-year-olds with OCD

1998
08/00
AnimalStudy Reduced activity of rat dopaminergic neurons in the VTA may explain "Akathisia"

1998
06/00
Case/Review Hypomania associated with mirtazapine augmentation of sertraline

1997
02/00
No Abstract Mania associated with serotonin selective reuptake inhibitors

1996
12/00
Case/Review Restless legs syndrome worsened by Paxil/Seroxat (paroxetine)

1996
10/00
Case/Review SSRI Side-Effects: Akathisia, Dystonia, Parkinsonism & Tardive Dyskinesia

1996
05/00
No Abstract SSRI-induced Akathisia

1996
03/04
Case/Review Akathisia: a review and case report following paroxetine treatment

1995
09/00
No abstract Paxil (Seroxat, paroxetine)-induced psychotic mania

1995
08/00
Case/Review Antidepressant-induced Mania and Cycle Acceleration: a controversy revisited

1994
11/00
Case/Review Antidepressant-associated Mania: a controlled comparison with spontaneous mania

1994
09/10
Case/Review Revisiting Fluoxetine: Akathisia & Suicidal Preoccupations

1992
11/00
Case/Review Akathisia, Suicidality and Prozac/Sarafem (FLUOXETINE)

1992
07/00
Case/Review Prozac (fluoxetine) treatment: Restlessness, Hyperactivity, Agitation, Insomnia

1992
03/00
Case/Review Mania associated with Prozac/Sarafem (fluoxetine) treatment in adolescents

1991
12/00
Case/Review Prozac-induced Serious Suicide Attempts by 3 patients: the Role of Akathisia

1989
09/00
Case/Review Typical Prozac/Sarafem-induced Akathisia: clinical and theoretical implications

1984
02/00
Case/Review A case of mania associated with Prozac/Sarafem (fluoxetine)

Medical reports, side-effects: SEROTONIN SYNDROME, NEUROLEPTIC MALIGNANT SYNDROME
2004
02/00
Case/Review Serotonin Syndrome and the use of SSRI's

2003
05/27
Case/Review Serotonin Syndrome: a brief review -case 1 fluoxetine

2003
05/06
Case/Review Serotonin Syndrome induced by Remeron/Remergil (Mirtazapine)

2003
05/00
Case/Review Fatal Serotonin Syndrome after combined treatment with linezolid

2003
02/00
Case/Review Serotonin Syndrome Induced by Low-Dose Effexor (venlafaxine)

2002
09/00
Case/Review Neuroleptic Withdrawal vs Serotonergic Syndrome in 8-year-old child on fluoxetine

2002
04/00
Case/Review Case of a patient with Fluoxetine & Selegiline induced Fatal Serotonin Syndrome

2002
04/00
Case/Review Severe Serotonin Syndrome induced by Mirtazapine monotherapy

2002
03/04
Case/Review Serotonin Toxicity with therapeutic doses of dexamphetamine and venlafaxine

2002
02/00
Case/Review Serotonin Syndrome present. as Hypotonic Coma & Apnea (fluoxetine & citalopram)

2001
10/00
Case/Review Serotonin Syndrome induced by Fluvoxamine and Mirtazapine

2001
09/00
Case/Review Neonatal paroxetine withdrawal syndrome or actually serotonin syndrome?

2001
03/00
Case/Review A Fatal Case of Serotonin Syndrome after moclobemide-citalopram intoxication

2000
04/00
Case/Review Venlafaxine-induced Serotonin Syndrome with relapse following amitriptyline

2000
03/00
Case/Review Serotonin Syndrome during fluoxetine-poisoning in a patient taking moclobemide

2000
02/00
Case/Review Case Report: Serotonin Syndrome with Serzone and Prozac

2000
01/22
Case/Review Neuroleptic Malignant Syndrome after venlafaxine

1999
09/00
Case/Review Serotonin syndrome associated to the use of paroxetine. Case report

1999
07/00
Case/Review Serotonin syndrome secondary to the use of sertraline and metoclopramide

1999
07/08
Case/Review Serotonin syndrome in a child associated with erythromycin and sertraline

1998
00/00
Case/Review Antidepressant drugs: disturbing and potentially dangerous adverse effects

1998
09/00
Case/Review Serotonin Syndrome due to venlafaxine overdose

1998
07/00
Case/Review Serotonin Syndrome induced by transitioning from phenelzine to venlafaxine

1998
07/08
Case/Review Serotonin Syndrome with Effexor and other SSRI-antidepressants

1998
04/00
Case/Review Serotonin Syndrome induced by venlafaxine and fluoxetine

1997
01/00
Case/Review Serotonin Syndrome following a single dose of Effexor (venlafaxine)

1996
07/12
Case/Review Isolated venlafaxine-overdose-induced Serotonin Syndrome

1995
07/08
Case/Review Serotonin Syndrome in a patient given fluoxetine and lithium

1994
11/00
Case/Review Fluoxetine induced Serotonin Syndrome

1994
11/00
Case/Review Prozac/Sarafem (fluoxetine)-induced Serotonin Syndrome in 48-year-old man

1994
11/00
Case/Review Serotonin Syndrome with Paxil/Seroxat, an OTC cold remedy, and vascular disease

1990
09/15
Case/Review Neuroleptic Malignant Syndrome with Prozac/Sarafem (fluoxetine)

Medical reports, side-effects: BLOOD/ORGAN DISEASES, STROKE, HEMORRHAGE, TIA, TUMOURS & BLEEDINGS
2004
04/00
Case/Review Transient ischemic attack (TIA) reported with Paxil/Seroxat (paroxetine) use

2003
00/00
Case/Review SSRI-Associated Bleeding: The Risk of Treating Hepatitis C-Infected Patients

2003
11/00
Case/Review Neonatal (baby) Large Intraventricular Haemorrhage with maternal use of Paxil

2003
05/06
Case/Review Severe Thrombocytopenia in a 66-year-old patient after Mirtazapine administration

2003
04/00
Case/Review Effexor-induced Pneumonitis (Lung Reaction) & Heart Failure simultaneously

2003
04/16
Case/Review Neonatal (baby) Convulsions & Subarachnoid Hemorrhage after exposure to Paxil

2003
02/00
Case/Review Respiratory Distress Syndrome & Renal Failure with overdose

2003
01/00
Case/Review Bupropion: Thrombotic Thrombocytopenic Purpura-hemolytic Uremic Syndrome

2002
12/00
Case/Review Ecchymosis with Prozac (hemorrhage under the skin, sign of liver dysfunction)

2002
09/00
Case/Review Massive peroperative haemorrhage, result of Paxil-induced thrombocytopathy

2002
09/00
Case/Review Mirtazapine-induced Severe Neutropenia

2002
05/00
Case/Review Effexor/Efexor (venlafaxine)-associated Vaginal Bleeding

2002
05/08
Case/Review Amotivational Syndrome (Frontal Lobe Syndrome) Link with SSRI Use in Youth

2002
03/15
Case/Review Rare Neurologic Syndrome (Call Fleming Syndrome) Linked to AntiDepressants

2002
03/05
Case/Review Male Breast Neoplasia (cancer) in association with SSRI therapy: report of 3 cases

2002
01/00
Case/Review Cerebral Vasoconstriction and Stroke after use of Serotonergic Drugs

2001
06/00
Case/Review Amotivational (Frontal Lobe) Syndrome with SSRI's in children & adolescents

2001
01/20
Case/Review Selective serotonin uptake inhibitors and Pancreatitis

2000
09/00
Case/Review Paroxetine and Irritable Bowel Syndrome

2000
05/15
Case/Review Paroxetine use associated with a substantial increase in Breast Cancer Risk

2000
04/00
Case/Review Hypertensive Urgency (high blood pressure) by Mirtazapine/Clonidine interaction

2000
03/00
Case/Review Bleeding and selective serotonin reuptake inhibitors in childhood and adolescence

2000
02/00
Case/Review Hemorrhagic syndromes related to SSRI's. 7 case reports & review of literature

2000
01/00
Case/Review Effexor: Eosinophilic Pneumonia (Lung/Blood Disease) & Respiratory Failure

1999
00/00
Case/Review Acute Ischaemic Event associated with the use of venlafaxine

1999
11/00
Case/Review Hyperthyroidism secondary to antidepressive treatment with fluoxetine

1999
05/00
Case/Review Ileus as a Possible Result of Bupropion in an Elderly Woman

1998
11/00
Case/Review Overdose: Severe Hypothermia, Cardial & Respiratory Function Compromised

1997
02/15
Case/Review Hemodynamic abnormalities & vasoconstriction following paroxetine 40mg per day

1991
03/00
Case/Review A fluoxetine-induced Frontal Lobe Syndrome in an obsessive compulsive patient

Medical reports, side-effects: HEPATO TOXICITY (Liver damage)
2003
00/00
Case/Review Paxil induced Cholestasis (liver disease where flow of bile from the liver is reduced)

2003
05/00
Case/Review Zoloft/Lustral-induced Hepatitis: a case report and review of the literature

2003
05/00
Case/Review Hepatic Injury & Pancreatitis during treatment with SSRIs & Effexor

2003
02/00
Case/Review Acute Liver Failure with concurrent Bupropion and carbimazole therapy

2003
02/00
Case/Review Antidepressant induced Cholestasis

2002
09/00
Case/Review Mirtazapine-induced Hepatotoxicity

2002
06/00
Case/Review Bupropion-induced Change CYP2D6 Extensive Metabolizer to Poor Metabolizer

