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Multiple meds -- polypharmacy


Rhiannon

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Just wanted to start a thread on this.

 

It sounds like (and Gianna says she's seen it to be true) the majority of people who take one psych med at some point or another are put on another one. Probably the most common is treating akathisia with benzos or treating benzo-caused depression with antidepressants, at least in the past, but now they're starting to prescribe all kinds of supplemental drugs "in case the first drug isn't working well enough by itself."

Started on Prozac and Xanax in 1992 for PTSD after an assault. One drug led to more, the usual story. Got sicker and sicker, but believed I needed the drugs for my "underlying disease". Long story...lost everything. Life savings, home, physical and mental health, relationships, friendships, ability to work, everything. Amitryptiline, Prozac, bupropion, buspirone, flurazepam, diazepam, alprazolam, Paxil, citalopram, lamotrigine, gabapentin...probably more I've forgotten. 

Started multidrug taper in Feb 2010.  Doing a very slow microtaper, down to low doses now and feeling SO much better, getting my old personality and my brain back! Able to work full time, have a full social life, and cope with stress better than ever. Not perfect, but much better. After 23 lost years. Big Pharma has a lot to answer for. And "medicine for profit" is just not a great idea.

 

Feb 15 2010:  300 mg Neurontin  200 Lamictal   10 Celexa      0.65 Xanax   and 5 mg Ambien 

Feb 10 2014:   62 Lamictal    1.1 Celexa         0.135 Xanax    1.8 Valium

Feb 10 2015:   50 Lamictal      0.875 Celexa    0.11 Xanax      1.5 Valium

Feb 15 2016:   47.5 Lamictal   0.75 Celexa      0.0875 Xanax    1.42 Valium    

2/12/20             12                       0.045               0.007                   1 

 

I'm not a doctor. Any advice I give is just my civilian opinion.

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compsports

Just wanted to start a thread on this.

 

It sounds like (and Gianna says she's seen it to be true) the majority of people who take one psych med at some point or another are put on another one. Probably the most common is treating akathisia with benzos or treating benzo-caused depression with antidepressants, at least in the past, but now they're starting to prescribe all kinds of supplemental drugs "in case the first drug isn't working well enough by itself."

 

I was put on Ritalin. It then caused depression so I got Prozac. When I developed suicidal ideation, my doses were doubled. I got worse and I was cold turkeyed off of both drugs on to Serzone.

 

When that didn't work and I also couldn't sleep, I ended up on Effexor and for sleep, Remeron, Trazadone, and Serzone. I am lucky I didn't get Serotonin syndrome. The gods were smiling on me.

 

I then was put on Zoloft, Adderall, and Remeron. Until the end, I was taking during the day, an AD, a stimulant, and Remeron. When I started having trouble sleeping, Doxepin was added.

 

And I also took Benzos on a PRN basis when I was getting agitation from drugs like Zoloft. I feared getting addicted so I never took too many.

 

That is my multiple meds story. Anyone else?

 

CS

Drug cocktail 1995 - 2010
Started taper of Adderall, Wellbutrin XL, Remeron, and Doxepin in 2006
Finished taper on June 10, 2010

Temazepam on a PRN basis approximately twice a month - 2014 to 2016

Beginning in 2017 - Consumption increased to about two times per week

April 2017 - Increased to taking it full time for insomnia

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Altostrata

Many of us, if not most of us, have been exposed to multiple psych meds, although not polydrugged.

 

There's been a lot of mis-medication as people searched for answers to their withdrawal syndrome. Where to go to first? A psychiatrist, of course. And then they do what they do -- which is to throw prescriptions at you, as many as you will accept.

 

As a side note: One of the reasons the psychiatric industry is slowing down in development of new psych drugs is that it's become harder and harder to find people who have not been exposed to psych drugs to be subjects in drug trials. We're running out of psych drug virgins!

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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cinephile

As a side note: One of the reasons the psychiatric industry is slowing down in development of new psych drugs is that it's become harder and harder to find people who have not been exposed to psych drugs to be subjects in drug trials. We're running out of psych drug virgins!

