![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 41 to 65 of 65. Go back in thread:
Posted by paulk on June 26, 2001, at 16:22:10
In reply to benzos » paulk, posted by Elizabeth on June 26, 2001, at 2:56:27
>“They do have other effects in addition to MAO inhibition, though: Nardil is also an inhibitor of GABA metabolism, while Parnate is *thought* to have some sort of dopaminergic effect (perhaps induction of dopamine release: Parnate is chemically extremely similar to amphetamine).
!@# Lawyers – I sure wish that information had been in the PDR. –The Nardil has just kicked in in the last week or so – I still question that the low BP is caused by other than the increase in the monoamines – from what I understood until 90% of the MAO is knocked out There isn’t enough rise in neuro transmitters to do anything.
I seem to be doing OK except I am starting to have trouble with word selection – and sometimes the wrong word will come out. I wonder if it is a side effect of the GABA? Perhaps I should take the med at night? I am still at the high dose 60/mg day – perhaps it will get better when they lower the does back down. Was the inhibition of the GABA metabolism a direct effect of the drug or secondary?
>
> > It isn’t pretty. I went to a funeral of a friend who had lost his hygiene habits after too many bezo over 15 years. He died choking to death on a hotdog. (this is not a joke)>That's terrible, but I do hope your example doesn't scare people unnecessarily! I really would be interested to know the details, if you're comfortable discussing them -- like the individual's age, why he was taking the benzos (and which ones and how much), whether he had other medical conditions that could have contributed, etc.
>Some people abuse benzos, and they can develop truly massive tolerance. The worst case of this I've heard of involved a guy who was using more than 100 mg of Xanax a *day*. Some people have general sedative abuse problems, and they often combine benzos with other CNS depressants, such as alcohol, barbiturates, meprobamate, industrial solvents (inhalants), etc. As I mentioned, most people who abuse benzos also abuse other drugs.
>However, most anxiety patients who take therapeutic doses (which can mean up to around 6 mg/day of Xanax or Klonopin) do not have problems with them. They certianly don't become demented or unable to care for themselves; on the contrary, benzos can eliminate crippling anxiety. It is true that some people suffer cognitive impairment (slowed thinking, memory problems) from benzos; these people usually end up taking alternative anxiolytics (such as antidepressants) instead (although most people I know who take ADs for panic disorder still occasionally need to take benzos).
He was taking – I think it was Restaril – (sp??) . He was very bi-polar yet a dear friend – very smart – didn’t usually go psychotic in his mania. He really needed to be in a halfway house to have someone monitor is medications. The lack of supervision is what I blame for his death. I think the benzos may have surpressed his gag reflex or dis-coordinated his swallowing enough to cause the problem. I don’t think this would be a common problem with people who can manage there own meds.
> > > I guess I’ve seen too many people who got in trouble with benzos when I was in hospital. That dosen’t mean everyone will, but some do.
> >That's rather surprising. Anxiety patients tend to use medication as directed or, if anything, to use *less* than the prescribed amount, not more.
Most of these people were in the hospital because they had benzo problems – sort of self-selected. Remember everyone reacts differently.> > I would humbly disagree; the short half-life of Xanex causes withdrawal symptoms of ‘panic and anxiety’ in some patients with a single dose.
It sure does it to me. – That’s why I’m interested in the slow release version. I would take it for anxiety and it worked – wonderfully – but then as it wore off I would feel even worse than before.>Some people might experience rebound anxiety (just as people who use short-acting benzos such as Halcion for insomnia may be subject to waking up in the middle of the night when the med wears off), but if they are truly taking the drug only on an occasional basis, rebound effects (if any) are unlikely to be serious. Also, people who have continuous anxiety (rather than, or in addition to, short-lived anxiety or panic attacks) will become anxious again after a benzo wears off: that's not a rebound reaction. Single, isolated doses of benzos do not cause dependence, by any definition you use.
I didn’t use Xanex after the prescription ran out because of that problem – I didn’t get addicted – but I sure wanted to keep taking more and more, but realized I shouldn’t. I really liked and hated the drug. Sure wish I could try the XR version.
> > When I took Xanex – I would get quite irritable as the drug wore off. This makes a drug spiral – take Xanex for anxiety – it works, but as it wears off anxiety is there, but worse – take more – and more. Now, this doesn’t happen to everyone – but it sure happens to some folks.
>Ahh. Irritability isn't an indication for benzos, and they have been known (and documented) to cause bad reactions in some people who had preexisting mood-regulation disorders (which often tend to manifest as irritability or atypical/mood-reactive depression).
I would say that irritability is a symptom of anxiety?? The irritability wasn't there until the drug was wearing off. You might be forgetting the wide variation of how these drugs effect people. (YMMV grin). I know the nasty discontinuation effects of Effexor – yet for many folks they can stop cold with out any problem.
> > They tapered – the anxiety returned – only treatment was CWSP.
>"CWSP?" (Is there something I'm supposed to know about here?)
CWSP = Cold Wet Sheet Packs – THE non-drug treatment for anxiety. (I wouldn’t want it done to me – its not fun to watch – but it seems to work a bit.
I’m thinking that there needs to be a new specialty in medicine – an endroconologist/pycopharmacologist. It sure would be nice if there were better and objective tests that could show what drugs to try first. – perhaps spinal fluid tests or long term urine collection for cortisal tests?
Reminds me – I ran into yet another old friend who tried Effexor – told me he went sort of manic (couldn’t sleep – roofed a house all night long in the dark) – his doc now thinks he may be a bit bipolar. – Perhaps putting someone on a SSRI for a couple of days and re running psyc evaluation would help spot hidden bipolar tendencies? I think that side effect may happen more than one would believe by reading the PDR.
Paulk
Posted by gilbert on June 26, 2001, at 20:26:17
In reply to Re: benzos » Elizabeth, posted by paulk on June 26, 2001, at 16:22:10
Well I just ever can't resist to jump into the whole benzo debate issues. The evil benzos, the addicitive benzos, people dying on benzos....what a load of crap. I'll tak my chances on benzos before you will get me on and MAO....How many people have died from bad reactions and hypertensive crisis from MAO"s....Study after study shows that panic patients don't abuse benzos. They always use the least dose possible and usually throw away half their damn pills. Also I am an ex junkie and drunk and I have felt way more stoned and I mean way more stoned on most antidepressants than xanax. I have been totally out of it like completely detached from reality...numb...no ability to cry even. I take two xanax per day and never have rebound, never have withdrawal and it is by far the most effective anti panic med I have ever had....and without side effects. Seems everyone is always trying to push an antidepressant or mood stabilzer down our throats. The side effect profile long term for xanax is mild compared to these other drugs. I am not sure I want my testosterone levels to drop below sea level from long term use of ssri's. I also don't want to have to ask the waiter if there is aged cheese in the lasagna so I don't have an MOA crisis. I sure as hell haven,t had any good experiences on other newer antidepressants, and the rap on benzos is simply political....no more patents. I know I have trouble with gaba shortages this is my chemical defiency...all the seratonin in the world didn't do me any good. So when the patent's run out on all of the ssri's we will be hearing about the wicked ssri's. The number of bad incidents from benzo use are microscopic compared to other drugs. Am I to believe all the bad press on ssri's....I mean there is loads of this stuff on the internet. Even lists of all the suicides of people on an ssri. I don't buy it. If your friend died from choking on a hot dog it sounds like he died from choking on a hot dog....he didn't choke on giant xanax pill did he? It is so easy to blame the drug....Or maybe he should have taken smaller bites when he ate. My pdoc even said xanax was long tested and one of the safest drugs for me to be on. Should everyone quit Effexor and Wellbutrin because of the lady in Texas killing her kids....She was on Effexor and Wellbutrin and I believe an antipyschotic as well. I don't think so.
Gil.
Posted by paulk on June 26, 2001, at 21:08:06
In reply to Re: benzos, posted by gilbert on June 26, 2001, at 20:26:17
>Well I just ever can't resist to jump into the whole benzo debate issues. The evil benzos, the addicitive benzos, people dying on benzos....what a load of crap. I'll tak my chances on benzos before you will get me on and MAO....
I think you should see some of the other stuff I have written – I like Benzos – and take one – I just was pointing out they can have bad effects on some – especially if they aren’t well monitored.
See what I wrote at
http://www.dr-bob.org/babble/20010605/msgs/65469.html
http://www.dr-bob.org/babble/20010605/msgs/65469.html>How many people have died from bad reactions and hypertensive crisis from MAO"s....