2002
02/00
Case/Review Hepatotoxicity (liver damage) associated with the new antidepressants

2001
11/00
Case/Review Acute Cholestatic Hepatitis induced by Bupropion. A case report

2001
08/00
Case/Review Severe hepatotoxicity with jaundice associated with paroxetine

2000
03/07
Case/Review Venlaxafine-Associated Hepatitis

1999
07/00
Case/Review Acute Hepatitis due to fluoxetine therapy

1999
06/01
Case/Review Venlaxafine-Associated Hepatitis

1999
04/00
Case/Review Effect of CYP2D6*10 genotype on venlafaxine in healthy adult volunteers

1998
04/00
Case/Review Symptomatic Liver Injury probably related to sertraline

1997
03/15
Case/Review Severe hepatitis attributed to paroxetine (Seroxat)

1996
11/00
Case/Review Reversible severe hepatotoxicity of paroxetine in a patient with major depression

1983
03/00
AnimalStudy SSRI-induced Lipidosis in Rats (fat infiltration into liver cells; can cause death)

1978
00/00
AnimalStudy SSRI-induced Hepatotoxicity in Rats and first-pass metabolism

Medical reports: CARDIOVASCULAR TOXICITY (Heart damage) & NEUROLOGICAL TOXICITY (Brain damage)
2004
06/21
AnimalStudy SSRI disrupts the development of neural circuitry during cortical synaptic formation

2004
04/00
Case/Review Amygdala volume reductions in pediatric patients with OCD treated with paroxetine

2003
04/00
Case/Review Effexor-induced Pneumonitis (Lung Reaction) & Heart Failure simultaneously

2003
03/00
No abstract Provoked bradycardia after Paxil/Seroxat (paroxetine) administration

2002
00/00
Case/Review Torsades de Pointes appeared to occur with Remeron (mirtazapine)

2002
08/00
Case/Review Acute Myocardial Infarction following Wellbutrin/Zyban (bupropion)

2002
04/15
Bio Study Neuronal Cell Death induced by Prozac/Sarafem (fluoxetine)

2001
12/00
Case/Review Celexa/Cipramil-Induced Bradycardia, Presyncope & Hypotension

2001
09/00
Case/Review Celexa/Cipramil-induced Torsades de Pointes, Prolongation of QT Interval

2000
02/00
Case/Review SSRI antidepressant drugs appear to Enhance Cocaine-induced Toxicity

2000
02/29
Animal Study Prozac & other SSRI's cause Shriveled & Corkscrew Shaped Brain Cells

1999
08/00
Case/Review Influence of CYP2D6 liver-enzymes & Cardiovascular Toxicity of Effexor (venlafaxine)

1999
02/00
Case/Review Celexa/Cipramil (citalopram)-induced Sinus Bradycardia

1998
09/01
Animal Study Brain cell (neuron) function in forebrain altered by prenatal exposure to Prozac

1998
08/00
AnimalStudy Reduced activity of rat dopaminergic neurons may explain "Akathisia" with SSRI's

1998
07/00
Case/Review Severe bradycardia an increase in QTc time observed with Paxil/Seroxat

1997
00/00
Animal Study Prenatal exposure to Prozac produces changes in brain serotonin (5-HT) neurons

1997
11/00
Case/Review Seizures, Tachycardia & Rhabdomyolysis following Effexor & Lamotrigine

1997
09/00
Case/Review Prozac (fluoxetine)-induced cardiovascular, neurovascular toxicity & seizure

1996
10/00
Case/Review Wellbutrin (bupropion) toxicity by CYP2D6 (liver enzymes) inhibition

1992
10/00
AnimalStudy Site specific malformations in mouse embryos following exposure to SSRI's

1992
09/00
Case/Review Case report of a Syncopal Episode associated with Prozac/Sarafem (fluoxetine)

1990
09/00
Case/Review Prozac/Sarafem (fluoxetine)-induced Bradycardia and Syncope in two patients

Medical reports: EPILEPTIFORM ACTIVITY, SEIZURES, REM SLEEP/MEMORY/EEG PROBLEMS, SLEEPWALKING
2003
12/00
Case/Review Memory Loss in a patient treated with Prozac/Sarafem (fluoxetine)

2003
09/00
Case/Review Wellbutrin/Zyban-induced Somnambulism (sleepwalking) & Amnesia

2003
04/16
Case/Review Neonatal Convulsions & Subarachnoid Hemorrhage after exposure to Paxil/Seroxat

2003
03/31
Case/Review SSRI-induced Epileptic Seizures

2003
02/00
Case/Review Seizure associated with sleep deprivation & Wellbutrin/Zyban (bupropion)

2003
01/14
Case/Review Remeron (mirtazapine) induces REM Sleep Behavior Disorder in parkinsonism

2002
00/00
Case/Review Effects of antidepressant drugs on seizure threshold

2002
00/00
Case/Review Celexa/Cipramil Induced Severe Hyponatraemia with Coma & Seizure

2002
04/00
AnimalStudy Proconvulsant Effects of high doses of Effexor (venlafaxine) in rats

2002
04/00
Case/Review Wellbutrin/Zyban common cause of Seizures presenting to Emergency Department

2001
09/10
Case/Review Bitemporal Epileptiform Discharges induced by Wellbutrin/Zyban (bupropion)

2001
07/00
Case/Review Acute Paroxysmal Dystonia induced by Prozac/Sarafem (fluoxetine)

2001
06/00
Case/Review Dose-dependent Seizure Activity associated with Prozac/Sarafem (fluoxetine) therapy

2000
12/00
Case/Review Seizures associated with therapeutic doses of Effexor (venlafaxine) & trimipramine

2000
03/02
Case/Review SIADH with Epileptic Seizures and Coma in Prozac/Sarafem (fluoxetine) therapy

1999
00/00
Case/Review Antidepressants and seizure susceptibility: from in vitro data to clinical practice

1997
00/00
Case/Review Toxic Delirium & general Tonic-Clonic Seizure with Prozac & low dose Trazodone

1997
11/00
Case/Review Seizures, Tachycardia & Rhabdomyolysis following Effexor & Lamotrigine

1997
09/00
Case/Review Prozac (fluoxetine)-induced cardiovascular, neurovascular toxicity & seizure

1996
00/00
Case/Review Nightmares and hallucinations after 2-month intake of tramadol & Paxil/Seroxat

1995
06/00
Case/Review Use of Wellbutrin/Zyban (bupropion) involves a Higher Seizure Risk

1995
01/00
Case/Review Worsening Tremor & Word-Finding Problems following Prozac (fluoxetine) treatment

1994
08/00
No Abstract Seizures and antidepressants

1994
06/00
No Abstract Antidepressant-associated Seizures

1993
12/00
Case/Review Seizures associated with Prozac/Sarafem (fluoxetine) therapy

1993
09/00
Case/Review Celexa/Cipramil-Induced Significant Decrease of EEG Power of NREM sleep (8-9hz)

1986
08/00
Case/Review A case of Wellbutrin/Zyban (bupropion)-induced Seizure

1986
06/00
Case/Review Marketing of Wellbutrin (bupropion) in US delayed after Epileptic Seizures in trials

Antidepressant Neurological Side-Effects: Addiction & Withdrawal

Antidepressant Neurological Side-Effects: Akathisia & Mania (Suicide & Aggression)

Antidepressant Neurological Side-Effects: Serotonin Syndrome

Antidepressant Neurological Side-Effects: Toxicity & Brain Damage

Antidepressant Neurological Side-Effects: "Anecdotal" Reports -Personal Experiences

Antidepressants: How To Wean/Taper Off

Antidepressants: How to Survive a Negative Reaction

Antidepressants: Conquering Depression and Anxiety

Aggressive marketing of depression and powerful brain/body harming mind-altering antidepressants,
is a very serious crime against parents, children and adolescents.

Back HOME

posted in Effexor Activists Tribe - 1 reply

hepatitis and effexor

2008-08-01T17:53:15Z

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1: Ann Pharmacother. 2006 Feb;40(2):323-7. Epub 2006 Jan 17. Links
Hepatitis associated with low-dose venlafaxine for postmenopausal vasomotor symptoms.Phillips BB, Digmann RR, Beck MG.
Department of Pharmaceutical Care, University of Iowa Hospitals and Clinics, Iowa City, IA 52242-1009, USA. beth-phillips@uiowa.edu

OBJECTIVE: To report a case of drug-induced hepatitis associated with low-dose venlafaxine. CASE SUMMARY: A 60-year-old white woman receiving venlafaxine 75 mg daily for vasomotor symptoms presented after one month of therapy with nonspecific complaints, including abdominal pain. A series of diagnostic and laboratory tests revealed an enlarged liver and elevated alanine aminotransferase (ALT) up to 372 U/L, aspartate aminotransferase (AST) up to 99 U/L, gamma-glutamyltransferase (GGT) up to 962 U/L, and alkaline phosphatase up to 758 U/L. All potential hepatotoxic medications were discontinued. Within one week after stopping venlafaxine, her liver function test results showed marked improvement. Almost 4 weeks after discontinuing therapy, venlafaxine 37.5 mg was reinitiated. Her ALT, AST, GGT, and alkaline phosphatase again increased to 269, 49, 256, and 263 U/L, respectively, 6 days after resuming therapy. Upon discontinuation of venlafaxine, her liver function abnormalities resolved. DISCUSSION: This case is significant due to the severity of symptoms and consequent liver function test results involved in diagnosing drug-induced hepatitis. It is also remarkable because of the hepatotoxicity that occurred initially and on rechallenge with low-dose venlafaxine. The hepatotoxic effects of venlafaxine have been characterized as rare and idiosyncratic. The Naranjo probability scale revealed that the adverse drug event was probable. CONCLUSIONS: Venlafaxine therapy can lead to drug-induced hepatitis, even when used at low doses. Clinicians should be aware of this possible adverse effect of venlafaxine therapy and monitor patients closely after initiation of therapy.

