Author Archive for Dr. David Healy

Dear Abby: Antidepressants and Marriage

News flash: A big-city American newspaper (the Chicago Sun-Times) has written about the side effects of antidepressants, and how they can destroy marriages.   It wasn’t on the Health page, or on the Business page where most of the important drug news appears.  It was in Dear Abby’s advice column.

You’ll find the letter from the unhappy husband below.  I wasn’t satisfied with Abby’s answer.  But my hat is off to her for taking the letter seriously and sharing it with her readers.  (There’s a lot of them, by the way – Dear Abby is the world’s most read advice column.  The current author’s mother was the original “Abigail Van Buren” who for decades shared top billing with her sister and rival, “Ann Landers.”)

You can send your own letter to Dear Abby through this link.  Tell her your experiences, thank her for raising the issue or share your opinions!  It couldn’t hurt – and just might raise some interest.  My own reply follows:

Dear Abby: Side effects of wife’s drug doom marriage after 40 years

As antidepressant takes away her ability to have a conversation or be intimate, husband is ready to move out.

DEAR ABBY: My wife and I have been married for 40 years. We were opposites who were attracted to each other and enjoyed a lot of the same things.

For the last 20 years, my wife has been taking an antidepressant (prescribed by her primary care physician, not a psychiatrist), and she has every side effect of the drug. For years I have tried without success to get her to seek help.

Although we still live in the same house, we have been going our own ways for the last year and a half. Even though my wife is a good person, I do not want to spend the rest of my life living with someone who is incapable of having a decent conversation, let alone being able to or having a need to be intimate.

I am going to move out. My question is, do I tell our children we are separating because their mom is addicted to a drug, or should I just be the bad guy and take the blame? — ENTANGLED IN NEW JERSEY

DEAR ENTANGLED: Your wife is not addicted to her antidepressant, and you shouldn’t say that to your children. The medication was prescribed for her by a well-meaning physician who obviously didn’t explain that there are alternative drugs with fewer side effects.

Your wife needs to consult a psycho-pharmacologist, a doctor with expertise in brain chemistry. Before moving out, please offer her the option of talking to one. Her doctor or insurance company should be able to give a referral. Or, your wife may be able to find someone who can guide her by contacting a university with a medical school. I am hoping she will, because it could change both of your lives for the better.


Dear Abby – Thanks for sharing the letter from “Entangled in New Jersey,” who was about to leave his wife of forty years because of her antidepressants.  She was unable to be intimate physically or emotionally; worse yet, she seemed to feel no need for intimacy.  In twenty years on the pills she had endured many other side effects as well, but would never ask her doctor for help.

My heart ached for “ENJ”.  It ached even more for his wife, because I have walked in her shoes myself, thanks to long-term antidepressant treatment.  Sexual side effects affect the majority of users, and include both physical obstacles (like genital numbness or trouble with erections) and a loss of interest or desire.

Emotional numbness and reduced ability to care about life is also common.  In fact, it’s how most antidepressants work: “numbing” is a feature, not a bug.  That’s why they actually do more for anxiety than depression, and why people considered “too sensitive” often find them helpful.  Especially in the short term.  It also explains why so many of us get trapped long-term in the “functional” but joyless limbo where ENJ’s wife is stuck.  About a quarter of US antidepressant users have been on the drugs for over ten years.

While I’m glad you believed ENJ and took his problem seriously, I wasn’t satisfied with your answer.  Let me explain why1

  1. Perhaps Mrs. ENJ is not “addicted” – but she might as well be. That’s why she won’t consider getting off the drug, and is probably terrified of trying.  Antidepressants are known to cause dependence.  Stopping them causes withdrawal symptoms, both physical and mental.  Some of these may feel like an extreme version of the mental distress that caused the person to seek help in the first place.  She may see this as proof that she needs the drug after all: “I thought it wasn’t doing me any good – but it must have been, because when I tried to stop I felt horrible!”
  2. Even a specialist from a top teaching hospital may not help. If ENJ’s wife believes, as I did, that she’ll always need these drugs “just like a diabetic needs insulin,” it’s likely because her doctor told her so.  Doctors, like patients, have been kept in the dark about withdrawal.  In fact, the peer-reviewed journals they trust have featured studies in which withdrawal was induced, by switching some patients from drug to placebo while others kept taking the drug.  The dismal results were then touted as “proof” that depression was a lifelong brain disease which would “relapse” without lifetime medication.

A huge problem is that most research on the drugs we take is now done by the drug makers themselves.  And they don’t share the raw data with anyone – not even the med-school professors who are often listed as “authors” when the results are published in a prestige journal.  Meanwhile, too many doctors think “evidence-based medicine” means listening to the rosy reports in those journal articles, and discounting what actual patients tell them if it doesn’t match.

3. Sexual and emotional numbing is often blamed on depression. If a patient who came in crying and wringing her hands a few months ago is calmer now, most doctors will call that success, and credit the drug. And if she isn’t doing anything to change her unhappy life situation, because she feels so flat and unmotivated?  Many will call that “residual depression.” Instead of blaming the drug, they may even raise the dose.  It’s likely the patient wasn’t enjoying a sparkling love life either, when she first showed up, so her current lack of interest in sex will not be put down to the drug.  Her partner will blame her, she will blame herself, her pain will increase, and the doctor will blame what will now be called “treatment-resistant depression.”

  1. The problems may persist even if she stops the drug. Almost everyone on antidepressants will have some sexual side effects, but these vary widely. A few lucky patients find they can simply stop the drug for a few days if they’re planning a romantic weekend.  For others, the problem persists until they stop the drug altogether.  However, a significant minority find their sex lives permanently wiped out or badly damaged, a condition now known as Post-SSRI Sexual Dysfunction or PSSD.   The same is true for drug withdrawal: Some people merely feel out-of-sorts for a few weeks.  Others suffer debilitating symptoms and struggle to get off the drug for months or years.

After decades of denial, the medical establishment is beginning to admit these problems are real:  In Europe, antidepressants now carry an official warning that sexual side effects can persist even when the drugs are stopped.  In the UK, patients fought for and won a parliamentary report on prescribed-drug dependence – and just this month, the Royal College of Psychiatrists officially admitted that antidepressant withdrawal can be severe and long-lasting.

Meanwhile, medical experts indignantly deny believing that depression is caused by a chemical imbalance in the brain.  We left that simplistic old hypothesis behind years ago, they say.  That would come as a shock to most of us, who still get this message nonstop from “experts” of all stripes, including our doctors.  So, it remains to be seen if all these official statements will change medical practice in real life.  If ENJ’s wife does decide to seek help, I still hope she finds a doc who is willing to question what s/he learned in medical school.

Abby, as a trusted advisor to millions, you are often approached to aid in health awareness campaigns.  These often focus on combating the stigma of mental illness, so that services will get adequate funding and people will not hesitate to seek help.  However, too often a simplistic narrative of “life-saving drugs” and “dramatic advances in brain research” is pushed, which dismisses any criticisms as based on “stigma.”

As you know, Abby, real life is a lot more complicated. Our current drug-centered treatment system helps some but does others more harm than good, and its claims to be based on settled science are exaggerated.   I thank you for listening to your readers, and encourage you to look beyond slick summaries of “what the science says.”

Sincerely, Uncomfortably Numb

(Post from regular RxISK contributor)

Grey Hair, Rotting Teeth, Semi-Blind and Demented

The Human Body is not meant to be taking ‘stuff’ all the time, whether medicines or biohack stuff or whatever.

Forget the image of a magic bullet that flies to the one spot where it is needed and causes no collateral damage, every medicine poisons. The trick is to use medicines only when the damage being caused by some condition outweighs the inevitable harms of the poison that might be used to counteract it.

Taken for too long, or when the harms of the drug likely outweigh the harms of the condition, we may end up paying a price.

Alcohol and nicotine are good examples of what can happen – and medicines are on prescription because they are thought to be more dangerous than alcohol and nicotine.

Sans Hair

A price like having our hair turn grey prematurely and getting brittle.  What’s the evidence for this – smoking is a great example.  Everyone who smokes is likely to turn grey earlier than they would otherwise have done.

It may be that drugs delivered in a way that reduces oxygen may make greying more likely but a very large number of drugs, possibly most of them, end up in hair.  While finasteride and bimatoprost can cause hair to grow, RxISK regularly gets reports from people complaining about hair falling out, not taking colour the way it should, changing texture and more on various treatments.

This is not something your hair stylist will ever warn you about – although it would be the easiest thing in the world for salons to install something like RxISK which would let them begin a discussion with their clients that could then be continued with their doctor.

From the first days of the oral contraceptives it has been clearer that women and their hairdressers can be quicker at spotting drug issues than doctors.

Sans Teeth

A price like rotting teeth. Antidepressants and antipsychotics seem particularly bad for this – After the Rot sets in – but its likely that any drugs taken for too long can cause problems.

This is not something dentists warn us about but it is something they should know something about and perhaps along with telling us to floss might tell us about whether there are any risks linked to any of the meds we are on – risks they can often spot but don’t usually mention to us.

Sans Eyes

A price like visual snow, astigmatism, blurred vision, cataracts, central vision loss, double vision, dry eyes, night blindness, flashes, glaucoma, hallucinations, halo vision, floaters, light sensitivity, reduced visual acuity, scintillations and tunnel vision.

Most drugs end up in our eyes.  Anyone on several drugs every day, especially the newer MABs like Humira, used for a range of inflammatory conditions mostly, likely has eyes popping with drugs.  Among antidepressants the SSRIs especially duloxetine are among the worst – which might help explain the high rates of nightmares both on these drugs and on stopping them. Note also that these drugs including the antipsychotics can cause visual hallucinations.

A 33 page list of visual reports sent into FDA for all leading drugs is Attached HERE.

Almost no doctor will ever tell you anything about these risks. In the case of the antidepressants, and the psychotropic drugs more generally, the usual story is pretty well all problems stem from the anti-cholinergic effects of the older drugs – this apparently causes urinary retention, constipation, blurred vision, dry mouth leading to teeth problems, and cognitive problems predisposing to dementia.

This is baloney.

Sans Mind

Without a hint of an anticholinergic effect in sight, the SSRIs and SNRIs cause all these problems – eye problems, teeth problems and cognitive problems.  The most common things anticholinergic drugs cause is a certain euphoria and if given with antidepressants and antipsychotics they usually make these more tolerable.

The place where dementia is becoming most obvious this month is with the antipsychotics.  For decades, particularly in North America the story was that psychosis causes brain damage and antipsychotics prevent brain damage and even cause brain cell growth.  This story got louder with the first brain scan studies that raised the possibility that it might be the drugs people were put on that led to the brain cell loss that was showing up on scans.

The evidence has been steadily accumulating however – with the most recent study appearing in JAMA this summer pointing strongly to the role of antipsychotic treatment in leading to brain cell loss – article here and see article HERE.

To get published, however, the authors had to add in what seems like a crazy rider – that even though antipsychotics cause brain cell loss, it still make sense to take them in order to ward off the brain risks of untreated psychosis.

There is no evidence that schizophrenia or any untreated psychosis led to brain cell loss before the antipsychotics.

It was recognised early on that antipsychotics lead to very obvious neurological damage in the form of tardive dyskinesia.

Antipsychotics may have a number of direct toxic effects but in addition to direct effects, by causing a profound lack of motivation, antipsychotics mean that people taking them daily vegetate physically and mentally.  The akathisia they cause also drives many to drink, which in its own right will cause brain cell loss.

It may make sense to take these risks in the case of someone who has a severe psychotic disturbance and where the meds really have a transformative effect. It makes much less sense when their effects are primarily sedative.

It makes no sense at all:

  • given to children
  • given as mood stabilizers – as with Olanzapine, Quetiapine, Latuda or others
  • used as add-ons to antidepressants – as with Abilify and Rexulti and Latuda.

Dementia Scare

When pharma is trying to replace a drug, one of the typical scare stories they come up with is that they cause dementia. This story was developed for the anticholinergics in the 1970s, and for the benzodiazepines in the 1990s.

There are a series of recent studies linking SSRI antidepressants to memory problems and dementia.  There are several ways SSRIs can cause dementia – one is through their ability to lower sodium levels our blood.  This causes fluid to migrate into our cells, and seemingly to mid-brain cells in particular, causing an osmotic demyelination syndrome ODS.

This may not be the only cause of problems but what seems clear is that SSRIs are linked to a number of neurological syndromes presenting in atypical form.

