Psycho-Babble Medication Thread 613775

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Re: oh » linkadge

Posted by Chairman_MAO on March 7, 2006, at 11:58:32

In reply to Re: oh » Chairman_MAO, posted by linkadge on March 7, 2006, at 11:36:28

I am not talking about depression; I am talking about the assertion that rats--and humans--will undoubtedly self-administer crack cocaine until death.

 

Re: oh » linkadge

Posted by Chairman_MAO on March 7, 2006, at 12:11:42

In reply to Re: oh » Chairman_MAO, posted by linkadge on March 4, 2006, at 9:27:34

Specifically, I am in agreement with the Rat Park investigator, who said:

" The disease model has been "embellished in the news media", to the point, he writes, "where the belief in drug-induced addiction has acquired the status of an obvious truth that requires no further testing." The widespread acceptance of this belief "is a better demonstration of the power of repetition than of the influence of empirical research ..." [9]

See also: http://www.szasz.com/addiction.pdf
and various works by Stanton Peele.

Mental illness CANNOT be a medical illness per se because physiological pathologies of the brain are the domain of neurology. A pathology is nothing except that which is identifiable post-mortem. My suffering of depression is irrelevant to this. The suffering in mental illness is real, and there certainly may be undetected abnormalities on a psychobiological level. However, until what such a problem is can even be defined--which it is has not, otherwise antidepressant monographs would not claim that the mechanism of action is unknown--there is no such thing as mental illness as defined by most psychiatrists and other professionals in the field. If you know of an argument to the contrary (especially in a peer-reviewed publication or other scholarly work) I am always interested in hearing it. Despite what you may think I have a very open mind about this, and have never heard anything that vitiates the Szasz argument.

 

Re: oh

Posted by linkadge on March 7, 2006, at 13:04:26

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 7, 2006, at 11:58:32

"am talking about the assertion that rats--and humans--will undoubtedly self-administer crack cocaine until death."

No arguments.

Linkadge

 

Re: oh

Posted by linkadge on March 7, 2006, at 13:16:40

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 7, 2006, at 12:11:42

I fully agree with you that mental illness is not something that has ever been made concrete in terms of its underlying malfunctioning or lack thereof.

But, simply because we lack the scientific language to fully describe or understand an abnormality does not mean that the abnormality is fabricated or nonexistant.

Dr. Peter Kramer argued two ways. While he made the point clear that the mechanisms of depression have never been fully elucidated, he also argued that this lack of knowledge is not proof, in any way that depression is not, in some cases, an entirely biological condition.

For instance, low thyroid can cause depression, thats biological. Many people on AD's could similarly have some sort of real, yet unidentified, biochemical abnormality. Its not inconcievable.

Sorry, I am a little unclear of what you are getting at, but thats o.k. I'm slow.


Linkadge

 

Re: oh » linkadge

Posted by Chairman_MAO on March 7, 2006, at 14:40:46

In reply to Re: oh, posted by linkadge on March 7, 2006, at 13:16:40

Dr. Kramer is not familiar with basic scientific epistemology, then. One is only allowed to make a positive scientific knowledge-claim regarding causal relations insofar as one is able to reason deductively from empirically validated propositions. Deductive reasoning entails making the claim that the conclusion could not be satisfied without the premeses being true. This is the spirit in which double-blind, placebo controlled studies are held as the most valuable evidence. Without a control group one can only reason inductively at best, and there are no firm rules for inductive reasoning. Dr. Kramer is conflating correlation with causation.
There has not been one cause of end-stage syphilis that does not feature a certain anatomical lesion detectable upon post-mortem examination. Indeed, a pathologist has no greater certainty that an individual's _behavior_ was due to syphilis than the presence of that lesion. The behavior is a symptom, not a cause. In the case of depression, Kramer is begging the question by treating the behavior as a symptom and then pointing to something which is merely a correlate with the symptom as a cause, e.g. low 5-HIAA levels. There are no data that I am aware of which shows that low 5-HIAA levels are anything but a CORRELATE of being depressed. That is, every conscious state has a complex neurobiological substrate; some folks who displayed depressive behavior turn out to have low 5-HIAA levels, some don't. In "real diseases", there is always an underlying set of pathologies without which the disease is not present. It would be absurd to say that someone who has low 5-HIAA levels and never claimed to be depressed nor acted depressed was depressed. There is no identified sine qua non of any mental illness; otherwise--as in neurosyphilis, Alzheimer's dementia, etc.--the behavior would be reclassified as symptoms of a neurological disorder. The psychiatric slight-of-hand involves taking what is considered to be the de facto pathology--such as drug addiction or depression-- and ascribing it to an underlying cause (it used to be demons, then humours, now it's biological, in keeping with the popular ideology of the time) which in reality is not a cause at all, but simply a correlate of the beahvior which is deemed pathological.

Below a certain density of dopaminergic neurons in the substantia nigra (MNs) WILL PRODUCE Parkinson's disease symptomology. There is no case in which there is 90% loss of MNs does not exhibit Parkinsonism that I am aware of. The link between hypothyroidism and mood is a CORRELATE; supraphysiological doses of T4 have an antidepressant effect in many people with "normal" levels. This does not indicate a pathology per se, only a hormonal influence on one's affective state.

I will agree with Kramer only insofar as there is no evidence that rules out psychobiological pathology. Certainly it is likely that some people diagnosed with many different mental illnesses have some heretofore unrecognized neurobiological abberation. However, many people without so-called "mental illnesses" do as well. The problem with psychiatric reasoning is that the beahvior is used to infer the abberation, which the psychiatrist in turn appeals to when asked about the cause of the disorder. This is called begging the question, and it is the antithesis of sound scientific reasoning.

This problem is further confounded by the entire medical notion of the norm. What is "normal"? The "normal" range of testosterone concentration, for instance, is so broad that many men who screen as normal exhibit symptoms of hypogonadism. Surely this is in part because of receptor insensitivity as well as things we have yet to or--here's the rub--never will be able to quantify. Despite the claims made to the contrary, there is no notion in neuroscience of what a "chemical imbalance" would even look like.
That does not mean such a thing does not exist. However, most people choose scientific theories based upon a synergy of two fundamental principles: (1) (Bayes' Theorem) which involves evaluating the likelihood of hypotheses given the weight of various pieces of evidence. (2) Occam's Razor, which states that the simplest plausible explanation of a phenomenon is likely to be the correct one. Biopsychiatric sophistry violates both of these principles some if not most (or all) of the time.

See:
http://www.szasz.com/manifesto.html
http://en.wikipedia.org/wiki/Bayesianism
http://www.peele.net/lib/blues.html
http://www.eliofrattaroli.com/main.asp

 

Re: oh

Posted by linkadge on March 7, 2006, at 15:51:26

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 7, 2006, at 14:40:46

"Certainly it is likely that some people diagnosed with many different mental illnesses have some heretofore unrecognized neurobiological abberation"

Thats all I am asserting. As far as seeking "treatment", or rather, "relief" goes, I don't really see it as being a prerequisite that one indeed has a firm grasp on the exact causes of their suffering.

So you have a problem with concentration. You take a stimulant. You have absolutely no conclusive evidence that your lack of concentration has anything do do with the biochemical mechanisms which the stimulant is purported to alter, but that doesn't factor much into your decision, because you know it can help - at least for now.

The same with MAO inhibitors. I realize that no conclusive evidence has linked overactive MAO to depression, but the medicine works for you.

So I guess what I am saying is, "so what" ?

I guess the, "so what" is in the possability that the medicines could make things worse long term.

Thats why my paranoid self got off everything.

Linkadge

 

Re: oh » linkadge

Posted by Chairman_MAO on March 7, 2006, at 16:28:25

In reply to Re: oh, posted by linkadge on March 7, 2006, at 15:51:26

There is a lot behind the "so what".

--Justification for involuntary mental hospitalization on the grounds that one has a "mental disease or defect" that renders them "dangerous". This is a way of incarcerating people who threaten those in power (politicians or a jury) but have committed no over crime. This is determined based upon expert testimony, considered scientific because it wears the mantle of neurobiology.
--Justification for the insanity defense, which provides for a "not guilty" verdict in case a person has a "mental disease or defect". This is a way of letting off those people who those in power (politicians or a jury) feel should not be punished though the law prescribes otherwise.
--Justification for forced drugging to protect people from themselves.
--Justification for government control over the administration of psychoactive drugs via psychiatrist proxy, e.g. it is OK to compel children to take Ritalin to eliminate behaviors considered undesirable in school, but an adult taking Ritalin of his own free will can be prosecuted and jailed for 10+yrs.
--Justification for arbitrary social norms disguised as scientific fact; the modern equivalent of religious people calling behavior that offends them "unnatural" or "unholy".
--Justification for state-mandated 12-step addiction treatment which somehow gets accepted as medical despite being anything but.
--Justification for the draconian drug policy that has created a veritable gulag of non-violent offenders in US Prisons (and around the world). Fifty percent of all US prisoners are non-violent drug offenders.

I'm sure there's more.

 

Re: oh » linkadge

Posted by Chairman_MAO on March 7, 2006, at 16:34:01

In reply to Re: oh, posted by linkadge on March 7, 2006, at 15:51:26

It is the notion of mental illness as a medical disease that makes it so a doctor can tell responsible adults which drugs he is entitled to in the pursuit of "life, liberty...and happiness". It is OK to take amphetamine, but only if a doctor deems it "medically necessary". I have languished for years waiting to have access to a doctor that was enlightened enough to see that I needed more than an SSRI+antipsychotic (as if more than a minority optimally benefit from that stuff).

Social control masquerading as medicine. This is the point that Thomas Szazs has been making for, oh, nearly fifty years now to no avail.

 

Re: oh » Chairman_MAO

Posted by linkadge on March 7, 2006, at 21:30:33

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 7, 2006, at 16:28:25

I don't see how my statement of "some people may have a genuine biochemical driven mental illness" gets extended to the notion that we should allow people be to invaulentarily hospitalized on the basis of a jury's assumption of mental illness.

Please keep in mind that my statement was intended to be narrow, short reaching, and not terrably indicative of anything global. I know where you stand on certain issues, and it is obviously a very complex and multifaceted issue. I don't stand for the concept of "mental illness" projected at large, if that is what you are assuming.

Linkadge

 

Re: oh

Posted by linkadge on March 7, 2006, at 21:59:04

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 7, 2006, at 16:34:01

Although we may be misguided about the safety of SSRI's, they do offer the benifit, that for some individuals their mood improving effects can last longer than those of a stimulant.

So, I cannot say a whole lot about your choice to medicate with a MAOI and a stimulant. If you believe that this will lead to unprecidented, and long lasting improvement in mood, then I can only wish you the best.

There are reasons beyond those which you have mentioned, why doctors tend to lean away from the use of stimulants and opioids to treat depression. I'm not going to venture to argue against your opinions on the use of stimulants and opioids to treat depression. If that is the path you wish to take, all of the best luck to you.

I *could* list a number of reasons why it might not be good idea, but I know you are familiar with all of those arguements, and would undoubtedly have a counterargument that would be feasable on at least some level. However, time will tell. Only time will tell if these drugs will actually make the cut for you.

One of the smartest men I know "Dr. Manji" said something allong these lines: 'The brain works to achieve homeostasis. Whenever you take a stimulant, or an antidepressant, you inevitably activate the systems which work to drive the brain into depression.'

The brain is infintely smarter than we are. It is *always* one step above.

Linkadge

 

Re: oh » linkadge

Posted by Chairman_MAO on March 7, 2006, at 23:49:17

In reply to Re: oh, posted by linkadge on March 7, 2006, at 21:59:04

Good luck driving the brain into depression at 80% MAO inhibition with modest doses of a catecholamine releaser! If this maxim really held true (I will pretend it does for the sake of argument, but my conclusion will show why it cannot), then psychostimulant+MAOI would not be one of the last bastions of antidepressant pharmacotherapy.

I know phenelzine brings about an unprecendented, long-lasting improvement in mood. The amphetamine helps out my concentration problems and gives me more energy to carry out tasks. I also know that the benefit of it does not build much tolerance, either. While there are of course some exceptions, those using psychostimulants for ADHD do not build tolerance to the therapeutic effect. The initial EUPHORIA fades as homeostasis sets in, but it is possible to have a new homeostasis that allows for better functioning than the old one. The increased focus/energy sticks around. Thus, I am combining the two drugs. I respond well to both for distinctly different purposes; why not put them together?

It is absurd to think that ABSOLUTE tolerance builds to a psychostimulant such that what once was an effective dose no longer has any effect whatsoever. There is no reason to believe that the new homeostasis created after administration of modest doses of d-amphetamine is inherently depressive. One could apply this logic to MAOIs (or SSRIs) as well; take away the MAOI too abruptly, and you could well have a rebound depression that is greater than what existed before. Furthermore, there are is actually SENSITIZATION to some amphetamine effects over time while others build tachyphylaxis (I LOVE THAT WORD).

Also, for his statement to have its implied theoretical import, one must assume that the mechanisms involved in psychostimulant action are the ones involved in the neurobiological substrate of the depression. In reality, the brain is far too complex for this to be the whole situation. I see his point, but it seems as if it could be expressed as "what goes up must come down". How far back down relative to the original level, though?

Ultimately, all this theoretical posturing is not worth much, as the problem actually lies in the mind, about which none of these hypotheses even apply.
Dr. Manji's statement, while obviously of value at least as a thought experiment, cannot be true because the mind is driven into depression, not the brain. And now we're back to square one: the impossibility of mental illness as a medical disease. For if the brain were the diseased entity, there would be some observed structural pathology indicating as such. However, depression is never diagnosed by observing the brain with diagnostic instruments alone. Rather, the patient's MIND is depressed--assume he's not faking it--not his brain. Minds can only be at most metaphorically sick, as they are metaphysicial entities which defy direct examination. Therefore, although use of certain drugs may activate certain mechanisms which could in theory lead to excacerbated depression, the important effect to evalute is "how do you feel", asked many times over the course of the therapeutic engagement.

There were many users of drugs such as Dexamyl (amobarbital/d-amphetamine) who used 3 caps regularly for 10+ years who did not build tolerance and attained a consistent therapeutic effect. Did it feel like the first day on the drug? I doubt it...but that doesn't mean Happy Hoover Lady (the Dexamyl 'mascot') didn't feel better than her default state most of the time while on the drug.

 

Re: oh » linkadge

Posted by Chairman_MAO on March 8, 2006, at 0:44:41

In reply to Re: oh » Chairman_MAO, posted by linkadge on March 7, 2006, at 21:30:33

I never figured you were, don't worry. ;)

Without going into anything else, let reiterate that a geniune biochemical abberation is not the domain of psychiatry. IF you have a neurobiological pathology--regardless of whether there are behavioral symptoms--the goal of the treating physician is to modify the functioning of the brain.
Ostensibly this is the goal of the psychiatrist. However, what the psychiatrist actually does is use drugs to alter behavior; he does not alter behavior with drugs vis a vis neurons. The behavior is examined, drugs are applied, and the behavior is re-examined. The psychobiological substrate is not referred to because it is unidentifable. Thus, psychiatry is not a medical discipline because the things it purports to treat--the mind--cannot EVER be observed.

I keep reiterating this point over and over because I hate saying it the simple way. OK, here it goes: there is no such thing as mental illness.
As Thomas Szasz so simply puts it, the term "mental illness" is a categorical mistake, like calling a whale a fish.

Mental: of the mind
illness: medical illness defined by physical pathology

"Medical illness defined by physical pathology of the mind?"
or is it
"Medical illness of the mind defined by physical pathology?"

Either way you have it, there can be no such animal, just like there can be no whalefish.

Let the flames wash over me and sanctify, O Lord!


**THIS DOES NOT MEAN THE PROBLEMS ARE NOT SERIOUS AND THAT THE SUFFERING IS NOT REAL**

 

Re: oh » Chairman_MAO

Posted by linkadge on March 8, 2006, at 15:10:11

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 7, 2006, at 23:49:17

I suppose you know yourself better than anyone else.

It all comes down to glutamate. You can mess around all you want with the neurotransmitters, but one is still confined by the upper bounds on the functionality of the cell. The cell only has so much energy, and can only work so hard before it must take a break, or die off.

I am sure you are aware of the fact that too much PEA neurotransmission, for instance, can create a neurotoxic environment.

It is good to have a healthy respect for the brain's homeostatic mechanisms, since oftentimes they are there for a reason. Trying to beat them, may not be in one's best interest for long term mental health.

Just my opinion.


Linkadge

 

Re: oh

Posted by linkadge on March 8, 2006, at 15:15:10

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 8, 2006, at 0:44:41

What's it matter who's domain it is in. If somebody else was handing out the pills, there'd be somebody else to blame.

I guess what I am saying is that I don't know "why" you are aruging what you are arguing.


Linkadge

 

Re: oh

Posted by linkadge on March 8, 2006, at 16:12:54

In reply to Re: oh, posted by linkadge on March 8, 2006, at 15:15:10

In your defence, people have been combining stimulants and MAOI's since the beginning of time. Namely tobacco smokers.

Tobacco ~ Nicotine + beta-carbolines.


Linkadge

 

Re: The Truth Do SSRI's and SSNRI's Work For Anyone?

Posted by sdb on March 8, 2006, at 21:22:47

In reply to The Truth Do SSRI's and SSNRI's Work For Anyone?, posted by Phillipa on February 27, 2006, at 13:12:49

Could be of interest concerning SSRI, TCA and so on. But in my opinion nothing new.

~sdb

http://psychiatry.uchicago.edu/grounds/011015/

 

Re: oh » linkadge

Posted by Chairman_MAO on March 8, 2006, at 22:31:14

In reply to Re: oh, posted by linkadge on March 8, 2006, at 16:12:54

The confusion on this issue arises due to the ill-fated "stimulant" classification. PSYCHOstimulants (d-amphetamine, methylphenidate, d-methamphetamine), viz. drugs that have a more potent CNS effect than peripheral effect, are far less dangerous to combine with MAOIs than _sympathomimetics_ or "stimulants" such as ephedrine, propylhexadrine, l-methamphetamine and l-amphetamine which have a primarily peripheral action.

Ironically, most doctors seem not to understand this. Then again, most doctors seem not to understand MAOIs very much at all. Personally, I don't understand how you couldn't find their antidepressant effect more interesting than that of uptake blockers, as--at least metaphysically speaking--levels of monoamine oxidase [A] have an intricate cascade of effects on personality and affect. Anyone who has experienced the phenomenon of the "phenelzine firecracker" effect (transition from seemingly hopeless despair to elated and socially effervescent literally overnight) will concur with me here. Studies show this happens after about 10 days at ~80%-90% MAO inhibition. Interestingly enough, while the hypomania usually subsides, there is a reliable euthymia or even hyperthymia which often remains for years or decades thereafter.

If you started Nardil at 1mg/kg and braved the side effects (and had some Nembutal to put yourself to sleep each night, haha), you'd notice it "kick in" a lot faster than 6-8 weeks.

 

Re: oh » Chairman_MAO

Posted by linkadge on March 9, 2006, at 9:13:01

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 8, 2006, at 22:31:14

Unless, Nardil was radically different from parnate, I'm not so sure it would be of any great benefit.

I made an argument before, that any agent that was capable of supressing REM sleep to the degree of the MAOI's would be bound to have pro-manic effects.

Despite what you say about the MAOI's I hear of them pooping out, and loosing effect all the time.

Even in my short run with parnate, which had a bit of a punch for the first little while, by the end of the trial, I just kind was in a zombie homeostatsis waiting for the next pill. IT made me a little psychotic too. Not my idea of bliss personally.

Anandamide reuptake inhibition, now that would be bliss IMO.