PMID: 16418323 [PubMed - indexed for MEDLINE]
is there an organ this drug doesn't harm????

posted in Effexor Activists Tribe - 0 replies

Wyeth Among 3 Firms Subpoenaed by U.S.

2008-07-28T19:45:10Z

January 31, 2004

IN BRIEF / HEALTH
Wyeth Among 3 Firms Subpoenaed by U.S.

The U.S. government has subpoenaed Wyeth in connection with its marketing to doctors of the antidepressant drug Effexor, making it the third drug company in a week to receive a subpoena in a widening federal investigation.

James Sheehan, assistant U.S. attorney in Philadelphia, said Wyeth, Johnson & Johnson and Forest Laboratories Inc. have been subpoenaed in a probe related to potentially over-aggressive marketing of psychiatric drugs.

The subpoenas came from the inspector general for the Office of Personnel Management, which investigates potential fraud involving the health benefits of about 10 million federal employees and retirees.

If you want other stories on this topic, search the Archives at latimes.com/archives.

Article licensing and reprint options

This is old but new to me.

posted in Effexor Activists Tribe - 0 replies

26 months after Effexor

2008-07-28T19:37:30Z

Here's an update to my last post on theeffexoractivist. (Leslee reprinted it below in her response to Wendy below.)
I took Effexor for 10 years, withdrew for 4 months and took my last dose on April 27, 2006. I still have a symptom similar to what Wendy describes in her post. It was much more acute during the withdrawal phase, but it hasn't improved in 2 years. It is triggered by head or eye movements like Wendy describes. In my case, it's also accompanied by a swooshing sound. If I have to move alot, I get full-blown motion sickness. I used to love to dance (couples and contra), but I can't anymore because I get too dizzy. I became very sick recently on a trip where I had to fly and drive a lot.
I still have other symtoms too, though they aren't as extreme as when I was going through acute withdrawal. I still have sleep disturbances, vivid dreams, waking up with anxiety and the feeling that I haven't really slept. My body still twitches when I'm laying in bed and I hear a sudden noise (I used to have intense full-body seizures). The worst symptom of all is the inability to feel pleasure or joy. In my research, I found that former long term meth users often lose the ability to feel joy. When we flood our brains with serotonin, the brain compensates by shutting down the receptors. No one seems to know if the receptors grow back after the flooding stops.
I will never again take antidepressants or any other drug. I hope I'll feel better someday, but in the meantime, I'm trying to adjust to a life without joy or pleasure.

posted in Effexor Activists Tribe - 4 replies

effexor and ulcer

2008-07-28T19:33:34Z

Antidepressants raise ulcer risk

Taking an antidepressant may increase the odds of developing an ulcer.

The study of 1,321 people with gastrointestinal bleeding found that such drugs as Eli Lilly's Prozac, Forest Laboratories' Celexa and Lexapro, GlaxoSmithKline's Paxil, Pfizer's Zoloft, and Wyeth's Effexor could trigger gastrointestinal bleeding in one of every 2,000 patients. The risk increased to 1 in 250 patients when aspirin or pain drugs also were taken, according to the report.

The medicines interfere with platelets, a critical part of the body's normal clotting process, researchers said. Drugs that suppress the production of acid in the stomach -- Prevacid, Prilosec, Nexium and Protonix -- may avert bleeding for those most vulnerable and should be considered, researchers said.

Article from the L..A. Times
too late for me but may help you....

posted in Effexor Activists Tribe - 0 replies

Neuroleptic malignant syndrome form non neuroleptic drugs yes it does exits......

2008-07-27T02:38:18Z

This is the closest I could access so we know nms is caused by antidepressants it is just a matter ot time before effexor and mns articles are easy to find. Last year at this time I couldn't find anything...it is filtering out now I think because they know the jig is up so to speak.
This is what I suspect anyway. Last couple of years when I have been very ill and getting no place fast with doctors I did a search on my symptoms. The resulting search gave me nms I have had it in my mind for a long time. I could never draw any lines to effexor or antidepressants. I was not taking any neuroleptic drugs so I was at a loss. It is one thing to find what you think is going on in your body but then to get a clinic doctor to listen that is another battle royal.
did a search on NMS and Effexor got this:
Neuroleptic malignant syndrome after venlafaxine (search got this) Mon, July 21, 2008 - 10:17 PM

Elsevier Article Locator

this is a page I can locate but cannot access so obviously effexor causes nms.

You have requested access to the following article:

Neuroleptic malignant syndrome after venlafaxine .
The Lancet , Volume 355 , Issue 9221 , Pages 2164 - 2165
E . Cassidy , V . O'Kearne

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I like to leave all the information so anyone can find it. I am not an ENTITLED so could not access the information in this site. Sooo I kept looking and ....

Next find:
Neuroleptic malignant syndrome: May be caused by other drugs..
EDITOR, - M F Bristow and D Kohen state that the neuroleptic malignant syndrome may occur in response to the sudden cessation of dopamine agonists as well as in patients treated with neuroleptic drugs.1 But the syndrome has also been reported after the administration of non-neuroleptic drugs, including lithium, metoclopramide, carbamazepine, antidepressants (including dothiepin and amoxapine), tetrabenazine, and metirosine.*RF 2-4*
The authors emphasise that the pathogenesis of the syndrome is unknown and mention several possible central mechanisms. Although dopaminergic hypofunction in the basal ganglia seems the most likely cause of the rigidity and tremor, peripheral mechanisms may give rise to the other features. Sustained rigidity and tremor are likely to produce considerable heat as a result of muscle metabolism, and this could account for the fever. Fever and metabolic changes secondary to rhabdomyolysis could contribute to autonomic dysfunction and clouding of consciousness, the two remaining key features of the syndrome. The beneficial effect of dantrolene, a skeletal muscle relaxant, in reducing the duration of the syndrome supports the importance of muscular mechanisms in pathogenesis. Central abnormalities may also play a part - in particular, decreased activity in dopaminergic pathways in the hypothalamus may lead to fever.

Awareness of the epidemiology of the neuroleptic malignant syndrome may help alert clinicians to early cases. The male to female ratio among patients is 2:1, and 45% of patients are aged between 20 and 39, although the condition occurs at all ages.2 Ninety per cent of cases begin within 10 days of the start of treatment with a neuroleptic drug, though not necessarily for the first time, and a rapid increase in the dose during this period is usual. Although all neuroleptic drugs have been implicated, half of all reports have concerned haloperidol.5

P M Haddad

Department of Psychiatry, Manchester Royal Infirmary, Manchester M13 9BX.

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

Bristow MF, Kohen D. How "malignant" is the neuroleptic malignant syndrome? BMJ 1993;307:1223-4. (13 November.)
Kellam AMP. The (frequently) neuroleptic (potentially) malignant syndrome. Br J Psychiatry 1990;157:169-73. [Free Full Text]
Burke RE, Fahn S, Mayeux R, Weinberg H, Louis K, Willner JH. Neuroleptic malignant syndrome caused by dopamine depleting drugs in a patient with Huntington disease. Neurology 1981;31:1022-6. [Abstract/Free Full Text]
Grant R. Neuroleptic malignant syndrome. BMJ 1984;i:1690.
Shalev A, Munitz H. The neuroleptic malignant syndrome: agent and host interaction. Acta Psychiatr Scand 1986;73:337-47. [Medline

This is the closest I could access so we know nms is caused by antidepressants it is just a matter ot time before effexor and mns articles are easy to find. Last year at this time I couldn't find anything...it is filtering out now I think because they know the jig is up so to speak.
This is what I suspect anyway. Last couple of years when I have been very ill and getting no place fast with doctors I did a search on my symptoms. The resulting search gave me nms I have had it in my mind for a long time. I could never draw any lines to effexor or antidepressants. I was not taking any neuroleptic drugs so I was at a loss. It is one thing to find what you think is going on in your body but then to get a clinic doctor to listen that is another battle royal.

for your information:

Definition of Rhabdomyolysis

Rhabdomyolysis: A condition in which skeletal muscle cells break down, releasing myoglobin (the oxygen-carrying pigment in muscle) together with enzymes and electrolytes from inside the muscle cells. The risks with rhabdomyolysis include muscle breakdown and kidney failure since myoglobin is toxic to the kidneys.

Rhabdomyolysis can occur from extensive muscle damage as, for example, from a crushing injury or an electrical shock. Drugs or toxins, particularly some of the cholesterol lowering medications such as cerivastatin (Baycol), may cause this disorder. Underlying diseases such as systemic lupus erythematosus can also lead to rhabdomyolysis. It is a common complication of major burns.

The key signs and symptoms of rhabdomyolysis include dark, red, or cola colored urine and muscle tenderness, stiffness, aching (myalgia) or weakness. Laboratory confirmation can come from the demonstration of myoglobin in the blood or urine.

Ideal treatment involves early and aggressive hydration with very large amounts of IV fluids to flush the myoglobin out of the kidneys. Diuretics may help. So may bicarbonate which makes the urine alkaline to prevent the breakdown of myoglobin into more toxic compounds.