There is also growing evidence that stimulant use can lead to early Parkinson’s disease – see Could your Stimulant Cause Dementia.

These studies along with the fact that brain scan studies linking cell loss to treatment can now be published makes you wonder if there are new drugs in the offing waiting to sweep in which pharma promise will save us from all these poisonous effects.


A big part of the problem is that most psychotropic drugs come with withdrawal effects that are worse than nicotine and alcohol.  Once on, never off.

Everything else you are put on gets added into these so that heading toward 50% of us over the age of 45 are on 3 or more drugs every day of the year and heading towards 50% of us over the age of 65 are on 5 or more drugs every day of the year.

Unless one of these drugs has some hidden anti-dementia effect, an earlier brain failure than would otherwise have happened seems likely.

Of course its all okay if I’m putting the poison in your mouth rather than my own.

It could all be so different – if we levelled with people.

The image above is from Sir Gawain and the Loathly Lady.  The Full Story is about What do Women Most Desire.  The denouement is in image form below.  The Answer is Control over our Own Lives.

Where’s Anonymous?

The following email arrived last week from someone who is unknown to me – has never filed a RxISK report about PSSD, never contributed to the RxISK Prize, never previously been in touch that I know of – at least under the name offered – doesn’t sign off, and is unwilling to engage in a public discussion but starts off on very familiar terms.


I have followed your work for years and have respected and appreciated you discussing PSSD. No one else at scale has discussed it like you. 

But the post you put up on biohackers discrediting them lost my respect for you, as well as the rest of the community. Have you been in the Facebook forums and YouTube posts on lately? 

The consensus is: you made a bad move discouraging people from actively trying to fix the issue working with people. Look up ergogenichealth YouTube channel and recent video. People think you’re acting moronic, and frankly I do too. 

If you want to be a champion for pssd sufferers, you need to be a champion for pssd sufferers. You don’t do that by discouraging recovery experimentation. I interact with many people prominent in the community, and the sufferers tone is that you made a grave mistake, and the now leaders in the field have been shown a large support by community members, in response to your post. 

I’m not sure what prompted you to turn your back against recovery protocols, but it has left a sour taste in the communities mouth around you, and sadly, me too. 

I used to respect you. Now I realize you’ve done nothing for us. Nothing at all. Your theories on it aren’t even correct, and you somehow seem against the idea of a resolution. After all if it was solved you’d have no more speeches and books to profit from. 

Use to respect you. So did the community. Now we do not. I think we now realize you never genuinely wanted to help us, but instead, yourself. 

Bad Move David

For the Record

The Bio-Rip-Off post was not discrediting bio-hackers. It was against vultures who rip people off.

High in the list of vultures who rip people and governments off are pharmaceutical companies.  Most of the people who end with Enduring Sexual Dysfunction are people who probably didn’t need the drugs they took, and who were not informed of risks that were known about in the 1980s.

As part of a marketing of their pills industry created a biobabble – loose and meaningless talk about neurotransmitters that replaced a psychobabble that had gone before it.  This junk was incorporated into the complementary medicine and healthfood industries who talk about how this and that can adjust your serotonin or dopamine – and increase the sales of drugs in the process.  And it also laid a basis for bio-hacking and wellness hacking.

Many of these who have been biohacked and bio-ripped off by pharmaceuticals are in Once Bitten Twice Shy country.  They will never go near a Rip Off merchant.  They are quite safe from the Ryan Ballows and Deyan Rabbies of this world.  Many put in a huge amount of work instead to raising the profile of the condition and getting research going rather than taking risks with more chemicals. Most of the work behind RxISK is done by people in this group.

There is another group – and I would probably fall into this group if I had an Enduring Sexual Dysfunction – who research the options and likely know more than any Ballow or Rabbie and who experiment with a variety of possible treatments.  Many get in touch with me for any thoughts I have about the wisdom of trying X or Y.  I respond to pretty well every query – several every week – usually supporting whatever it is that is being tried and asking for feedback on the outcomes. In some cases that look promising I pass on the information to others to try – but nothing interesting in one person so far has appeared to generalise to others.

There have been a huge amount of things tried but no solid leads so far – other than confirmation that many things can produce a temporary response, typically after they have been stopped. This suggests that PSSD does not involve permanent damage or that at least the damage can be counter-balanced.

There is another group of people – much smaller, perhaps younger, maybe less confident in their own research abilities, who have fallen into the clutches of the Ballows and Rabbies.  The post was about alerting them to the risks.

Never Wanted to Help Us

RxISK has been running for nearly 10 years now. The Enduring Sexual Dysfunctions (EDS) came on our radar very early on along with a host of serious problems that antidepressants and other drugs can cause.

We feature the work of people affected in identifying the culprit drug, and sometimes an answer to the problem as with Anne-Marie and SSRI induced alcoholism, which is the most read post we have ever had.  We have people at present working on putting a grid in place that might offer possible leads for people with EDS or SSRI withdrawal to try, which hopefully will be posted soon.  Vanishingly few academics or doctors featured on these posts.

In the case of EDS, all the contacts with people have been done for free.

Hyper-concerned about people’s privacy, when we get in touch with the 800 or so people on our books we email each individually – there is no group mailing. This is an incredibly time-consuming and close to physically painful procedure – something that would be a lot easier if people ‘came out’ but we respect the difficulties almost everyone has with this.

In a lot of this work, RxISK acts as a focus for a growing number of people who are doing the work – chasing leads, chivvying people to commit to doing things and sharing information about what might work to raise the public profile of EDS and steering people away from reinventing wheels based on things we have learned from committing to the task for the long run.

In terms of the RxISK Prize, all funds are held in trust.  Not a cent has been spent on anything or would be spent on anything other than rewarding a genuinely effective and safe treatment/cure. As part of the price of rewarding whoever finds an answer we would insist on making the knowledge of what works available for free to everyone who suffers with EDS.

Another part of the Prize is its role in perhaps saving lives. Someone looking at what the Ballows and Rabbies have to offer might just pause for thought – if they haven’t claimed the prize, do they really have something that works.

If the Prize is not claimed we envisage handing back all moneys to all donors. We will alert people so that even anonymous donors, if they can show what they donated and when, will get their money back.

In a sense we are not holding money.  We are holding pledges and if there is a very wealthy person out there who wants to pledge money rather than donate, this might be an inexpensive way forward for everyone.

If the Prize Fund were half a million dollars, mostly made up of pledges, perhaps that  would incentivize more research.  Something for potential pledgers to consider.

High Stakes

Something else to consider is that people are dying.  Younger people mostly.  They have done research and figure that certain hypotheses like the very widely cited epigenetic hypothesis has nailed the problem and that there therefore must be treatments to reverse these epigenetic changes. They are prepared to take risks with drugs like this.  Failing that they can’t see a point in living.

David Stofkooper was one such person.  He got in touch.  We listened to him and didn’t persuade him not to biohack.  We set up a meeting with some very serious researchers who looked like the best bet to be able to let him know how solid these epigenetic ideas actually are and what treatments if any might do what he wanted.  All of this was done for free.

I don’t know if things were free with the researchers he met – it’s likely he paid nothing. Ultimately however he felt nothing could be done and he took his own life.  David’s mother is now one of those doing the most to raise the profile of the condition and the researchers he saw are now actively engaged in research in this area.

What keeps the RxISK effort going is trying to avoid more deaths like David’s and a hope that it might be possible instead to end the terrible suffering of those who are affected.

There is no effort to stop people taking stuff. But it is unquestionably the case that wherever there is suffering there will be people who spot an opportunity to make a fast buck.  Ballow seems to me to fit this bill.

What next?

Does Anonymous figure the Ballows and Rabbies should just be given a free pass?  A group of people willing to celebrate rip off merchants is not my idea of a community.  Judge for yourself.


I am asking you to be accountable to ME. A member of the community. You’re further making things difficult.
Just shows you have no regard for any of us. At all. What the fuck kind of pssd leader are you if you’re not into LEVELING with the community?
Get me your response. Why discourage experimentation when you and your seemingly smart colleagues are doing nothing to help the community.
Why post articles about people that are, with negative slants?
Why act as if you actually know what meso is doing and knows, or Ballow, when you don’t?
How could you post that blog without communicating with them on it all?
Extremely suspicious.
Answer my email openly. That is what I ask. I am not asking you to answer it in a blog post. I am reaching out directly to YOU.
Be a man. Respond.


If you were a man you’d be able to cope w a public response


Dude you are a fucking total dick. YOU DO NOT CARE ABOUT PASD SUFFERERS.




James T. O’Donnell PharmD (Rush University Medical Center) and James J. O’Donnell PhD (Rosalind Franklin University of Medicine and Science),

The field of pharmacology is an important area of medicine that focuses on the effects of drugs in different biological systems. This field of study is especially relevant when considering drug-related side effects and adverse events in patients. Even with advancements in medication development, the potential for a drug-related side effect is always possible. Most side effects are considered minor and mostly just inconvenient, but there are drugs that can have serious and potentially deadly side effects. A pharmacologist is an expert in this arena and can provide useful interpretation of how these effects occurred and why the clinical manifestation appears as such.

As a pharmacologist, we have spent our careers studying the intricate interactions between the human body and drugs. We are frequently sought out to provide expert opinions in medical settings that involve drug complications. Medication errors are common in clinical settings and can contribute to serious side effects causing significant patient harm. A medication error can include prescription, omission, unauthorized drug, improper dosing, incorrect dose preparation and drug administration into the wrong place in the body.  Depending on the severity of the error, the mistake can go unnoticed or contribute to damage and even death of the patient. While sometimes devastating, medication errors can provide a unique opportunity to learn more information on the effects of the administered drug and its impact on particular tissues.

We have been consulted in numerous interesting cases that demonstrate that even drugs deemed generally safe for use can show serious side effects if certain factors go wrong. If the drug dosing is incorrect, if the drug is not administered properly, if too much drug is given (overdose), if the patient has a condition in which the drug is contraindicated (not supposed to be used); these all can negatively impact how the drug effect will be seen in the patient and how serious unwanted, toxic side effects can be. There are two cases that we were asked to provide expert opinions on that showed very significant and debilitating effects of a generally safe class of drugs used for imaging (radiology) procedures. In both cases, the patients experienced medication errors in which they were incorrectly administered contrast agents in their myelography imaging procedures.  The summaries provided below highlight the acute and long-term complications which developed. Following the summaries, we have provided our interpretations on how these drugs may have caused the injuries and our commentary on medication errors in myelography procedures.

While these toxic reactions are rare, more information is needed on the understanding of long-term ramifications following such incidents. There is relatively no information available on residual toxic effects, since the majority of available reports discuss acute findings in these cases, and an unfortunate majority of patients that receive overdoses or inadvertent (accidental administration into the body/spinal cord) injections of contrast agents die.

Myelography is a type of radiographic (X-ray or CT scan) imaging examination that doctors use to see inside the spinal cord and assess for spinal cord injury, cysts, tumors and other abnormalities. Myelography is generally regarded as a safe procedure with minimal possible risks when dosed and administered correctly. To perform the procedure, the doctor injects a contrast agent – a drug that acts as a type of dye – into the patient’s spinal canal to visualize the images of the spinal cord. Myelographic dyes temporarily change the way the imaging interacts with the body. Contrast agents make certain structures or tissues in the body appear more defined compared to the surrounding tissue. By improving the visibility of specific organs, blood vessels or tissues, contrast agents aid doctors in the diagnosis of medical conditions. Contrast materials are delivered into the body in one of three ways. They can be swallowed (taken by mouth or orally), administered by enema (given rectally) or injected into a blood vessel (vein or artery; also called given intravenously or intra-arterially). Intrathecal (spinal canal) iodinated contrast agents are commonly employed during myelography imaging procedures and are considered to be generally safe and effective when administered correctly.

CASE #1 (CH)

This first case involves a middle-aged woman – CH. CH was scheduled for a myelogram procedure. During her procedure, she was administered an intrathecal injection overdose of Isovue-M, a non-ionic iodinated contrast agent. CH was administered 2-3 times the recommended dose of Isovue-M and two times the recommended maximum dose for the myelogram procedure. Following the procedure, CH developed altered cognitive (thinking) ability, memory loss and seizure activity while hospitalized. Upon discharge she was released with ongoing medical problems including “altered mental status”, “contrast-induced seizures” and “status epilepticus”. A brain scan was performed 18 hours’ post-procedure which showed that the Isovue-M contrast agent was in spaces surrounding the brain, and images of the cerebral spinal fluid (CSF) were 200x higher than normal. Moderately high contrast agent in CSF was still observed two days later. It was clear to us that excessive levels of the contrast agent was exposed to brain tissue for an extended period of time. This brain exposure to toxic levels of the contrast agent was responsible for the serious effects that CH experienced immediately following the procedure. Unfortunately, CH suffered permanent damage from this toxic exposure and continues to experience significant medical complications including cognitive deficits, seizures, impairments in memory function, and significant hearing loss.

