• N&PD Moderators: Skorpio

Benzo's are nerotoxic!!!?

i'm pretty sure all drugs are neurotoxic to some degree. you can't just keep putting chemicals in your brain over and over and have it not have any lasting affects.

my question is to those who have been on benzos long term, have you noticed any signs or symptoms of brain damage? if so, what?
 
Benzos neurotoxic. I have access to academic journals, so I'll dig up the references when I'm more sober. This is new and is very different from what i learned in biopsychology.

ebola
 
burn out said:
i'm pretty sure all drugs are neurotoxic to some degree. you can't just keep putting chemicals in your brain over and over and have it not have any lasting affects.

my question is to those who have been on benzos long term, have you noticed any signs or symptoms of brain damage? if so, what?

I think the question is if any changes will be permanent upon cessation.
 
I don't know about neurotoxic effects on the cellular level. A different issue is that permanent sedation could lead to a lack of "brain exercise", which I think will have negative effects itself.
 
entropy90 said:
Sir, I wish to offer my sincerest apologies. I made an honest mistake and did not bother to look at what I posted. If there is anyway I can make this up to you I would be more then greatfull to do so.

In a perfect world this would be the quote I would have used:


However in an attempt to keep this thread about the nerotoxic affects of Benzodiazepines and not about the validty of a quote or the education level of the quotee, I will refrain from posting any further on the aforementioned topic and pertain all futher posts to the original content of this thread.
Is this formality all in a mocking way? I'm sorry if my reply back to you sounded harsh, I was just pissed off. Sorry. :|
 
rnd.id. said:
I don't know about neurotoxic effects on the cellular level. A different issue is that permanent sedation could lead to a lack of "brain exercise", which I think will have negative effects itself.
I agree with this.
 
burn out said:
i'm pretty sure all drugs are neurotoxic to some degree. you can't just keep putting chemicals in your brain over and over and have it not have any lasting affects.

my question is to those who have been on benzos long term, have you noticed any signs or symptoms of brain damage? if so, what?
I have noticed a general cognitive decrease since I started taking them, when I stopped for about 5 months once I did felt that like I had "lost" somewhat of my "brains". Specially with hypnotic benzodiazepines I've noticed that the amnesia produced is not only anterograde but sometimes also posterior to use you will forget things done recently, that you'll have to do or even events that happened in the past; thus I really do think from experience that there certainly are long term abuse post use neurolophysiological changes in your system.
 
closedeyevision said:
this is priceless, a good enough question about benzos hijacked by someone who started taking them at age 11. 11!!! for. fuck. sake
Do you mind if I ask what's so bad about that? :\
 
following the example of basically every other drug, its likely that longterm use of benzodiazapines will kill GABA receptors via over-stimulation. however thats just speculative. honestly i've never heard anything about benzos being neurotoxic, except that they arent, or at the very least many, many times less toxic than barbiturates.

and you damn children need to leave your personal crap out of this thread. take it to pm and stfu.
 
narutokun said:
Is this formality all in a mocking way?

Not at all I was just trying to get across that I was actually sorry. sorry if it sounded like I was being a bit of a dick. And really I am sorry about getting in the middle of that tiff between you and Ham-milton.
 
^No if you meant it that way there's nothing to be sorry about. I'm the one's who sorry. I probably misinterpreted that you were backing him up by thinking that you were talking about the school thing and not the age thing, while you actually were talking about the other part of the post; sorry.
 
>>following the example of basically every other drug, its likely that longterm use of benzodiazapines will kill GABA receptors via over-stimulation.>>

This is not the example of every drug. This is following the example of amphetamines and their derivatives, basically.

Opioids and cannabinoids, for example, have not been shown to kill cells with endorphin and anandamide receptors, respectively.

ebola
 
ebola said:
This is not the example of every drug. This is following the example of amphetamines and their derivatives, basically.

Glutamate receptors can die from overstimulation, as can dopamine receptors, and possibly serotonin receptors. and its possible that more than just those can be killed by overstimulation. there isnt nearly enough data, but its still possible
 
like w/ a lot of drugs... only time will tell, clever science brainiacs can speculate and use fancy words, but as far as i'm concerned, some benzos have been around for a while now... the more "dangerous" ones which are more likely to cause amnesia and rebound w/D effects months or even years in some cases after havin taken them are slowly being taken off the general market and only used in extreme cases (Halcion, rohypnol, nimetrazepam....)

(i don't understand any of that psycho-babble on wiki so fukit... i dunno... i can't back up what i said scientifically, so it's jus an opinion really)
 
Receptors can definitely be downregulated with overstimulation, but this does not necessarily lead to the death of the neuron on which they are found. As long as the cells remain healthy, they can homeostatically upregulate receptors upon cessation of drug use. Long-lasting brain plasticity has been found in response to chronic treatment with most psychoactive drugs, and any effects that persist after drug use stops are probably due either to neurotoxicity or, if no cells die, changes in gene regulation in the affected brain areas. In the latter case, there should be ways of either reversing or compensating for this plasticity.
 
A lot of things..

could be said about the nitro group in its pharmacokinetics/dynamics. First, the nitro moiety is a rare beast in the pharmacopea. You just don't find many nitro groups on synhetic pharmaceuticals or on natural products. The electron withdrawing groups of choice (electron withdrawing by induction[-I] or by resonance[-R]) seem to be electron withdrawal by induction (halogens,ie., fluorine, chlorine, bromine, or in a few cases the most unstable, iodine). The nitro group has both properties, it is electron withdrawing (on aryl rings) by both -I and -R effects. The reason why Clonazepam exists as a widely prescribed drug is because the nitro group substitution just happens to impart both more of an antiseizure effect and lowered toxicity. Most benzos have halogens attached to the aryl rings to make them more potent, more toxic, and more metabolically stable (longer half-lives). The nitro group gets metabolized in stages where free radical production occurs, but that's why Ubiquinone (CoEnzyme -Q) exists in every cell ( along with other antioxidants), is to catch the little free radical buggers. WE are essentially "burning up"by oxidative transformations. Life processes produce a lot of free radicals simply because single electron transfer is what nature chose as a mechanism for a lot of the bond making and breaking in our bodies. What worries me more about the nitro group is it getting fully reduced (by reductase enzymes) in the areas of high MAOI (monoamine oxidase inhibition), to an aniline, which could possibly be a carcinogen.
 
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There are a few mentions of neurotoxicity

Effect of GABA agonists on the neurotoxicity and anticonvulsant activity of benzodiazepines.
Chweh AY, Swinyard EA, Wolf HH, Kupferberg HJ.
Progabide (50 mg/kg, i.p.), a GABA receptor agonist, significantly decreases the median minimal neurotoxic dose (TD50) of clobazam, chlordiazepoxide, and diazepam; the receptor binding of these substances is highly enhanced by muscimol. Progabide has no significant effect on the TD50 of clonazepam and triazolam; the receptor bindings of these substances is either only slightly enhanced or not altered by muscimol. Progabide also significantly decreases the median antimaximal electroshock dose (MES ED50) of all the benzodiazepines tested. However, progabide has no effect on the median antipentylenetetrazol dose (PTZ ED50) of the benzodiazepines. Likewise, THIP (2.5 mg/kg, i.p.) significantly decreases the TD50 of chlordiazepoxide but not that of triazolam. THIP significantly decreases the MES ED50 of chlordiazepoxide and triazolam but has no effect on the PTZ ED50 of these two substances. The above data suggest that benzodiazepine receptors linked to GABA receptors contribute to the minimal neurotoxicity and anti-MES activity but not to the anti-PTZ activity of benzodiazepines.

PMID: 2983169

Open study of clobazam in refractory epilepsy.

Munn R, Farrell K.

Clobazam is a 1,5-benzodiazepine reported to have a wide spectrum of antiepileptic activity and is associated with less neurotoxicity than the 1,4-benzodiazepines, nitrazepam and clonazepam. The effect of clobazam on seizure control and neurologic behavior was examined prospectively in 115 children (average age: 8.4 years) with intractable seizures. Eighteen children (16%) became seizure free and a further 35 (31%) demonstrated a greater than 90% decrease in seizure frequency. Tolerance to the antiepileptic effect of clobazam was observed in 30 of 79 children (38%) who demonstrated an initial improvement in seizure control. Complete tolerance was observed in 9 patients, partial tolerance in 9, and partial tolerance that responded to an increased dose of clobazam in 12. Seventy-two percent of patients reported improvement and 26% worsening in at least one parameter of neurologic function after beginning clobazam. The improvement in neurologic function correlated poorly with change in seizure control. Patients who discontinued 1,4-benzodiazepine (n = 37) had a greater improvement in attention span, alertness, balance, drooling, and mood compared to the remainder of the group. These data suggest that clobazam is effective in the treatment of children with a wide range of epilepsies and seizure types and support the clinical impression that clobazam is associated with less neurotoxicity than the 1,4-benzodiazepines.

PMID: 7605555

^Looks like the term though is not 100% defined & given that copious amounts of MSG & aspartame are used in food & drink as well as other environmental pollutants, food additives & alcohol - the idea of neurotoxicity becomes a relative issue rather than absolute.

Personally SWIM agrees with most views in this thread that addiction, withdrawal, tolerance and side effects are far more clinically relevant (&potentially serious) when using benzodiazepines.
 
Ubiquninone. I like that one.

I think it can be agreed (no?) that whatever neurotoxicity-risk benzos represent, it's gotta be rather minimal. These aren't exactly new drugs, and considering the general idea among doc's that once benzo dependent, always benzo dependent, there has to be thousands of benzo-dependents out there who've been taking them since they hit the market.
 
er...

unubiquinone? iniquinubone? inquinunone? UBIQUINONE? got it:o =D
You should see my freudian e-slips=D .
Benzos, just like barbiturates and alcohol, and all the other downs in the world, they are all DUM-DUM concoctions and take away the edge of reality by making one oblivious to it. Why intelligent people want to make themselves less intelligent is beyond me, but we all do it, don't we?:|
BTW- Ham-milton.. Blessed are the dyslexic because they never know whether they are ahead or behind of you =D
 
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