From the Greek roots rhabdo-, striped (striated) + -myo-, muscle + -lysis, breakdown = the breakdown of striated muscle (skeletal muscle).

Last Editorial Review: 3/14/2003

yes I had that too red urine was told it was likely form eating beats aaarrrgghh

posted in Effexor Activists Tribe - 1 reply

bleed to death or be depressed hmm...if only we knew before we took the drug

2008-07-20T00:45:51Z

This article explains how and why ssri's cause us to bleed... finally. I have been looking for 4 years and asking doctors. Though it is good to find it makes me sick that it is too late. Maybe it will be in time to help another, but I think we at this tribe know most will not seek out this site or this information as they think the drugs are safe that the powers that be would not allow such dangers on the market!!!!!!! We know better What To Do?!

Do SSRIs cause gastrointestinal bleeding?[No authors listed]
Selective serotonin re-uptake inhibitor antidepressants (SSRIs) can inhibit uptake, and therefore storage, of serotonin by platelets. This is significant because release of serotonin from platelets augments their aggregation; so use of SSRIs could, in theory, predispose patients to bleeding disorders. Case reports have suggested a link between SSRIs and easy bruising, nosebleeds, menorrhagia, petechial, ocular, small bowel, rectal and cerebral haemorrhages, and a prolonged bleeding time. Also, the summaries of product characteristics (SPCs) for all SSRIs include warnings about use in patients with a history of bleeding disorders or concomitant use with drugs known to affect platelet function. Here we review the risk of gastrointestinal bleeding associated with the use of SSRIs.

PMID: 15038078 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/15038078?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=4&log$=relatedarticles&logdbfrom=pubmed

posted in Effexor Activists Tribe - 1 reply

effexor and mucocutaneous hemorrhage

2008-07-18T04:07:14Z

sites can be found at serotonin and macocutaneous hemorrhage
google it
From PubMed
1: Rev Med Interne. 2000 Feb;21(2):152-60. Links
[Hemorrhagic syndromes related to selective serotonin reuptake inhibitor (SSRI) antidepressants. Seven case reports and review of the literature

Nelva A, Guy C, Tardy-Poncet B, Beyens MN, Ratrema M, Benedetti C, Ollagnier M.
Centre Régional de Pharmacovigilance et de Renseignements sur le Médicament, Saint-Etienne, France.

PURPOSE: Selective serotonin reuptake inhibitors (SSRIs) are widely prescribed. Since their release unexpected adverse effects such as bleeding disorders have been described. METHODS: Thirty patients with either hematoma or muco-cutaneous bleeding have been selected from case reports of the Saint-Etienne Pharmacovigilance center and from a literature review. RESULTS: The female/male sex-ratio was 3:4 and the mean age 42 years. Two newborns who had been exposed in utero to SSRIs were also included in the study. Eleven patients presented an underlying disease or were at risk. Various adverse effects such as bruising, hematoma, petechiae or purpura, epistaxis, and more rarely intestinal hemorrhage, ocular bleeding or cerebral hemorrhage were encountered. Symptoms were sometimes associated with prolonged bleeding time and platelet aggregation disorders and usually resolved within two days to four months after treatment discontinuation. CONCLUSION: Hematoma and muco-cutaneous bleeding would therefore be related to treatment, including selective serotonin reuptake inhibitors. However, these adverse effects are still poorly known and rarely reported. The main mechanism suggested would be a decrease in serotonin platelet leading to a defect in platelet aggregation. However, an increase in capillary fragility or susceptibility related to the patient's condition might be involved. Study of hemostasis history in patients requiring treatment with SSRIs might be of value.

PMID: 10703071 [PubMed - indexed for MEDLINE]

Postmarketing Reports
Voluntary reports of other adverse events temporally associated with the use of venlafaxine that have been received since market introduction and that may have no causal relationship with the use of venlafaxine include the following: agranulocytosis, anaphylaxis, aplastic anemia, catatonia, congenital anomalies, impaired coordination and balance, CPK increased, deep vein thrombophlebitis, delirium, EKG abnormalities such as QT prolongation; cardiac arrhythmias including atrial fibrillation, supraventricular tachycardia, ventricular extrasystole, and rare reports of ventricular fibrillation and ventricular tachycardia, including torsade de pointes; toxic epidermal necrolysis/Stevens-Johnson Syndrome, erythema multiforme, extrapyramidal symptoms (including dyskinesia and tardive dyskinesia), angle-closure glaucoma, hemorrhage (including eye and gastrointestinal bleeding), hepatic events (including GGT elevation; abnormalities of unspecified liver function tests; liver damage, necrosis, or failure; and fatty liver), interstitial lung disease, involuntary movements, LDH increased, neuroleptic malignant syndrome-like events (including a case of a 10-year-old who may have been taking methylphenidate, was treated and recovered), neutropenia, night sweats, pancreatitis, pancytopenia, panic, prolactin increased, renal failure, rhabdomyolysis, serotonin syndrome, shock-like electrical sensations or tinnitus (in some cases, subsequent to the discontinuation of venlafaxine or tapering of dose), and syndrome of inappropriate antidiuretic hormone secretion (usually in the elderly).

There have been reports of elevated clozapine levels that were temporally associated with adverse events, including seizures, following the addition of venlafaxine. There have been reports of increases in prothrombin time, partial thromboplastin time, or INR when venlafaxine was given to patients receiving warfarin therapy

posted in Effexor Activists Tribe - 0 replies

SSRIs induce extrapyramidal side-effects EPS

2008-07-17T22:21:32Z

SSRI-Induced extrapyramidal side-effects and akathisia: implications for treatment
Roger M. Lane
Pfizer Inc., 235 East 42nd Street, New York, NY 10017, USA

The selective serotonin reuptake inhibitors (SSRIs) may occasionally) induce extrapyramidal side-effects (EPSand/or akathisia.This maybe a consequence of serotonergically-mediated inhibition of the dopaminergic system. Manifestations of these effects in patients may depend on predisposing factors such as the presence of psychomotor disturbance, a previous history of drug-induced akathisia and/or EPS, concurrent antidopaminergic and/or serotonergic therapy, recent monoamine oxidase inhibitor discontinuation, comorbid Parkinson's disease and possibly deficient cytochrome P450 (CYP) isoenzyme status. There is increasing awareness that there may be a distinct form of melancholic or endogenous depression with neurobiological underpinnings similar to those of disorders of the basal ganglia such as Parkinson's disease. Thus, it is not surprising that some individuals with depressive disorders appear to be susceptible to developing drug-induced EPS and/or akathisia. In addition, the propensity for the SSRIs to induce these effects in individual patients may vary within the drug class depending, for example, on their selectivity for serotonin relative to other monoamines, affinity for the 5-HT2C receptor, pharmacokinetic drug interaction potential with concomitantly administered neuroleptics and potential for accumulation due to a long half-life. The relative risk of EPS and akathisia associated with SSRIs have yet to be clearly established. The potential risks may be reduced by avoiding rapid and unnecessary dose titration. Furthermore, early recognition and appropriate management of EPS and/or akathisia is required to prevent the impact of these effects on patient compliance and subjective well-being. It is important that the rare occurrence of EPS in patients receiving SSRIs does not preclude their use in Parkinson's disease where their potentially significant role requires more systematic evaluation.

Key Words: akathisia • basal ganglia • CYP2D6 • dopamine • extrapyramidal side-effects • SSRIs • serotonin syndrome

Definition of Extrapyramidal side effects

Extrapyramidal side effects: Physical symptoms, including tremor, slurred speech, akathisia, dystonia, anxiety, distress, paranoia, and bradyphrenia, that are primarily associated with improper dosing of or unusual reactions to neuroleptic (anti-psychotic) medications
http://www.medterms.com/script/main/art.asp?articlekey=11354
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Dystonia Index Glossary

Dystonia
What are the dystonias?
What are the symptoms of dystonias?
How are dystonias classified?
What do scientists know about the dystonias?
When do symptoms of dystonias occur?
Are there any treatments for dystonias?
What research is being done on dystonias?
Where can I get more information about dystonias?

What are the dystonias?

The dystonias are movement disorders in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures. The movements, which are involuntary and sometimes painful, may affect a single muscle; a group of muscles such as those in the arms, legs, or neck; or the entire body. Those with dystonia usually have normal intelligence and no associated psychiatric disorders.

What are the symptoms of dystonias?

