![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 61 to 85 of 183. Go back in thread:
Posted by rod on May 3, 2005, at 5:36:17
In reply to Re: Survector, posted by sukarno on May 1, 2005, at 19:05:38
> I was reading some French website about Stablon where a French doctor was giving his opinion of it. He was saying that it isn't well-studied and only a minority of patients benefit from it, and because there are many other "proven" antidepressants already on the market, he doesn't prescribe Stablon.
>
> Another doctor there said it was more of a "light" antidepressant and is well-tolerated.
>he there, vienna calling :-)
Yes exactly. I live in Austria and doctors say the same here. They did not have much success with Stablon, and they rarely use it anymore. Also the insurance "caontrolles" the drug, because for most patients its a waste of time and for the insurance a waste of money. But if you tried nearly everything else, they grant permission to get it.
And its the same here like anywhere else. Effexor is quite the most prescribed AD here....bye
Roland
Posted by sukarno on May 3, 2005, at 6:31:22
In reply to Re: Survector expired » sukarno, posted by ed_uk on May 2, 2005, at 10:48:00
Hi Ed! :-)
How are you doing now? Are you still off medication? I went off nortriptyline abruptly years ago and the only "withdrawal" effect I felt was a sensation of pressure in the head, but that didn't happen all the time. I wonder if you are experiencing any withdrawal reactions from discontinuing lofepramine.
"Btw, Seroxat was the last drug to receive bad publicity in the UK. Effexor hasn't received any bad publicity yet, most people will not have heard of it. Doctors are prescribing a lot of Effexor at the moment, I imagine there'll be a documentary about the withdrawal symptoms soon!"
Is it difficult to get Seroxat now in the UK?
Effexor has a nasty reputation among patients with regards to withdrawal symptoms/reactions upon tapering or rapid/abrupt discontinuation. I'm sure they'll restrict that one too in due time.
Do you know if amphetamine is metabolised by CYP2D6?
Oh, last night I had a severe headache...well, I've had headaches for the entire month I've been on Stablon and last night was too intense for me so I went to two different doctors. The first doc said my BP was 140/80 and prescribed captopril 12.5mg but I didn't take it. I took another Xanax instead and an hour later I got a second opinion at another clinic and my BP was 120/80.
He prescribed tramadol 50mg, but I didn't fill the prescription because I'm afraid of side effects.
I wonder if tramadol is metabolised by 2D6... I was reading that it is pain killer, but also a mild inhibitor of reuptake of norepinephrine and serotonin, so taking it with TCAs can increase the risk of seizure. (I read that from Rxlist.com)
I've never tried MAOIs because of the strict diet. I've heard of people having hypertensive crisis even though they didn't eat tyramine-rich foods and reports of liver damage with phenelzine. Hmm... then again, I've heard that phenelzine is great for panic attacks. Seems risky because I am already prone to fluctuations in BP.
I remember before I was on medication for anxiety and panic disorder that I had BP of 145/90.. I was quite nervous though. After getting on Tranxene the BP went down to normal but over the years my BP has risen..not to what anyone would consider "high". I think the highest I've seen it is 150-something/95 when I was having severe headaches from low dose Effexor (6.25mg).
I asked my doctor friend to help me find Survector since I know it was produced here in 2004, so she said she called the pharmacist and he is checking other pharmacies.
I wonder if manufacturer destroys the drug when it is expired and/or banned.. or if they sell the remaining stock. I'm not sure, but I hope I can at least try a small amount to see if I'll have headaches or other side effects.
It is strange that Survector was made the "black sheep" and scapegoated like that, when drugs of abuse like Xanax are still widely prescribed in almost all countries. Despite all the misprescribing of Valium, that was never pulled off the market despite reports of jaundice and abuse, but with Survector the whole world went nuts over a few hundred cases of abuse and liver problems... the vast majority did just fine on it.
I guess the SSRI manufacturers saw Survector as a threat to their market share and pushed the FDA and WHO to have it withdrawn.
:-(
It's sad to read stories where antidepressants have failed people, but Survector helped them....yet they struggle to find it because of their government's decision to ban it.
Very unfortunate. Barbiturates are still on the market. hmm... but they target Survector... sorry for the rant, it just seems fishy to me why it was pulled.
Paul
p.s. I have found that Survector is still being produced in Uruguay and Brazil...that is confirmed. I might check with the Philippines too, since they still sell methaqualone (Quaalude/Mandrax/Revonal)..I figure if they still sell rubbish like that, they should sell Survector.
Posted by sukarno on May 3, 2005, at 7:27:03
In reply to Re: Survector expired, posted by sukarno on May 3, 2005, at 6:31:22
"..... Rasagiline (Agilect, Azilect) is a potent, selective, irreversible monoamine oxidase (MAO) type-B inhibitor. It is a useful agent in the symptomatic treatment of Parkinson's disease. Rasagiline and its analogues are under investigation for Alzheimer's disease. They apparently enhance memory and learning. Rasagiline may also improve mood, motivation and age-related memory decline in the ageing but nominally well adult population.