Less than you would think.
>Study after study shows that panic patients don't abuse benzos
I agree – but I have also see the few who get into trouble. I think doctors are way to restrictive about Benzos.
>Also I am an ex junkie and drunk and I have felt way more stoned and I mean way more stoned on most antidepressants than xanax.
I agree again – The biggest problem with Benzos is that they can interfere with learning and memory – I remember a pre med student who took 1mg/day of valium for a semester – had poor final scores and tells me he can’t remember much of that semester.
>I take two xanax per day and never have rebound, never have withdrawal and it is by far the most effective anti panic med I have ever had....and without side effects.
Wish it worked that way for me YMMV.
>Seems everyone is always trying to push an antidepressant or mood stabilzer down our throats.
>I am not sure I want my testosterone levels to drop below sea level from long term use of ssri's.
Hadn’t heard of this side effect??? The SSRI do interfere with sex – but I didn’t know they lowered Testosterone?? Where did you read this? Benzos can kill sex for some people. Again YMMV.
>I also don't want to have to ask the waiter if there is aged cheese in the lasagna so I don't have an MOA crisis.
I don’t think MOAIs are for most folks – but they have been reported to work very well for people with atypical depression – and the diet restrictions vs my depression is an easy trade – I really hate my depression. My take so far is I have less side effects than with Effexor – (Effexor would kill my sex life)
>I sure as hell haven,t had any good experiences on other newer antidepressants
Again, I say that our neuro chemistry is probably much more variable that the way we look – and the effects of the drugs vary greatly form one person to another thus YMMV. I found that on Effexor I knew what it was like to be normal for the first time in my life – made me sad to realize all I had missed. For others SSRIs don’t do a thing.
> and the rap on benzos is simply political....no more patents.I agree to a point – Benzos had a bad rap even when the patent was in place.
> The number of bad incidents from benzo use are microscopic compared to other drugs.
I would have to disagree. Some depressed folks are pushed farther into depression with Benzos – so for them it can be bad – there have been many suicides with benzos plus alcohol. I would like to see suicide statistics of SSRIs vs Benzos. I bet SSRI would have fewer.
>Even lists of all the suicides of people on an ssri. I don't buy it. If your friend died from choking on a hot dog it sounds like he died from choking on a hot dog....he didn't choke on giant xanax pill did he?
I don’t think he was a typical benzo user – he didn’ t have it together enough to manage his own meds – really should have been in a halfway house and given benzos when he was in mania – he took a LOT of benzos – more than anyone else I have known.
>It is so easy to blame the drug....Or maybe he should have taken smaller bites when he ate. My pdoc even said xanax was long tested and one of the safest drugs for me to be on. Should everyone quit Effexor and Wellbutrin because of the lady in Texas killing her kids....She was on Effexor and Wellbutrin and I believe an antipyschotic as well. I don't think so.
Some one taking an antipyschotic is in a whole differnt world that folks with anxiety and depression - they have breaks with reality - don't know what is real or in their head. Effexor is not listed for use for Schizophrenia or Mania.
I would be much more worried about the memory and learning effects of benzos than the choking risk. My point remains, that there are SOME people who have big time trouble with benzos. Most people use them very well, and IMHO benzos are under prescribed.
paulk
Posted by grapebubblegum on June 26, 2001, at 21:10:53
In reply to Re: benzos, posted by gilbert on June 26, 2001, at 20:26:17
And Gilbert knows that I just have to jump in when he posts. You said: "They always use the least dose possible and usually throw away half their damn pills."
True, how true... I just cleaned out my cabinets and found a forgotten old dusty bottle of klonopin, and there were about 25 of the 30 originally prescribed pills still in there, prescribed and filled sometime in '99.
Posted by grapebubblegum on June 26, 2001, at 21:24:10
In reply to Re: diet pills » paulk, posted by Elizabeth on June 26, 2001, at 1:54:50
Elizabeth, I think you missed my question or I missed your answer so I'll reprint it: "Elizabeth: I missed it if you stated this before, but are you a physician or some sort of professional other than a plain old layperson like myself? I'm just curious since you seem to know your shizzit."
Also to whoever mentioned this: What is the cold wet sheetpack treatment and how does it work, if it does? Could someone explain how it supposedly works, scientifically?
Posted by gilbert on June 27, 2001, at 10:27:00
In reply to Re: benzos » gilbert, posted by paulk on June 26, 2001, at 21:08:06
I would agree people that have a diagnosis of depression would not probably do well on benzo monotherapy....however for all of us panic and anxiety patients and for me personally I feel my depression is a direct result of the inability to do things because of fear...I >E > agoraphobia. In this case if I am able to function on xanax my depressive episodes lift because I can now be functional. I aslo think that benzos are not without some drawbacks as are all drugs. I would rather over sleep a little or be midly depressed once in a while than have no sex life or be unable to sleep at all. Like I said in my last post I have felt my mood was more altered by antidepressants than xanax. I felt completey stoned on luvox. I was quick to temper and detached on the other ssris's. I did have sexual dysfunction on all of them including effexor which took my blood pressure up. So I feel I am using the least of all evils so to speak. I am sorry I am so defensive but it just always seems that the benzos get no credit and it get kicked around a little more than other drug classes. I have to defend what has given me my life back.
P >S > benzo suicides are almost always in combination with other drugs be it alcohol or whatever. I have a feeling that if those same people had a bottle of inderol they would have swallowed it down with some vodka. Also being alcoholic myself I know very rarely do people kill themselves without a chemical primer. The prevalence of benzo scripts versus beta blockers or some other downer would indicate it was simply the tool available to end their life not necessarily the tool that caused them to end their lives.
Gil
Posted by Elizabeth on June 27, 2001, at 10:31:20
In reply to Re: benzos, posted by paulk on June 26, 2001, at 16:18:19
> >“They do have other effects in addition to MAO inhibition, though: Nardil is also an inhibitor of GABA metabolism, while Parnate is *thought* to have some sort of dopaminergic effect (perhaps induction of dopamine release: Parnate is chemically extremely similar to amphetamine).
>
> !@# Lawyers – I sure wish that information had been in the PDR. –Lawyers? Quoi?
> The Nardil has just kicked in in the last week or so – I still question that the low BP is caused by other than the increase in the monoamines – from what I understood until 90% of the MAO is knocked out There isn’t enough rise in neuro transmitters to do anything.
No, the increase in neurotransmitter concentrations takes place immediately. That's not directly responsible for the antidepressant effect of the drug, but a lot of the side effects, direct or indirect, happen sooner, orthostatic hypotension being one of these. MAOIs (and tricyclics) decrease the compensatory cardiovascular response to changes in posture.
> I seem to be doing OK except I am starting to have trouble with word selection – and sometimes the wrong word will come out.
That's a common effect of antidepressants, especially tricyclics and MAOIs. Anticholinergic drugs are the worst that way, but norepinephrine has some effects that oppose those of acetylcholine. MAOIs upset the reciprocal interaction between NE and ACh; as a result, they virtually abolish REM sleep. In light of this, their effects on implicit or associative memory are surprisingly subtle.
> I wonder if it is a side effect of the GABA?
In the case of Nardil, that might have something to do with it too. (I had the word-finding problems on Parnate as well, although it wasn't a big deal with any of the MAOIs.)
> Perhaps I should take the med at night?
I tried taking Nardil on every imaginable dosing schedule. Didn't make any difference in any of the side effects.
> I am still at the high dose 60/mg day – perhaps it will get better when they lower the does back down.
I don't think that's such a good idea. First of all, 60 mg is *not* a "high" dose; it's a normal dose. Also, although it was once thought that the right way to give people antidepressants was to start with a high "loading" dose and then decrease it down to a very low "maintenance" dose, this has proven not to work very well. (My own experience with MAOIs bears this out: at one point I tried decreasing the Nardil to 30 mg, and my depression and panic started coming back. I've also tried dropping the Parnate down to 30, 20, and even 10 mg, and it just doesn't work very well when I do that.)
> Was the inhibition of the GABA metabolism a direct effect of the drug or secondary?
I'm still not sure what you mean by that (although I know what *I* would mean < g >). I'm also not sure the mechanism is known. But I believe it's an early effect, not one that takes a week or more to happen.
On to the benzos....