Dystonia can affect many different parts of the body. Early symptoms may include a deterioration in handwriting after writing several lines, foot cramps, and/or a tendency of one foot to pull up or drag; this may occur "out of the blue" or may occur after running or walking some distance. The neck may turn or pull involuntarily, especially when the patient is tired or stressed. Sometimes both eyes will blink rapidly and uncontrollably, rendering a person functionally blind. Other possible symptoms are tremor and voice or speech difficulties. The initial symptoms can be very mild and may be noticeable only after prolonged exertion, stress, or fatigue. Over a period of time, the symptoms may become more noticeable and widespread and be unrelenting; sometimes, however, there is little or no progression.

more about dystonia here

www.medicinenet.com/dystonia/article.htm
For me the dystonia seemed to be with my back or ribs (both) I felt torched pulled way off balance.... I suspect causing pain and disfunction of my right side and organs there in. Of course I can't prove a thing and only have my word to go on.
I also get the jerking leg, the whole body jerk that wakes me from sleep, tooth grinding, swooshing head, kicking, panic waking, delayed reaction from my eyes balls being behind my head. movements...been to the hops and clinic so many times for dizzyness so bad I could barely walk... was given a variety of drugs that didn't work and the cause was never discovered...who knows fish oil helps I think I am getting better... afraid to speek too soon don't want to jinx myself.
Good luck to you all. Peace Sandy

Wed, July 16, 2008 - 8:07 PM

posted in Effexor Activists Tribe - 1 reply

This stuff sucks

2008-07-13T23:48:31Z

Discovered I have been depressed for over 35 years, doc put me on Effexor XR in 2003. 37.5 mgs/day -> 75 -> then I quit cold turkey in 2004? 2005? I forget, but quickly realized that you can't DO that. Went back on it and then weaned myself off of it more slowly. Things got bad again in 2005 and I went back on it. 75 -> 150 -> 225 -> 300 mgs day! Was horribly depressed back then, and the E XR really did help IMHO. In 2007, I found my BP skyrocketing off the charts and then found an article about E XR and high BP, so I decided to wean myself off the stuff again, with my neuro's approval. It's taken me several months now to get from 300 down to 75, and recently I find myself getting nauseous almost every day. I'm in the middle of getting diagnosed for something, not sure what, Fibromyalgia? MS? Parkinsons? We don't know yet. I already experience a lot of the withdrawal symptoms listed, and was experiencing them before I started cutting back.

How long does it take to get off this crap!!!!!

posted in Effexor Activists Tribe - 4 replies

What was the point?

2008-07-07T01:36:42Z

I have been slowly cutting down on the effexor in hopes of "kicking" this drug once and for all... and once again I am finding my body is fighting harder to keep me on it. I am really hurting this time around.. my eyes are so tender and sensitive to anything including this computer screen to the sun...to the TV.. my brain actually feels pain.. like a headache but slightly different. I have spoken to a few people and I feel as if they think I am crazy. It is almost refreshing to read some of the posts and articles (as sick as that is) as it is validating what I am feeling. I have taken Paxil in the past and thought that was a NIGHTMARE to get off of... but Effexor takes the cake. How long is this going to last?
Funny I needed help with my anxiety and I am anxious about getting off the THING that was suposed to HELP the anxiety....
Now on top of all of that: I need to workout to drop the weight, fight this war my body is waging against me and my head, and also manage my stress and anxiey drug free---? What was the point? I didn't progress I REgressed!

posted in Effexor Activists Tribe - 1 reply

Physician Testifies that Man Went Insane on Effexor

2008-06-28T07:01:40Z

Fourth paragraph from the end reads: "Lewis said she had received a report from the medical doctor who had examined Henry. 'It is my opinion, with reasonable medical certainty, that Mr. Henry suffers from a bipolar disorder that was exacerbated by the antidepressant Effexor, leading to a manic state, that included psychotic features,' the doctor said in the court documents. 'This psychotic state interfered with him being able to have substantial capacity to know the wrongfulness of his behavior'."

http://bangornews.com/news/t/news.aspx?articleid=166314&zoneid=164

Suspect in machete threat skips court, may have fled to Caribbean

By Diana Graettinger
Thursday, June 26, 2008 - Bangor Daily News

MACHIAS, Maine - A 36-year-old man who was charged with terrorizing his wife with a machete last year may have skipped the country and gone back to his home in Saint Lucia.

Saint Lucia is one of the Windward Islands of the Lesser Antilles in the eastern Caribbean Sea.

Kirk Henry, most recently of Machias, was charged with two counts of terrorizing, criminal threatening and assault in August 2007. He was scheduled to appear in Washington County Superior Court on Monday but never showed up.

Henry’s attorney, Carol Lewis of Lubec, told Judge E. Allen Hunter that she had not had contact with her client.

Hunter issued a warrant for Henry’s arrest. If Henry returns to Washington County he will be arrested.

First Assistant District Attorney Paul Cavanaugh said Wednesday the county still did not know where Henry was.

"We have a suspicion that he has returned to Saint Lucia, where he is from," he said.

"He was held in jail from the date of the offense in August 2007 until he posted bail in May 2008," Cavanaugh said.

A Whiting man posted the $5,000 cash bail, Cavanaugh said, which will be forfeited because of his failure to appear.

According to court documents, on Aug. 25, 2007, Henry was at the Indian Lake Cottage in Whiting that he shared with the victim until around 8 p.m., when he left to go to a bar in Eastport.

After learning that Henry was to meet another woman in Eastport, the victim called the bar and spoke with Henry, an affidavit on file with the Washington County Superior Court states.

Henry returned to the couple’s cottage around 2 a.m. Sunday and an argument ensued. "[Henry] then became physically abusive, throwing [the victim] about the kitchen, her body breaking glasses and dishes as she was attacked," the affidavit says. "During the attack, [the victim] sustained a cut to her finger. She sustained injuries to her eye, lip, nose, ribs, hip and thigh."

When the victim wiped some of the blood from her finger on Henry, he became "enraged," the affidavit says. "He grabbed the telephone and destroyed it and threw another object through the front window of the cottage," court documents say.

The victim tried to hide in the bathroom.

Henry grabbed a machete and began to hack at the bathroom door, the affidavit says.

The victim tried to run out of the bathroom and out the front door, but Henry blocked her escape. She then ran to the bedroom. Henry pushed his way into the bedroom. "Holding [the victim] by the throat with one hand, [Henry] screamed at her [that] he was going to kill her as he held the machete above her head with the other hand," the affidavit states. The victim begged for her life, "dropping to her knees and telling [Henry] she was sorry for ever questioning him," the affidavit says.

Sometime later, the assault ended and Henry fell asleep on the couch, the machete beside him.

Afraid, the defendant remained at the cottage and then drove Henry to a boat-building class that morning. "Back at the cottage, she tried to clean some of the blood and glass left from the attack earlier that morning," the affidavit states. "She then left the cottage for her house in Machias."

Although the victim went to the hospital that night, she did not call police. She did contact domestic violence support services the next day, but still did not report the incident to police.

Three days later, the victim reported the incident to the Washington County Sheriff’s Department.

Henry then contacted the victim’s daughter and told her the situation was putting him "between a rock and a hard place" and he might do "something crazy, like burn the house down," the affidavit says.

The Machias Police Department investigated the incident.

When police questioned Henry, he admitted to police that he had threatened to burn the house down. He was arrested.

On Sept. 25, 2007, Henry’s attorney filed a motion with the court requesting a forensic evaluation. In her request, Lewis noted that Henry had been under a lot of stress and had recently suffered a loss, which may have affected his reasoning. The motion was granted.

On March 24 of this year, Lewis filed a request to enter a plea of not criminally responsible by reason of insanity, the court document says.

Lewis said she had received a report from the medical doctor who had examined Henry. "It is my opinion, with reasonable medical certainty, that Mr. Henry suffers from a bipolar disorder that was exacerbated by the antidepressant Effexor, leading to a manic state, that included psychotic features," the doctor said in the court documents. "This psychotic state interfered with him being able to have substantial capacity to know the wrongfulness of his behavior."

In April, Lewis filed a motion for a Stage Three Forensic Evaluation. Two weeks later, a letter was filed with the court from the Department of Health and Human Services’ Adult Mental Health Services notifying Riverview Psychiatric Center in Augusta that Henry could be admitted to its facility for 60 days. "At the end of 60 days or sooner, the State Forensic Service shall forward a report to the court ... relative to the defendant’s competence and criminal responsibility, with respect to the court’s order," the letter said.

Although a judge signed the order for commitment, Henry never showed up.

Henry remains on the lam. "He could be gone forever or caught tomorrow," Cavanaugh said. "He sits in the drawer until we find him."

bdncalais@verizon.net

454-8228

posted in Effexor Activists Tribe - 0 replies

Class Action Lawsuit?

2008-06-26T22:26:04Z

I'm not the litigious type, but with all this alarming info about this drug, has there been any talk of a CAL?

posted in Effexor Activists Tribe - 1 reply

celexa and death from brain bleed

2008-06-24T15:09:47Z

Had a freind who died this month he was taking celexa and fell down he said he fainted. Woke in his own bed didn't recall getting to bed I went to his house the next day after he woke and cleaned up the blood. He had a headache and was dizzy. He fell twice while I was there the second time knocked himself out. I called an ambulance. At hosp they inserted a cathadar when they did that he had a major brain bleed went silence stopped breathing they inserted an breathing tube put him on a machine operated on his brain he never woke up.
I took celexa for 4year along with effexor I have quit both. I had warned him about these drugs. I found out he had started taking celexa again when we were in emerg. I had excessive vaginal bleeding and stomach bleed while on celexa and effexor.
What do you think are these drugs killing people???!!!

posted in Effexor Activists Tribe - 2 replies

We have NO control over Tribes ad content.