It was clear that the high levels of ISOVUE-M resulted in profound levels of the contrast agent to enter into the brain. The drug manufacturer specifically warns against entry of the drug into the brain and states that entry of a large or concentrated amount of the contrast agent increases the risk of neurotoxicity. Her reported side effects were consistent with those listed by the manufacturer for adverse events for the nervous system. Given the greatly excessive dose that CH received, the drug was able to access the brain causing significant and irreversible contrast neurotoxicity – death of brain cells – contributing to each of the neurologic and cognitive deficits experienced. As stated earlier, most patients do not survive, so the medical community does not have a lot of experience in assessing and predicting residual and long-term toxicities from such overdoses.

CASE #2 (DP)

This second case involves a middle-aged man – DP. DP was scheduled for a myelogram procedure as part of a workup for brief episodes of vertigo, or the sudden sensation that your head is spinning. During his procedure, he was inadvertently administered an intrathecal overdose of Conray, a non-ionic iodinated contrast agent that is not to be used (contraindicated) in this type of procedure. Following injection, DP exhibited signs of contrast-induced neurotoxicity including lower limb disturbances, seizure activity, cognitive dysfunction and memory loss. He also presented with burning and prickling sensations, tingling and spasms. It was quickly determined that he had been administered the incorrect contrast product for intrathecal use in myelography. Conray contrast media is never to be administered intrathecally and contraindicated for use in myelography. In attempts to remove the contrast agent, attempts were made to flush and drain the drug out of his system. DP was also treated with Keppra, an anti-epileptic drug, to control his seizure activity. DP was released four days following the procedure. Following discharge, he continued to experience persistent cognitive impairment, including the inability to concentrate and multitask, and dull tension-like headaches. He continues to exhibit neuromuscular impairments, including overactive or overresponsive reflexes, dizziness, unsteadiness, generalized weakness and muscle spasms.

In this case, it was immediately acknowledged that the wrong drug was delivered and emergency steps were taken to remove the drug from the central nervous system. Due to the known pharmacology of Conray contrast agent, intrathecal use and direct application in the CNS is contraindication -never to be used. The manufacturer warns against the use of intrathecal administration and states serious neurological adverse events, including death, convulsions, cerebral hemorrhage, coma, paralysis, seizures and brain edema. The accidental administration of a highly toxic and contraindicated agent resulted in direct entry of the agent into the brain and significant and irreversible contrast neurotoxicity.

Medical errors resulting in neurotoxicity

In the first case, the medication error that occurred resulted in the wrong dose of ISOVUE-M being delivered causing a significant overdose of the contrast agent. In the second case, the medication error that occurred resulted in the wrong contrast agent being injected  into the spinal cord of the patient, one that was not to be used in this type of procedure. Both medication errors resulted in significant neurotoxicity causing permanent damage to brain structures and subsequent clinical manifestations.

The exact mechanisms underlying neural insult following contrast agent administration remains uncertain. It seems likely that these contrast agents were able to access the brain, either directly or by crossing through the blood brain barrier, and then acted to disrupt normal brain signaling and caused brain cell death. These agents are poisonous to the brain. Complications that result in aberrant brain activity can also lead to permanent damage. A causal relationship is often suggested between seizure-like behavior and deficits in cognitive abilities, i.e., impaired thinking and memory dysfunction. Both patients immediately experienced seizure activity following their procedures. It is likely that the seizures contributed to memory loss. The severity and permanent dysfunction that both patients continued to display support our opinions that the contrast agents contributed to significant damage of brain structures involved in information processing, thus leading to permanent memory impairment. Persistent damage to sensory and motor capabilities also most likely reflect damage to components of the spinal cord and brain regions involved in motor control.

A critical point in these cases is that contrast agents are CYTOTOXIC – meaning that they kill cells.  If enough of the cells are killed or damaged, the function of that cell or brain structure, or region of the brain is damaged. Unfortunately, and notoriously, brain tissue and function does not regenerate like many other systems in the body.


The neurotoxicity experienced by both patients is multifaceted and caused by:

  • Toxic nature of the drug’s pharmacology/chemistry
  • Relative dispersion of the agent in the brain
  • Cell death and damage to important CNS structures

The permanent contrast-induced damage to specific brain structures, e.g., mesial temporal, occipital and temporal cortical structures, likely correlates to cognition, memory, vision and hearing problems observed in these patients. Given the toxicity of the contrast agent and the exposure of the agent to the brain during this procedure, it is highly probable that the adverse reactions, both transient and permanent, are contrast-induced toxic reactions. Recall that both patients were being seen by doctors for issues unrelated to any neurological impairment. A reasonable, clinically valid, and scientifically sound explanation of their current neurological deficits is the acute neurotoxicity, from which both patients did not fully recover.

These cases highlight the devastating effects of medication errors. While these patients are fortunate to be alive, the long-term effects are serious and debilitating. More than 100,000 medication errors are reported to the FDA each year and most of these are preventable. In the cases discussed above, it appears that proper oversight on many levels was overlooked leading to these tragic drug induced injuries. In the hospital, dosing and drug administration should be quality checked by multiple people to ensure that patients are not at risk for potential life-threatening complications due to medication errors.

RxISK and Sharks


Two posts last week on RxISK Biohacking and david healy Stormy Weather raised issues about the Enduring Sexual Dysfunctions (ESD) linked to SSRIs and related drugs (PSSD and PGAD), finasteride and related drugs (PFS), and isotretinoin (PRSD).

In the biohacking post both sides of the “debate” were concerned about the people with these conditions who had taken their own life and the many who were thinking about doing so. We’re desperate, was the framing – What are you doing?  What are we supposed to do – just lie down and die?  Why isn’t someone doing research to help us?


  • A group in New York are looking at PRSD but not chasing the biology of the condition.
  • A group in Queen’s University Ontario are looking at PGAD – again not chasing the biology but doing impressive work.
  • Irwin Goldstein in San Diego and Anne Oaklander in Boston are looking closely at these conditions and helping to raise their profile. The US scene/culture doesn’t lend itself to co-operative research.
  • A group in Baylor College Houston working on PFS.
  • Roberto Melcangi in Milan has been working in this area for some time – mostly on PFS but he recognises links to PSSD.
  • The Dept of Neuroscience in Maastricht University and Mario Negri Institute in Milan are co-operating but at the moment its only on how best to investigate PSSD.

This might sound like a lot but it’s almost nothing and these groups are not linking up with each other – not even the two groups in Milan.  The perception sufferers have that nothing is happening, and nothing is likely to happen soon, is correct.

How Long Must We Wait?

In the case of a similar type of problem in the 1960s – Tardive Dyskinesia – the thing that made a difference was a legal action.  All of sudden everyone took TD seriously.

At RxISK we are better placed than most to put out feelers about possible legal actions.  The inclusion of a mention of PSSD in drug labels in Europe last year should help with this.

But legal actions are usually against pharmaceutical companies and up till this you have had to have hundreds of people affected by the one drug all from the same country – essentially the United States as its impossible to take an action against Pharma anywhere else.

A group of those with sexual dysfunction on Propecia did put together enough people to take an action against Merck, but it made little difference.  I’m not privy to the details of what happened but what is needed from this kind of action is not the pittance of money that might be on offer but information on when a company like Merck knew about the issues and their thinking about the problem.

The Post-Finasteride Syndrome (PFS) Foundation have been intensely secretive about anything they learnt from this action – likely nothing because they were chasing the wrong thing or their silence was bought with a pittance.  They have also been intensely secretive about the results of research into which they’ve poured millions probably because the research didn’t bear out the original hunch of a small group of insiders.

Aside from the PFS group, no-one has been able to put together a big enough list of sufferers for several reasons.

The requirements to have several hundred people all affected by the same drug from same country makes it difficult to get anywhere.

In the case of the USA, RxISK could likely put together 200+ people on citalopram – escitalopram (same drug) and 100 + in the US but Forest who used to market this were just marketers and know very little about the drugs they sold so the documents are less likely to be of much interest and now they’ve sold out to Actavis who can hold their hands up and say – we’ve never heard of PSSD.

It might be possible to overcome some of these problems if the PSSD and PGAD communities got together.  The commonest cause of PGAD appears to be withdrawal from SSRI and related drugs.  This would almost immediately double the known numbers of people on each of the drugs involved.  But at the moment we have rigid PFS, PRSD, PGAD and PSSD silos.

Another reason is anonymity.

How Long?

Those with Enduring Sexual Dysfunction (ESD) face a situation similar to the one facing those with AIDs in the 1980s.  Then as now people were dying.  Then as now there was stigma linked to the illness. Then as now the need was to get the world to listen.

The AIDs community Came Out.  They put their names in the frame.

Apart from a very few people like Kevin Bennett almost no-one with any ESD has done so. The world just about came round to listening to the AIDs community.  It is not going to pay any heed to a faceless, nameless nothing.  Nameless, faceless – dead, never existed; what’s the difference?

The recent Stormy Weather posts on davidhealy makes the point.  Those with ESD are pretty well all decent people, who took their pills when told to, never expected anything like this to happen them, and never expected sex to become such a big part of their lives.  They blend into the mainstream far more than those affected with AIDs ever did and should be even better able to say to everyone else – look we are just like you.  We never did promiscuous sex or intravenous drugs or tried to subvert your morality.  You could be pretty sure you’d never catch AIDs but there’s a very good chance you or your children will get this or already have but don’t know it.

But to make a difference people need to put their names and faces in the frame.  They need to appear in person in front of politicians or outside the offices of regulators or researchers and do outrageous things as the AIDs activists did – daub buildings with blood, sit in meetings with politicians and bureaucrats dangling a ticking watch in front of them while they talk.

But instead, when a post with Stormy Daniels in it, followed up by a powerful image of Stormy and DJT appears on, I get complaints from nameless PSSDers claiming to represent other nameless PSSDers, who say this is not us, we have nothing to do with porn – take it down.

What gives someone with no face or name the right to ask something like this?

Stormy Daniels and Venus O’Hara and others in the “industry” are exactly where people with these problems are likely to go – not to nice people like the Pope.

I’m sure having even the remotest links to porn and Jeffrey Epstein (and Bill Clinton and British Royalty) is not anyone with ESD, just as much as I am sure few if any of the ESD communities are ever likely to murder but to raise the profile of this problem someone is going to have to get close to murderous.  The scammers who prey on your vulnerabilities have no problem being murderous.  But the ESD communities (not the PGAD community so much) are inward looking. Everybody is caught in their own Hell when the times need you to Die on your Feet rather than Exist on your Knees.

Stormy reappeared in the news a few days ago when DJT confirmed her reports from years ago that he hates Sharks.  Many in the ESD communities seem happy to float in the water with sharks circling around them – with notable exceptions like those linked to RxISK who have written most of the PSSD posts, created the images for the Stormy Weather posts, and spend a lot of time writing to and camping out in front of regulators and politicians and calling into pharmacies to distribute literature.

Oh Lord, How Long?

Every day that goes by confirms that these ESDs are a new – never seen before type of problem.

People with PSSD, PGAD, PFS and PRSD cleverly and systematically, taking risks on the way, have done all the obvious things that conventional medicine and pharmacology would suggest they do without this making any difference.

This leaves pleading with Heaven as the only option but the pleas remain unanswered because there is no Expert up there who knows what is going on or how to put it right.

We don’t even know where these problems are.  Everybody thinks the brain but this seems unlikely.  Everyone thinks serotonin or androgen receptors but this is almost certainly not right.

The flip side to this should be that there is a chance to rewrite the pharmacology, and neurology and medical books here, a chance to discover new treatments that work without the drug having to be in your body and a Nobel Prize waiting for someone or some group who can solve the puzzle,

The flip side is that answering these problems might tell us far more about who or what we are than any amount of brain scanning neuroscience.  Albert Camus said that the ultimate philosophical problem is why not commit suicide. Giving life is the other side of this why go on living coin. The drugs that cause ESD cause suicide and stop us giving life – they smash into these central philosophical questions.  Nearly 1 in 6 of us is taking them – where are the philosophers when the Joker sets up a Philosophical Magic Show in broad daylight?

