SSRIs as a treatment for drug addiction (especially benzos).

[Okiv99]

SSRIs have been shown to promote neurogenesis and bdnf (brain derived neutrophic factor) in the brain (both of these things are increased by exercise which it is so beneficial after quitting drugs). Upregulating neurogenesis is important after addiction as we know because the brain is in a plastic state (almost frozen state ) after addiction and so is rigid and not adjusting to new behavioural patterns well.

Additionally its been shown SSRIs enhance GABAergic transmission in the brain and elevate Gaba levels (this would be beneficial for all recovering addicts) but it is my belief that this may additionally help ex benzo addicts that have damage their GABAergic system with long term use.

Ofcourse we know SSRIS can have bad effects for the short adjustment period but im wondering you guys thoughts on this. Reading into the scientific literature they look very promising and I have been experimenting on myself. I have found my drug cravings have massively reduced, I am getting enjoyment out of normal life much quicker than on my previous quits and I have a sense of well being that I haven't had for years.

 

[Deleted member 81238]

Which specific SSRI s? Prozac ? Lexapro?

 

[Okiv99]

Which specific SSRI s? Prozac ? Lexapro?

They all have slight nuances. Fluoxetine is the most studied SSRI in terms of neurogenic effects but setraline and paroxetine also show effects. A bunch of others do too but are lesser studied.

Fluvoxamine is shown to have the strongest gabaergic effect followed by paroxetine and setraline.

For this reason if wanting both effects id choose setraline or paroxetine but also remember theirs an adjustment period and each person requires an individual dose for the drug to work. A good doctor will titrate the dose up very slowly and monitor you closely (monthly check ups) at first.

There is also some other nuance in terms of sides people experience but Ive found as long as people start low and up the dose slowly sides are pretty limited apart from during the initial 2 weeks when start or upping the dose.

These changes also take a long time im talking 3-6 months for increases in bdnf and changes in gaba receptor expression.

 

[Allylbenzene]

Reading into the scientific literature they look very promising and I have been experimenting on myself.

I'd be careful when interpreting research showing benefits of SSRI drugs. The non-serotonin effects of SSRI drugs are more likey to be responsible for the positive effects. These include increasing BDNF and allopregnanolone which can be done in much safer ways. A well-known drug that increases BDNF is ketamine, called a "fast-acting antidepressant". Pure allopregnanolone is prescribed for depression (the body naturally makes it from pregnanolone too).

The serotonin theory of depression remains a dubious theory.

The rudimentary approach of increasing serotonin is a highly questionable approach for treating drug addiction and could easily make things worse.

To anyone considering this:
PLEASE BE CAREFUL before using SSRI drugs.
At least learn about the common side effects so you can make an informed choice.

Three years before Prozac received approval by the US Food and Drug Administration in late 1987, the German BGA, that country's FDA equivalent, had such serious reservations about Prozac's safety that it refused to approve the antidepressant based on Lilly's studies showing that previously nonsuicidal patients who took the drug had a fivefold higher rate of suicides and suicide attempts than those on older antidepressants, and a threefold higher rate than those taking placebos.
Using figures on Prozac both from Lilly and independent research, however, Dr. David Healy, an expert on the brain's serotonin system and director of the North Wales Department of Psychological Medicine at the University of Wales, estimated that "probably 50,000 people have committed suicide on Prozac since its launch, over and above the number who would have done so if left untreated.
...
Dr. Joseph Glenmullen, a clinical instructor in psychiatry at Harvard Medical School and a clinician at the Harvard University Health Services, says he wrote the book ["Prozac Backlash"] because he was alarmed by the number of patients who were reporting severe side effects from the serotonin-boosting antidepressants including Prozac, Paxil, Zoloft, and Luvox. "The two most upsetting side effects were patients becoming suicidal on the drugs, and the development of disfiguring facial tics," he said in an interview.

The Boston Globe, 2000.