2008-06-24T07:07:35Z

Please be aware that the effexor activist has no control over the ads displayed by Tribes.

posted in Effexor Activists Tribe - 4 replies

Affected by Anti- Depressants

2008-06-18T21:14:40Z

[X]1. Crying spells
[X]2. Worsened mood
[X]3. Low energy (fatigue, lethargy, malaise)
[X]4. Trouble concentrating
[X]5. Insomnia or trouble sleeping
6. Change in appetite
[X]7. Suicidal thoughts
8. Suicide attempts
[X]9. Anxious, nervous, tense given clonazepam (Klonopin) panic, phobias, social phobia
[X]10. Panic attacks (racing heart, breathless) " "
[X]11. Chest pain
12. Trembling, jittery,or shaking
[X]13. Irritability blamed on peri menopausal
14. Agitation (restlessness, hyperactivity)
[X]15. Impulsivity
16. Aggressiveness
[X]17. Self-harm
[X]18. Homicidal thoughts or urges
19. Confusion or cognitive difficulties
[X]20. Memory problems or forgetfulness
21. Elevated mood (feeling high)
[X]22. Mood swings blmaed on menopausal symptoms and age
23. Manic-like reactions
24. Auditory hallucinations
25. Visual hallucinations
[X]26. Feeling detached or unreal
27. Excessive or intense dreaming
[X]28. Nightmares
[X]29. Flu-like aches and pains
[X]30. Fever
[X]31. Sweats
[X]32. Chills
33. Runny nose
34. Sore eyes
[X]35. Nausea
[X]36. Vomiting
[X]37. Diarrhea
[X]38. Abdominal pain or cramps blamed on IBS (Irritable bowel syndrome)
[X]39. Stomach bloating
40. Disequilibrium
41. Spinning, swaying, lightheaded
[X]42. Hung over or waterlogged feeling
[X]43. Unsteady gait, poor coordination
44. Motion sickness
[X]45. Headache
46. Tremor
47. Numbness, burning, or tingling
[X]48. Electric zap-like sensations in the brain
[X]49. Electric shock-like sensations in the body
[X]50. Abnormal visual sensations
[X]51. Ringing or other noises in the ears
[X]52. Abnormal smells or tastes --metallic
53. Drooling or excessive saliva
[X]54. Slurred speech
[X]55. Blurred vision
[X]56. Muscle cramps, stiffness, twitches given flexeril
[X]57. Feeling of restless legs
58. Uncontrollable twitching of mouth

I had all the symptoms checked with [X]
I was on a variety of medications none of which seemed to help me, I was diagnosed with PTSD (post traumatic stress disorder) I stopped taking all the medications in 2003 most of the symptoms listed above have disappeared. Whats awful with these drugs is they give you another one to mask the symptom from the first and it gets worse and worse.
I thank you for giving me a voice and wish you the best in what is and was a huge undertaking in getting the word out.
MeShell Hazard

posted in Effexor Activists Tribe - 3 replies

more on the Soldiers on SSRIs

2008-06-13T02:54:34Z

Thank you Brad Good find. will post at activist tomorrow. Here is more on the subject.

Paragraph 13 reads: "At least 115 soldiers killed themselves last year, including 36 in Iraq and Afghanistan, the Army said on May 29. That's the highest toll since it started keeping such records in 1980. Nearly 40% of Army suicide victims in 2006 and 2007 took psychotropic drugs overwhelmingly, selective serotonin reuptake inhibitors (SSRIs) like Prozac and Zoloft. While the Army cites failed relationships as the primary cause, some outside experts sense a link between suicides and prescription-drug use though there is also no way of knowing how many suicide attempts the antidepressants may have prevented by improving a soldier's spirits. "The high percentage of U.S. soldiers attempting suicide after taking SSRIs should raise serious concerns," says Dr. Joseph Glenmullen, who teaches psychiatry at Harvard Medical School. 'And there's no question they're using them to prop people up in difficult circumstances'."

Paragraph 12 reads: "Such questions have assumed greater urgency as more is revealed about the side effects of some mental-health medications. Last year the U.S. Food and Drug Administration (FDA) urged the makers of antidepressants to expand a 2004 "black box" warning that the drugs may increase the risk of suicide in children and adolescents. The agency asked for and got an expanded warning that included young adults ages 18 to 24, the age group at the heart of the Army. The question now is whether there is a link between the increased use of the drugs in the Iraqi and Afghan theaters and the rising suicide rate in those places. There have been 164 Army suicides in Afghanistan and Iraq from the wars' start through 2007, and the annual rate there is now double the service's 2001 rate."

http://www.time.com/time/nation/article/0,8599,1811858,00.html

America's Medicated Army

Thursday, Jun. 05, 2008 By MARK THOMPSON

Enlarge Photo
Illustration by Lon Tweeten and D.W. Pine for TIME

Seven months after sergeant Christopher LeJeune started scouting Baghdad's dangerous roads acting as bait to lure insurgents into the open so his Army unit could kill them he found himself growing increasingly despondent. "We'd been doing some heavy missions, and things were starting to bother me," LeJeune says. His unit had been protecting Iraqi police stations targeted by rocket-propelled grenades, hunting down mortars hidden in dark Baghdad basements and cleaning up its own messes. He recalls the order his unit got after a nighttime firefight to roll back out and collect the enemy dead. When LeJeune and his buddies arrived, they discovered that some of the bodies were still alive. "You don't always know who the bad guys are," he says. "When you search someone's house, you have it built up in your mind that these guys are terrorists, but when you go in, there's little bitty tiny shoes and toys on the floor things like that started affecting me a lot more than I thought they would."

So LeJeune visited a military doctor in Iraq, who, after a quick session, diagnosed depression. The doctor sent him back to war armed with the antidepressant Zoloft and the antianxiety drug clonazepam. "It's not easy for soldiers to admit the problems that they're having over there for a variety of reasons," LeJeune says. "If they do admit it, then the only solution given is pills."

While the headline-grabbing weapons in this war have been high-tech wonders, like unmanned drones that drop Hellfire missiles on the enemy below, troops like LeJeune are going into battle with a different kind of weapon, one so stealthy that few Americans even know of its deployment. For the first time in history, a sizable and growing number of U.S. combat troops are taking daily doses of antidepressants to calm nerves strained by repeated and lengthy tours in Iraq and Afghanistan. The medicines are intended not only to help troops keep their cool but also to enable the already strapped Army to preserve its most precious resource: soldiers on the front lines. Data contained in the Army's fifth Mental Health Advisory Team report indicate that, according to an anonymous survey of U.S. troops taken last fall, about 12% of combat troops in Iraq and 17% of those in Afghanistan are taking prescription antidepressants or sleeping pills to help them cope. Escalating violence in Afghanistan and the more isolated mission have driven troops to rely more on medication there than in Iraq, military officials say.

At a Pentagon that keeps statistics on just about everything, there is no central clearinghouse for this kind of data, and the Army hasn't consistently asked about prescription-drug use, which makes it difficult to track. Given the traditional stigma associated with soldiers seeking mental help, the survey, released in March, probably underestimates antidepressant use. But if the Army numbers reflect those of other services the Army has by far the most troops deployed to the war zones about 20,000 troops in Afghanistan and Iraq were on such medications last fall. The Army estimates that authorized drug use splits roughly fifty-fifty between troops taking antidepressants largely the class of drugs that includes Prozac and Zoloft and those taking prescription sleeping pills like Ambien.

In some ways, the prescriptions may seem unremarkable. Generals, history shows, have plied their troops with medicinal palliatives at least since George Washington ordered rum rations at Valley Forge. During World War II, the Nazis fueled their blitzkrieg into France and Poland with the help of an amphetamine known as Pervitin. The U.S. Army also used amphetamines during the Vietnam War.

The military's rising use of antidepressants also reflects their prevalence in the civilian population. In 2004, the last year for which complete data for the U.S. are available, doctors wrote 147 million prescriptions for antidepressants, according to IMS Health, a pharmaceutical-market-research firm. This number reflects in part the common practice of cycling through different medications to find the most effective drug. A 2006 federally funded study found that 70% of those taking antidepressants along with therapy experience some improvement in mood.

When it comes to fighting wars, though, troops have historically been barred from using such drugs in combat. And soldiers who are younger and healthier on average than the general population have been prescreened for mental illnesses before enlisting.

The increase in the use of medication among U.S. troops suggests the heavy mental and psychological price being paid by soldiers fighting in Iraq and Afghanistan. Pentagon surveys show that while all soldiers deployed to a war zone will feel stressed, 70% will manage to bounce back to normalcy. But about 20% will suffer from what the military calls "temporary stress injuries," and 10% will be afflicted with "stress illnesses." Such ailments, according to briefings commanders get before deploying, begin with mild anxiety and irritability, difficulty sleeping, and growing feelings of apathy and pessimism. As the condition worsens, the feelings last longer and can come to include panic, rage, uncontrolled shaking and temporary paralysis. The symptoms often continue back home, playing a key role in broken marriages, suicides and psychiatric breakdowns. The mental trauma has become so common that the Pentagon may expand the list of "qualifying wounds" for a Purple Heart historically limited to those physically injured on the battlefield to include posttraumatic stress disorder (PTSD). Defense Secretary Robert Gates said on May 2 that it's "clearly something" that needs to be considered, and the Pentagon is weighing the change.

Using drugs to cope with battlefield traumas is not discussed much outside the Army, but inside the service it has been the subject of debate for years. "No magic pill can erase the image of a best friend's shattered body or assuage the guilt from having traded duty with him that day," says Combat Stress Injury, a 2006 medical book edited by Charles Figley and William Nash that details how troops can be helped by such drugs. "Medication can, however, alleviate some debilitating and nearly intolerable symptoms of combat and operational stress injuries" and "help restore personnel to full functioning capacity."

Which means that any drug that keeps a soldier deployed and fighting also saves money on training and deploying replacements. But there is a downside: the number of soldiers requiring long-term mental-health services soars with repeated deployments and lengthy combat tours. If troops do not get sufficient time away from combat both while in theater and during the "dwell time" at home before they go back to war it's possible that antidepressants and sleeping aids will be used to stretch an already taut force even tighter. "This is what happens when you try to fight a long war with an army that wasn't designed for a long war," says Lawrence Korb, Pentagon personnel chief during the Reagan Administration.

Military families wonder about the change, according to Joyce Raezer of the private National Military Family Association. "Boy, it's really nice to have these drugs," she recalls a military doctor saying, "so we can keep people deployed." And professionals have their doubts. "Are we trying to bandage up what is essentially an insufficient fighting force?" asks Dr. Frank Ochberg, a veteran psychiatrist and founding board member of the International Society for Traumatic Stress Studies.

Such questions have assumed greater urgency as more is revealed about the side effects of some mental-health medications. Last year the U.S. Food and Drug Administration (FDA) urged the makers of antidepressants to expand a 2004 "black box" warning that the drugs may increase the risk of suicide in children and adolescents. The agency asked for and got an expanded warning that included young adults ages 18 to 24, the age group at the heart of the Army. The question now is whether there is a link between the increased use of the drugs in the Iraqi and Afghan theaters and the rising suicide rate in those places. There have been 164 Army suicides in Afghanistan and Iraq from the wars' start through 2007, and the annual rate there is now double the service's 2001 rate.

At least 115 soldiers killed themselves last year, including 36 in Iraq and Afghanistan, the Army said on May 29. That's the highest toll since it started keeping such records in 1980. Nearly 40% of Army suicide victims in 2006 and 2007 took psychotropic drugs overwhelmingly, selective serotonin reuptake inhibitors (SSRIs) like Prozac and Zoloft. While the Army cites failed relationships as the primary cause, some outside experts sense a link between suicides and prescription-drug use though there is also no way of knowing how many suicide attempts the antidepressants may have prevented by improving a soldier's spirits. "The high percentage of U.S. soldiers attempting suicide after taking SSRIs should raise serious concerns," says Dr. Joseph Glenmullen, who teaches psychiatry at Harvard Medical School. "And there's no question they're using them to prop people up in difficult circumstances."

The Trauma of WarBefore the advent of SSRIs Lilly's Prozac was the first to be approved by the FDA, in 1987, followed by Zoloft from Pfizer, Paxil from GlaxoSmithKline, Celexa from Forest Pharmaceuticals and others existing antidepressants had many disabling side effects. Impaired memory and judgment, dizziness, drowsiness and other complications made them ill suited for troops in combat. The newer drugs have fewer side effects and, unlike earlier drugs, are generally not addictive or toxic, even when taken in large quantities. They work by keeping neural connections bathed in a brain chemical known as serotonin. That amplifies serotonin's mood-brightening effect, at least for some people.

In 1994 then Major E. Cameron Ritchie, an Army psychiatrist, was among the first to suggest that SSRIs should deploy with Army combat units. In a paper written and published after she returned from a combat deployment to Somalia, Ritchie noted that the sick-call chests used by military doctors "contain either outdated or no psychiatric medications." She concluded, "If depressive symptoms are moderate and manageable, medication may be preferable to medical evacuation."

By 1999, military docs were debating the matter among themselves. Nash, a Navy psychiatrist, wrote that Navy doctors who also provide Marines with medical care had "sharp differences of opinion" over letting troops in war zones use SSRIs. Skeptics argued that their "real safety" in combat had not been proved. Supporters countered that their use could "avoid depleting manpower resources and damaging individual careers through unnecessary removals from operational duty." Nash reviewed the medical literature and reported that SSRIs "can be safely administered to deploying and deployed personnel."

The trickle of new drugs became a flood after the invasion of Iraq in 2003. Details of America's medicated wars come from the mental-health surveys the Army has conducted each year since the war began. If the surveys are right, many U.S. soldiers experience a common but haunting mismatch in combat life: while nearly two-thirds of the soldiers surveyed in Iraq in 2006 knew someone who had been killed or wounded, fewer than 15% knew for certain that they had actually killed a member of the enemy in return. That imbalance between seeing the price of war up close and yet not feeling able to do much about it, the survey suggests, contributes to feelings of "intense fear, helplessness or horror" that plant the seeds of mental distress. "A friend was liquefied in the driver's position on a tank, and I saw everything," was a typical comment. Another: "A huge f______ bomb blew my friend's head off like 50 meters from me." Such indelible scenes and wondering when and where the next one will happen are driving thousands of soldiers to take antidepressants, military psychiatrists say. It's not hard to imagine why.

Repeated deployments to the war zones also contribute to the onset of mental-health problems. Nearly 30% of troops on their third deployment suffer from serious mental-health problems, a top Army psychiatrist told Congress in March. The doctor, Colonel Charles Hoge, added that recent research has shown the current 12 months between combat tours "is insufficient time" for soldiers "to reset" and recover from the stress of a combat tour before heading back to war.

Colonel Joseph Horam says antidepressants have made "a striking difference" in the way troops are treated in war. A doctor in the Wyoming Army National Guard, Horam served in Saudi Arabia during the first Gulf War and has been deployed to Iraq twice during this war. "In the Persian Gulf War, we didn't have these medications, so our basic philosophy was 'three hots and a cot'" giving stressed troops a little rest and relaxation to see if they improved. "If they didn't get better right away, they'd need to head to the rear and probably out of theater." But in his most recent stint in Baghdad in 2006, he treated a soldier who guarded Iraqi detainees. "He was distraught while he was having high-level interactions with detainees, having emotional confrontations with them and carrying weapons," Horam says. "But he was part of a highly trained team, and we didn't want to lose him. So we put him on an SSRI, and within a week, he was a new person, and we got him back to full duty."

It wasn't until November 2006 that the Pentagon set a uniform policy for all the services. But the curious thing about it was that it didn't mention the new antidepressants. Instead, it simply barred troops from taking older drugs, including "lithium, anticonvulsants and antipsychotics." The goal, a participant in crafting the policy said, was to give SSRIs a "green light" without saying so. Last July, a paper published by three military psychiatrists in Military Medicine, the independent journal of the Association of Military Surgeons of the United States, urged military doctors headed for Afghanistan and Iraq to "request a considerable quantity of the SSRI they are most comfortable prescribing" for the "treatment of new-onset depressive disorders" once in the war zones. The medications, the doctors concluded, help "to 'conserve the fighting strength,'" the motto of the Army Medical Corps.

These days Ritchie now a colonel and a psychiatric consultant to the Army surgeon general thinks the military's use of SSRIs has helped destigmatize mental problems. "What we're trying to do is make treating depression and PTSD especially PTSD, which is quite common for soldiers now fairly routine," she says. "We don't want to make it harder for folks to do their job and their mission by saying they can't use these medications." Ritchie, who communicates "six times a day" with her colleagues in the war zones, says she is unaware of "any bad outcomes" resulting from soldiers taking SSRIs.

William Winkenwerder Jr., who issued the 2006 policy as the Pentagon's top doctor before stepping down last year, says the new medicines are working well. "Combat presents some unique and important caveats obviously, those who are being treated have access to firearms, and they may be under significant stress, so they need to be very carefully evaluated, and good clinical decisions need to be made," Winkenwerder tells TIME. "It's my belief that is happening."

"In a Total Daze"
And yet the battlefield seems an imperfect environment for widespread prescription of these medicines. LeJeune, who spent 15 months in Iraq before returning home in May 2004, says many more troops need help pharmaceutical or otherwise but don't get it because of fears that it will hurt their chance for promotion. "They don't want to destroy their career or make everybody go in a convoy to pick up your prescription," says LeJeune, now 34 and living in Utah. "In the civilian world, when you have a problem, you go to the doctor, and you have therapy followed up by some medication. In Iraq, you see the doctor only once or twice, but you continue to get drugs constantly." LeJeune says the medications combined with the war's other stressors created unfit soldiers. "There were more than a few convoys going out in a total daze."

About a third of soldiers in Afghanistan and Iraq say they can't see a mental-health professional when they need to. When the number of troops in Iraq surged by 30,000 last year, the number of Army mental-health workers remained the same about 200 making counseling and care even tougher to get.

"Burnout and compassion fatigue" are rising among such personnel, and there have been "recent psychiatric evacuations" of Army mental-health workers from Iraq, the 2007 survey says. Soldiers are often stationed at outposts so isolated that follow-up visits with counselors are difficult. "In a perfect world," admits Nash, who has just retired from the Navy, "you would not want to rely on medications as your first-line treatment, but in deployed settings, that is often all you have."

And just as more troops are taking these drugs, there are new doubts about the drugs' effectiveness. A pair of recent reports from Rand and the federal Institute of Medicine (iom) raise doubts about just how much the new medicines can do to alleviate PTSD. The Rand study, released in April, says the "overall effects for SSRIs, even in the largest clinical trials, are modest." Last October the iom concluded, "The evidence is inadequate to determine the efficacy of SSRIs in the treatment of PTSD."