Wow, this is astonishing! Not surprising, of course, but it speaks volumes to how effective the mainstreaming of psychiatry has been. Do you have an article or report on this finding, sur? I'd love to read it.

 

I think another reason the development of new psych meds is slowing down is simply because big pharma sees the writing on the wall: the market is becoming saturated (hell, even KIDS -- not just adolescents -- are being sucked into the psych vortex) and the companies are realizing many of their "blockbuster" drugs are going off patent in a few years. And, of course, they're running out of ideas for new meds: after all, how many times can you tweak the molecules until you reach diminishing returns?

 

I'm with the boring old man in that "personalized medicine", genetics, and biomarkers for mental disorders will be the new cash cow for psychiatry. Of course pills will play a large role in personalized medicine (of course! how could they not?) but the pills alone won't be the big money-makers anymore: it will be the expensive diagnostic testing of a patient's genes to test how well a patient will respond to pills. 'Whoo boy, glad I won't be a part of that mess!

Been on SSRIs since 1998:

1998-2005: Paxil in varying doses

2005-present: Lexapro.

2006-early '08: Effexor AND Lexapro! Good thing I got off the Effexor rather quickly (within a year).

 

**PSYCHIATRY: TAKE YOUR CHEMICAL IMBALANCE AND CHOKE ON IT!

APA=FUBAR

FDA=SNAFU

NIMH=LMFAO

 

Currently tapering Lexapro ~10% every month:

 

STARTING: 15 mg

11/7/10: 13.5 mg

12/7/10: 12.2 mg

1/6/11: 10.9 mg

2/3/11: 9.8 mg

3/3/11: 8.8 mg

4/1/11: 7.8 mg

4/29/11: 7 mg

5/27/11: 6.4 mg

6/24/11: 5.7 mg

7/22/11: 5 mg

8/18/11: 4.5 mg

9/14/11: 4 mg

10/13/11: 3.6 mg

11/9/11: 3.2 mg

12/7/11: 2.6 mg

1/3/12: 2.1 mg

2/2/12: 1.8 mg

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Altostrata

I'm going to give myself a good medal for Googling. I knew I read this somewhere (emphasis mine):

 

https://www.ft.com/content/7688bcee-77e8-11df-82c3-00144feabdc0

 

No room for gloom

 

By Clive Cookson and Andrew Jack

 

Published: June 15 2010 03:00 | Last updated: June 15 2010 03:00

 

....

Caroline has joined the small band of people willing to risk what is widely seen as the stigma attached to depression and similar mood disorders. Another recent example is the writer Allison Pearson. They are the visible tip of a growing pandemic of what the biologist Lewis Wolpert memorably called " malignant sadness ". According to the World Health Organisation , depression causes more disability than any other disease, affecting more than 120m worldwide. The cost of all this is thought to exceed $100bn (£68bn, €82bn) a year.

 

On the face of it, then, depression presents a classic "unmet medical need" with a vast potential market that should be a priority for increased pharmaceutical research and development. In reality, quite the opposite is happening. Several of the largest drugmakers have recently decided to curb or cease research in the field, reducing the funding and expertise available to find better treatments.

 

The withdrawal reflects growing financial pressures on the industry to cut spending on high-risk low-profit areas such as mental health, where there are few new scientific leads in the laboratory and many cheap generic drugs are coming on to the market. Yet neuroscientists say research into the biology of depression, funded by public agencies and smaller biotechnology companies, is on the brink of breakthroughs.

 

In February Andrew Witty, chief executive of GlaxoSmithKline, said his company would stop work on antidepressants, bringing an end to research by the developer of drugs such as Wellbutrin and Seroxat. GSK denied that its decision was related to the public criticism, regulatory scrutiny and litigation over suicidal feelings and other alleged side-effects generated by Seroxat in recent years.

 

Rather, Mr Witty said there were more promising and productive areas of research in its portfolio, while antidepressants were "among the most expensive, high-risk" drugs to develop, with weak "endpoints" that made it difficult to measure likely success until late in the development process. AstraZeneca took a similar view a few weeks later, winding down its discovery work on depression and other mental disorders as it pared back in-house research spending.

 

At the heart of the problem is the difficulty in first identifying appropriate patients to take part in clinical trials and then proving that they do better on the new drug candidate than on placebo (dummy pills). "That is the number one reason why we as an industry are moving away from an area that has an incredible burden of disease," says Frank Yocca, AstraZeneca's head of discovery for central nervous system drugs.

 

Clinical trials are particularly hard to organise for antidepressants because, for a start, medical definitions of depression and its severity are not as clear-cut as for most other diseases. In addition, reliable "bio-markers", objective measurements of disease progress such as brain scans or blood tests, are unavailable.

 

Then there is the large - and mysteriously growing - placebo effect, which makes it hard to demonstrate statistically that patients taking the active drug are doing better than those on dummy pills. Psychiatrists have long recognised that patients with depression and other mood disorders are susceptible to the suggestion that they will get better. But it is not clear why placebo power should have increased, as analysis of clinical trials over the past 30 years shows it has.

 

"It would be like invoking magic to suggest that people are becoming more suggestible," says John Geddes, professor of psychiatry at Oxford University . "The change is more likely to be an artefact of the way patients are recruited to clinical trials."

 

Finding trial volunteers - who are depressed, not taking an existing drug and willing to try an experimental one - has become harder over the years, says Chris Thompson, chief medical officer for the UK's Priory hospital group. In response, investigators have been (unconsciously) upgrading the level of depression of potential subjects, so that they meet the criteria for inclusion.

 

But once the trial is under way, researchers no longer have a motive to exaggerate the volunteers' symptoms. Everyone, whether on drug or placebo, seems to get better - "which is catastrophic if you are trying to discover how effective the drug is", says Prof Geddes, who chaired the depression and anxiety part of the UK Medical Research Council's recent mental health research review. "Everyone in the field knows that this happens." So researchers are discussing ways to reduce the problem - for example, dropping placebo-controlled trials and comparing new drugs with the best existing treatments.

 

Yet even if clinical trials were easy to organise, drug companies might not have a great incentive to innovate, given the downward trend in the antidepressant market. Although prescriptions are rising, their value is falling as the new generation of antidepressants introduced during the 1980s and 1990s, such as Eli Lilly's Prozac and Wyeth's Effexor, lose their patent protection and cheaper generic versions appear.

 

IMS, a provider of healthcare data, says global antidepressant sales peaked in 2006 at $20.2bn. Last year the market was worth $19.2bn and Datamonitor projections show a 4 per cent annual fall until 2014, when slow growth may resume. With the overall pharmaceutical market growing more than 5 per cent a year, the share taken by antidepressants is shrinking.

 

Existing classes of antidepressant - known as "selective serotonin reuptake inhibitors" (SSRIs) and "serotonin norepinephrine reuptake inhibitors" (SNRIs) because of the way they function in the brain - work reasonably well for 60-70 per cent of people. Their side-effects are less serious than the previous generation.

 

....

 

Some smaller pharmaceutical and biotech companies are still looking for better antidepressants. "I'm almost encouraged by big competitors pulling out," says Jacques Servier, founder of France's privately owned Servier Laboratories. "They are often dominated by financial pressures. We are independent, have more liberty and can afford to be more daring."

 

Mr Servier's commitment to antidepressants was inspired by his background in psychiatry: "I saw depression was a real hell, with people waking up at 3 or 4am in atrocious discomfort, feeling a loss of activity and sometimes suicide."

 

Mr Servier's research led to the launch of Valdoxan (agomelatine), a new class of antidepressant that claims improved sleep and fewer side-effects. Though the drug has been used by about 100,000 patients, he concedes it is not easy to compete with low-cost generic alternatives: "Generics are very good for those who respond to them but the price is very low and the companies don't contribute to research."