Everyone thinks scientists, philosophers and our rulers (if only to hang onto our vote) are interested in what reality is all about – in this case they either aren’t naturally interested or aren’t forced to be interested.  We who are about to Die prefer to Salute those who are going to give us the thumbs down rather than group together and force reality on them.

Make America White Again

Maybe very few people think DJT is interested in reality.  But he keeps on about Making America Great Again which lots of people figure this means Make America White Again – MAWA.  Well the single biggest thing likely to sabotage his plan is the drugs that cause ESD.  They are primarily taken by white communities and even if they don’t cause ESD are inhibiting sex so that people don’t make love so much and aren’t having children, in addition to dying from suicide more than other communities.

About 10-15% of the population take these drugs – this means 20% (in some poorer white communities likely closer to 50%) are not making love the way they would wish to.  And these figures may actually be a lot higher if you take into account other ethnic communities are not taking them and are instead multiplying away happily.

Worse again if you are white and do manage to make love on these drugs, you are more likely to have an abortion, more likely to miscarry or if you carry your baby to term, more likely to have a child born with autistic spectrum disorder or a serious birth defect.  It would be difficult to devise a more effective Great Replacement strategy than SSRIs, Propecia and Accutane.

Perhaps this is where Ryan Ballow, the Cortical Kid, could help.  He’s an army Vet, and a DJT supporter.  Rather than give vulnerable white people junk that risks harming them, he could get in touch with DJT whom he idolises and point out the obvious to the Chief – hey Boss what are we going to do about this.  Look at what the Deep State is doing to our community.

Would it be wrong to ally with Trump on an issue like this or the NRA on the issue of guns don’t kill people, its idiots taking SSRIs who do?  Depends on whether you think Joe and Kamala are more likely to bring this problem out of the darkness into the light.

Maybe Joe as a Catholic should be concerned.  But hey, we’ve already contacted Jose Mario Bergoglio about the issues and several Catholic dignitaries and got nowhere.  Reproductive rights – who us?  That’s not something we recognise.

Hunger strike outside the Vatican for Lent next year?

The Endgame

Here’s how this is likely to play out.  Sometime very soon, a company or companies will bring a new antidepressant or nerve pill on the market.  Part of their marketing will be claims that it doesn’t cause sexual dysfunction or suicide.

They will make an offer you can’t refuse to some ESDers.  We are going to fly you first class round the world, to conventions with audiences of thousands of doctors, put you up in the best hotels and all we want you to do is tell these doctors about your condition, how grim it is, the people you know who have committed suicide, the people injured by sharks taking advantage of them – we might take a risk and let you talk about the ridicule you’ve had at the hands of doctors.   That’s all – you don’t need to do anything else.  Just raise the profile of this awful problem.

What could be wrong with this?  This is how the issue of benzodiazepine dependence was recognised – how all problems with older drugs come to light.

This is how the problem gets buried.  Nobody bothers to even talk about doing any more non-existent research when Zacpro rides into town to solve the problem.  Time to be scientific and move on to some unsolved problems.   Not even the sharks will be interested to circle around you any more.

Which is a disaster.  Never in the course of human history have a group had so much potential leverage.  Up to a quarter of our communities are affected.  Many of these think they’ll be okay when they get off the drugs – soon – but in fact they can’t get off and if they did their ability to make love might well be even worse than it is on the drugs.  The wealth, privilege, access to media outlets and power that those affected with ESDs have way outstrips anything people with AIDs had.

The so called scientific literature on which these drugs are based is junk – ghostwritten, with no access to the data.  There are company documents showing obliteration of sexual function in young healthy men in 2 week studies done in the 1980s.  Companies knew about these problems back then.  The supposedly solid walls of Jericho just need a few people to march around them a couple of times and they will fall.





Bio Rip-off, Bio Delusions, Bio Hack?

This ambiguous picture comes up when you search under grave robbing – nothing you can make money out of is sacred.  But its entitled grave digger. Digger, robber, it can be hard to tell.

We had an email a few days ago about a young man desperately seeking help who had in good faith took something he thought would help with hair loss and was now several years later suffering appallingly – both the sexual side effects some drugs and over-the-counter meds, can cause and the social isolation that comes with this.

RxISK began working on PSSD, PFS, and PRSD and the wider withdrawal issues they are linked to to help with cases like this.  There is at present very little we can say to young men like this – or young women in the case of PSSD or PRSD.

The RxISK Prize was set up to increase awareness, foster research and prevent people who are in a nightmare situation from turning to ghouls for help.  There have always been people willing to trade on the fears and hopes of those who are in a state like this – take their money and expose them to things that don’t work and risk damaging them further.

Many people complain about the pharmaceutical industry who effectively  operate a pay us what we want or you will die business model.  Few mention the Alternative Medicine, Complementary Medicine, Harley Street Medicine, and Transition Medicine rip-off people who can be just as ruthless.  The pharmaceutical industry we have today was shaped by efforts to tame the quacks and hucksters who were making ridiculous money from dangerous stuff touted as cure-alls (a lot of psychotherapy can be chucked in here too).

What FDA and EMA and MHRA and Donald Trump and Joe Biden need to realise in doing nothing about PSSD and related conditions they are laying the ground for a return to hucksterism.  See Stormy Weather.

One of the problems taking the next step with this post is that RxISK has avoided criticising others trying to do something for PSSD and related conditions – because we know we don’t have the answers and its important not to cut off any avenues of research or support.  But the two scenarios below are concerning.

Scenario 1

A few weeks ago we had this email:

…. back in October I sent you a link from the PSSD Forum regarding potential PSSD research by a pharmacist who also has the condition – Deya Rabbie. Mr Rabbie has experience working in community pharmacies and majored in neuropharmacology. He plans to continue his education in the future. I’m contacting you today on his behalf to share some exciting news and also ask for your help. Mr Rabbie has been in contact with his former university in Egypt regarding PSSD and they have granted him permission to conduct rat studies there with the hope of finding the root cause of PSSD and hopefully a cure. I’ve posted a link to the university website below. He is being assisted by an expert (Mr. Ali) who works at the university and received his MSc in pharmaceutics, excellent with honours. He has experience with cancer research and epigenetic pharmacology They will also be getting aid from several other professors.

(Research proposal as well as CV and certificates are attached)

He promises to be 100% transparent throughout the research. He has come up with these steps after talking at length with the community.

Before the research begins, he will hold a Q&A on the PSSD forum where people can ask him any questions related to the study. Also, he’ll release the one year roadmap for the research and outline how he plans to spend the money that is donated. On top of this, there is a legal notice from the university stating that the research can take place specifically mentioning PSSD.

During the research he will continue to communicate with the community by hosting a bi weekly Q&A about the month’s research and a monthly vlog including footage from the lab. The vlog will focus on the previous months progress and outline the plan for the following month.

On top of this photos of the lab will be shared occasionally and he will also publish a monthly financial report of money in and out.

As you know, we have been waiting for an opportunity like this for a long time and this is a once in a lifetime opportunity for sufferers. It could help to raise awareness of the condition and also lead to a cure which would save many lives. The issue we have is funding. We need to raise $23,000 for laboratory equipment as well as salaries for those involved. This will cover a year of research. Mr. Rabbie has given up his pharmacy job to research PSSD and is only taking the minimum salary required to survive in his country. Mr. Ali has also agreed to work on this full time.

Is there anything that RxISK could do to help like send an email to all sufferers to gain support? Is there anything else that you could offer or suggest? Your endorsement and help would be very much appreciated and are essential for this much needed research to happen. This will put us a big step closer towards finding a cure.

A GoFundMe page will be set up for the research which if funded, can begin with no delay as baseline tests have already been conducted on the rats.

Please don’t hesitate to contact myself or Mr Rabbie ( with any questions you have or if you require any additional information.

Perhaps its not but this looks like a scam.  The person who sent the email seems taken in by rather than part of what’s going on but he protested vigorously that no this was not a scam.  And then another person who really has PSSD jumped in – saying no it wasn’t a scam.  Neither have been helped but both seem to think there are lots of people who have been helped, even tho Rabbie himself seems not to have been helped.  

What do you think?  Would you take help from this source?

Scenario 2

A few weeks ago we had this email from someone with genuine PSSD

… could really do with some advice. I’m thinking of taking up a 3 month course with ‘Ryan Michael Ballow‘ he’s a bio hacker and the owner of ‘cortex labs’ have you heard of this man or been on his Web page? nootropics are used in the the 3 month course. Just wanted to know your view as I dont want to waste 3k for nothing? I’m desperate that’s why I’m willing to take risks.

Then we had this email from Ryan Ballow:

I’ll make this brief. I am a biohacker that has been recruited to solve the PSSD puzzle but a handful of men that have the syndrome. I believe the issue is curable. So far, I have gotten some pretty promising results with clients on this. I am not interested in the “prize,” as I work with people on a consulting basis for this, and run an international company. However – I’d like to be in touch with you to share ideas, and generally discuss the matter.

I have had success targeting 5ht1a autoreceptor function, up-regulating dopamine receptor function, fostering hypothalamus release of Oxytocin, and some other targeted approaches. As far as a “cure” goes, to me, at this stage, that seems more like a set of protocols designed to reverse the underlying “bad chemistry,” if you will. I am at the forefront of this. It is a major part of my life.

Shortly afterwards another person with genuine PSSD emailed

I want to introduce you to Ryan Ballow. He is a bio hacker who is working with clients in resolving PSSD. He would like to communicate with you, so I thought I would introduce you guys through email.
Followed immediately by RB again 
I’ve come across your website and research several times throughout the last few years. As you probably understand, there aren’t many people talking about PSSD, and the severity of the issue, as well as the moral dilemma with the medical establishment prescribing SSRI.
At any rate, I believe we will cross paths eventually, as I am at the forefront of mechanistically solving this issue, and run client work with it, so far having a good degree of success.  Let’s try to get on a call sometime in September.

Hack Attack

The first scenario looks like a scam.  The second is more complex.

One of the reasons for a RxISK Prize is to try and keep people and their money and their hopes safe from dodgy research and for what of a better word biohackers.  RB doesn’t appear to know much about PSSD – the ideas mentioned are far from cutting edge.  Whatever about that, taking 3K off people who will take terrible risks to get better from an horrific condition and then giving them things he knows little about for a condition he likely knows nothing about other than what his clients have told him – fits the Harley Street Medicine bill.

If we on RxISK become aware of anything that genuinely seems to help, we will put it up on the website and tell the world about it instantly and email everyone we know who is affected to let them know and it will all be done for free.  These conditions are not something to gouge people over.

But there is another issue here.  The marketing by pharma has left many people thinking we can do almost anything with the drugs we have.  June Raine the current boss of MHRA seems to think there is no need to warn about PSSD, PRSD, PFS because doctors can cure anything with drugs – after all they can change men into women and women into men.   She apparently really said this.

One way to view the current epidemic of Rapid Onset Gender Dysphoria in young women, wanting to be men or at least not women, is in terms of a massive biohack – based on the idea we can do anything with the techniques we have.  We just need to fiddle around with your bits and we’ll sort you out.

This seems to be a distinctively American way of thinking.  Not American only but America first where a belief in techniques and technologies is stronger than anywhere else in the world.  The rest of the world almost always follows.

The ROGD epidemic likely links into an American Wellness epidemic – a $4 billion industry where people get checked for all kinds of trace metals and have their hormones tweaked.  An industry that corporations fuel as a perk of employment,

The kind of thinking that seems to underpin it is caught (somewhat endearingly) in the Americana musings below.  Americans have been thinking this way about their bodies for well over a century and for over 30 years now as Joseph Davis’ Chemically Imbalanced brings out have been talking this way about their emotions too.  Many no longer seem to have emotions – they have serotonin and dopamine levels instead.


I’m off X completely…  After a couple days, I was randomly emotional and had some memories return that I hadn’t felt/recalled from many years ago.  There was a day or two where I could actually feel music, feel the notes.  Then came the flu symptoms but of course without a fever.  I was always worse at night.  Fatigued, achy and anhedonia, and dark thoughts.  This really robs you of your empathy and feel like you could witness violence, even happen to someone close to you, and not blink.  It’s truly sad.  Makes me realize a few small microscopic chemicals and metabolites are what determines being human or not and being a lost soul or not.

The worst of the aches stopped probably 17 days of being completely off.  However, I’m still numbed and downregulated or insensitive to much.  I have little to no sexual function.  Penis is nearly always cold, no erections (except maybe at night when I’m sleeping which makes me question a lowered cortisol level then too).  I was on X for about Y years with my increase from xmg to xxmg that really changed me.  I gained a couple inches of belly fat shortly after going to xxmg where I used to be slim.  Some could be age related… but I’m a bit doubtful as you’ll see.

I share this because I’ve really been reflecting on what’s changed.  I’m racking my brain.  What characteristics do I remember of myself from my 20s and early 30s when normal compared to now post-SSRI?  I used to get colds much easier, had sinus and allergy type issues, was far more excitable, emotional, cried at sentimental things, was creative and could compose music on my guitar/tell jokes off my cuff.  I was giddy many times.  I had a high libido/probably hypersexual (I saw a study where a group of individuals were considered hypersexual and found to consistently have both high cortisol and ACTH levels compared to the control group).  I was also very driven, a bit obsessive compulsive at times, nervous, socially anxious and competitive.  Now, often times, I can’t be bothered to be motivated.  I’m not nervous or anxious anymore about really anything.  I’m usually only physically present but more zombie-like than attached or engaged in the moment.  My allergies seem mostly gone.  Colds far more seldom.  I don’t produce sinus drainage constantly like I used to.  I’m not really emotional anymore, good or bad.

This will seem very odd but I remembered a very peculiar trait from before being on X.  Please forgive me but I guess it has to be part of the conversation.  When I was healthy, whenever I felt the highest libido and when getting aroused, I often felt a wave of drowsiness come and go during that time.  Or it happened the most when I felt drowsy.  Then I got thinking about antihistamines and that drowsy feeling you get.  So it made me research histamine.  Did I once have high histamine followed by my body counteracting and is this what I no longer produce well?  Is this what is holding me back?  Being once under-methylated to now over-methylated?  How can I test/tell if this is what happened?

I keep reading people’s stories that they were once hypersexual, maybe had an overly sensitive HP-Axis, always would get anxious, etc.  But now after chronic treatment, some people with PSSD only feel anything when extremely hungover if ever.  Copious amounts of alcohol raise histamine during hangover, correct?  I recall reading people’s stories about only feeling anything after drinking a lot red wine, which raises histamine.

All I can really find is information about wanting to take antihistamines, lower histamine, etc.  What if the key is to doing the very thing opposite to what most people without PSSD are trying to do?  Rather than lower histamine, we raise it somehow?  Force excitability.  We are in some repeating loop of insensitive receptors and downregulation.  What can we administer to break the repeating loop?  Would high histamine possibly re-sensitize the 5-HT1a receptors?

Also, how can I possibly test if X lowered my allopregnenolone levels?   Is this not an important neurosteroid that’s often depleted upon chronic ?  The men’s clinic I’m working with wants me to start taking pregnenolone 30mg daily, which I would guess could raise my progesterone (which is low at 0.1 ng/ml) and perhaps my allopregnenolone and cortisol?  I know I probably don’t want too much progesterone, because I read for males, high doses are what they use to chemically castrate sex offenders in prison.

Some other folks say they took low dose hydro-cortisone over many months (no more than 10-15mg a day perhaps to not necessarily fully suppress or shutdown endogenous production).  They then tapered, and their sexual function eventually came back.  I just feel like things somehow revolve around breaking this stuck state and rebooting things.  Forcing anxiousness over a period of time.

No longer fully naive, I told my wife I will teach my child to take full hormone panel when they are 25 and at peak health to capture their best “settings” in case they ever find themselves needing to “dial” back in someday.  Now that data is lost for me since I’m in PSSD and I don’t know where my markers and “settings” are best configured.

The end note is endearing but crazy.



Editorial Note:  This post by Stevie Lewis raises a very tricky area.  There is no doubt that SSRIs cause movement disorders and not just temporary disorders but permanent problems like atypical Motor Neurone Disorder (ALS), Steele-Richardson Syndrome, Osmotic Demyelination Sydrome (Pontine Myelinolysis) and Multiple System Atrophy.  There is also little doubt that most neurologists have a blind spot for these problems – which is bizarre. 

Various aspects of the roller coaster ride which is protracted SSRI withdrawal have been concentrated on at different times by different campaigners; akathisia, suicide, PSSD. I want to flag up another part of the jigsaw puzzle which doesn’t receive much attention – SSRI induced movement disorders.  You are going to read a bit about my movement disorder, and about Sharron’s and K’s.  You will also see short videos of me and Sharron losing control of our bodies.

Sharron, K and I would like you to share this post and encourage feedback from anyone you know who is an “expert” on the subject:

  1. Expert either because he/she has developed a movement disorder after taking or going into withdrawal from an antidepressant. Doesn’t matter if the movement disorder got better – those stories are just as important, particularly any insights on how and why they got better.
  2. Or expert because he/she has any thoughts or evidence on what causes some of us to develop movement disorders. And what we might do about it.

Both Sharron and K are still in the acute phase of their journey and need any help and advice that can be given.

My first movement disorder episode occurred in November 2009.  Some time in 2010 I did my first Internet search on movement disorders.  Interestingly, when I put in the same search criteria today “SSRI induced movement disorders”, three of the same papers that I read at the time have come straight up.  Which leads me to believe that not a lot of research has subsequently been done on the subject.  Here are those three;

Leo 1996

Gerber and Lynd 1998

Koliscak and Makela 2003

The writer in the third publication thinks:  “Recognizing akathisia is important because it can be very bothersome”.  Only a dispassionate scientist could put the words “bothersome” and “suicide ideation” in the same sentence.

One reason the incidences of SSRI movement disorders are hard to track down is due to the fact that they are also known in the business as Extrapyramidal Reactions (EPRs). This more recent research (2015) concludes: “Case reports associating serotonergic antidepressants with EPRs continue to be published. Practitioners are advised that monitoring for such is important. Rigorous research efforts are needed to better understand the clinical risk factors for these adverse drug reactions.”  Hawthorne and Caley 2015

It is clear that SSRIs cause movement disorders, if you look in the right places.  Equally it is clear that SSRIs cause withdrawal if you look in the right places, but we know from experience that those who prescribe them are shielded by the system from seeing such reports.  Drug companies, medical journals and medical guidelines have made sure of that.

However, the movement disorder that Sharron, K and I have doesn’t match any described in articles or research on the subject.  We don’t seem to have akathisia, dystonia, dyskinesia, tardive or otherwise, myoclonus or tics.

Stevie’s Story

My movement disorder came out of the blue.  I had been taking Seroxat for just over 12 years, and I had tried and failed many times to withdraw with worsening symptoms each time.  In January 2009 I started on alendronic acid for osteoporosis.  In September 2009 I took 3 metoclopramide tablets.    The first episode was two months later.

The movement disorder starts with a trigger, my muscles tense and tighten and I start to feel afraid.  Then my body doubles up and I lose control as my core muscles and pelvic and buttock muscles jerk violently.  I am continually flooded with waves of fear.  Afterwards I feel in shock, and my gut responds with extreme diarrhoea.  I lost a lot of weight in a short amount of time.

You can see the movements here – Stevie Lewis

Whilst writing this article I found something I had written 10 years ago. I had drawn lightening strikes all over the page.  That is what an episode feels like – constant physical bolts and shocks. It is an entirely physical experience.

In 2013 I decided I had to stop taking Seroxat whatever the withdrawal consequences in the hope that if I did, the movement disorder would eventually go.  In the early days and during the worst years of my withdrawal, the trigger for an episode could be movement (walking, bending, stretching), something I ate or drank, something I smelt or saw or unexpectedly heard, and usually as I was dropping off to sleep. I was routinely jerked and jolted awake and I hardly slept. I can’t give a set amount of time for the length of a jerking episode.  The longest was 7 hours, the shortest 30 seconds and the rest anywhere in between.   Today I am very fortunate that I jerk rarely and if I do it is related to movement or something I swallow.  Medication or supplements are still a trigger.

I have seen 3 neurologists over 5 different visits and ended up with diagnoses of Extrapyramidal Symptoms (EPS), “stress”, Medically Unexplained Symptoms (MUS), Functional Neurological Disorder (FND) and “anxiety”.

From the many stories I have read and my own experience, where neurology is involved the patient’s experience worsens.  Not because they throw additional drugs at the problem, but because they seem wilfully blind to the role that the antidepressant, or any psychiatric drugs may have played in the symptoms presented to them.  The finger is pointed at the person rather than the ingestion of a chemical.  You can imagine them having no problem saying “It’s the heroin you’ve been injecting”.

The third neurologist I saw, when I asked him if he thought that long term use of Seroxat was causing my movement disorder, said “I don’t know about those drugs, it’s psychiatry that knows about them”.  Really?  Someone whose specialism is the nervous system claims not to know about a drug whose intended function is to alter it?

I think it is time that neurology stepped up to the plate and openly acknowledged the number of patients they now see who have developed functional neurological disorders after taking antidepressant drugs. And I think it is important to point out here that, as many people who are prescribed an antidepressant end up on other drugs which are thrown at the many side effects and withdrawal effects that arise, neurology must be regularly seeing patients with what can best be described as chemical toxicity.  Which I suspect goes unacknowledged.

Sharron’s story is next.  My claim that our movement disorders seem identical is based on meeting her, watching her body jerk and holding her as she went through an episode.

Sharron’s Story

I was prescribed Sertraline for ‘low mood’ in 2013 by a psychiatric nurse prescriber from our local Mental Health team. My first prescription was for 50mg of Sertraline and diazepam. The diazepam was for two weeks to settle me into the Sertraline. Over the coming weeks because I felt no better, my prescription for Sertraline was increased to 150mg. Which I continued to take for six years.

My prescription for Sertraline was often given with Omeprazole over the six years.  I later developed gut problems which caused prolonged vomiting and often saw me in A & E. During these bouts of vomiting I was given various drugs to rehydrate and stop the vomiting. They finally settled on Ondansetron, the only medication that would stop the vomiting.

Whilst on holiday in Mexico I started vomiting again and was taken to hospital where I was given Dexamethasone, Ondansetron, Zyprexa, Metoclopramide, Ketoralac and Pantoprazloe.  On my return home various tests, CT scans, X-rays showed nothing that would cause the vomiting.  Months later I concluded Sertraline was causing my problems, so after six years of taking it, I decided to stop. I was unaware of tapering schedules and stopped suddenly.

Within days I developed numbness and tingling in my hands and my body began to twitch and shake. Some weeks after this began my GP decided I should see a neurologist. My GP was adamant withdrawal from the Sertraline was not the cause of my shaking and jerking, saying symptoms of withdrawal usually last only a few weeks.

My GP wrote to a psychiatrist on my behalf to ask if it was possible that my problems were due to Sertraline withdrawal. The reply was No, it was more likely to be my gut causing problems and maybe I should see a gastrointestinal specialist.  I was diagnosed with dyspepsia, no known cause. My appointment with a neurologist concluded I had FND. He was certain it was nothing to do with my sudden withdrawal from Sertraline. My MRI of my neck and brain showed no problems.  I felt very strongly that FND was not the problem and that I was not being listened to.

My gut problems continued after I stopped Sertraline. But in a different way. I had no appetite. The smell of food would start me shaking and my shoulders jerking. When I could eat, I would often start shaking and vomit. This did improve over several months and I was able to eat without vomiting and shaking. The shaking and jerking continued, for months it was a daily occurrence. I struggled to find triggers. In total I have lost 5 stone.

It starts with my buttocks tensing up, I can feel it work its way up my body. Everything tightens up, my arms go rigid, my hands and fingers became distorted, my neck and shoulders tighten, and then like a sudden release, I shake and jerk violently. Often, when the violent jerking stops, I continue to shake. The shaking often goes on for hours and often leads to more of the tense jerking.   During these episodes, I experience extreme fear, terror, panic everything becomes loud and I want to get up and run. I start to cry/sob as my body slowly relaxes again.

You can see Sharron’s movements here – Sharron

For the past year I have struggled with sleep. On occasions my body will tense up and I jerk myself awake. The fear and terror this brings with it is enough to keep me awake along with a tremor/shiver, which is more like something you experience when you are cold rather than the jerking.  This tremor/shiver is external and internal and includes palpitations and heart flutterings. I have since found the cold, pain, sudden noise, or a sudden movement can bring it on. I also have episodes where I cannot pinpoint it to anything.