Chris LeJeune could have told them that. When he returned home in May 2004, he remained on clonazepam and other drugs. He became one of 300,000 Americans who served in Iraq and Afghanistan and suffer from PTSD or depression. "But PTSD isn't fixed by taking pills it's just numbed," he claims now. "And I felt like I was drugged all the time." So a year ago, he simply stopped taking them. "I just started trying to fight my demons myself," he says, with help from VA counseling. He laughs when asked how he's doing. "I'd like to think," he says, "that I'm really damn close back to normal."

posted in Effexor Activists Tribe - 0 replies

Increased U.S. Soldier Suicide Attempts and Deaths linked to Antidepressants

2008-06-13T02:52:41Z

A drastic increase in suicide attempts and deaths have been attributed to soldiers taking antidepressants to cope with war violence and extended tours of duty.

http://www.theaustralian.news.com.au/story/0,25197,23848691-26397,00.html
http://www.voanews.com/english/2008-05-29-voa64.cfm
http://www.cnn.com/2008/US/02/01/military.suicides/index.html

posted in Effexor Activists Tribe - 3 replies

has anyone else had syptoms of ms while still on effexor....I did had the mri...need info....

2008-05-22T04:35:15Z

150mg for seven years.quit cold turkey 4.5 months ago
I have been ill with reocurring infections sinus lung kidney -this started around 2004. Four years after starting effexor. In two years I had 14 rounds of antibiotic for kidney infections. Add to that the sinus and lung infections and I was on an antibiotic almost constantly for two years. Even with the drugs I was too ill to keep my life going. Lost my home my job ect. 2006-07 couldn't seem to get to the bottom of the illness despite several hospital emerg and clinic visits.
I am going to back up a bit here to 2004 this year I had one gastly bout of vomitting blood.aprox 2 litres after about a year of waiting seen by a gastroentologist eventually ended up on pariet for esophagitis. This same year I had an ovary removed for excessive vaginal bleeding. I did not know at the time that effexor could cause stoamche bleeds or excessive vaginal bleeding hence did not consider quitting then I would have in a heartbeat had I known.
2007 my blood pressure was rediculously erratic. I finally bought my own bp machine to check it at home. often it was over 190! HEADACHES!!!
I was put on verapamil a vasodialator - a few months later I was put on lipitor to lower my high cholesteral. In November last year 07 I became very ill again. I was told a couple different things it could be by a couple of different doctors but somewhere in this time I came to the conclusion that I was not taking another pill.
That was 4.5 months ago I have been thru hell. I found effexor activists a couple of months after quitting. I keep finding validation and am gobstruck that such a dangerous and for me damaging medication is allowed on the market. I am too angry for words but also in no shape for a fight. Now getting healthy /staying alive-is my priority - I am now forced to do this on my own as I no longer trust the medical community or their drugs.
I feel there are many dangers to this drug and there are other side effects including liver that are not talked about. i spent the better part of the last 18 months prior to quitting in bed sick as a dog. Vommitting green slime ect. there is more I just don't have the energy now....good luck to you folks. peace sandy
Sun, March 30, 2008 - 6:24 PM — permalink - 0 comments - add a comment

posted in Effexor Activists Tribe - 4 replies

Ineffective with loads of bad side effects

2008-05-18T06:12:31Z

This is even more pathetic when you are aware of the fact that the recent studies have shown that for the vast majority of people,

EFFEXOR is NO BETTER THEN A PLACEBO

http://theeffexoractivist.org/forum/viewtopic.php?t=2296

So I guess if you think the republicans are working for you, you are either seriously mentally ill or it is all in your mind.
________________________________________________________________

http://www.huffingtonpost.com/2008/05/12/gops-new-slogan-already-b_n_101376.html

GOP's New Slogan Already Being Used To Market Anti-Depressant

Leave it to the tone deaf GOP to find a way of attaching themselves to this election cycle's "change" mandate that simultaneously reinforces the fact that their failed policies have messed up the world to such an inhuman extent that many Americans now live their daily lives in a state of free-floating panic and paralyzing anxiety.
In today's New York Times' Caucus blog, Carl Hulse reports that House Republicans have got themselves a brand-new slogan:
It looks like Republicans will counter the Democratic push for change from the years of the Bush administration with their own pledge to deliver, drum roll please, "the change you deserve." The first element of the party agenda developed over the past few months by the leadership and select party members will focus on family issues.

"Through our "Change You Deserve" message and through our "American Families Agenda," House Republicans will continue our efforts to speak directly to an American public looking for leaders who will offer real solutions for the challenges they confront every day," said the memo prepared for lawmakers.

What the GOP doesn't seem to realize, because they are idiots, is that "the change you deserve" is the registered advertising slogan of Effexor XR, a drug that many of you might have started taking as a result of all the...you know -- terrorism. (Hat tip to Bluestem for catching this gem.)
Effexor, also known as Venlafaxine, is approved for the treatment "of depression, generalized anxiety disorder, social anxiety disorder, and panic disorder in adults." Its common side effects are very much in keeping with the world the House Republicans have striven to build: nausea, apathy, constipation, fatigue, vertigo, sexual dysfunction, sweating, memory loss, and - and I swear I am not making this up - "electric shock-like sensations also called 'brain zaps.'"
Its less common side effects are equally awesome in their appropriateness.
And when the Food And Drug Administration reviewed the ad copy that included the tagline, "The change you deserve," it took issue with Wyeth Pharmaceuticals, which manufactures Effexor, saying that the company made "unsubstantiated superiority claims." Sounds like the GOP have picked an ironically accurate tagline for their efforts!

Effexor slogan stolen by House Republicans.

May 12, 2008
Anxiety disorders: House Republicans swipe marketing slogan.

We knew the National Republican Congressional Committee, its chair Tom Cole, and House minority leader John Boehner were not enjoying Congress like they used to when they had control back in 2006.

And their get-up-and-go had diminished to procedural games and time chewing motions to adjourn. Their gloom was so bad last week, the caucus by and large voted against Motherhood, as the WaPo reported.

Nonetheless, we were alarmed by the slogan for the minority caucus's re-branding campaign, for it directly addresses the depressed opportunities House Republicans might be feeling of late.

In the New York Times article, House G.O.P. Adopts Change Theme, we learn:

It looks like Republicans will counter the Democratic push for change from the years of the Bush administration with their own pledge to deliver, drum roll please, “the change you deserve.” The first element of the party agenda developed over the past few months by the leadership and select party members will focus on family issues.

“Through our “Change You Deserve” message and through our “American Families Agenda,” House Republicans will continue our efforts to speak directly to an American public looking for leaders who will offer real solutions for the challenges they confront every day,” said the memo prepared for lawmakers.

We think the slogan will only heighten the public's perception that the House Republican caucus needs help. After all, Americans have heard that slogan time and again.

Unfortunately, it wasn't pimped for political discourse, but to market an anti-depressant.

According to Wikipedia, the prescription drug "Venlafaxine is used primarily for the treatment of depression, generalized anxiety disorder, social anxiety disorder, and panic disorder in adults."

The brand name version, Effexor, is sold by Wyeth, which marketed it using the slogan, "The Change You Deserve™."

According to a December 2007 Alternet article, Are You One of Big Pharma's Lab Animals?, the drug company's ad agency came up with this marketing slant:

Wyeth's ad agency serenaded the nation with the message in its "The Change You Deserve™" campaign that, if we were not enjoying things the way we used to do, if we were lacking in what agencies used to call get-up-and-go, it was time to go on the antidepressant Effexor.

Are these symptoms of depression interfering with your life?

Not involved with family and friends the way you used to be?
Low energy, fatigue?
Not motivated to do the things you once looked forward to doing?
Not feeling as good as you used to?

We don't intend to make light of depression or any mental illness, for we've known far too many people who have suffered from them. Nonetheless, using a well-known shrug drug's advertising slogan for rebranding is unfortunate at best. A Freudian slip? Self-sabotage? Who knows. Somehow, we doubt the slogan for a red pill with "W" on it will help the GOP much in November.

posted in Effexor Activists Tribe - 0 replies

Hi Leslee, I got here in the end

2008-03-10T20:25:43Z

Quite quickly considering, for me LOL. Its only taken 5 months :)

I don't know if I'll be able to find my way back here again though...but at least I made it!

Paula

posted in Effexor Activists Tribe - 1 reply

Why this tribe was created

2007-10-30T08:46:41Z

In the beginning it was our intention to set aside one part of http://theeffexoractivist.org as a true forum for our members. However because the site has been repeatedly hacked, this has become impossible and the entire site is now read only. We apologize to our sincere members for the difficulty. The site, like many of the big pharma awareness sites has been repeatedly attacked in a number of ways.

We would love to read about your personal experiences with drugs and doctors and articles you have found.

We will be resuming our activist news letters soon, If you would like to receive our updates Please register with us. You will need to check your bulk mail as Our email at
admin@ theeffexoractivist.org
has been been used to send out tons of spam. (NOT BY US!)
This is just more of the harassment this site has endured. It seems this type of harassment is happening at most of the sites that expose big pharma.

Remember: Nobody on this site is a doctor, therapist, or a pharmacist. .

posted in Effexor Activists Tribe - 2 replies

Welcome to our brand new forum

2007-10-16T19:39:02Z

Hello and welcome
To return to our home page
http://theeffexoractivist.org/

We will not be promoting this tribe any where but at theeffexoractivist.org and to a few friends.
You might want to check out
http://tribes.tribe.net/depressionhelp

Wile you are here you might want to check out some of the other thousands of tribes. It is an amazing place where you can talk about every thing under the sun.

posted in Effexor Activists Tribe - 3 replies

Effexor half life....

2007-10-13T03:24:19Z

Effexor has a half life of 4-5 hours...

by comparison....

Meth has a half life of ten hours
Crack and cocaine, 1 hour.

Wyeth Pharmaceuticals...HOW are they any different from street drug dealers? THEY LIE MORE!

posted in Effexor Activists Tribe - 8 replies