Prozac Revisited [Boston Globe]

 

[Okiv99]

I'd be careful when interpreting research showing benefits of SSRI drugs. The serotonin theory of depression is questionable. The non-serotonin effects of these drugs include increasing BDNF and allopregnanolone which can be done in many other safer ways. The most well-known drug that increases BDNF is ketamine, called a "fast-acting antidepressant". Pure allopregnanolone is prescribed for depression.

The blunt strategy of increasing serotonin is a highly questionable approach for treating drug addiction and could easily make things worse.

To anyone considering this:
PLEASE BE CAREFUL before using SSRI drugs.
At least learn about the common side effects so you can make an informed choice.

Prozac Revisited [Boston Globe]

Oh yeah im not saying they are a magic cure/bullet or they come with no side effects. I miss-worded my post if it came across that way. Mainly just that in people who are having issues with adjusting/changing habits over the medium-long term the neurogenesis effect could be beneficial. I wouldn't recommend them when in initial withdrawal at all and anybody who decides to use them should start with as small a dose as possible and slowly titrate up under doctor supervision.

Exercise increases neurogenesis/bdnf aswell and its believed this is why it improves/speeds up recovery.

 

[shreddedlettuce]

Ok not an SSRI, but a Tricyclic antidepressant, Mianserin, which is similar but not the same as Mirtazapine. and pasting this here for the scientists out there

*Mianserin is closely related to mirtazapine, both chemically and in terms of its actions and effects, although there are significant differences between the two drugs (for example, its higher noradrenergic activity and lower 5-HT3 receptor antagonism)"

*******

Point being the withdrawals even over 10 weeks of slow weaning, the last few days hit me harder then any other withdrawal to many hectic substances, in my experiences.

It lasted at least two months after it was out of my system.

And I am not referring to mental anguish, but physical, flu like weakness, even on my Vyvanse.

It was bizarre, they helped me for over a decade though, but after my first 13 months on Vyvanse, I knew what was missing my whole life (subjective, I know but it is true).

I requested to be taken off the Mianserin as I was feeling "depressed", only depressed by having to take antidepressants.

I stuck it out, but was so close to just giving in and take them like vitamins for the rest of my life.

Would never have happened without the right medication finally.


Just wanted to share with anyone who is pondering about the reason why they are on antidepressants.

There should be no doubt.

There's no right or wrong answer.

Or if they are needed for life (chronic), that's cool too.

Stay safe everyone.


AND to answer the OP IME, it can help, but as a really long term treatment, not for me. but I got lucky. Information is power and hope this didn't de-rail the thread.

 

[emkee_reinvented]

SSRIs have been shown to promote neurogenesis and bdnf (brain derived neutrophic factor) in the brain (both of these things are increased by exercise which it is so beneficial after quitting drugs). Upregulating neurogenesis is important after addiction as we know because the brain is in a plastic state (almost frozen state ) after addiction and so is rigid and not adjusting to new behavioural patterns well.

My preference naturlal HQ herbelb s maybeybe exracts.
Lot s of herb are neoplastic ao Weed.

Additionally its been shown SSRIs enhance GABAergic transmission in the brain and elevate Gaba levels (this would be beneficial for all recovering addicts) but it is my belief that this may additionally help ex benzo addicts that have damage their GABAergic system with long term use.

Likewise lots f herb s do this, free of side effect s.
Lots of GAABA-t inhibitors and GABA-a modlators.
Non additive and most of em have a wider spectrum off effect s.
Many also anti-oxidant s. Eryrhrina Mulungu intrigues me.

As it out-competes Western medicine, and at the same no side effect s.
Only good ones when used as anti- Epileptic.

Ofcourse we know SSRIS can have bad effects for the short adjustment period but im wondering you guys thoughts on this. Reading into the scientific literature they look very promising and I have been experimenting on myself. I have found my drug cravings have massively reduced, I am getting enjoyment out of normal life much quicker than on my previous quits and I have a sense of well being that I haven't had for years.