 

Another company committed to depression research - and shielded by a non-profit foundation from short-term financial pressures - is Lundbeck of Denmark. Lundbeck sells Cipralex, which it also argues has fewer side-effects than generic alternatives. Two other compounds in late-stage trials have a new mechanism of action.

 

Ulf Wiinberg, chief executive, hopes that within a decade, more targeted therapies for different subgroups of patients, "just like we have for cancers", will emerge. "The first time patients present with depression, they will definitely receive a generic," he says. "But after the first or second failure, they need new drugs. We should be treating with the best available therapy."

 

Two US companies with promising candidates are Clinical Data Inc (CDI) and Targacept. CDI has applied for Food and Drug Administration approval of vilazodone, which could reach the market next year. Targacept is about to start the final trial of TC-5214 in collaboration with AstraZeneca, which agreed in December to pay $200m up front for rights to the drug - demonstrating that, while big pharma companies are winding down their research into antidepressants, they are prepared to pay for promising candidates developed elsewhere.

 

Many mental health experts are less concerned with the pharmaceutical industry than with what Dr Thompson calls the "scandal of how little public money there is for research into the biology of depression". A better understanding of what happens in the brain when people feel seriously depressed would give researchers a lead to develop better drugs. One promising avenue, says Prof Geddes, is to use powerful new brain imaging techniques to probe the neural processing of emotion.

 

Like all complex disorders, depression results from many genes and environmental factors working together. The genes remain largely unknown and so do the environmental triggers that might explain the rise. "There is evidence that the incidence of depression is increasing and that this is over and above better recognition," says Prof Geddes. Its onset may on average be earlier in life than it used to be, adds Dr Thompson. Possible causes range from the stresses of modern life - if anything exacerbated by recession - to excessive eating.

 

....

Hope lies in cells that spring eternal in the neurone zone

 

The bleakest dogma of 20th-century neuroscience held that the adult brain never grows: we can only lose neurones (brain cells) as we get older.

 

But research led from the Salk Institute in California and Columbia University in New York has overthrown the dogma. New neurones do form in parts of the brain - and the process, known as neurogenesis, offers a promising way of fighting depression.

 

Scientists showed in 2003 that existing antidepressants achieve some of their effect by stimulating growth in the hippocampus, a brain area involved in learning and memory. The discovery seems to solve a pharmacological puzzle.

 

Antidepressants such as Prozac are supposed to work by increasing the level of certain brain chemicals (such as serotonin) that transmit signals between neurones. But the drugs raise neurotransmitter levels very quickly, so why do they take several weeks to lift the sufferer's mood?

 

The explanation for the delay - that it reflects the time taken for new cells to grow in the hippocampus - has been confirmed by brain imaging, animal studies and post-mortem examinations of human brains. It is now possible to track neurogenesis through scans that show increased blood flow in the living human brain.

 

So the hunt is on for new antidepressants designed specifically to maximise neurogenesis. Leader of the pack is a San Diego company, Brain Cells Inc , founded by academics from Salk and Columbia. After screening more than 1,000 chemicals for their neurogenic effect on brain cell cultures, BCI has discovered two drug candidates that are giving encouraging results in early clinical trials. One of them is a combination of two chemicals, melatonin and buspirone, which have little effect individually on depression or neurogenesis but work well together.

 

Although the first application of neurogenesis will be depression, it may be useful for treating other brain conditions.

 

NeuroNova , a Swedish company, is testing two protein drugs that stimulate neural growth in patients with Parkinson's and motor neurone disease. Syngis Pharma of Germany has started a trial of a growth-stimulating factor that is injected into the brain following a stroke. Animal experiments show that it might both reduce cell death immediately after the stroke and then help blood vessels and neurones to grow, reducing the patients' long-term disability.

 

Another intriguing possibility, says Carrolee Barlow, chief scientist at BCI, is that stimulated growth of the hippocampus will improve memory and cognition in diseases such as Alzheimer's.

 

....

Edited by Altostrata
updated link

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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