Linkadge

 

Re: The Truth Do SSRI's and SSNRI's Work For Anyon

Posted by Cairo on March 9, 2006, at 20:44:27

In reply to Re: The Truth Do SSRI's and SSNRI's Work For Anyon, posted by linkadge on February 27, 2006, at 17:42:53

In many families, support is there for depression/anxiety before meds are tried, so I think you can tell if it's the medication that is helping.

We have jumped through hoops with social skills training, CBT, diet, etc. for my daughter's social phobia. Tried Librium, and school refusal disappeared immediately. Started her later on Lexapro and she was a different kid (not 100%, but at least 40% better). Same social skills training, same CBT, etc. Switched her to Zoloft because Lexapro was way too sedating and voila, we've added another 30% within a week. I don't believe she is that disingenuous to fake getting better or not.

I think in some people who are sensitive to doses, the side effects or quitting prematurely prevent them from ever reaching a therapeutic level so they don't see improvement, but label it a "failure". In others, it just simply may not be the right SSRI/med. Granted, there are those whose situation is so multifaceted that they may not do well on any med. But why generalize about meds? You'll get the good, the bad, and the ugly with all meds, depending on the patient you're looking at. We're still in the dark ages, as far as meds go.

"Can'st thou not minister to a mind diseased?
Pluck from the memory a rooted sorow,
Raze out the written troubles of the brain,
And with some sweet oblivious antidote
Cleanse the stuff'd bosom of that perilous stuff
Which weighs upon the heart?" - MacBeth

We all wish.

Cairo


> Well, just to play the devils advokate:
>
>
> >Friend #1: Same family and social circle as >before Paxil. There were mprovements in his >social life that kicked in after his depression >improved.
>
> Depression resolved on its own, or due to the system of reassurance provided by a caring physician plus placebo effect.
>
>
> >Friend #2: Given the same life circumstances, >she is calmer and more balanced on meds. She's >gone on and off enough to clearly know the >difference.
>
> She's gone on and off enought to know she's addicted.
>
>
> >Same friends, same family, same doctor, same >job. Different drug.
>
> Different drug = new placebo with a less burdonsom side effect profile.
>
>
> >Her husband and kids were always good. She said >had a good life and was chronically depressed >and anxious for no apparent reason. Enter Prozac.
>
> Again. Enters a system of support.
>
>
> >At least for these folks, it's not coincidence.
>
> Theres no way to proove either way. The placebo effect is very strong. So strong, that study designers look for good ways to downplay their effects. I watched a show. Its funny to see how people will swear by their placebo's!
>
>
>
> Linkadge
>
>

 

Re: oh » linkadge

Posted by Chairman_MAO on March 9, 2006, at 23:29:33

In reply to Re: oh » Chairman_MAO, posted by linkadge on March 9, 2006, at 9:13:01

What dose of parnate were you taking?

What you are describing sounds like an initial response to the psychostimulant effect that waned.
Yes, many people on all sorts of medications experience waning effectiveness; is it the medicine or different life conditions? Probably both...

That said, MAOIs+d-amphetamine probably is a little more robust than effexor in terms of poop-out. ;)

If you were at 1.5mg/kg Parnate and told me it pooped out, I'd be surprised. Then I Would urge to try an augmentation strategy or perhaps switch to Nardil + psychostimulant/etc. You will not have that same "psychotic" feeling that you had.

BTW, that "psychotic" feeling could have been taking too LOW a dose such that the dopaminergic effects of TCP and metabolites wasn't counterbalanced enough by increased concentrations of intrasynaptic SE. When I took 30mg (over a day) once after being on 60mg for about a week before, I found myself feeling paranoid. Back up to 60 (0.7mg/kg, right on target) and it went away.

 

Re: oh

Posted by linkadge on March 10, 2006, at 16:05:34

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 9, 2006, at 23:29:33

I was on 60mg, which for me, was about 1mg/kg.

The doctor was uncomfortable going any higher. Its not so much that it pooped out, it was more that I didn't get much AD effect past the intial stimulant effect. It wasn't really a mood brightener for me. It certainly made the world more "interesting" however. It was an anhedonia buster.