Rasagiline was first synthesised and developed by the Iranian-born Israeli researcher, Professor Moussa Youdim. It will shortly be licensed for sale by Teva Pharmaceuticals under the brand name Agilect in the USA and Azilect in Europe. In the USA, Agilect will be co-promoted with Eisai, Inc, but Eisai upper management are reportedly resisting an FDA request for a [probably unnecessary] "black box" warning on the labelling. In Europe, Azilect will be co-promoted by Danish-based drug giant Lundbeck. Barring unexpected hitches, rasagiline is expected to gain a product license in the first quarter of 2005. Professor Youdim believes that a few years hence we may mix a spoonful of drugs into our daily cereal bowls to protect the brain from neurodegenerative disease. Possibly in future we will take a cocktail of neuroprotective pills to retard the ageing process itself. Pitfalls doubtless lie ahead, and timescales may prove optimistic; but neither senescence nor age-related disease are inevitable.
Rasagiline can be taken orally both on its own in early Parkinson's disease, and as an adjunct to levodopa (L-DOPA) treatment in later stages of the disorder. There is tentative evidence that rasagiline can slow the progression of Parkinson's disease itself as well as offer symptomatic relief. This has been shown in vitro and in non-human animals, though not yet conclusively in controlled clinical trials of human subjects.
Parkinson's disease is a degenerative disorder of the central nervous system of unknown origin. Both environmental and genetic factors play a role in its onset. Symptoms include stiffness, tremors, slowness of movement, impaired balance, decreased facial expression, fatigue, apathy and sometimes pain. A slowing down of mental processes is sometimes mistaken for dementia; but as a rule of thumb, "if you give a Parkinson's patient time to answer a question, they will answer. If you give an Alzheimer's patient time to answer a question, they will forget the question".
Parkinson's disease is often foreshadowed by diminished vitality and depression. These tend to worsen as the disease progresses. Some 50% of Parkinsonians become clinically depressed; there is accumulating evidence that the depressive symptoms of "dopamine deficiency disorder" are directly tied to the neuroanatomical degeneration.
Overt signs of Parkinson's disease are associated with an 80%-plus loss of dopamine-producing neurons in the substantia nigra of the midbrain. Sub-clinical signs and symptoms may appear earlier. Some researchers suspect that all of us would all go on to develop Parkinsonian symptoms if we lived long enough. This is because of disproportionate nigral dopamine cell loss during every decade of adult life. Increased dopamine catabolism is associated with oxidative stress and neuronal cell death. Selective MAO-B inhibitors delay this process, but the molecular mechanisms of neuroprotection appear to be independent of MAO-B inhibition itself, lying in the interference by propargylamines with apoptosis signalling pathways.
By inhibiting MAO-B, rasagiline prevents the deamination of the monoamines dopamine and phenethylamine (PEA), thereby increasing their concentration in the synapse and curbing production of the reactive oxygen species, hydrogen peroxide. High concentrations of hydrogen peroxide are associated with increased oxidative stress. Rasagiline both raises levels of striatal dopamine produced from levodopa and improves the survival prospects of ailing dopaminergic neurons themselves. This salvage job helps restore a measure of normal locomotion, gait and coordination in Parkinsonian patients while delaying their physical decline.
In the brain, dopaminergic neurons in the substantia nigra project to the basal ganglia. The basal ganglia regulate bodily movement, but also play a role in thinking and emotion. To function adequately, basal ganglia cells require a proper balance between the dopamine and acetylcholine signalling systems. This balance is lost in Parkinson's disease as the dopamine neurons die off. Parkinson's patients are sometimes given anticholinergic drugs like benztropine (Cogentin), trihexyphenidyl (Artane), and ethopropazine (Parsitan) to control their tremor. At worst, these drugs are dementing; at best, they impair memory and cognition. Anticholinergics were the mainstay of treatment before the advent of levodopa. Fortunately, the benefits of rasagiline, either as monotherapy or an adjunct to levodopa treatment, extend beyond restoring motor activity. For rasagiline (modestly) improves cognitive performance on a range of tests, suggesting a role in improved central cholinergic function that is still obscure. More speculatively, a low-dosage regimen of rasagiline may prevent or retard the onset of Parkinsonian symptoms, dementia and diminished vitality in the wider, notionally healthy community as a whole. Such usage is likely to remain off-label for the foreseeable future.
The main therapeutic advantage of rasagiline over the other selective irreversible monoamine oxidase-B inhibitor selegiline (l-deprenyl, Eldepryl) is that rasagiline does not have the perhaps toxic amphetamine metabolic breakdown products of the structurally similar selegiline. Selegiline is metabolised to R(-)-methamphetamine and R(-)-amphetamine, whereas rasagiline is metabolised to R(+)-1-aminoindan. There is no evidence that these trace amphetamine metabolites contribute to selegiline's neuroprotective action.
Both selegiline and rasagiline are neuroprotective via multiple mechanisms that are poorly understood. However, their role in stabilising mitochondrial membrane potential is critical. The propargylamine moiety rather than MAO inhibition per se apparently holds the key to their neuroprotective action: the S isomer of rasagiline is some 1000 times less potent as an MAO inhibitor, but it's still protective against neurotoxic insults. Rasagiline inhibits activation of the apoptotic cascade triggered by dopamine neurotoxins and oxidative stress. Apoptosis is an active process of programmed cell-death induced by exposure to neurotoxins. Rasagiline and other propargylamines can rescue deteriorating dopaminergic neurons by inhibiting the "death signal" transduction-mechanism of mitochondrial permeability transition. Current evidence suggests that rasagiline may be more effective than selegiline in salvaging dopamine nerve cells from the usual neurological carnage of later life.