One year on, I still suffer with the movement disorder. The extreme episodes are more spaced out and not happening as often. But I do not know from day to day how I will be. The longest gap between episodes is about three weeks. During that time, I had sudden jerks, my body tensed but then relaxed without going into full jerking and shaking.  A year on and I feel abandoned by the medical profession. I have been told repeatedly its nothing to do with Sertraline.   My life has changed beyond recognition. I am unable to do the job I loved. I battle daily with the frustration, loss and emotions any sudden illness/disability would bring.”

K’s Story

K approached me via social media having read my story and seen my and Sharron’s videos.

My name is K and I am 51 years old. I went to see my doctor for  help sleeping when my work schedule changed.   He prescribed Xanax .25 mg at night once in a while a few times a month. I never had any problem with that but then he added in paroxetine (Paxil/ Seroxat) without any reason.  I took it for five years as prescribed by my doctor.

Three months after stopping I developed a movement disorder which is still getting worse after two years off the drug.  It happens all day and into the night so I can’t sleep longer than 1 hour because of my whole body jolting and jerking so much with waves of fear.  The symptoms calm down and then come back up in a matter of minutes or hours.  The movement disorder that I have is very like Stevie and Sharron’s – I have seen both their videos and that is what prompted me to get in touch with Stevie.

Five months after stopping paroxetine I voluntarily admitted myself to rehab due to psychosis, and because I couldn’t control my body and mind anymore.

I went to see a movement disorder specialist; he didn’t know what was wrong with me and I was told to go back on the paroxetine.  I made multiple trips to ER and they and the mental hospital treated me like a drug addict and made me feel like I was overreacting.

When my symptoms from withdrawal were so severe I was told the movement disorder look like Parkinsons.  They put me on so many antipsychotic medications I decided to not take any after I came out of the mental hospital. Nobody believed my symptoms are caused by withdrawal not a mental health issue.  I don’t want to be more damaged than I already am.

I never had a mental health problem before taking paroxetine, I never asked for this drug in the first place. Please help me, I really feel like death alive, I have lost all hope and I feel so helpless right now.

Editorial Note:  These movements look choreiform – the point is they do fit inot recognisable neurological patterns.  We are interested to get as much input as possible from people with neurological issues on or withdrawing from any drug – not just psychotropic drug and not just antidepressants.

Helping H: SSRI Withdrawal

The expert inputs Managing Efexor and SSRI Withdrawal and Protracted Antidepressant Withdrawal to and comments on H’s case Side Effexor Withdrawal have been wonderful to get and hopefully will be a resource for others.

Helping H

H’s original problem and the idea of a commentary came about because 3 of us considered her case in response to a request she sent to RxISK for a consultation and we all figured this was not a problem that had any easy answers.  Getting and giving H a range of views seemed the best way forward.  It risked leaving her more hopeless if there were no answers, but a recognition of her difficulties and that they are widely shared might help nevertheless.

I’ve seen almost no more correspondence from H than readers of this blog have seen. My sense is that she is a competent woman, perhaps very competent.  Her difficulties getting off Efexor, or anything that happened before leading her to be on it, don’t change my view.

I have known a lot of extraordinarily competent people have problems getting off these drugs – competent here doesn’t mean lawyers, doctors or professionals, although these can be competent too.  It means I have met people who impress me greatly who have had tremendous difficulties getting off and have taught me most of what I know about getting off – or not getting off – from using lower potency drugs, to splitting doses, using liquids and being active.

H is in her 40s. The difficulties in getting off appear worst of all for women in their 40s and 50s, who may have been put on paroxetine (Paxil/Seroxat) or venlafaxine – desvenlafaxine (Efexor/Effexor/ Pristiq) for perimenopausal issues – as a treatment for hot flashes for which these drugs have been promoted. In this case, totally normal women, with no hints of nervous problems ever, can end up suicidal, beyond agitated and in complete disbelief – facing doctors who pass their problems off as depression or anxiety and in need of a tweak to the meds.

Tardive Dependence

Another aspect of what shapes my view is that women in the same age group put on SSRIs for this and related reasons, end up with Persistent Genital Arousal Disorder (PGAD) on stopping.  This is clearly related to withdrawal in some way – it can start on treatment but usually declares itself on stopping.  The discomfort can be so intense it leads women to have ECT, have the nerves to their genital area cut, to injections of botulinum or cholecystokinin or other remedies into their vulva (injections means up to 100 at a time), and clitoridectomy.

There is or potentially is an element of PGAD and PSSD – a tardive element as in tardive dyskinesia – in every withdrawal syndrome and at present we have no answers for this element of withdrawal.

There are almost certainly other tardive components that can happen on treatment – affecting the bladder, gut, respiratory system, peripheral nerves and other parts of the body.

There are things we seem to be able to do if there is no “tardive” element to a withdrawal, but at the moment very little we can do for any tardive elements that may be present.

Central or Peripheral?

My exposure to withdrawal syndromes – including PSSD and PGAD – has left me leaning toward viewing these states as peripheral in origin rather than central.  People tend to worry that these drugs have fucked their brains – and point to very real memory, emotional and other cognitive problems as evidence of this.

These ideas are totally understandable given the heavy marketing of these drugs aimed at creating the impression they go straight to one little spot in the brain and correct a problem there – they don’t.  The serotonin in all of us is primarily in our body not our brain.

It is also not clear to me that withdrawal or at least the tardive component has anything much to do with serotonin.  Fifty years of research has failed to link tardive dyskinesia to the dopamine system on which antipsychotics act, and my hunch is the same will apply to drugs active on the serotonin system.

This seems to have implications for proposals to reduce in decrements of 10% and for hyperbolic rather than linear reductions.  These models hinge on an understanding that we are dealing with rates of separation from the serotonin reuptake site or related receptors, which might hold when there is no tardive element but seem less likely to hold when there is.

So if not serotonin, what?

RxISK has floated ideas about Transient Receptor Potential (TRP) channels/receptors here before primarily in connection with PSSD.

Someone linked to RxISK who cannot get off the SSRI he is on has been doing a lot of digging in this area and we hope to post something more soon about these bits of us that were almost completely unknown when the SSRIs were first launched.

Labels and Guidelines

One of the issues that has featured in comments is the issue of doctors prescribing off label or not keeping to guidelines or not recognising obvious withdrawal. The anger at this runs deep and seems to fit with complaints against pharma companies who push drugs for off-label use.

The actions of doctors like H’s doctors can be viewed with incomprehension.

Part of the problem here is some doctors are, or feel they are, stuck.  There is no drug licensed for the SSRI-induced toxicity that killed Stephen O’Neill – see The Perfect Killing Machine and The Death of Stephen O’Neill.  There are no guidelines for managing H’s or Stephen’s situations.  I don’t want anyone to comment saying there are NICE guidelines or there is a recognition of the problem by the Royal College of Psychiatrists – there isn’t.  There is a certain amount of fig-leafing going on but nothing worth anything to anyone having to live with these problems.

Many doctors who want to treat H or Stephen O’Neill will figure they have little option but to diagnose a case of depression or anxiety and treat accordingly – the complaints H and Stephen voice include depressed mood, anxiety and perhaps even suicidality after all.  Taking matters into their own hands, these doctors feel, could be risky – there are so many people out there from regulators to politicians to guideline makers to bioethicists to most people on Mad in America who will figure going off-label is just about the greatest sin there is.

No guidelines, no regulator, no academic, or senior clinician, no pharmaceutical company is ever going to say – here’s what you can do for withdrawal – other than perhaps mention tapering which doesn’t involve going off label.  Pharmaceutical companies could get sued or fined heavily for recommending anything that shows any originality.

SSRI dependence, withdrawal, addiction, raises profound political problems.  The system knows people with these problems are there – in their hundreds of thousands, perhaps millions – and it would prefer you die rather than recognise the issue and grapple with it.

Those affected find it incomprehensible that those in positions to help just don’t seem to listen – they really wish you would go away.  The surprising thing is “we” never get the message, or see their fingers stuck in their ears.  It needs something more drastic than nice letters or talking to them.

Pain and will power

The tardive point above seems to argue against the will-power, mind over matter, point that has come up in several comments.

It does and it doesn’t.  People who work with pain say that it can be very important for the person affected to recognise that their opioid or other analgesic is causing the problem for which they want more treatment. The same case can be made for some anxiety and depression states.

It’s not just a matter of recognising a particular drug is the source of much of the problem but that the act of turning to any drug can be a problem.  There is something about embracing the pain, or anxiety, or depression without figuring there is a magical solution somewhere that can be a help – this is not the same as mind over matter or of will-power.  I say this as someone who isn’t sure I would be able to deal with significant pain or withdrawal without a stack load of meds.

It is much more intuitive, it seems, to figure there must be something out there that can put this right.  Resigning ourselves to seemingly doing nothing doesn’t seem right – just like staying still in quicksand doesn’t seem right.  But trying to get out of quicksand by doing the obvious thing is what will kill us.

That said, the problems linked to withdrawal may be beyond willpower.  As Annie notes, the desperation of akathisia or PGAD doesn’t leave much room for the exercise of willpower.


Do you think this lady has Effexor withdrawal?


Are her “skin” difficulties anything you have come across before?

Skin issues linked to SSRIs yes but not particularly to withdrawal

When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

I don’t know what to do.  The worry is going back on treatment will cause further problems.

Do you see people who can’t increase or decrease?

Yes.  And a lot of doctors see things getting worse as the dose goes up and can’t make the link to an increased dose, leading to the prescribing cascade we see in H’s case.

How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

I’m not sure it does.

What would you do for this woman now?

When the problems get to this point there are no guidebooks.  You want someone you can work with.  This will almost certainly involve someone willing to prescribe off label and willing to give what you think might work rather than what s/he thinks, and maybe even giving something s/he is somewhat against.

There are people who have been helped by drugs I would never give in a million years, and options I can make a good case for that don’t work as well as I think they should. Some options are available in some countries and not others.


There should be a common interest between people with protracted withdrawal syndromes and those with PSSD and PGAD which represent very clear forms of tardive withdrawal.  Find an answer for PGAD and PSSD and we will likely be able to make a big difference for people stuck in withdrawal also.

How did we get Here?

In the 1980s, companies like GSK ran healthy volunteer trials in which it was clear volunteers exposed to these drugs could have withdrawal symptoms after only 2 weeks on treatment.  The symptoms included anxiety, depression, sexual dysfunction, suicidality, dizziness, gut and other problems.

These drugs were sold as non-dependence producing in contrast to the benzodiazepines.  There were however more reports of dependence/ withdrawal linked to paroxetine in 3 years of paroxetine being on the UK market than there were from all benzodiazepines combined in the previous 20 years. Yet regulators, politicians, guideline makers and others exhorted us to continue taking out pills. We did and now 10% of our populations are on them semi-permanently – they can’t get off.  Worse again, many of these same people claim these drugs are saving their lives because they feel so much better when they start taking them again after a brief stop.

One of the few things that may lead to increased recognition of SSRI withdrawal is a new drug –  there is growing interest it seems to me in the sexual dysfunction and suidicality linked to SSRIs that smells like premarketing for some new compound.

The company will have some experts get up on platforms to talk about the well-known sexual and suicidal problems SSRIs cause which might seem like recognition for people like H.  It won’t be recognition – it will be one last use of her distress to boost the sales of some new compound that will cause its own problems.

H and others concerned about people who are dependent on these drugs will be left barking while the pharma caravan moves on.

The worrying thing is there isn’t more interest at the moment in dependence on SSRIs which may mean that companies know these new drugs will also cause dependence.




Protracted Antidepressant Withdrawal

Following H’s report of difficulties with Effexor, we asked Will Hall, Altostrata, Bob Fiddaman and Josef Witt-Doerring, all experienced in this area, how they would Manage her Withdrawal.

We also asked Peter Groot who helped develop the first Tapering Strips for Antidepressant withdrawal – who with colleagues has demonstrated that this can help many people – not all – unfortunately not all he would say.

Before answering the questions, all were asked, Peter offered some more general views that have been paraphrased here.

General Thoughts

What does H’s mild depression mean, why the increase in dose, were other treatment options discussed?

How did or can H’s doctor know that her sleep difficulties are not related to the use of Effexor?

Temazepam looks like it was prescribed indefinitely. How does this relate to what guidelines say?

H’s withdrawal was linear tapering as opposed to ‘hyperbolic tapering’, which is predicted to lead to ever larger problems at each following tapering step (1).

When she had difficulties, the tapering should have been halted, regardless of whether the problems she reported were thought to be physical or mental (2).

How many withdrawal symptoms can a patient report without them being recognised as such?

When doctors believe that certain symptoms are not related to withdrawal of a drug and do not report it, the effect will be that in the literature these symptoms will indeed not be related to the drug!  The result is a self fulfilling prophecy!

How do these doctors know, other than their gut feeling that these symptoms are probably transient? Where is the evidence?

In the case of adding gabapentin etc, H’s problem is not that Effexor does not work well enough but that it is causing major harm. Ever more medications to try to solve problems caused with wrongful prescribing of medications in the first place.

Were are the guidelines that support these solutions? If these are not there, what are these physicians doing? What is the difference with African medicine men we use to laugh at?

I don’t know what ‘Movical’ is. It is added to all the other medications in a desperate attempt to solve problems caused by previous medications without knowing if this could lead to yet more problems. This is clear example of a disastrous prescribing cascade causing iatrogenic harm

When H tries to come off again and the skin problems return so quickly (after what is essentially a rechallenge) this is strong evidence that these are withdrawal problems.

If this patient wants to taper, she should be enabled to do this very slowly and in very small steps allowing for proper self monitoring.

A huge problem for H now is that so much damage has been done to her, it is difficult to predict what approach could be successful for her current complaints.

I am not able to give good advice here, other than to do things gradually and – very important – on the basis of shared decision making in which the doctor is honest about what is known and what is not known and is willing to listen to and guide the patient.

In the case of her doctor – she ‘told me that people can experience depression in a very physical way. For example, some people get back pain even though there is nothing wrong with their back. She said my skin feeling was my version of that.’

The patient is told that she has a major depression and this explains her complaints away by saying that the complaints of the patients can occur ‘even though there is nothing wrong‘.  If there is nothing wrong, how can the patient be diagnosed with ‘major depression’?  How is this helpful?

Increasing the dose so quickly:

  • is asking for problems, because this goes way too fast, especially given the precious problems the patient had when she tried to taper
  • makes it impossible to determine what could be a helpful dose for the patient (if there is one)

Increasing the dose to 375 mg:

  • is irresponsible and wrong, given the fact that the patient functioned on 75 mg for 2 years and 150 mg for 8
  • What reason could there be to increase the dose to 375 mg? This is iatrogenic damage

In conclusion:

I find this case a very sad example of a prescribing cascade leading to iatrogenic harm, which could have been prevented if her doctors had been willing to listen to her and had taken seriously what she was telling them, instead of relying on beliefs or even prejudices for which there is little or no proof at all, which are often called ‘expert-opinion

I hope it will be possible to help her to improve her situation, but I suspect this may take a long time.

Specific Questions

1.     Do you think this lady has Effexor withdrawal?

She suffered from withdrawal at the very beginning. Because the withdrawal was handled so badly, she now suffers from the iatrogenic consequences of overmedication which is the result of a terrible prescribing cascade. This makes it much more difficult to deal with than the withdrawal problems she had at the beginning.

By at the beginning, I mean the moment during the tapering when she experienced the first problems: ‘When I dropped to 75 mg problems started‘. Patients who are currently being prescribed tapering strips or the stabilisation strip we developed in the Netherlands will see that they come with a simple self monitoring form which patients are asked to fill in. We ask them to do this to help themselves and their doctor to guide the tapering.

What they are asked to do is to fill in how they rate there own subjective experiences about possible complaints they might have on a scale of 1 (no complaints) – 7 (severe complaints). They are asked to describe their complaints especially when they are new or when they suddenly become much worse or improve. But they are not obliged to do this. Our primary motivation is to help the patient because we consider this to be more urgent than trying to answer scientifically interesting questions. We explain this is the review which is about to appear  (3).

The reason to ask for subjective experiences is that these are what matter for the patient. Whether their complaints have been recorded previously by other patients may be scientifically interesting but is not the first concern of the patient. As this case demonstrates, making clinical decision based on whether certain symptoms have been reported previously can harm patients. In this particular case doctors have telling the patient fairy tales – that the complaints the patient had had nothing to do with (tapering of) the venlafaxine – without knowing if these fairy tales were true. But my main criticism is that such an approach does not help the patient.

To go back to the tapering. The way we feel this should be done – which is actually in agreement with all the not concrete advice in guidelines and patient leaflets – is to taper at a rate which helps the patient. In this particular case, the fact that this lady was experiencing problems when she reduced the dose from 112,5 mg to 75 mg very strongly predicted that the perhaps still manageable withdrawal problems she experienced would become much worse if she continued to taper further to 37,5 mg and even much much worse after that. Which is precisely what happened.

With the knowledge we have – and already had – this could have been prevented by halting the tapering at 75 mg. Or perhaps by increasing the dose, perhaps even a little bit. And by continue tapering when the patient felt better and up to it. And without prespecifying how long the taper should last. Because we must accept that we are not able – and perhaps never will be – to predict this for an individual patient.

Patients are much better helped if a doctor guides the tapering on the basis of the information the patient provides and by listening to what the patients wants. If that would have happened in this case, a lot of the damage that has now been done could – and should – have been prevented.

2.     Are her “skin” difficulties anything you have come across before?

Complaints from patients when coming off patients can be very different from each other and I doubt if a really good inventory has ever been made. A problem here are circular arguments that are often being used. Doctors who say “that’s not something which is normally reported as an Effexor withdrawal symptom” may be inclined not to ascribe these symptoms not normally reported to (withdrawal of) Effexor. As a result the symptoms may not be reported as a possible side effect. And this will lead future doctors to conclude “that’s not something which is normally reported as an Effexor withdrawal symptom”. Leading to harmful self fulfilling prophecies.

It is my view that the attitude of the medical profession in cases like this should change. Doctor should telling something completely different to their patient: ‘I do not know if your complaints have been reported before, but because you started having them while you were tapering I consider this as a signal that your tapering is going too fast for you’.

This leaves a scientific question open which is not really relevant for the patient in the first place. Because the first concern of the patient is to be helped properly. Such an helpful approach is in strong contrast with what sadly often still happens, where patients are being treated badly on the basis of theoretical considerations and ‘expert-opinion‘, which in this particular this case clearly was not worth very much.

3.     When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

This depends on the situation. The sooner a patient reports complaints, the easier it is to help them. Therefore it is so important that a patient self monitors and reports upcoming complaints during tapering to the doctor as soon as they start occurring. In such cases the advice can be relatively straightforward. The doctor can then ask the patient if the complaints are still bearable and if the patient wishes to stay on the same dose (stabilise) for a while or perhaps to increase the dose again, perhaps even a little bit in order to let the complaints go away. Outcomes will differ depending on the situation and patient, but changes to help the patient are much better if this approach is followed than based on the doctor’s beliefs or prejudices.

The longer a patient waits before asking for help, the more difficult it will become to determine what will be the best approach to continue. Because the more harm will have been done.

Whatever the advice of a doctor will be, it is crucially important that the doctor honestly discusses the uncertainties of different approaches and really listen to what a patient tells and what a patient wants. Clearly, in this particular case none of this has happened.

4.     Do you see people who can’t increase or decrease?

For me this question is too open to give a straightforward answer. Patients differ from each other as do their circumstances. Depending on these circumstances a patient may be able to increase or decrease in certain circumstances and not in other circumstances. Generally speaking we can say that until now tapering has never been done and could not be done properly. Because the medication to do this has never been made available. I think we have changed this by developing tapering medication. We are now gathering data about their use in daily clinical practice from as many patients as we can. And are working hard to publish about this in the near future. I hope this will help us to give meaningful answers to questions like this. But at this point in time I find this difficult.

5.     How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

It fits more or less, but certainly not completely. Things are definitely more complicated than that. For instance, the way people try to come off benzo’s using the Ashton protocol in which very slow tapers are shown to be helpful for some patients, cannot be explained by looking at the receptor occupancy only. The same is true for tapering of fluoxetine, where there are people who experience severe withdrawal symptoms who are being helped by gradual tapering using tapering strips. Which cannot be explained on the basis of receptor occupancy.

It is my strong view that for the time being it is most helpful to leave aside all sorts of theoretical considerations and agree that the most helpful approach for helping patients is to listen to them and to allow them to taper at a speed they agree with.

6.     What would you do for this woman now?

I am afraid I have no clear answer here. I can only hope she finds a doctor who is helpful and willing to guide her in a probably difficult and perhaps long process to recover from all the iatrogenic damage that has been done to her.


  1. Horowitz, M.A. & Taylor, D. Tapering of SSRI treatment to mitigate withdrawal symptoms. Lancet Psychiatry 6, 538-546 (2019).
  2. Chouinard, G. & Chouinard, V.A. New Classification of Selective Serotonin Reuptake Inhibitor Withdrawal. Psychotherapy and Psychosomatics 84, 63-71 (2015).
  3. Groot, P.C. & van Os, J. How user knowledge of psychotropic drug withdrawal resulted in the development of person-specific tapering medication. Therapeutic Advances in Psychopharmacology. Accepted for publication. Preprint available at withdrawal/. (2020).

To be continued with a final entry next week

Managing Effexor and SSRI Withdrawal

H’s nightmare with Effexor withdrawal was laid out in last week’s post.  Experts on antidepressant withdrawal were asked to comment – Will Hall, Altostrata, Peter C Groot, Bob Fiddaman, Josef Witt-Doerring have generously given time to do so.  James Moore, Stevie Lewis and Ed White, administrator for a Facebook venlafaxine withdrawal group, who have substantial international profiles on withdrawal have also added comments to last week’s post.

Most of those commenting have had lives touched by withdrawal. I’ve designated them as experts but they would likely see themselves as ordinary people who have had to grapple with two awful problems – the effects of a drug and a betrayal by the medical profession and the pharmaceutical industry – and they would likely say to any readers going through similar problems that your motivation is more likely to lead to answers than waiting for expertise to ride to the rescue.

The issues in these posts apply to all SSRI and SNRI antidepressants, but also antipsychotics, gabapentinoids and other drugs.  The withdrawal button beside the RxISK blog brings up 50+ posts on withdrawal issues with some on Sertraline and Prozac having hundreds of comments.  RxISK also has a Complex Withdrawal panel with more information.

Will Hall

Will has long been regarded as one of the leaders in the Recovery Movement and researchers on withdrawal. 

A few quick thoughts – skin rash is associated with venlafaxine and is considered very serious; she’s also on a high dose, I think this might need urgent addressing even if the risk and struggle of withdrawal is high given past experience.

She mentions a number of other drugs but it’s unclear whether still on them or not.

Doctors are consistently dismissing the role the drugs might be playing.

Sounds like she is long term benzo user which can have big implications.

Because a drug reaction isn’t reported in the clinical literature doesn’t mean it couldn’t be drug related.

Her self report is very limited and I’d want to know more about the rest of her life. Tolerance of withdrawal, like tolerance of pain, varies widely between people.

People frequently have physical ailments that are best addressed psychosocially – doesn’t mean they aren’t “real” only that we are humans and our entire lives come to play in our physical health.

Because of skin rash being associated with venlafaxine I’d consider it likely this is effexor related even if unusual.

I think the withdrawal process has to be understood and approached specific to the person’s life in general and ways for them to gain greater control and connection; many people have used 12 step and addiction groups for example to endure withdrawal. We know from addictionology and placebo studies that the body is extremely responsive to larger life context and so addressing that could be key, for example, is she alone with this.

  1. Do you think this lady has Effexor withdrawal?


  1. Are her skin difficulties anything you have come across before?

Skin problems, akathisia in general absolutely, not sure specific venlafaxine and these specific symptoms, but I consider it plausible

  1. When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

I present pros and cons and advise them outcome is unpredictable. She’s on a very high dose right now that would be a concern. She’s gotten bad direction from professionals so I’d steer her towards finding her own leadership in all this.

  1. Do you see people who cant increase or decrease?

Yes of course, I don’t know a biological standard for this but it’s consistent with the idea that there are people who can and can’t make changes in life

  1. How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

I think the role of the benzos and the sleep suggest to me that there is far reaching toxic impact in her body. nobody is really modeling this bc so complicated and existing models too rudimentary

  1. What would you do for this woman now?

With the rash I’d encourage her to consider significant dosage reduction, soon, despite discomfort. The rash is very troubling and would indicate abrupt withdrawal. Then I’d find out more about her life and emotional state and work on gaining more power to ease relaxation and “letting go” during a time of difficulty. I’d work with how to proceed best you can given a life out of control. I’d try to focus on areas of her life where she can get satisfaction and empowerment outside of the drug process. This would then allow the drug process to become more clear, her decision making to get clearer, and to be more tolerable. I’m especially concerned if she is alone and who is on her side, where does she go with her emotional inner world – people often just export all this onto a drug struggle.

Here is a paper I wrote that presents some of my overall learning and how it applies to how we think about drug research.


Altostrata set up Surviving Antidepressants – the best known website for people grappling with antidepressant dependence.  She has probably linked with more people about withdrawal than anyone else.

It’s not common, but we have a cohort of people who got skin symptoms and sensitivities as this woman describes, while tapering or after going off antidepressants. Itching is not uncommon. She may always have had a lurking allergic reaction to Effexor that tipped over when she was hypersensitized by withdrawal.

She should not have continued tapering through “mild” withdrawal symptoms. Continued tapering makes mild withdrawal symptoms worse.

If she had asked me, I might have suggested a reinstatement of 5 beads of Effexor. That is correct, 5 beads. This is to evade the hyper-reactivity that seems to be almost universal in withdrawal syndrome and which she’s already evidenced. We often find a very low dose reinstatement is enough to reduce withdrawal symptoms to a tolerable level; after that, improvement is gradual over months — not days or weeks. To repeat: Very low-dose reinstatement is sufficient. (With SSRIs, particularly paroxetine, I would take the occasion to substitute perhaps 1mg fluoxetine instead.)

Currently, she clearly is suffering from an unnecessary but typical prescription cascade from her psychiatrist. Her current symptoms (Effexor and Lyrica?) may be an allergic reaction to any one or a combination of her drugs, or it could be a universal hypersensitivity reaction to the absurdly high doses of all of them. To find out which drugs are causing the problem, I would ask her to submit a daily diary over several days including when she takes each drug, the dosage, and her symptoms after each dose.

If it’s a single drug causing the reaction, symptoms will be more severe shortly after taking the dose or at peak plasma. To find a drug-drug reaction, I would map the P450 cyp requirements of each drug she’s taking.

She didn’t say how much Lyrica she’s taking, but I’ll bet it’s a lot. As she observes, it causes constipation. If she weren’t taking an unholy amount of Effexor, it’s likely a lower amount of Lyrica would help her sleep. As this woman observed, Effexor always interfered with her sleep.

My guess is that gradually reducing Effexor will help quite a bit. She may have to cope with “psychological” symptoms. I imagine she feels terrible physically and will be further traumatized when she realizes the drugs are making her sick. Feeling “depressed”, angry, helpless, and betrayed in these situations is a normal reaction.

So, overall, she’s overdrugged by a typical psychiatrist who thinks more is better and all the patient’s complaints are due to “depression”. As ever, I am disgusted and appalled at the utter cluelessness of a profession that throws psychotropics into people with wild abandon.

Would like to point out that very low dose reinstatement for post-discontinuation withdrawal symptoms conforms to theory underlying hyperbolic taper. As demonstrated in the SERT occupancy literature, you don’t need a lot of drug for partial receptor occupancy.

Shapiro, Bryan B. Subtherapeutic Doses of SSRI Antidepressants Demonstrate Considerable Serotonin Transporter Occupancy: Implications for Tapering SSRIs.

Psychopharmacology 235, 9 (2018): 2779–81.

Bob Fiddaman

Bob Fiddaman is a wee known SSRI activist. Over the years, The Fiddaman Blog has discombobulated the UK regulator and many others and his account of withdrawal from Seroxat/Paxil in The Evidence However is Clear shaped perceptions of the problem – See Here

I suspect we may all have different opinions but I write these down as someone who has gone through a 19 month taper of Seroxat (Paxil) and three month period of cold-turkey.

  1. Do you think this lady has Effexor withdrawal?


  1. Are her “skin” difficulties anything you have come across before?

Absolutely. ‘Skin-itching’ is otherwise known as ‘crawling skin sensation’, which is a classic symptom of akathisia.

It’s sometimes difficult to explain. I’ve read many first hand accounts where people describe it as small worms crawling under their skin.

Even the National Alliance on Mental Health (NAMI), who are a pharma funded organisation, admit this. They write:
“The symptoms you are experiencing could be due to your medication. These types of symptoms are consistent with a side effect referred to as akathisia. Those with akathisia experience an inability to sit still and a constant urge to move. Due to a feeling of inner restlessness, a patient may experience fidgeting, pacing, rocking while standing or sitting, crossing and uncrossing legs while sitting, and constant movement of the feet. Patients have also described these feelings as “wanting to jump out of my skin” and as a “crawling skin sensation.” ~

  1. When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

This is a good question and, for me at least, very difficult to answer as I am not a healthcare professional. Do we tell a heroin addict going through cold-turkey to take a shot of heroin if their withdrawal gets intolerable? The advice I normally give is to taper at your own pace and not at the pace of what a prescribing physician tells you  to. I use the mantra, ‘Your body, your rules’.

  1. Do you see people who can’t increase or decrease?

Decrease, yes. In my experience of increasing the dose after an initial drop, the withdrawal effects seem to disappear. Decreasing is a whole different ball game because the only crutch one has is to go back to the original dose. When a person increases, it, in essence, gives the brain what it wants because the prior dose was ‘wearing off’, or rather ‘losing its strength’. There’s a train of thought on kids who smoke weed – On first trying weed, one may get a high after four or five ‘tokes’. As they become more experienced in smoking weed, those four or five tokes barely make a dent – so they take more draws until they reach their ‘high’. – Eventually they can smoke a whole joint, then two, three, four etc. In other words, a drug doesn’t have the desired effect if a person stays on the same dose, although I’m still baffled at what a ‘desired effect’ is when it comes to drugs like Effexor.

  1. How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

As I said, ‘Your body, your rules’. Nothing is set in stone regarding drug withdrawal. The 10% rule is merely a guidance. I, myself, came down ultra slowly because 10% would have been too drastic for me to tolerate. A smoker who smokes 40 cigarettes a day and wants to quit, may jump to just 20 a day – this would be too much of a drastic drop. He may then try 30, or 35 a day and still find he struggles. Cutting down to 39 a day for 7 days, then 38 a day for 7 days may be the only way he can beat his reaction to nicotine craving. This is basically the rule I used when tapering from Seroxat (Paxil)

6. What would you do for this woman now?

The electric zaps she is experiencing are what I have also experienced. I found a way to combat them – worked for me but may not work for her.

First, in my experience, it’s best to taper during the colder months of the year – for some reason my withdrawal was worse in the summer months – I can’t quite put my finger on this, I just know it was easier during the winter.

Second, drink lots of water – I drank up to 8 pints of water a day – this may be a placebo effect – I told myself I was flushing out poison.

Thirdly, if at all possible, go for walks, really push yourself – wear loose clothing and focus on what’s in front of you. Turning your head during withdrawal can be problematic as it can cause visual problems, dizziness and a nauseous feeling.

Finally, when the zaps start run a bath or sink of cold water, the colder the better. Place a large towel in the bath, wring it out then wrap it around your head like a turban. This, for me at least, gave me immediate relief. Also, running cold water on your wrists (the pulse part).  There is something about the cold that helps. Has any study ever shown the brain to be hotter during any kind of drug withdrawal?  This may be why it’s easier, for some, to taper during the winter months.

Josef Witt-Doerring

Josef is a medical doctor who in 2018 had a feature on the front-page of Psychiatric Times with an inside spread on Antidepressant Withdrawal and the need to listen to patients and patient groups – astonishing views to see expressed in the heart of US psychiatry.  

  1. Do you think this lady has Effexor withdrawal?

I believe this lady has a tardive (late onset) and chronic sensory disorder likely caused by Effexor. The descriptions of the sensory disturbance sound partially similar to akathisia and restless leg syndrome (minus the confinement to the legs of course). The sensory pain in those conditions appear to match what this woman is describing: a hard to explain, deep scaly, crawling, agonising sensation. It has become more recognized recently that antidepressants have the potential to cause these types of disturbances – tardive sensory problems.

The onset of the sensory difficulties also fits a pattern common with tardive syndromes caused by long term use of certain monoamine modulating drugs (antipsychotics and antidepressants) : onset during withdrawal and persistent for many months after discontinuation and thankfully for this lady partial remittance on reinstitution of treatment – there are reports of these syndromes persisting despite reinstitution of the causative drug.

2. Are her “skin” difficulties anything you have come across before?

I haven’t heard about the red-pin spots before as being a common symptom directly stemming from these tardive syndromes, but I have heard of emergent drug sensitivity (such as with antibiotics). If this isn’t simply a symptom of these tardive syndrome I’m yet to encounter, it may be worth looking for other exposures in her environment which, did not precipitant skin reactions in the past but may now be doing so. Perhaps, other drugs, laundry detergents etc.

3. When people have enduring difficulties on withdrawal – do you advise them to go back on treatment and taper even more slowly?

Hard to say. Depending on the experience during the withdrawal. If for example there was absolutely no improvement in 6 months, that appears to me to be a reasonable sign that the condition may be permanent. E.g the body does not appear to be capable of correcting whatever biological aberration that has been induced.  If there was a trend towards improvement, but the withdrawal failed due to the enduring difficulty of the symptoms, despite slight improvements, then I would be more hopeful in re-attempting withdrawal again in the future at a much slower pace. Additionally, in conditions such as Tardive dyskinesia which can often be permanent, old age can be a poor prognostic sign for recovery, I would be more encouraging in younger patients than older ones in reattempting withdrawal with the hope of cure. Also, the level of support someone has would be important in gauging how well they would tolerate another withdrawal.

4. Do you see people who can’t increase or decrease?

I’ve read many cases and heard from many individuals first-hand about being unable to decrease without severe symptoms. However I have not read cases like this where even dropping half a pellet from a very high dose — 375 mg, causes symptoms to emerge, typically these small drops only cause problems at the lower end of tapering.

5. How does a case like this fit into current models – like reducing receptor occupancy in 10% steps?

A good question. The idea behind reducing dosages in increasingly small amounts in order to drop receptor occupancy in a controlled linear fashion is that it will give the brain a greater chance to modulate receptor expression/sensitivity as previously modulated synaptic neurotransmitter levels return to normal. This is intuitively appealing and does appear to be the experience of many people who taper of psychiatric drugs – smaller drops confer better chance of success and reduced severity of withdrawal symptoms.

The problem here that I can see is that there does exist tardive syndromes which simply don’t improve, regardless of the time that someone is off the drug: Tardive Dyskinesia being the paradigm. Although it is very bleak and disheartening, I think there might need to be a place where some, after attempting to discontinue for long periods of time, might have to come to the conclusion that the problems will not go away. In these cases, hopefully reinstitution of the drug can improve these symptoms.

6. What would you do for this woman now?

There appears to be two options: One which manages symptoms and one which tries to cure the condition.

1)    Symptomatic Management:
Persist with the Effexor which is at least masking the sensory disturbance and work on finding a combination of therapies: pharmacologic and others which allow this lady to live as comfortable as is possible.

2)    Curative:
Proceed on the assumption that a long taper of miniscule decreases might allow this lady to come off the medication. Liquid formulations might be useful for titration, switching to fluoxetine might be useful as it could have less inter-dose fluctuations given the long half-life. Although given this patients demonstrated sensitivity to even minuscule changes in Effexor dose, this sounds frightening to attempt.

There would likely need to be pharmacologic and other therapeutic treatments to be used regularly and as needed if the withdrawal symptoms are severe during the taper.

Both are hard choices, with 1 there is always a chance the symptoms might break through in the future necessitating higher and potentially more dangerous doses of Effexor to suppress them, and with 2 there is a chance it may not work, or simply be too be excruciating.

Both plans would need a knowledgeable doctor who can be flexible as treatment proceeds. The worst-case scenario would be getting treated by someone who simply throws meds at her off an algorithm or writes these symptoms off as hysteric manifestations of her depression.


The picture above comes from Heather’s Life Moments – created by Heather to reflect her hell coming off Paxil.  Like H in this post, Heather appears to have been on a road to a prescription cascade.

To be Continued with 2 more posts…