I wasn't sleeping well, and I felt a paranoid feeling like I was trapped in a different world that I didn't recognize or understand. Objects about me became very dark and otherworldly. I felt a low grade fear that I describe as kind of a smouldering fear. My doctor and I independantly came to the conclusion that it was PEA overload, since I was exercising excessivly at the time too.

Linkadge

 

Re: oh » linkadge

Posted by Chairman_MAO on March 12, 2006, at 1:11:08

In reply to Re: oh, posted by linkadge on March 10, 2006, at 16:05:34

Tranylcypromine has a substantially stronger serotonergic effect at 1.5mg/kg and above. Lower doses do not induce downregulation of 5ht2 receptors.

 

General comments, mostly to the ChairmanMAO

Posted by Questionmark on March 13, 2006, at 2:34:37

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 8, 2006, at 22:31:14

Chairman,
While i'm not sure i necessarily agree with some of what i think you were trying to refute (such as others' statements regarding placebos and drugs), but...
i just had to tell you that you made SO many brilliant posts in this thread. i want to print out a lot of your posts in this thread and read them to people every chance i get (not quite literally, but..). MAN!
SERiously though. Including things that have not occurred to me before-- such as the ridiculous question-begging that occurs in psychiatric diagnoses, and psychiatry in general.
Uh, i might have had more but oh well. i'll shut up now.

 

Linkadge-- question.

Posted by Questionmark on March 13, 2006, at 2:45:34

In reply to Re: oh, posted by linkadge on March 7, 2006, at 15:51:26


>" Thats why my paranoid self got off everything.
>
> Linkadge"


Linkadge, you got off everything?! As in, every pharmaceutical?? That's great! i'm sorry, since you've probably discussed this so much already, but i've not been able to spend much time on pbabble at all in recent months. But.. so how do you feel??? i remember you being extraordinarily depressed for awhile before.
Would you mind telling me what all you are currently taking and how you have been feeling?
If you are feeling even close to okay i am astounded.
But great to hear.

 

Sorry, more questions! (Regarding Parnate) » Chairman_MAO

Posted by Questionmark on March 13, 2006, at 3:16:08

In reply to Re: oh » linkadge, posted by Chairman_MAO on March 12, 2006, at 1:11:08

> Tranylcypromine has a substantially stronger serotonergic effect at 1.5mg/kg and above. Lower doses do not induce downregulation of 5ht2 receptors.


This is fascinating-- and very significant potentially. However:

1. Don't the psychostimulant-like effects dose-dependently increase too? So would not those effects continue to overpower the increased serotonergic effects (at least for the most part)?

2. Believe me, i'm definitely one who believes that the classical dietary restrictions lists for MAOIs are vastly overstated (i think there might be some good ones out here and there though, such as a section i read in a modern clinical psychpharmacology book recently), but
wouldn't 1.5mg/kg Parnate (not exactly sure how much that is since i've been trained by the absurd American measurement system-- i'm assuming from what you've said before this could easily be around and over 100mg/day?) put one at a very high risk of a hypertensive reaction or crisis??
i had one on, i think, 20mg during the first month on Parnate from some mac & [albeit cheddar] cheese. It wasn't quite severe enough to scare me to going to the hospital, though i maybe should have, but it was still bad-- a wretched, pounding headache & the like (i won't go into the details too much). In ~3 years on Nardil, however (although i was smarter and more cautious this time around), i only had one hypertensive reaction and that was only when i had a moronic lapse in ... thought.. and took 50mg ephedrine (yeah, i went to the ER for that one).
So, i guess i'm just saying that i feel like all i'd have to do is smell some Monterray Jack and i'd have a hypertensive crisis, if i was on 100+mg Parnate.

3. i guess there's no real "3.", but i would have to get a really strong serotonergic effect from Parnate at some dose (especially a higher one) if i were to be helped by it. On just 20mg, i was hoerrendously obsessive-compulsively perfectionistic, at times more more anxious than i would normally have been-- rarely any less anxious-- and after awhile my depression became horribly intense and painful and emotional.

Sorry for the excessive writing. i have a problem with wanting to make my thoughts sufficiently clear and.. well, nevermind.


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