Good they help you, btw that 1 till 4 weeks are tricky.
Suicidal can, some people go loco, No personal exp though.
But they dont work for you at the smart.

 

[Deleted member 585202]

Interesting topic. They always throw tons of SSRIs at me when I'm in rehab. I don't take them, because their efficacy is dubious and because of side effects of course. But if they promote neurogenisis and enhance GABA, that sounds great, but I'm very skeptical. I have dozens of bottles of various SSRIs laying around untouched.

 

[Allylbenzene]

They always throw tons of SSRIs at me when I'm in rehab. I don't take them, because their efficacy is dubious and because of side effects of course. But if they promote neurogenisis and enhance GABA, that sounds great, but I'm very skeptical. I have dozens of bottles of various SSRIs laying around untouched.

The "side" effects are caused by increasing serotonin.
I edited my post to make that more clear...

Dr. Joseph Glenmullen, a clinical instructor in psychiatry at Harvard Medical School and a clinician at the Harvard University Health Services, says he wrote the book because he was alarmed by the number of patients who were reporting severe side effects from the serotonin-boosting antidepressants

The Boston Globe, 2000.

 

[Deleted member 585202]

The "side" effects are caused by increasing serotonin.
I edited my post to make that more clear...

I'm aware of that. My dilemma is that I feel like therapeutic benefits are outweighed by the side effects. I think placebo effect is baked into their therapeutic design.

Another issue is that I don't want anything messing with my LSD therapy sessions, heh.

 

[Allylbenzene]

My dilemma is that I feel like therapeutic benefits are outweighed by the side effects.

Calling them "side" effects is a bit misleading imo. They are caused by the primary effect of increasing serotonin.

 

[jambabomba]

The "side" effects are caused by increasing serotonin.
I edited my post to make that more clear...

Right. Just like you said it is allopregnanolone that helps with depression - if SSRI's help at all in the first place.

Serotonin theory is a bunch of bullshit that scientists have abandoned like 20 years ago. Indeed, using SSRI's for benzo withdrawal would be ultimately stupid as they rise so much serotonin that it will upregulate glutamatergic signalling in cerebral cortex and frontal lobes through 5ht-2a/5ht-2c which is a receptor that about 70% of glutamatergic neurons have and about 40% of neurons are glutamatergic.

So in general SSRI's cause anxiety&depression to go worse in the first 2 weeks until ex. 5ht-2a&5ht-2c downregulates and after 2 weeks the total net excitatory serotonin effect is diminished and allopregnanolone has some chances to shine but nevertheless I would say SSRI meds at full dose is like raping your mind.

Allopregnanolone and thus BDNF and neurogenesis is even increased at so small doses that do not even rise serotonin at all. So maybe 1-5mg of ex. Fluoxetine might be a worth trying. At least you would not get increased suicide risk and bad anxiety for the first 2 weeks until serotonin receptor downregulation and less excitatory serotonin -> glutamatergic transmission to cerebral cortex and frontal lobes and thus less anxiety.

 

[jambabomba]

Edit: And if SSRI's increase GABA directly it is because of mind's own compensation mechanism from overstimulated glutamatergic signalling through serotonin. Not direct effect of the SSRI as they increase first glutamatergic signalling to a point of suicide. So of course your mind tries to compensate.

But that is like saying that benzo or alcohol withdrawal increases GABA and GABA receptor density - yes it does but at what cost.

Edit: And BDNF too I suspect is majorly because of stressed brain by too much serotonin - a compensatory mechanism to overloaded excitatory serotonin system.

Just like Ketamine it first overstimulates your brain with high amplitudes&high glutamatergic tone and then brain compensates and creates theta&delta states and that is where the anabolic actions like BDNF, NGF and mTor stimulation happens. Not during overstimulated phase but because of mind's compensatory mechanisms to stress it causes.

 

[Allylbenzene]

Serotonin theory is a bunch of bullshit that scientists have abandoned like 20 years ago.

This article is a great all-round biochemistry take on the misconceptions of serotonin in modern medicine, but I get the impression you might always know of this author.