> He was taking – I think it was Restaril – (sp??) . He was very bi-polar yet a dear friend – very smart – didn’t usually go psychotic in his mania. He really needed to be in a halfway house to have someone monitor is medications. The lack of supervision is what I blame for his death. I think the benzos may have surpressed his gag reflex or dis-coordinated his swallowing enough to cause the problem.
It's really horrible to think about this, but the fact is, people with serious mental illness who don't have family to take care of them are at high risk of death for a whole lot of reasons. For example, a person with bipolar disorder, especially one who has trouble functioning to the point where he needs to live in a halfway house, is pretty much guaranteed to be on a lot of medications, possibly including neuroleptics (and perhaps anticholinergics to offset the side effects), lithium, and/or anticonvulsants. All of these have known risks, some of which can be quite serious. Bipolar disorder is associated with a high risk of suicide attempts and substance abuse as well.
Restoril (temazepam) is generally prescribed only for insomnia, not for daytime anxiety. It is unlikely that your friend was prescribed this medication in very large doses.
> I don’t think this would be a common problem with people who can manage there own meds.
Well, it isn't. It also isn't a common problem with benzodiazepines in general. The other medications used to treat bipolar disorder are much more dangerous. A lot of times I hear of people dying from polydrug overdoses, but some particular drug (usually a controlled substance) is singled out as the cause. When someone dies from an overdose of benzos and alcohol, it's not because benzos are dangerous or toxic. If either drug by itself is to blame in such a case, it's the alcohol -- an incredibly toxic drug (several characteristics of ethanol make me want to label it a solvent rather than a drug, and it certainly has no place for systemic use in modern medicine).
> Most of these people were in the hospital because they had benzo problems – sort of self-selected. Remember everyone reacts differently.
Fair enough. But I bet that most of those people abused other drugs, not just benzos. I've known a few people who abused benzos, but without exception they were addicted to alcohol or heroin and abused other drugs (cocaine, amphetamines). Addicts sometimes use benzos to substitute for their DOCs when supply is short, and they can easily become dependent because they tend to self-medicate (i.e., take the benzos in an unsupervised fashion) with very large doses (some people apparently can get high on benzos, but I've never known anybody who could get high on the usual prescribed doses!).
[re withdrawal symptoms:]
> It sure does it to me. – That’s why I’m interested in the slow release version.Well, remember, slow release doesn't mean slow elimination. A lot of people have a hard time getting off of Effexor XR, for example. Xanax SR would be great for people who need to take it every day, though.
> I would take it for anxiety and it worked – wonderfully – but then as it wore off I would feel even worse than before.
I guess I'm confused. What sort of anxiety were you taking it for? (Any diagnosis?)
> I didn’t use Xanex after the prescription ran out because of that problem – I didn’t get addicted – but I sure wanted to keep taking more and more, but realized I shouldn’t.
"Wanting" to take increasing doses of a drug is always a good sign that you're headed for addiction, yes.
> I really liked and hated the drug. Sure wish I could try the XR version.
If you're going to take it for a while and then stop, it's still going to cause withdrawal symptoms. I don't know about this rebound anxiety that you speak of, because I don't think I've ever heard of that before even with regular Xanax.
> I would say that irritability is a symptom of anxiety??
I guess it depends on your definition. I usually think of anxiety as involving inhibition, and irritability as involving disinhibition.
However you want to slice it, the people who have these weird reactions to Xanax (I looked into it, and some of them seemed to involve self-injury in people with a history of cutting, etc.) are people who have problems with emotion regulation. Sometimes that looks a lot like anxiety (presumably that's how they got prescribed Xanax in the first place).
> The irritability wasn't there until the drug was wearing off. You might be forgetting the wide variation of how these drugs effect people. (YMMV grin).
I'm not forgetting. I've known dozens of people who took benzos, mostly Xanax and Klonopin. None of them ever had this problem. Some people experience irritability or peevishness during benzo withdrawal, but that's after discontinuing chronic use.
Did this "rebound anxiety" happen the very first time you took Xanax? And how often were you taking it? (Frequent use, even if it's not around-the-clock, can lead to some degree of dependence.)
> I know the nasty discontinuation effects of Effexor – yet for many folks they can stop cold with out any problem.
Yeah, I didn't have a problem stopping it, but I'd only been on it for a month or so. (Plus, I had to stop because of a rather nasty reaction, so even if I had withdrawal symptoms I might not have noticed them!)
> CWSP = Cold Wet Sheet Packs – THE non-drug treatment for anxiety. (I wouldn’t want it done to me – its not fun to watch – but it seems to work a bit.
Remind me never to submit to "inpatient detox." < g >
> I’m thinking that there needs to be a new specialty in medicine – an endroconologist/pycopharmacologist. It sure would be nice if there were better and objective tests that could show what drugs to try first. – perhaps spinal fluid tests or long term urine collection for cortisal tests?
Oh, that would be great, but reliable tests of the type you're talking about (even those involving lumbar puncture, which, BTW, is not a practical test to do routinely) just don't exist, with few exceptions (the dexamethasone suppression test can be used to determine which depressed patients are potential candidates for steroid-suppression therapy; urinary levels of the norepinephrine metabolite MHPG are pretty consistently elevated in depressed patients who respond to alprazolam).
> Reminds me – I ran into yet another old friend who tried Effexor – told me he went sort of manic (couldn’t sleep – roofed a house all night long in the dark) – his doc now thinks he may be a bit bipolar.
Not conclusively by any means. Unipolar depressives -- no family history of bipolar disorder, no personal history of mania or hypomania, and no subsequent spontaneous manias or hypomanias -- can sometimes have this kind of reaction to antidepressants. It's idiosyncratic, but not unheard of. Some people are sensitive to a particular AD or class of ADs, and some ADs have a greater tendency than others to trigger mania. (Tricyclics have a particularly bad reputation for this, and my pdoc says he thinks Effexor is a bit worse than the other new-generation ADs.)
-elizabeth
Posted by Elizabeth on June 27, 2001, at 10:44:30
In reply to Re: benzos, posted by gilbert on June 26, 2001, at 20:26:17
> Study after study shows that panic patients don't abuse benzos. They always use the least dose possible and usually throw away half their damn pills.
Yeah. People with panic disorder tend to be really afraid of meds and really sensitive to side effects. They're *not* prone to overusing them.
But don't go jumping on MAOIs. They're good broad-spectrum antidepressants, and they're very safe if you use them properly (rather like benzos, no?). (Plus, it's a great opportunity to learn about different types of cheese!)
> It is so easy to blame the drug....
It's especially easy to blame controlled drugs, even though they're controlled because of "abuse potential," not because of toxicity. (I mean,
antineoplastics -- the most toxic drugs used in modern medicine -- are not controlled substances, because nobody would ever take them unless they had to.)> Should everyone quit Effexor and Wellbutrin because of the lady in Texas killing her kids....She was on Effexor and Wellbutrin and I believe an antipyschotic as well. I don't think so.
Yeah, lately it's become fashionable to blame SSRIs and other modern ADs for all kinds of crazy incidents. Occasionally, ADs do cause mania or agitation. People need to know about the possibility so they can get treatment if there's any sign of such a reaction. It's not like these things happen all of a sudden with no warning whatsoeer. I had an undeniable case of serotonin syndrome, complete with delirium and vomiting, while I was taking Effexor, but it wasn't like I just woke up in the morning completely psychotic. As soon as I started feeling sick, I recognised the symptoms and got myself to a hospital, and by the next day I was feeling a little bit spacey but otherwise fine. (Plus, I certainly wasn't with-it enough to hurt anybody seriously, even if I'd been inclined to.)
-elizabeth
Posted by Elizabeth on June 27, 2001, at 11:31:23
In reply to Re: benzos » gilbert, posted by paulk on June 26, 2001, at 21:08:06
> >Study after study shows that panic patients don't abuse benzos
>
> I agree – but I have also see the few who get into trouble.The question I'd ask is, were these patients diagnosed with panic disorder?
> I agree again – The biggest problem with Benzos is that they can interfere with learning and memory – I remember a pre med student who took 1mg/day of valium for a semester – had poor final scores and tells me he can’t remember much of that semester.
People who have that sort of problem tend to notice it pretty quickly. (Although I have to say, I've encountered a lot of pre-meds who weren't on any Valium and whose grades probably would have been better if they had been. < g >)
> Benzos can kill sex for some people. Again YMMV.
CNS depressants seem to have opposing effects on men's and women's sexuality (at least, alcohol and barbiturates do).
A common side effect of benzos, which most people don't seem to know about, is that they can make you really hungry. On several occasions, I've found myself getting really hungry after coming down from a panic attack with the aid of Xanax or Ativan. And once, when I was really depressed and wouldn't eat or drink anything, a concerned friend convinced me to take a Xanax. Within 30 minutes I was not only up and about, but fixing myself some pasta. *That* was impressive.
> I don’t think MOAIs are for most folks – but they have been reported to work very well for people with atypical depressionThey work for a wide variety of types of depression, not just atypical (although they haven't been tested adequately in melancholic depression, the existing data are positive). I definitely don't have atypical depression, but of all the standard antidepressants that I've tried, the MAOIs have come the closest to fixing whatever's wrong with me. Most people with melancholia take tricyclics, Effexor, or Remeron, etc. I couldn't tolerate tricyclics or Effexor, and Remeron didn't seem to work.
> I agree to a point – Benzos had a bad rap even when the patent was in place.
Like SSRIs and Ritalin, they were vastly overused. That probably accounts for a lot of it.
> I would have to disagree. Some depressed folks are pushed farther into depression with Benzos
Yes. Xanax seems to be superior in this regard (it even acts as an antidepressant for some).
> there have been many suicides with benzos plus alcohol.
Yeah, but blaming the benzos for that is kind of silly. There've been many suicides with any-drug-you-name-it plus alcohol. There've also been plenty of accidental deaths from alcohol poisoning, no other drugs required. Alcohol is just plain toxic.
> I would like to see suicide statistics of SSRIs vs Benzos. I bet SSRI would have fewer.
Let's leave out polydrug overdoses; those can get really complicated. The number of suicides committed with SSRIs alone is incredibly low. But so is the number with benzos alone. In order to get enough benzos to commit suicide, you would have to acquire a huge amount, by hoarding them, getting them on the black market, going to multiple doctors, etc. -- even an entire month's supply for someone taking them regularly would be very unlikely to kill a normal healthy adult.
Also, let's not forget that benzos have been around for more close to 50 years, while SSRIs have been around for about 15 years. (I'm not sure exactly when fluvoxamine, the first marketed SSRI, first became available, but it was only after Eli Lilly's impressive marketing of Prozac in the USA that the use of SSRIs became widespread.)
> I don’t think he was a typical benzo user – he didn’ t have it together enough to manage his own meds – really should have been in a halfway house and given benzos when he was in mania – he took a LOT of benzos – more than anyone else I have known.
How many? You said he was on Restoril -- that's a sleeping pill. Was a cause of death ever determined? Was there a quantitative toxicology screen? If not, it's hardly reasonable to attribute his death to any one thing. Like I said, people in that situation -- severely mentally ill, nobody to support them, probably don't have access to the best medical care, etc. -- are endangered in all sorts of ways.
> Some one taking an antipyschotic is in a whole differnt world that folks with anxiety and depression - they have breaks with reality - don't know what is real or in their head. Effexor is not listed for use for Schizophrenia or Mania.
Lots of people with bipolar disorder can't get by on mood stabilisers alone; they need to take an antidepressant too. There's also something called schizoaffective disorder -- schizophrenia plus major depression or bipolar disorder. Psychotic depression needs to be treated either with a combination of antidepressants and antipsychotics or with ECT. Many people with schizophrenia suffer from major depressive episodes following psychotic episodes ("crashes," you could say; the research diagnostic criteria set is labelled "postpsychotic depressive disorder of schizophrenia"), and they need to be treated with antidepressants. Some people with OCD and certain types of severe nonpsychotic depression need antipsychotics in addition to antidepressants. People with borderline personality disorder or complex posttraumatic stress disorder often need a combination of several different types of drugs (which may include antipsyhotics) in addition to intensive psychotherapy.
Mental illness is not an either-or thing, not by any means.
> I would be much more worried about the memory and learning effects of benzos than the choking risk.
I think that the high-potency benzos cause less cognitive impairment than the low-potency ones --although Halcion, the most potent benzo of all the marketed ones, is known to cause memory lapses -- which is why it's only used as a sleeping pill; while Librium, a very low-potency benzo, doesn't seem to cause much impairment at all.
Also, a lot of people *don't* suffer these side effects at all, especially those who are able to get by on low doses. Even when I was taking Klonopin (4 mg) every day, I didn't have a problem with memory or learning (and as a science student, I'd certainly notice any such impairment). I think I mentioned that I know someone who used to abuse Xanax and was at one point taking over 100 mg/day. Guess what? He's a scientist too (we went to school together), and he was actually functioning surprisingly well on that amount of Xanax. (Today he's stable on I think somewhere around 10 mg/day -- for depression as well as panic disorder -- and is completely functional, much more so than he was without medication. He's also stopped self-medicating altogether.)
> My point remains, that there are SOME people who have big time trouble with benzos. Most people use them very well, and IMHO benzos are under prescribed.
Most people use them properly *and* don't have significant side effects. Most people who have panic disorder would choose benzos over antidepressants any day. In fact, I bet that a lot of people with depression would prefer to take high doses of Xanax or Deracyn than have to deal with all the side effects of antidepressants.
-elizabeth
Posted by Elizabeth on June 27, 2001, at 11:36:41
In reply to pssst: Elizabeth! and sheetpacks, posted by grapebubblegum on June 26, 2001, at 21:24:10
> Elizabeth, I think you missed my question or I missed your answer so I'll reprint it: "Elizabeth: I missed it if you stated this before, but are you a physician or some sort of professional other than a plain old layperson like myself? I'm just curious since you seem to know your shizzit."
I didn't miss the question, but I did avoid it. I'm a student; I'd rather not go into any more detail than that. (Bad past experiences with internet harrassment and namecalling, you know.)
But thank you for the kind words. It's nice to be appreciated.
> Also to whoever mentioned this: What is the cold wet sheetpack treatment and how does it work, if it does? Could someone explain how it supposedly works, scientifically?
I think it's a form of torture inflicted on all those evil drug addicts by their "treaters." :-)
(I've known a fair number of drug addicts in my time, and although there were a few bad apples among them, by and large they were decent, caring, sensitive people -- perhaps too sensitive for this world.)
-elizabeth
Posted by grapebubblegum on June 27, 2001, at 15:15:49
In reply to Re: benzos » paulk, posted by Elizabeth on June 27, 2001, at 11:31:23
Sorry, Elizabeth, but I knew nothing of harrassment and name calling or I would not have asked my question twice.
As for sheet packs, I am still intrigued: does anyone else know how this practice started and what its supposed mechanism is? I am simply curious.
Also, Elizabeth, you said "A common side effect of benzos, which most people don't seem to know about, is that they can make you really hungry. On several occasions, I've found myself getting really hungry after coming down from a panic attack with the aid of Xanax or Ativan. And once, when I was really depressed and wouldn't eat or drink anything, a concerned friend convinced me to take a Xanax. Within 30 minutes I was not only up and about, but fixing myself some pasta. *That* was impressive."
I won't argue because I've had similar experiences, plus I noticed that when heading off a panic attack that was really brewing up into a doozy, the klonopin, once it started working, liberated TEARS and rendered me verbose, which led me to believe that perhaps some pent-up anxiety or stress of some sort was behind the panic attack and the klonopin had somehow un-blocked a dam. Sounds like a "duh," perhaps, but this was major Sherlock Holmes stuff to me, being a person who is, overall, pretty aware of her feelings but I suppose not aware at every point in time which feelings are being suppressed and what they are doing under the surface.
About the eating, though: I was wondering about this just recently. Everyone has heard me brag that since I started on a very low-dose regimen of klonopin, I have lost weight with minimal effort, which makes me question how strong an appetite-stimulant effect benzos have, if any. My theory is that perhaps there APPEARS to be an appetite increase when in reality, the benzos lower the anxiety which had previously made you feel too anxious, sick or depressed to eat, thus liberating a healthy appetite. I also remember suffering for months walking a panic-attack tightrope daily until I finally gave in to my doctor's suggestion and took .25 mg klonopin and suddenly I was able to eat a big plate of food and it was the nicest feeling to have an appetite again instead of feeling sick at the sight of food.
So, if you don't mind my expanding this idea of tears and appetite into one more branch...
I wonder also if benzos actually CAUSE depression or if they only APPEAR to. Remember, I'm just a lil' ole layperson so I'm not challenging anyone's proven medical facts but I'm just putting up for examination the possibility that it could be more complicated than that. i.e., in a person who tends to suffer from anxiety at times of greatest weakness (panic attacks being a concentrated form of anxiety or depression for purposes of this theory) I wonder if constant low or medium-level anxiety masks underlying depression and when the anxiety is alleviated, as it can be with benzos, the depression that seems to emerge with benzo use may have been there all along as a substrata of the anxiety. Just a theory for anyone who wants to ponder it. I'm not even sure if I agree with my own theory: it's just in the "hmmm...?" stage for me.
Posted by Elizabeth on June 27, 2001, at 23:47:47
In reply to Paulk, posted by gilbert on June 27, 2001, at 10:27:00
> I would agree people that have a diagnosis of depression would not probably do well on benzo monotherapy....
You'd be surprised. Some have no luck with standard ADs and find relief with Xanax. And Deracyn (adinazolam) is actually labelled as an antidepressant in some countries. (It's not available in the US.)
> I aslo think that benzos are not without some drawbacks as are all drugs.
I'm suspicious of any drug that has no side effects. It usually turns out they have no effects at all! (I'm thinking of things like Tylenol, the nondrowsy antihistamines, etc.)
> I am sorry I am so defensive
People who need benzos constantly feel put on the defensive, and understandably so, too. You're not alone -- not at all.
-elizabeth
Posted by Elizabeth on June 27, 2001, at 23:55:29
In reply to benzos and appetite, posted by grapebubblegum on June 27, 2001, at 15:15:49
> Sorry, Elizabeth, but I knew nothing of harrassment and name calling or I would not have asked my question twice.
Oh no, it's just that I don't like to reveal personal information, like my geographic location or what I do, on the net. No offense taken.
> I won't argue because I've had similar experiences, plus I noticed that when heading off a panic attack that was really brewing up into a doozy, the klonopin, once it started working, liberated TEARS and rendered me verbose, which led me to believe that perhaps some pent-up anxiety or stress of some sort was behind the panic attack and the klonopin had somehow un-blocked a dam.
Well, like I said: people with panic-anxiety are inhibited and fearful. Benzos liberate them from their inhibition.
> About the eating, though: I was wondering about this just recently. Everyone has heard me brag that since I started on a very low-dose regimen of klonopin, I have lost weight with minimal effort, which makes me question how strong an appetite-stimulant effect benzos have, if any.
YMMV. But I've known a lot of people who get the munchies on them. Especially inhibited, depressed, social-phobic/isolating types. I think your theory about the mechanism of benzo-induced appetite increase is probably right. I don't binge on junk food when I get hungry on benzos: I just eat a good healthy normal meal.
> I wonder also if benzos actually CAUSE depression or if they only APPEAR to.
For starters, some people can confuse depression with sedation. They think that because they feel tired when they take Klonopin or Valium or whatever, they must be getting more depressed.
> I wonder if constant low or medium-level anxiety masks underlying depression and when the anxiety is alleviated, as it can be with benzos, the depression that seems to emerge with benzo use may have been there all along as a substrata of the anxiety.
Anxiety and depression frequently go hand in hand. It's often hard to say which, if either, is primary. Your idea is intriguing. I have no idea how we'd go about testing it, though!
> Just a theory for anyone who wants to ponder it. I'm not even sure if I agree with my own theory: it's just in the "hmmm...?" stage for me.
All theories start as hypotheses, and all hypotheses start as speculation. :-)
-elizabeth
Posted by gilbert on June 28, 2001, at 0:28:49
In reply to Re: benzos and appetite » grapebubblegum, posted by Elizabeth on June 27, 2001, at 23:55:29
Thanks Elizabeth for putting into word my thoughts and feelings about benzos and backing it up with good sound data. I always seem to get caught up in the emotional defense of these drugs...you fill in the blanks more inteligently than I can.......I missed you last week. Me and grapebubblegum had to go it alone.....LOL
Gil
Posted by paulk on June 28, 2001, at 3:33:00
In reply to Re: benzos » paulk, posted by Elizabeth on June 27, 2001, at 11:31:23
>How many? You said he was on Restoril -- that's a sleeping pill.
Yes – He was also on another benzo at the same time – be would take several of the resoril and had very slurred speech, stuble around, and would pass out – unable to be roused.
> Was a cause of death ever determined?
They removed a half a hotdog ->Was there a quantitative toxicology screen? If not, it's hardly reasonable to attribute his death to any one thing.
No screen that I know of – there was some kind of investigation – they found a lot more benzos that someone in his state should have had.
I’m guessing - but he was a extremely biolar – he would get manic and march the streets for days – the police knew him as quite crazy but harmless – and then crash - I was always amazed that he never seemed to break with reality as far as I knew. I used to stop by and get him food sometimes. – He had a trust set up, but still couldn’t keep his apartment clean and stocked with food. He would sometimes be quite filthy – sounds strange, but he was still a dear friend to me – he never would be afraid to tell things straight – frank to a fault – not what many would like, but we shared a love for classical music – he was quite smart – got a commercial license to run radio stations when he was only 13. As time went by his intellect deterrioted – much like a long term drunk (he didn’t drink probably would have killed him with all the benzos on board. )
I'm guessing - he probably needed very large doseages of benzos whren he was manic - and abused them at other times.
>Like I said, people in that situation -- severely mentally ill, nobody to support them, probably don't have access to the best medical care, etc. -- are endangered in all sorts of ways.
He used to be in a state hospital before they turned them all out – He probably would have done a lot better permanently in a half way house with someone metering out his drugs.
Posted by paulk on June 28, 2001, at 5:11:25
In reply to MAOIs, benzos, etc. » paulk, posted by Elizabeth on June 27, 2001, at 10:31:20
> > The Nardil has just kicked in the last week or so – I still question that the low BP is caused by other than the increase in the monoamines – from what I understood until 90% of the MAO is knocked out There isn’t enough rise in neuro transmitters to do anything.>No, the increase in neurotransmitter concentrations takes place immediately.
This is not at all what my doctor told me??? He said that the reason they ramp the drug up to 60mg/day is that it takes some time to knock out enough MAO to effect the monoamines – after that, the MAO level can be kept low by a lower dosage that is only knocking out the amount that the body is replacing.
>That's not directly responsible for the antidepressant effect of the drug, but a lot of the side effects, direct or indirect, happen sooner, orthostatic hypotension being one of these. MAOIs (and tricyclics) decrease the compensatory cardiovascular response to changes in posture.
I’m going to have to check into this – I always want to understand how a drug is working – you have raised some doubts about the model I had in my head (of what the drugs were doing in the same place.< grin >)
> > I seem to be doing OK except I am starting to have trouble with word selection – and sometimes the wrong word will come out.
>That's a common effect of antidepressants, especially tricyclics and MAOIs. Anticholinergic drugs are the worst that way, but norepinephrine has some effects that oppose those of acetylcholine. MAOIs upset the reciprocal interaction between NE and ACh; as a result, they virtually abolish REM sleep. In light of this, their effects on implicit or associative memory are surprisingly subtle.
Hmmm – I have had the same effect on higher dosages of Effexor – 150mg/day
> I wonder if it is a side effect of the GABA?
In the case of Nardil, that might have something to do with it too. (I had the word-finding problems on Parnate as well, although it wasn't a big deal with any of the MAOIs.)> >Perhaps I should take the med at night?
>I tried taking Nardil on every imaginable dosing schedule. Didn't make any difference in any of the side effects.
That’s what my doctor said also.
> > I am still at the high dose 60/mg day – perhaps it will get better when they lower the dosess back down.
>I don't think that's such a good idea. First of all, 60 mg is *not* a "high" dose; it's a normal dose. Also, although it was once thought that the right way to give people antidepressants was to start with a high "loading" dose and then decrease it down to a very low "maintenance" dose, this has proven not to work very well.
I’ve only seen this dosing scheme suggested for Nardil?? If the idea is to bring down the level of MAO and then maintain it there; it makes sense. That is the pills knock out so much MAO enzyme – after which you just need to knock out what the body replaces – thus a lower dose. I’m going to have to dig into this deeper.
> (My own experience with MAOIs bears this out: at one point I tried decreasing the Nardil to 30 mg, and my depression and panic started coming back.
Now, if the drug has a dual MAO plus a GABA effect. I could see that the MAO level could be maintained at a low dose, but to maintain a higher level of GABA might require a higher dose, which would explain return of panic attacks. (That’s a lot of ifs, but I don’t remember seeing that the increase in GABA was due to the missing MAO – so I could imagine that it could have a different dose dependency than the increase in Monoamines.)
> > Was the inhibition of the GABA metabolism a direct effect of the drug or secondary?
>I'm still not sure what you mean by that (although I know what *I* would mean < g >). I'm also not sure the mechanism is known. But I believe it's an early effect, not one that takes a week or more to happen.
OK, a primary effect of a MAOI would be the knocking out of the MAOI – the secondary effect would be a resulting increase of mon-amine transmitters – (Seritonin, Dopamine, Ne) due to the missing MAO.
Another example – a SSRI has a primary effect blocking the reuptake – the secondary effect would be the increase in seritonin level, a terserary effect could be a resulting promotion of new neuron generation, a fourth level effect would be improved memory function. Each of these effects has a different time frame associated with it.
My hunch, which could easily be wrong, but I hope to find the answers, is that the lowBP is not caused by the increase in Monoamines, but is a different effect of the drug. And I wonder if the same is true for the GABA effects of Nardil.
On to the benzos....> > He was taking – I think it was Restaril – (sp??) . He was very bi-polar yet a dear friend – very smart – didn’t usually go psychotic in his mania. He really needed to be in a halfway house to have someone monitor is medications. The lack of supervision is what I blame for his death. I think the benzos may have surpressed his gag reflex or dis-coordinated his swallowing enough to cause the problem.
It was my understanding that he had been using only benzos for the last 5 years.>Restoril (temazepam) is generally prescribed only for insomnia, not for daytime anxiety. It is unlikely that your friend was prescribed this medication in very large doses.
He may have been getting them from 2 or three doctors at once. Probably not the best medicine for a Biopolar – but he seemed to enjoy his manias – might have just wanted to be able to sleep and return to his mania the next day.
> Most of these people were in the hospital because they had benzo problems – sort of self-selected. Remember everyone reacts differently.
> > I would take it for anxiety and it worked – wonderfully – but then as it wore off I would feel even worse than before.
>I guess I'm confused. What sort of anxiety were you taking it for? (Any diagnosis?)
GAD with mixed depression – probably better called atypical depression in my case.
> > I would say that irritability is a symptom of anxiety??
>I guess it depends on your definition. I usually think of anxiety as involving inhibition, and irritability as involving disinhibition.
I define anxiety as fear/worry – some people try to control fear by avoiding the stimulus, others by fighting it (sounds like fight / flight adrenalin). I have done a bit of both – getting irritable /angry has the advantage of giving the illusion of being in control. At times I have had panic attacks –light headed, heart palpitations, shaky hands and voice. – But I can go long times with out those symptoms – and will get quite irritable if I feel I’m getting pushed into a situation that will cause me anxiety.
I wonder if depression is an adaptation to anxiety – hypersomnia, not eating, less active, fatigue, low self estemem would all help a cave man avoid anxiety producing situations.
>Did this "rebound anxiety" happen the very first time you took Xanax? And how often were you taking it? (Frequent use, even if it's not around-the-clock, can lead to some degree of dependence.)First time – half pill in the morning – that evening I had rebound anxiety – and even edgy the next day.
Paulk
Posted by Elizabeth on June 28, 2001, at 21:33:49
In reply to Re: benzos » Elizabeth, posted by paulk on June 28, 2001, at 3:33:00
> Yes – He was also on another benzo at the same time – be would take several of the resoril and had very slurred speech, stuble around, and would pass out – unable to be roused.
People with bipolar disorder are at increased risk for (among other things) drug abuse. Especially when they can't afford to see a good doctor on a regular basis so their medication use will be monitored properly.
> >Was there a quantitative toxicology screen? If not, it's hardly reasonable to attribute his death to any one thing.
>
> No screen that I know of – there was some kind of investigation – they found a lot more benzos that someone in his state should have had.I'd wonder about the details. See, I was found in a coma a few months ago, and the doctors jumped to the conclusion that I had taken a benzo overdose just because I tested positive for benzos and negative for the (few) other drugs they tested for. (I didn't take any sort of drug overdose, BTW, and no cause was ever determined. But I had taken Klonopin the night before...and the paramedics had given me Ativan, too!)
Anyway, I really feel for you about what happened (tragically, it's not a unique story at all), but it's a leap to assume that benzos caused it.
-elizabeth
Posted by Elizabeth on June 29, 2001, at 8:44:13
In reply to Re: MAOIs, benzos, etc. » Elizabeth, posted by paulk on June 28, 2001, at 5:11:25
> >No, the increase in neurotransmitter concentrations takes place immediately.
>
> This is not at all what my doctor told me???"Immediately" is imprecise: what I mean is that it doesn't take a few weeks (or even days) for the increase in monoamine levels to be observable; as with reuptake inhibitors, this effect happens rapdily.
> He said that the reason they ramp the drug up to 60mg/day is that it takes some time to knock out enough MAO to effect the monoamines – after that, the MAO level can be kept low by a lower dosage that is only knocking out the amount that the body is replacing.
This idea hasn't been borne out by practice. Despite the labelling (which hasn't been changed much since the drug's original approval in 1959, BTW), current clinical experience seems to support the continued use of the effective initial dose in maintenance therapy. I don't know of any evidence supporting the idea that a lower maintenance dose is clinically effective. A dose of around 45 mg/day typically results in 80% inhibition of MAO, incidentally. MAO begins to return to normal levels within a few days; the two-week washout period recommended between stopping MAOIs and starting other serotonergic ADs is really very conservative.
> Hmmm – I have had the same effect on higher dosages of Effexor – 150mg/day
That's consistent with the reciprocal interaction model (considering the dose-dependent effects of Effexor on NE reuptake).
> I’ve only seen this dosing scheme suggested for Nardil??
It's actually in the labelling for Nardil. But there are an awful lot of errors in the labelling for Nardil. It's an old drug. They really should just rewrite the product monograph entirely, but who wants to waste the time and money on that when a drug is old, off-patent, not very popular in the first place, etc.?
> If the idea is to bring down the level of MAO and then maintain it there; it makes sense. That is the pills knock out so much MAO enzyme – after which you just need to knock out what the body replaces – thus a lower dose. I’m going to have to dig into this deeper.
For one thing, MAO is regenerated faster than one might expect. When you drop down to 15 or 30 mg, you might not experience an immediate clinical effect (and MAO levels won't increase too much in a single day), but in the long-term, an altered equilibrium will be established where you have a level of MAO inhibition less than what is required keep neurotransmitters from being metabolised sufficiently to maintain the cellular changes thought to be responsible (hand wave, hand wave) for the antidepressant effects of these drugs. (Are you with me here? < g >)
Also, as I noted, although monoamine concentrations increase rapidly in response to MAO inhibition, increased MA concentrations are not directly responsible for the clinical effects of monoaminergic antidepressants.
> Now, if the drug has a dual MAO plus a GABA effect. I could see that the MAO level could be maintained at a low dose, but to maintain a higher level of GABA might require a higher dose, which would explain return of panic attacks.
The increase in GABA levels occurs via a similar mechanism to that responsible for increases in monoamine levels: phenelzine (as well as many other hydrazine-related compounds) inhibits an enzyme that catalyses a major metabolic pathway of GABA. Allowing this enzyme to return
(BTW, in case this is of any relevance, I have primary depression, while the panic may be primary or it may result from the depression and other factors. It's definitely not the case that my depression is the result of panic disorder, because I was depressed long before I ever had a panic attack.)
> (That’s a lot of ifs, but I don’t remember seeing that the increase in GABA was due to the missing MAO – so I could imagine that it could have a different dose dependency than the increase in Monoamines.)
That's right. Non-hydrazine MAOIs, like Parnate and selegiline, don't increase GABA. Phenelzine inhibits GABA transaminase (the enzyme alluded to above -- this mechanism is analogous to MAO inhibition and makes phenelzine a novel anxiolytic).
> My hunch, which could easily be wrong, but I hope to find the answers, is that the lowBP is not caused by the increase in Monoamines, but is a different effect of the drug.
It's caused by NE increase, though not directly.
About your friend...
> It was my understanding that he had been using only benzos for the last 5 years.
That explains why he was doing poorly. A person with severe bipolar disorder needs to be on, at a minimum, a mood stabiliser of some sort. (Often they need a combination of multiple mood stabiliers, antidepresants, antipsychotics, and/or benzos.)
> He may have been getting them from 2 or three doctors at once.
That's a hallmark of drug abuse (although it doesn't prove drug abuse, it's highly suggestive). My guess is that he was trying to self-medicate his moods (to less-than-adequate effect) with benzos. This can be tempting, as they are fast-acting and have few side effects compared to lithium and most anticonvulsants and antidepressants (and certainly compared to all currently used antipsychotics).
> Probably not the best medicine for a Biopolar – but he seemed to enjoy his manias – might have just wanted to be able to sleep and return to his mania the next day.
That's not uncommon. Bipolars are notorious for going off their meds because they miss the manias and don't feel "productive" in a normal mood. It would be nice if mild hypomania were sustainable, but for most people it isn't.
> >I guess I'm confused. What sort of anxiety were you taking it for? (Any diagnosis?)
>
> GAD with mixed depression – probably better called atypical depression in my case.GAD covers a lot of territory. Can you be specific?
> I define anxiety as fear/worry – some people try to control fear by avoiding the stimulus, others by fighting it (sounds like fight / flight adrenalin). I have done a bit of both – getting irritable /angry has the advantage of giving the illusion of being in control.
Perhaps anxious people who have a "control freak" < g > response or personality type are likelier than others to have weird reactions when the anxiety is relieved?
> At times I have had panic attacks –light headed, heart palpitations, shaky hands and voice.
That's common in depression, especially atypical, anxious, or mood-reactive depression.
> But I can go long times with out those symptoms – and will get quite irritable if I feel I’m getting pushed into a situation that will cause me anxiety.
That's, I suspect, a temperamental thing -- an individual trait -- perhaps related to the atypical depression. It's not the anxiety itself, but how you react to it. Atypical depressives are said to be "mood-reactive" in that they can sometimes be cheered up; they also tend to be unusually sensitive or emotionally reactive as a trait, even when not depressed.
> I wonder if depression is an adaptation to anxiety – hypersomnia, not eating, less active, fatigue, low self estemem would all help a cave man avoid anxiety producing situations.
I think that hypersomnia and lethergy in atypical depression could be avoidance responses, yes. (Atypical depression is most commonly associated (by definition, but also by statistical study of symptom clusters that tend to occur together) with overeating, not undereating.)
> First time – half pill in the morning – that evening I had rebound anxiety – and even edgy the next day.
Wow. You seem to be very sensitive to benzos. (Half of what strength pill, BTW?) I think that if a drug has that profound effect on you, it's not too surprising that you will experience a rebound effect. I also would hazard a guess that perhaps this type of rebound puts certain people at increased risk for addiction.
-elizabeth
Posted by paulk on June 29, 2001, at 19:29:43
In reply to Re: MAOIs, benzos, etc. » paulk, posted by Elizabeth on June 29, 2001, at 8:44:13
> > >No, the increase in neurotransmitter concentrations takes place immediately.
> >
> > This is not at all what my doctor told me???
>
> "Immediately" is imprecise: what I mean is that it doesn't take a few weeks (or even days) for the increase in monoamine levels to be observable; as with reuptake inhibitors, this effect happens rapidly.
>I was told it takes about three weeks to knock out enough MAO to raise the level of monoamines. I experienced the loss of accommodation I always notice with an increase in seritonin level at about 3-4 wks. I saw a decrease in BP the first couple of days that seems to correlate with the short half-life of the drug comes on in the first 30min and goes away in 3-4 hours.
> > He said that the reason they ramp the drug up to 60mg/day is that it takes some time to knock out enough MAO to effect the monoamines – after that, the MAO level can be kept low by a lower dosage that is only knocking out the amount that the body is replacing.
>
> This idea hasn't been borne out by practice. Despite the labeling (which hasn't been changed much since the drug's original approval in 1959, BTW), current clinical experience seems to support the continued use of the effective initial dose in maintenance therapy.Sort of what my doctor just told me yesterday – the drug is so cheap – and there doesn’t seem to be a problem with knocking out too much of the MAO so why not just keep the dose up for an incremental improvement.
>I don't know of any evidence supporting the idea that a lower maintenance dose is clinically effective. A dose of around 45 mg/day typically results in 80% inhibition of MAO, incidentally.
That’s not enough from what I understand.
>MAO begins to return to normal levels within a few days;
Yes, but getting down to 90% can take much longer – 80% probably is not enough to do any good.
Think of a flooded basement up to the first floor with water still coming in through the walls – you turn on a small pump that has to pump out the basement AND any water that is still coming in.
After three weeks you get 90% of the water out - now the water comes in a bit quicker so you approch an equilibrium. If you turn off the pump it takes very little time for the water to go back up to 80%.
The monoamines only start to increase after the MAOs are down to about 90% This explains the slow onset of the drug – especially when you realize that the monoamines need to be higher for another 3 – 6 weeks for the drug to reach maximum effectiveness.
>the two-week washout period recommended between stopping MAOIs and starting other serotonergic ADs is really very conservative.I sort of though so – I asked about that and my doc said it had more to do with lawyers – in theory you should be able to switch between MAOIs without waiting – probably the attitude is that it would cost a lot to study – so they go ultra conservative and reduce risk of a lawsuit and reserve an extra excuse.
> It's actually in the labelling for Nardil. But there are an awful lot of errors in the labeling for Nardil. It's an old drug. They really should just rewrite the product monograph entirely, but who wants to waste the time and money on that when a drug is old, off-patent, not very popular in the first place, etc.?
Not to mention the liability costs of doing so. If it weren’t for all the lawsuits, I bet it would have been rewritten already.
> Also, as I noted, although monoamine concentrations increase rapidly in response to MAO inhibition, increased MA concentrations are not directly responsible for the clinical effects of monoaminergic antidepressants.I would have to see numbers on this – the body is replaces MAO constantly – but sort of slowly – to reach a steady state of 90% is supposed to take weeks. The tertiary effect of the increase in neuro-transmitters is immediate AND long term – I respond in a better mood quite rapidly to SSRIs. There is evidence that while the Seritonin levels are higher, new neurons are formed (I think it was near the hippocampus) and over the course of weeks to many months cause long-term changes one could think of as healing. For atypicals like myself – there is probably some genetic or endocrine system defect that makes effective treatment it a lifelong deal.
> The increase in GABA levels occurs via a similar mechanism to that responsible for increases in monoamine levels: phenelzine (as well as many other hydrazine-related compounds) inhibits an enzyme that catalyses a major metabolic pathway of GABA. Allowing this enzyme to returnI have looked for this GABA effect written somewhere – where did you see it? (not in the PDR of course)
>
> (BTW, in case this is of any relevance, I have primary depression, while the panic may be primary or it may result from the depression and other factors. It's definitely not the case that my depression is the result of panic disorder, because I was depressed long before I ever had a panic attack.)Atypical depression?
>
> > (That’s a lot of ifs, but I don’t remember seeing that the increase in GABA was due to the missing MAO – so I could imagine that it could have a different dose dependency than the increase in Monoamines.)
>
> That's right. Non-hydrazine MAOIs, like Parnate and selegiline, don't increase GABA. Phenelzine inhibits GABA transaminase (the enzyme alluded to above -- this mechanism is analogous to MAO inhibition and makes phenelzine a novel anxiolytic).I’m confused – if we inhibit GABA transaminase – wouldn’t there be an increse in GABA?
>
> > My hunch, which could easily be wrong, but I hope to find the answers, is that the lowBP is not caused by the increase in Monoamines, but is a different effect of the drug.
>
> It's caused by NE increase, though not directly.I’m Confused again – I would think that an increase in NE would cause an increase in BP – as happens with Effexor????
>
> About your friend...
>
> > It was my understanding that he had been using only benzos for the last 5 years.
>
> That explains why he was doing poorly. A person with severe bipolar disorder needs to be on, at a minimum, a mood stabiliser of some sort. (Often they need a combination of multiple mood stabiliers, antidepresants, antipsychotics, and/or benzos.)Yes – but he loved his manic state – couldn’t work or anything, but seemed not to get psychotic or nasty at the top – just outrageous and uninhibited -
> thing -- an individual trait -- perhaps related to the atypical depression. It's not the anxiety itself, but how you react to it. Atypical depressives are said to be "mood-reactive" in that they can sometimes be cheered up; they also tend to be unusually sensitive or emotionally reactive as a trait, even when not depressed.
Yep – that’s me. Even the very small dose of Clonazepam sure helps dampen the reactivity – just enough to keep me from moving from appropriately angry to feeling threatened and escalating the conflict. My wife had to adjust to it – she used to depend on me blowing up and eventually feeling guilty. She would even light the fuse to move the blame on to me. Now that doesn’t work anymore.
-Paulk
Posted by Zo on June 29, 2001, at 19:58:07
In reply to MAOIs, benzos, etc. » paulk, posted by Elizabeth on June 27, 2001, at 10:31:20
Just thought I'd add, I had a spell of high hypomania for two weeks after stopping Effexor abruptly a few years back. .when I was still doing dumb things with my meds. . and thought that meant that I was per se Bipolar II. This has not proved to be the case; my understanding is that coming off any number of ADs abruptly can indude mania. . .and that this is something most people aren't aware of. True?
Zo
Posted by paulk on June 29, 2001, at 22:53:07
In reply to Re: Effexor Mania - Eliz Paul , posted by Zo on June 29, 2001, at 19:58:07
I've only heard of it setting off mania on starting a SSRI.
Posted by Zo on June 29, 2001, at 23:21:47
In reply to Re: Effexor Mania - Eliz Paul » Zo, posted by paulk on June 29, 2001, at 22:53:07
> I've only heard of it setting off mania on starting a SSRI.
I think on the PI sheets of most ADs, there in the fine print, you'll see the word manic tucked away. Elizabeth would know better than I. .
Posted by Elizabeth on June 30, 2001, at 1:29:53
In reply to Re: MAOIs, benzos, etc. » Elizabeth, posted by paulk on June 29, 2001, at 19:29:43
> I was told it takes about three weeks to knock out enough MAO to raise the level of monoamines.
Huh. This must be the same as the spiel pdocs give their overly-curious SSRI patients about how the reason it takes the drugs so long is because you have to "build up therapeutic levels in your blood." (In fact, transporter blockade -- and resulting increases in extracellular serotonin -- occurs within hours of the first dose. This is why a single dose causes side effects but no therapeutic effect. < sigh > :-) )
> Sort of what my doctor just told me yesterday – the drug is so cheap – and there doesn’t seem to be a problem with knocking out too much of the MAO so why not just keep the dose up for an incremental improvement.
Yeah. You're not going to be able to maintain adequate MAO inhibition if you drop down to an ineffective dose.
> >I don't know of any evidence supporting the idea that a lower maintenance dose is clinically effective. A dose of around 45 mg/day typically results in 80% inhibition of MAO, incidentally.
>
> That’s not enough from what I understand.80% is a standard number that's tossed around a lot, although the truth is probably that the therapeutic level is not exactly the same for every individual. (45 mg isn't usually a high enough dose, anyway.)
> >MAO begins to return to normal levels within a few days;
>
> Yes, but getting down to 90% can take much longer – 80% probably is not enough to do any good.The point (whether or not it's 80 or 90%; estimates vary) is, when you have 80% (or 90%) inhibition, and then you cut the dose of the inhibitor by 75%, the MAO is going to start returning. You're not going to be able to maintain that level of enzyme inhibition on the reduced dose.
> Think of a flooded basement up to the first floor with water still coming in through the walls – you turn on a small pump that has to pump out the basement AND any water that is still coming in.
No thanks. I hate metaphors and analogies. :-) (Seriously, there's a reason I don't like argument by analogy -- the analogy could have a major flaw.)
> The monoamines only start to increase after the MAOs are down to about 90%. This explains the slow onset of the drug – especially when you realize that the monoamines need to be higher for another 3 – 6 weeks for the drug to reach maximum effectiveness.
MAOIs, work faster than other ADs, if anything. It doesn't take weeks for neurotransmitter levels to increase; that happens early, as with the reuptake inhibitors. MAO is the major pathway for removal of extraneous extracellular monoamines; other enzymes like the methyltransferases are relatively minor, and even the monoamine transporter pumps do not play as great a role as MAO. There may be some time delay in percent inhibition, but it isn't going to play a major role in the onset of action, which is due to the effects of chronic increase in neurotransmitter levels.
> I sort of though so – I asked about that and my doc said it had more to do with lawyers – in theory you should be able to switch between MAOIs without waiting
In theory. There have actually been cases which resembled what is now known as serotonin syndrome. Interestingly (perhaps), they all seemed to occur when the switch was between tranylcypromine and phenelzine or isocarboxazid (i.e., a non-hydrazine and a hydrazine).
> – probably the attitude is that it would cost a lot to study – so they go ultra conservative and reduce risk of a lawsuit and reserve an extra excuse.
Precisely! < g >
> Not to mention the liability costs of doing so. If it weren’t for all the lawsuits, I bet it would have been rewritten already.
I wonder if we can sue them for not rewriting it? < chuckle >
> I would have to see numbers on this – the body is replaces MAO constantly – but sort of slowly – to reach a steady state of 90% is supposed to take weeks.
It's rather complicated, but the long and short of it is that antidepressant effects don't result (directly) from increased NT levels, but from long-term (several weeks) effects of increased NT levels. (At least, that's the current understanding. < g >)
> The tertiary effect of the increase in neuro-transmitters is immediate AND long term – I respond in a better mood quite rapidly to SSRIs.
That's not the usual time course of recovery on any drug currently labelled for depression.
> I have looked for this GABA effect written somewhere – where did you see it? (not in the PDR of course)
Textbooks, articles...I don't know where I first read of it. Try Medline?
> > (BTW, in case this is of any relevance, I have primary depression, while the panic may be primary or it may result from the depression and other factors. It's definitely not the case that my depression is the result of panic disorder, because I was depressed long before I ever had a panic attack.)
>
> Atypical depression?No. "Major depressive disorder with melancholic features" and "panic disorder without agoraphobia." (IOW, tricyclics would be indicated if I could tolerate the bloody things. < g >) I should add that the depression was early-onset (around age 10, unusual for melancholia) and that I have a mixed family history of typical and atypical depressions (the latter also sometimes being associated with panic disorder, alcoholism, and/or migraine). This makes everything terribly complicated, and it's one of the reasons I think I will end up needing a combination of medications (perhaps MAOI + TCA).
> I’m confused – if we inhibit GABA transaminase – wouldn’t there be an increse in GABA?
Exactly! And that's what Nardil does. (I'm not sure about Marplan, though.)
> I’m Confused again – I would think that an increase in NE would cause an increase in BP – as happens with Effexor????
You'd think that, wouldn't you? NE has different effects at different receptor subtypes. For example, the antihypertensive drug clonidine is an alpha2-adrenergic autoreceptor agonist (Remeron is an alpha2 antagonist). I'm not sure what the details are in the case of MAOIs; it's not that they decrease blood pressure, but rather, they decrease the autonomic response to change in posture, resulting in lowered blood pressure upon rising.
Explanations for the side effects of these drugs are often as woefully lacking as the explanations for their therapeutic effects.
> Yes – but he loved his manic state – couldn’t work or anything, but seemed not to get psychotic or nasty at the top – just outrageous and uninhibited -
That's bad enough, believe me.
> Yep – that’s me. Even the very small dose of Clonazepam sure helps dampen the reactivity – just enough to keep me from moving from appropriately angry to feeling threatened and escalating the conflict.
I've encountered this kind of mood-reactivity associated with atypical depression before. It interests me a great deal. I'm just glad to hear you've found relief.
-elizabeth
Posted by Elizabeth on June 30, 2001, at 1:32:23
In reply to Re: Effexor Mania - Eliz Paul , posted by Zo on June 29, 2001, at 19:58:07
> my understanding is that coming off any number of ADs abruptly can indude mania. . .and that this is something most people aren't aware of. True?
True. Weird, but true.
I had an episode of serotonin syndrome which occurred after I had increased the dose of Effexor XR from 150 to 225 mg, then decreased it to 187.5 (due to jitters). One of the main features of the syndrome was mixed mania.
-elizabeth
Posted by TPirog on May 8, 2008, at 18:05:59
In reply to Re: ANTI-BENZO DOCTORS: ANYONE ELSE HAVE ONE?? » royce, posted by Elizabeth on June 10, 2001, at 10:23:11
Just thought you might be interested in a list of Benzo Wise Doctors and therapists that might be helpful at http://www.benzodocs.com
Thanks
Tony
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