Chronic rasagiline use increases the activity of the antioxidative enzymes superoxide dismutase (SOD) and catalase (CAT), both in the dopaminergic systems of the brain and also in the heart and kidneys. Professor Youdim speculates that one day rasagiline will be used not just as a prophylactic against neurodegenerative disease but as a cardioprotectant.
Rasagiline is typically well tolerated if used within the therapeutic dosage range. In one study, the efficacy of 1mg rasagiline taken once daily was similar to 200mg of the COMT inhibitor entacapone (Comtan) administered with each levodopa dose: the only adverse event reported to be significantly more common with rasagiline than with the placebo was postural hypotension. Professor Youdim, profiled in Haaretz, observes that rasagiline [taken at a low MAO-B selective dosage] typically has no adverse side-effects. Most recently, the well-controlled PRESTO study of the Parkinson Study Group confirmed an improvement in motor fluctuations and Parkinson's disease symptoms in levodopa-treated patients; the only adverse events significantly more common with rasagiline than with the placebo were reportedly balance difficulties in the 0.5 mg rasagiline group, and anorexia, vomiting and weight loss in the 1 mg group. Fewer patients reported depressive symptoms. In the LARGO study, the frequency of adverse side-effects in patients using rasagiline or entacapone as adjuncts to levodopa treatment was similar to those in patients taking the placebo. At dosages above around 2mg per day, rasagiline loses its selectivity for MAO type B and also inhibits MAO type A. An MAO-B selective regimen does not cause significant tyramine potentiation, the dreaded "cheese effect" common to users of older unselective and irreversible MAOIs who eat tyramine-rich foods. Thus low-dosage rasagiline demands no special dietary restrictions.
The optimal dosage of rasagiline has yet to be exactly established, whether for Parkinsonians, or for depressives who may benefit from higher rasagiline dosages that inhibit both types of MAO enzyme, or for use of rasagiline prophylactically as a neuroprotectant by the "worried well", i.e. sufferers from the fatal hereditary disorder we know as the ageing process. Over the clinical dosage range, rasagiline displays a more-or-less linear pharmacokinetics. An excessively high dosage of rasagiline apparently shrinks the cell sizes of nigral tyrosine hydroxylase-positive neurons. This is currently of unknown significance, but suggests a dose-effect graph with an inverted U shape, possible toxicity, and consequently the need for caution.
The effects of a long-term regimen of rasagiline on human life-expectancy and maximum lifespan are unknown. Yet since selegiline can increase both life-expectancy and maximum lifespan in a number of non-human animal species, it is possible, though again unproven, that rasagiline's superior metabolic profile may offer advantages for life-extension. The only other current routes to enhanced longevity are either caloric restriction (CR) - which takes brutal self-discipline and can compromise mood, virility and vitality - or, hypothetically, the use of compounds like resveratrol which mimic the effects of caloric restriction without provoking its troublesome side-effects. But they remain clinically unproven too.
Rasagiline doesn't displace catecholamines from their intracellular stores. It lacks any significant "abuse potential", though this is seldom a problem with selegiline either. Neither acute nor chronic rasagiline taken at MAO-B selective dosages increase tissue levels of the monoamine neurotransmitters noradrenaline, serotonin and dopamine. In common with selegiline, rasagiline may be protective against the serotonergic damage caused by the widely used drug MDMA (Ecstasy). Unfortunately, the risks of taking any MAOI with MDMA probably statistically outweigh any neuroprotective benefit. A post-E fluoxetine (Prozac) or other SSRI may offer a less hazardous form of neuroprotection; but this carries theoretical risks too. Until safe and sustainable insight-and-empathy drugs are developed, it may be prudent either to use them only very sparingly or avoid them altogether. An enriched conception of mental health is of limited use until we have the means to sustain it.
If rasagiline is good news, then other pharmaceutical products on the horizon are better. Perhaps most notable is the neuroprotectant ladostigil (TV3326), again designed by the redoubtable Professor Youdim. Ladostigil inhibits both cholinesterase and MAO activity, enhancing cognition and mood alike. Ladostigil is cunningly designed with a propargyl group for MAO inhibition and a carbamate moiety to inhibit cholinesterase. Both the MAO type A and MAO type B inhibition of ladostigil are relatively selective to the brain: liver and small intestine enzymes are less affected.
This advance is important for several reasons. One reason is obviously the plight of a rapidly growing population of elderly Parkinsonian and Alzheimer's patients in need of more effective drug therapies with fewer risks and adverse side-effects. But the potential range of therapeutic application is broader. Most people would like to feel happier, smarter, younger and sexier. Sadly, contemporary antidepressants and nootropics are badly flawed. It's not just that they are often ineffective. They either have anticholinergic "dumb drug" effects like the older tricyclics, or they flatten emotions and kill libido, like the SSRIs. Older unselective, irreversible MAOIs like tranylcypromine (Parnate) and phenelzine (Nardil) can elevate mood, but their risks and accompanying dietary restrictions make them unattractive even for the clinically depressed and their wary physicians. Meanwhile classic nootropic agents such as cholinergic boosters are liable to subdue mood and cause behavioural inhibition. The attraction of dual action agents like ladostigil, on the other hand, is that they promise to lift mood and intellectual performance alike, while offering a measure of protection against the ravages of ageing.
Even so, tomorrow's neuroprotective smart mood-brighteners are just stopgaps. They offer only palliative relief on the route to germ-line gene therapy in decades to come, and perhaps the wholesale genomic rewrites of the era beyond. The global pandemic of human ageing can ultimately be cured; but eradicating the lethal disorder we call old age may still take several centuries. In the meantime, rasagiline and its derivatives are potentially valuable drugs that can improve the quality of life of sick and ageing Darwinians in the years ahead ...."
Posted by sukarno on May 3, 2005, at 17:33:36
In reply to Re: Stablon (tianeptine) and hepatotoxicity » sukarno, posted by ed_uk on April 24, 2005, at 12:00:30
Tianeptine treatment induces regionally specific changes in monoamines.
Frankfurt, McKittrick, McEwen, Luine
Encephale 1995 Oct, 23 696 (1-2)1-6
ABSTRACT
Tianeptine is an atypical tricyclic antidepressant that facilitates serotonin (5-HT) reuptake. Tianeptine (10 mg/kg) or saline was administered intraperitoneally to male rats daily for 4 days. Monoamine levels were measured in micropunches of discrete brain nuclei that are implicated in mood and cognition. In addition, the rates of 5-HT and norepinephrine (NE) accumulation were determined by the pargyline method. Few changes were noted in the 5-HT system. 5-HT levels were increased by short-term tianeptine in the CA3 region of hippocampus, and 5-hydroxyindoleacetic acid (5-HIAA) was increased in the ventromedial nucleus of hypothalamus, while 5-HT turnover was decreased in preoptic area (POA). In addition, short-term tianeptine treatment increased NE levels in POA, parietal sensory cortex (SCTX) and dorsal raphe (DR), and decreased NE in dentate gyrus. NE turnover was also decreased in DR, SCTX and parietal motor cortex. These data suggest that the short-term neural and behavioral actions of tianeptine may be attributable, in part, to alterations of the norepinephrine system.
===Maybe this is why I have an "Effexor headache" and slightly raised BP. I had no idea that Stablon (tianeptine) increased norepinephrine levels and that this is the mechanism of action with regards to its antidepressant effect.
Servier says it works on the HPA axis (Hypothalamic-Pituitary-Adrenal axis), reducing its response to stress, among other things, but no mention on their website about norepinephrine.
One would think that by increasing NE, you would help motivation, but that didn't happen to me.. I still feel a serious lack of motivation.. but at least I'm not depressed.
I lowered the dose to 2 tablets a day after I had that severe headache 24 hours ago.
When I woke up I felt "slowed down" and when I moved my head it felt like a strange sense of vertigo..(room felt like it was moving when I moved my eyes or head.. a slight "visual lag" I suppose... but that's stretching it). I certainly felt depressed until an hour or so after I took the first Stablon of the day.
I wonder if this headache is dangerous.
Posted by hok on May 3, 2005, at 18:23:25
In reply to Rasagiline (Azilect) useful for motivation?, posted by sukarno on May 3, 2005, at 7:27:03
anybody tried it yet? it's supposed to be like selegiline but without the amphetamine metabolites. I guess it won't be available in europe or the u.s. until later this year. I was only able to find it online through some of the pharmacies in Israel, where it was recently launched.
Posted by sukarno on May 3, 2005, at 19:07:56
In reply to Re: Rasagiline (Azilect) useful for motivation? » sukarno, posted by hok on May 3, 2005, at 18:23:25
So you can buy it from an Israeli online pharmacy? I might try that.
My interest in dopamine agonists stems from persistent lack of motivation and low libido. I don't suffer from erectile dysfunction (impotence) though, just lack of interest.
Does anyone here find dopamine agonists or dopamine reuptake inhibitors (e.g. Survector...how I wish I had that! argh!) useful for increasing libido (sex drive)?
I think Stablon may have helped, but only marginally.
A lot of people say l-deprenyl (Eldepryl/selegiline) and Dostinex (cabergoline) are great for reviving one's sex life, in addition to helping boost motivation and lift depression.
:-)
Posted by sukarno on May 3, 2005, at 23:04:40
In reply to Survector, posted by sukarno on May 1, 2005, at 3:24:03
Hi everyone.
I just called PT Darya-Varia Laboratoria, the local manufacturer of Survector and they informed me that it is no longer being produced here, so they told me to call Servier, which I just did.
Servier told me that they quit making it "a long time ago" but they have a new one called "Stablon"... that wasn't news to me.
Anyway, I went to Servier's website and they have a Parkinson's drug which boosts dopamine D2 and D3 and also norepinephrine! :-)
Sounds like a good Survector substitute I suppose, because Survector boosted dopamine and also norepinephrine and serotonin (somewhat).
This is a link to product information of Trivastal (Piribedil):http://www.servier.com/pro/Neurosciences/trivastal/trivastal_press.asp
Might be worth a shot.
Posted by ed_uk on May 5, 2005, at 6:16:15
In reply to Re: Survector expired, posted by sukarno on May 3, 2005, at 6:31:22
Hi Paul,
>How are you doing now? Are you still off medication?
I'm ok thank you, no withdrawal symptoms :-) I won't be going back on lofepramine in the near future.
>Is it difficult to get Seroxat now in the UK?
It's still prescribed a lot, some docs prescribe it like candy... others are more cautious.
>BP
If you stick to the appropriate diet, Nardil reduces blood pressure.
>I have found that Survector is still being produced in Uruguay and Brazil...
Is that definite? I thought they were just using the remaining stocks in Brazil.
Kind regards,
Ed.
Posted by sukarno on May 5, 2005, at 8:51:58
In reply to Re: Survector expired » sukarno, posted by ed_uk on May 5, 2005, at 6:16:15
Hi Ed! :-)
I've always wondered why Nardil and TCAs such as imipramine are more effective at blocking panic attacks, because SSRIs and many other drugs target the same neurotransmitters as the older MAOIs and TCAs.
Is there some mode of action that Nardil and Tofranil (imipramine) have that is separate from their effects on 5-HT and to a lesser extent NE that causes them to have much higher efficacy than the SSRIs?
I remember that imipramine was heavily sedating and that was good for me because I needed a good night's sleep after all that anxiety and panic. I've heard Nardil is not sedating though.
Tofranil is said to be the gold standard in treating panic disorder anyway (or used to be).
Survector is still being produced in Uruguay according to an online pharmacy, but I'd bet that they are wrong about it after doing more searching on Google.
I think it was forced off the market due to the SSRIs. I've never heard of a medication that was on the market for 21 years and then suddenly pulled like that.
We, the sufferers/victims of anxiety/depression, are not the ones who are considered when the big decisions are made by the top drug companies, etc.
I remember when I had told the first psychiatrist I saw here in Indonesia about my panic disorder, he ignored what I had said about my bad reactions to SSRIs and prescribed me Zoloft anyway. Of course I didn't fill it.
I'm still taking Stablon, but lowered the dose to 2 tablets a day.. headache is much improved. Is that headache caused by serotonin?
I feel quite depressed though. I'm hoping to find some antidepressant that will work and not be chock full of sexual side effects or anxiety like SSRIs or the cardiotoxicity of TCAs, etc.
I guess I'm afraid to try Nardil. What foods _can_ I eat on Nardil? I know to avoid tyramine-rich foods, but what I eat now is:baked beans, spaghetti noodles, high fiber wheat bread, olive oil.
That's my vegan diet. lol... Is that free of tyramine?
Thanks Ed. I think you are a psychopharmacologist in reality, eh? hehheh. You know your stuff about medications and mechanisms of action, etc.
Best regards,
Paul:-)
Posted by Chairman_MAO on May 5, 2005, at 16:54:45
In reply to Re: Survector expired, posted by sukarno on May 5, 2005, at 8:51:58
After approximately a three-day adjustment period where I had some mild "brain shocks" and emotional lability, the 75mg phenelzine I switched to from the 120mg tranylcypromine kicked in. Wow, I am impressed! It's a lot like the mild euphoria the parnate gave me without any of the stimulant side effects. I still do miss Parnate's DA "push" that gave me a little extra motivation and "go get em'" attitude, but I am really loving how calm I am. Also, my libido is slightly dampened, but performance and the enjoyment of "the act" are intact. Pretty nice. Now, if I don't start gaining weight exponentially, I'll be all set! My sleep is also vastly improved on phenelzine over tranylcypromine.
I really can't say enough good things about the irreversible MAOI + buprenorphine combination. I really feel someone should do a study of it in treatment-resistant depression or anxiety disorders.
That said, please don't be afraid of the diet nor the drug interactions. It's really very easy to follow. Everyone's different, but I ignore the diet except for the following, which I strictly observe:
NO:
1) Fermented Soy Products
2) REAL aged cheeses. Processed cheddar, etc. that one finds in 75%+ of all food in the USA are safe. As a matter of fact, the tyramine reaction was first discovered when MAOIs were introduced in Europe, because their aged foods are actually significantly aged, so people started having terrible headaches and stroking out all over the place. No one really noticed this in the US because most of our food is slop. ;)
3) Tap beer anywhere other than bars that I am certain clean their taps. If I'm going to a savory restaurant, especially one I frequent, I simply explain to the bartender that I am highly allergic to fermented beer residue in the taps and to simply be straight up with me about whether they clean the taps or not. It's never led me wrong yet, probably because no bartender wants to risk a lawsuit after I tell them what the reaction would be. Of course, I always carry around some chlorpromazine just in case (want to get phentolamine amps /w syringe to carry while I travel, but I dont know if doc will rx that, heh)
4) REAL air-dried sausages and aged meats
5) fava/broad beansThat's pretty much it for me. Simply avoid stuff that's really aged, spoiled, or otherwise old, and you'll do fine. You can carry medication with you to abort a hypertensive crisis, too. I think you'll find that, if you respond to an MAOI, you will never want to go back. I have ingested one or more representatives from just about every class of illicit and licit psychoactive drug, and have yet to find something that reliably produces anywhere near as course or robust a mood lift as the irreversible MAOIs. Any drug that's ever come along (at least in the US) that's ever stood a chance at rivaling the MAOIs has been taken off the market because of "abuse potential". I feel today the MAOIs would've never been FDA approved because of abuse potential, but they got in the door before the insanity convention of 1972 when they signed the CSA into law. I'm happy about that, too, because otherwise I would be a more-or-less miserable dysfunctional wreck.
Posted by ed_uk on May 6, 2005, at 5:28:39
In reply to Re: Survector expired, posted by sukarno on May 5, 2005, at 8:51:58
Hi Paul!
>Is there some mode of action that Nardil and Tofranil (imipramine) have that is separate from their effects on 5-HT and to a lesser extent NE that causes them to have much higher efficacy than the SSRIs?
Nardil raises levels of 5-HT, NE, dopamine and GABA in the brain. Parnate raises 5-HT, NE and dopamine but not GABA. Also, it is important to bear in mind that MAOIs affect 5-HT via a completely different mechanism to the SSRIs.
In addition to 5-HT reuptake inhibition, the noradrenergic properties of imipramine may help to suppress panic attacks.... SSRIs do not share this effect.
>Survector is still being produced in Uruguay according to an online pharmacy, but I'd bet that they are wrong about it after doing more searching on Google.
Can you find out who the manufacturer is, call them, and find out whether they're still making it??
Kind regards,
Ed.
Posted by pro_social_soon on May 6, 2005, at 5:40:31
In reply to Re: Survector » sukarno, posted by ed_uk on May 6, 2005, at 5:28:39
> Hi Paul!
>
> >Is there some mode of action that Nardil and Tofranil (imipramine) have that is separate from their effects on 5-HT and to a lesser extent NE that causes them to have much higher efficacy than the SSRIs?
Dr.Liebowitz observed in comparison studies between the TCA "imipramine" (Tofranil) and the MAOI "phenelzine" (Nardil) that while phenelzine was extremely effective in treating Social Anxiety, imipramine showed no efficacy - with the primary difference in the two drugs being the marked pro-DA effect of Nardil. Recent studies also show low levels of sex steroid "pregnenolone sulphate" in those with generalized Social Phobia and GAD (generalized anxiety disorder). Low PS levels are linked with abnormal dopamine function and passivity.
Posted by sukarno on May 6, 2005, at 12:16:21
In reply to Nardil,Imipramine » ed_uk, posted by pro_social_soon on May 6, 2005, at 5:40:31
Hi Ed! :-) I sent off an email a few days ago to Uruguay but have not received a reply. I even wrote it in Spanish. Oh well. *sigh* I guess it's gone for good!
" Dr.Liebowitz observed in comparison studies between the TCA "imipramine" (Tofranil) and the MAOI "phenelzine" (Nardil) that while phenelzine was extremely effective in treating Social Anxiety, imipramine showed no efficacy - with the primary difference in the two drugs being the marked pro-DA effect of Nardil. Recent studies also show low levels of sex steroid "pregnenolone sulphate" in those with generalized Social Phobia and GAD (generalized anxiety disorder). Low PS levels are linked with abnormal dopamine function and passivity."
Would this explain low libido in some folks with GAD?
I'm also interested to see if l-deprenyl (selegiline, trade name "Eldepryl" and in Indonesia "Jumex") since it is an MAO-b inhibitor in doses <10mg, could have the same effects as Nardil on panic disorder. I'm assuming it doesn't affect GABA...perhaps it is more like Parnate?
Also, DA agonists tend to lower prolactin levels which can increase libido and motivation.
I wonder if l-deprenyl is a better idea for me than Nardil. I'm afraid also of what dose I should take since all of these drugs are metabolised by CYP2D6.
I highly suspect that I'm a "poor metaboliser".
I've also considered amphetamine but it too is metabolised by 2D6.
The rule of thumb I went by with Prozac and Effexor was to take 1/20 the standard dose and that worked, except I couldn't find an Effexor elixir to take, so I took 1/4 of 25mg dose and it gave me hypertension and severe headache.
Posted by sukarno on May 6, 2005, at 14:57:57
In reply to Developing side effects to tianeptine (Stablon), posted by sukarno on March 25, 2005, at 5:30:58
Atypical antidepressants
Enclosed in 16/02/2005Until it appears a better term, the antidepressants that do not characterize as Tricíclicos, as Inhibiting Selective of the Recaptação of the Serotonina and nor as Inhibiting of the MonoAminaOxidase are atypical.
Some of these Atypical Antidepressants increase the noradrenérgica transmission, through the antagonism of receivers a2 (daily pay-sinápticos) in the central nervous system, at the same time where they modulate the central function of the serotonina for interaction with the receivers 5-ht2 and 5-ht3, as it is the case of the Mirtazapina.
The antagonistic activity in the histaminérgicos receivers H1 of the Mirtazapina is the responsible one for its sedative effect, even so is practically unprovided of anticolinérgica activity.
Other atypical ones are inhibiting of the recaptação of Serotonina and Norepinefrina, some also inhibiting, the recaptação of dopamina. It is the case of the Venlafaxina, the Mirtazapina. Some of these drugs also costumam to reduce the sensitivity of the receivers beta adrenergics, also after acute administration, what it can suggest a beginning of faster clinical effect.
Also they are here the inhibitors of the recaptação of the Norepinefrina (Noradrenalina), as it is the case of the Riboxetina. Some atypical ones, as it is the case of the Tianeptina, even so are serotoninérgicos, do not inhibit the recaptação of the Serotonina in the neuron daily pay-sináptico but, induce its recaptação for the neurons of the cortex, hipocampo and the límbico system.
The Amineptina, another atypical one, is a molecule derived from the tricíclicos but its mechanism of action is essentially dopaminérgico, while that the other tricíclicos antidepressants are essentially noradrenérgicos and serotoninérgicos. Unhappyly its production in Brazil was discontinued in 2005.
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Posted by ed_uk on May 7, 2005, at 8:57:08
In reply to Re: Nardil,Imipramine, posted by sukarno on May 6, 2005, at 12:16:21
Hi Paul!
I'm sorry to hear about amineptine being discontinued in Brazil :-(
>selegiline.....
Selegiline can sometimes cause considerable anxiety as a side effect. I haven't heard of anyone benefitting from it as a treatment for anxiety.
Kind regards,
Ed.>
Posted by Chairman_MAO on May 7, 2005, at 12:00:08
In reply to Nardil,Imipramine » ed_uk, posted by pro_social_soon on May 6, 2005, at 5:40:31
ARe you sure the neurosteroid in question was not allopregNANolone? Pregnenolone is a negative GABA-A modulator, while allopregnanolone is a positive GABA-A modulator, acting at a binding site on the GABA-A receptor distinct from benzodiazepines and barbiturates. Interestingly enough, allopregnaolone builds cross tolerance to diazepam, but not to itself. It is also more potent than benzos. The investigational drug ganaxolone is a methylated synthetic derivative of allopregnanolone that is being studied for epilepsy, but I predict will have profound value in treating PTSD, mood disorders related to the menstrual cycle, as well as SAD, GAD, etc.
Posted by Chairman_MAO on May 7, 2005, at 12:11:17
In reply to Re: Nardil,Imipramine, posted by sukarno on May 6, 2005, at 12:16:21
Unfortunately, selegiline does not have the same magical effect (at least for me) on social anxiety that Nardil does. Perhaps somewhat motivating, but anxiety was increased. I took up to 15mg/day on top of Celexa and then Lexapro years ago. I wish I knew then what I know now, because I Would've asked my shrink then--who was extremely accomodating to my needs--to try an irreversible MAOI. I brought it up in passing, but he told me he'd rather not deal with it because of the diet unless we had to. In retrospect, if I pushed the issue, I'm sure he would've gone for it. Oh well,gotta look to the future now. :)
I have to say, now that the adjustment "brain shocks" have subsided (after only about 5 days), Nardil (75mg/day) is slightly superior to tranylcypromine (200mg/day) for social phobia. Parnate would be better for someone with absolutely no other anxiety complaints except social phobia, I think, because it has such a great dopaminergic "push" to it. At around 120mg/day and above, it is really like no other medication; I feel for anyone (like SLS) whose depression is so recalcitrant that it doesn't respond to that because it is so damn effective. However, phenelzine has somewhat of an effect like that for me, although it's more subtle. The main difference is that phenelzine is so effective for the physiological manifestations of anxiety, general anxiety, etc. that it's superior--again, for me--in social phobia. It is better than a benzo for me, because it gives me motivation instead of takes it away. I'm noticing that it makes me want to go up to people I don't know and just talk to them. I have never felt that before. Is that what it's like to be an "outgoing" person? Wow, there's a whole world out there ...
Posted by sukarno on May 20, 2005, at 3:40:04
In reply to Re: Nardil,Imipramine » sukarno, posted by Chairman_MAO on May 7, 2005, at 12:11:17
Hi everyone! :-)
Well, I've figured out that 2 tablets a day doesn't quite cut it for my depression, but 3 tablets gives me a headache and some slight jitters, so I'm going to have to "fine tune" the dose some more.
I'm guessing that 2 1/2 tablets per day is optimal dose for me.
This is good stuff...much more tolerable than an SSRI and I definitely don't worry like I used to.
:-)
I did have a major panic attack, but that was a few days after I moved to a new house, so all the moving, etc, could have caused that.My Xanax dose is 1mg at 9am, 1mg at 3pm, 1.5mg at 9pm and another 1.5mg at 3am/5am (depending on when I wake up).
5mg seems to stop the nighttime panic attacks. I'm getting more used to the weird dreams I guess. hehheh.
Posted by ed_uk on May 20, 2005, at 5:09:53
In reply to Stablon (tianeptine) update, posted by sukarno on May 20, 2005, at 3:40:04
Hi Paul!
I hope you're not having any side effects from the increased Xanax :-)
Ed.
Posted by Declan on May 20, 2005, at 7:33:11
In reply to Re: Stablon (tianeptine) update » sukarno, posted by ed_uk on May 20, 2005, at 5:09:53
Hi there, so its worth taking, you reckon? Like it's one I can actually get . Does it help you get organized and motivated at all?
Declan
Posted by sukarno on May 20, 2005, at 8:09:17
In reply to Re: Stablon (tianeptine) update, posted by Declan on May 20, 2005, at 7:33:11
Hi Declan. :-)
I find it helps me concentrate better or think clearer. I don't really feel more motivated unfortunately.
I was thinking of trying dopamine agonists like Survector *grin* or some of those Parkinson's drugs since they seem to really boost motivation from what I've read.
Other than that, I've read that amphetamines like Adderall are good for lack of motivation, but they have quite a few side effects and would probably worsen my anxiety. Not sure if the benzos would cover for the anxiety caused by amphetamines.
The price of Stablon is quite high I think, especially since you have to take it 2 to 3 times a day. Here in Jakarta it is about 40 to 60 cents per tablet...so multiply that by 2 or 3 and the cost is substantial, but to me it is worth it...and I don't have insurance so I pay the full price.
Maybe in a larger dose it will motivate you. I like the good feeling it gives me in the higher doses, but I'll end up with a headache later on. Gives me some jitters but not as bad as caffeine or anything of that sort. Feels like adrenaline and my breathing improves.
It has been investigated in treatment of asthma and the few studies I've read are promising, so if you have asthma you might want to give it a try.
I took 3 yesterday and feel pretty good now...not depressed at all.
No side effects from increasing the Xanax to 5mg/day. My doctor said it was ok to do that.
One thing about Stablon I've noticed is that it has reversed some of the cognitive deficits caused by Xanax and/or anxiety. I feel "smarter" than I used to.
Posted by sukarno on May 25, 2005, at 6:56:53
In reply to Developing side effects to tianeptine (Stablon), posted by sukarno on March 25, 2005, at 5:30:58
I ran out of Stablon a few days ago and had to resort to taking an expired batch (exp. 1/2004) which I got as a free sample from a pdoc in 2002.
This stuff appears to be made in France by the "real" Servier, hehheh.
Seems to be stronger...I feel a bit "hypomanic" and irritable.
Can Stablon become more potent with age? Does anyone know?
Of course, I also just recently moved (on 8 May) so I've felt quite stressed out...maybe it's just the stress.
Posted by sukarno on May 25, 2005, at 7:00:46
In reply to Re: Nardil,Imipramine » sukarno, posted by Chairman_MAO on May 7, 2005, at 12:11:17
Chairman MAO said:
> I have to say, now that the adjustment "brain shocks" have subsided (after only about 5 days)I've been wanting to ask you about that but kept putting it off. Sorry.
Can you describe those "brain shocks"? Is it anything like the "zaps" you get during SSRI withdrawal?I wonder if zaps are a result of SSRI neurotoxicity or because of serotonin fluctuations.
Posted by sukarno on June 24, 2005, at 5:16:10
In reply to Developing side effects to tianeptine (Stablon), posted by sukarno on March 25, 2005, at 5:30:58
I'm curious if anyone else here has taken Stablon (tianeptine, an atypical tricyclic antidepressant...supposedly with no anticholinergic action).
Have you ever felt thirsty on it? I never have until recently. I had raised the dose from 25mg to 37.5mg (2 to 3 tablets respectively) and noticed some thirst, sometimes intense. I now drink double (3 litres) the amount of water than I used to.
Is this something I should be concerned about? I thought Stablon doesn't have anticholinergic or antihistaminic effects.
Ed, are you still around? You know a lot about psychopharmacology. :)
I also have been steadily raising my Pepcid (famotidine) dose to quite a high level. I'm on 20mg 6 to 8 times a day since I'm developing a tolerance to it and the acid was coming back (I have GERD).
I'm not sure which drug is responsible...or maybe both are.
Can Pepcid, since it is an H2 receptor antagonist become *nonselective* and target H1 histamine receptors too?
Thanks in advance! I drink a lot of water but it doesn't seem to help, but if I lower the Pepcid, the acid will come back with a vengeance and if I cut the Stablon down I'll get some headaches as a withdrawal reaction.
Thanks again. :)
Paul
Posted by ed_uk on June 24, 2005, at 10:26:25
In reply to Dry mouth.... Stablon (tianeptine) side-effect?, posted by sukarno on June 24, 2005, at 5:16:10
Hi Paul!
Apparantly, 20% of patients treated with tianeptine get a dry mouth. I expect the true figure is higher though because this study seems to underestimate side effects! Only 17% got drowsy on amitriptyline - I think not LOL!
The incidence of dry mouth (38 vs 20%), constipation (19 vs 15%), dizziness/syncope (23 vs 13%), drowsiness (17 vs 10%) and postural hypotension (8 vs 3%) are greater with amitriptyline than with tianeptine. Insomnia and nightmares occur in more tianeptine than amitriptyline recipients (20 vs 7%).
>thirst, sometimes intense.......
>Is this something I should be concerned about?Probably not ...but I think it would be worth seeing your doctor and getting a few tests done eg. blood glucose for diabetes etc.
>I also have been steadily raising my Pepcid (famotidine) dose to quite a high level.
Dry mouth is listed as a side effect of Pepcid but I don't think it's common.
> I'm on 20mg 6 to 8 times a day since I'm developing a tolerance to it and the acid was coming back (I have GERD).
I hope the high dose is helping :-) Perhaps you should see a gastro-enterologist. Have you tried a proton pump inhibitor eg. lansoprazole? They can be more effective than H2 antagonists for some people.
Kind regards
~Ed
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