 

[Allylbenzene]

Just like Ketamine it first overstimulates your brain with high amplitudes&high glutamatergic tone and then brain compensates and creates theta&delta states and that is where the anabolic actions like BDNF, NGF and mTor stimulation happens. Not during overstimulated phase but because of mind's compensatory mechanisms to stress it causes.

Have you ever looked into agmatine? It's an endogenous alpha-2 adrenergic agonist, 5-HT2A partial agonist and mimics many of ketamines key properties eg NMDA¡ and mTOR.

 

[jambabomba]

And by the way, nicotine, alcohol, GHB and morphine all increase allopregnanolone much more than any SSRI. GHB is much better antidepressant than any SSRI - GHB increases allopregnanolone up to 10-20 times. Alcohol also increases allopregnanolone several folds. Moderate Alcohol + nicotine is good allopregnanolone booster.

I bet allopregnanolone combined to small dose/micro dose of naltrexone, high dose of Baclofen and high dose of Vitamins like Vitamin C could cure many addictions and cravings. Basically it seems that what human are addicted to (when addicted to drugs) could be reduced to endogenous steroids + endorphins and other peptides. So stimulating those + adding GABA-b agonist could be a cure. Gaba-b system is out of balance in most addicts and they have reduced sensitivity to baclofen like also depressed and schizophrenics have.

And allthough allopregnanolone is PAM at GABA-a like benzodiazepines it has equal and superior affinity to all subreceptors.

 

[Allylbenzene]

I bet allopregnanolone combined to small dose/micro dose of naltrexone, high dose of Baclofen and high dose of Vitamins like Vitamin C could cure many addictions and cravings.

Agreed. Regular pregnenolone is OTC btw which is the sole precursor for all other neurosteroids including allopregnanolone. Although pregnenolone has some GABA antagonist MOA iirc.

So stimulating those + adding GABA-b agonist could be a cure.

This is essentially the key metabolic element which is missing from most drug recovery protocols. Metabolic function drives steroidogenesis which is the synthesis of neurosteroids like pregnenolone and allopregnanolone.

 

[jambabomba]

Agreed. Regular pregnenolone is OTC btw which is the sole precursor for all other neurosteroids including allopregnanolone. Although pregnenolone has some GABA antagonist MOA iirc.


This is essentially the key metabolic element which is missing from most drug recovery protocols. Metabolic function drives steroidogenesis which is the synthesis of neurosteroids like pregnenolone and allopregnanolone.

Yes indeed. I recently needed to taper my benzodiazepines very quickly as I was running out of them.

I tapered them very quickly in a week and then started to take Pregnenolone 500-800mg/d. I also took DHEA 100-200mg which raises endorphins too and also increases allopregnanolone. On top of those I also took conversion (to allopregnanolone) boosters like Propranolol, PEA, Tribulus, Choleus forskoli (not so sure about that one) Vitamin C 5-10g/d, Amitriptyline&Olanzapine. All of the mentioned affect positevely to allopregnanolone synthesis by increasing either 3hsd or 5-alfa enzyme activity.

I really had the most easiest taper I've ever had. And pregnenolone certainly needs fat to absorp and affect well.

Btw, do you know other effective conversion boosters than mentioned?

 

[jambabomba]

Have you ever looked into agmatine? It's an endogenous alpha-2 adrenergic agonist, 5-HT2A partial agonist and mimics many of ketamines key properties eg NMDA¡ and mTOR.

Thank you for the link. Yes I know Ray Peat and have read also his material.

He used to take 2grams daily of pregnenolone :D

Agmatine is not so familiar with me. I know it but have never used it.

 

[Allylbenzene]

You can always tell when someone is familiar with Rays perspective...

I also took DHEA 100-200mg

It's a GABA antagonist afaik...(!) Ray didn't recommend it.

Btw, do you know other effective conversion boosters than mentioned?

For what, boosting steroidogenesis you mean? See blue below: