The Tianeptine myth?
doug123 19 Jul 2006
I've seen it frequently hyped that Tianeptine is supposed to induce neurogenesis; but there is no evidence for this in healthy humans...so I would assume it's another myth...until someone can disprove it....
I did my best to disabuse folks of this hype here
An otherwise healthy individual who might be considering a pharmaceutical drug to induce neurogenesis or improvements in neuroplasticity should be aware such activity can in fact be quite dangerous; and that such benefits have never been demonstrated in a single human trial in healthy subjects.
Does anyone have any evidence to suggest otherwise?
ikaros 19 Jul 2006
http://www.servier.c...cation_olie.asp
And I think you've gotten it wrong. Tianeptine does not induce neurogenesis, but it RESTORES neurogenesis in individuals who have this normal process disturbed (e.g. depressed, stressed, neurotic population). In other words if everything in your brain is normal and OK, then it is very unlikely (this has been also said by Servier itself) that you'll get extra braincells, though tianeptine becomes a nootropic if one wants to restore brain's neuroplasticity in old age when that function seems to decline, also the ability to maintain neurogenesis at top level in old age is another question, though it should be possible in theory.
doug123 19 Jul 2006
Take care.
ikaros 19 Jul 2006
http://www.pnas.org/...ourcetype=HWCIT
As for other claims (old age and maintaining neurogenesis), they remain speculative due to lack of studies.
opales 19 Jul 2006
http://www.tianeptin...tianeptine.html
I do think it has been perhaps a little undeservedly (not that I don't think there is any promise to it) heralded in the smart drugs (i.e. amateur psychiatry) circles, IMO in the end it comes down to this:
Like reboxetine1 and milnacipran2 and consistent with its primarily European development, most of the published trials of tianeptine have been active rather than placebo-controlled and results were not published in full with rigorous peer review, compromising the ability to critically assess efficacy.
Some people seem to have the tendency to rather opt for wishful extrapolations from preliminary/poor data rather than face the cold reality with substances that have better testing. Better testing means better knowledge of efficacy (or lack of it), and yes, better knowledge of adverse effects too.
doug123 19 Jul 2006
Some people seem to have the tendency to rather opt for wishful extrapolations from preliminary/poor data rather than face the cold reality with substances that have better testing. Better testing means better knowledge of efficacy (or lack of it), and yes, better knowledge of adverse effects too.
The real, "bottom line" issue is that there is zero evidence that tianeptine can or will induce neurogenesis in a "healthy" human -- or a "disordered" human.
dopamine 19 Jul 2006
If you took the average person off the street, there would probably be something wrong with his/her health (this line of argument goes). If supplements and drugs can reverse these maladies, we should use them, while at the same time being educated as to how they work. The flaw in this line of reasoning is that self-diagnosis is often psychologically problematic - leading to a "misdiagnosis" and subsequent mistreatment.
doug123 19 Jul 2006
If supplements and drugs can reverse these maladies, we should use them, while at the same time being educated as to how they work. The flaw in this line of reasoning is that self-diagnosis is often psychologically problematic - leading to a "misdiagnosis" and subsequent mistreatment.
There is but one trial in which Tianeptine was studied under randomized, double blind, placebo controlled conditions; and there is no data whatsoever that demonstrates neurogenesis effects in humans -- disordered or healthy.
Lithium seems to demonstrate a neurotrophic effect in HUMAN bipolar patients...but not healthy patients -- and this is a QUALITY study published in the Lancet:
http://www.sciencedi...bbb737d81b081a0
Lithium-induced increase in human brain grey matter
DrGregory J Moore PhDa, b, , , Joseph M Bebchuk MDa, Ian B Wilds MSca, Guang Chen MDa and ProfHusseini K Menji FRCP©a, c
aDepartments of Psychiatry and Behavioural Neurosciences, Wayne State University School of Medicine, 4201 St Antoine, UHC-9B, Detroit, MI 48201, USA
bDepartment of Radiology, Wayne State University School of Medicine, 4201 St Antoine, UHC-9B, Detroit, MI 48201, USA
cDepartment of Pharmacology, Wayne State University School of Medicine, 4201 St Antoine, UHC-9B, Detroit, MI 48201, USA
Summary
Rodent studies have shown that lithium exerts neurotrophic or neuroprotective effects. We used three-dimensional magnetic resonance imaging and brain segmentation to study pharmacologically-induced increases in grey matter volume with chronic lithium use in patients with bipolar mood disorder. Grey-matter volume increased after 4 weeks of treatment. The increases in grey matter probably occurred because of neurotrophic effects.
It is considered unethical (and even basis for a malpractice suit!) to treat humans for an alleged condition with a pharmaceutical drug based on zero evidence.
johnmk 20 Jul 2006
doug123 20 Jul 2006
Structural plasticity and tianeptine: cellular and molecular targets.
* McEwen BS,
* Magarinos AM,
* Reagan LP.
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY 10021, USA. mcewen@rockvax.rockefeller.edu
The hippocampal formation, a structure involved in declarative, spatial and contextual memory, undergoes atrophy in depressive illness along with impairment in cognitive function. Animal model studies have shown that the hippocampus is a particularly sensitive and vulnerable brain region that responds to stress and stress hormones. Studies on models of stress and glucocorticoid actions reveal that the hippocampus shows a considerable degree of structural plasticity in the adult brain. Stress suppresses neurogenesis of dentate gyrus granule neurons, and repeated stress causes remodeling of dendrites in the CA3 region, a region that is particularly important in memory processing. Both forms of structural remodeling of the hippocampus are mediated by adrenal steroids working in concert with excitatory amino acids (EAA) and N-methyl-D-aspartate (NMDA) receptors. EAA and NMDA receptors are also involved in neuronal death that is caused in pyramidal neurons by seizures, head trauma, and ischemia, and alterations of calcium homeostasis that accompany age-related cognitive impairment. Tianeptine (tianeptine) is an effective antidepressant that prevents and even reverses the actions of stress and glucocorticoids on dendritic remodeling in an animal model of chronic stress. Multiple neurotransmitter systems contribute to dendritic remodeling, including EAA, serotonin, and gamma-aminobutyric acid (GABA), working synergistically with glucocorticoids. This review summarizes findings on neurochemical targets of adrenal steroid actions that may explain their role in the remodeling process. In studying these actions, we hope to better understand the molecular and cellular targets of action of tianeptine in relation to its role in influencing structural plasticity of the hippocampus.
PMID: 15177088 [PubMed - indexed for MEDLINE]
And once again, if one has not experienced atrophy in their brain due to a depressive illness, taking a drug to induce neurogenesis is silly...and can be dangerous....
The side effects from tianeptine are QUITE terrible and occur in WAY too many patients for MDs to prescribe without getting a million calls...geez....20% of patients experience dry mouth, 15% constipation, dizziness 13%, drowsiness 10%, postural hypo tension 3%, Insomnia and nightmares 20%! It's no wonder this drug never caught on!
http://en.wikipedia....wiki/Tianeptine
Side effects
Tianeptine was both studied for short-term (3 month) and long-term treatment (12 months) and equally well tolerated. The studies encompassed 1,300 to nearly 3,000 patients each.
Side effects are as follows (Amitriptyline vs Tianeptine):
* dry mouth (38 vs 20%)
* constipation (19 vs 15%)
* dizziness/syncope (23 vs 13%)
* drowsiness (17 vs 10%)
* postural hypotension (8 vs 3%)
* Insomnia and nightmares occur more often in tianeptine than in amitriptyline recipients (7 vs 20%)
Costa e Silva and colleagues at the Jardim Botanico in Rio de Janeiro, Brazil reported a greater frequency of headaches in the tianeptine group as compared with placebo.[11]
So far neither seizures nor kidney or bone marrow damage have been noted.
Liver toxicity has been observed very rarely, as is the case with amineptine, however, this is thought to be due to genetic predisposition and is often preceded by rash, itching, fever, and/or abdominal pain.
Sema Gülen Yýldýrým and colleagues reported in 2004 of a case of hypomania caused by tianeptine.[12]
So: if you are depressed or not, Tianeptine would probably be something to look at if compounds with better research don't work...
Dude: if you want to induce neurogenesis -- excercise! Get off your lazy ass!
http://www.stanford....ogress/ae4.html
Research in Progress
HD and Lifestyle
Running for Your Life
Researchers have shown that exercise greatly improves health in people with HD. Regular exercise can increase the level of chemicals in the brain called growth factors, or neurotrophic factors, that promote the growth of neurons, especially brain-derived neurotrophic factor (BDNF). BDNF is found in the hippocampus, the part of the brain that regulates memory, emotion, and thought.
Mice that voluntarily ran on a wheel for several days showed higher levels of BDNF in the hippocampus than their more sedentary counterparts. It seems that exercise maintains brain function and plasticity, making the brain more resistant to the damage caused by HD. Neuroplasticity, or plasticity, is the ability of the brain to reorganize pathways between neurons as a result of new experiences. As we acquire knowledge throughout our lives, our brain changes to accommodate new learning. For more information on neuroplasticity, click here.
Since environment influences neuroplasticity, getting enough exercise is important throughout life, especially beyond middle age. Incorporating exercise into your daily routine will help maintain neuroplasticity over time. With increased neuroplasticity comes an increase in the survival of neurons, and thus, a resistance to brain deterioration. Maintaining an adequate plasticity also enhances learning and prevents a decrease in awareness, perception, and memory with age. Experts recommend getting a minimum of 30 minutes of moderate-intensity exercise at least five days a week or 20 minutes of vigorous exercise three days a week.
http://www.ncbi.nlm....l=pubmed_docsum
Full paper available here: http://www.cma.ca/mu...-2/pdf/pg84.pdf
Abstract:
J Psychiatry Neurosci. 2006 Mar;31(2):84-92.
Antidepressant effects of exercise: evidence for an adult-neurogenesis hypothesis?
Ernst C, Olson AK, Pinel JP, Lam RW, Christie BR.
Neuroscience Program, UBC Hospital, University of British Columbia, Vancouver, BC.
It has been hypothesized that a decrease in the synthesis of new neurons in the adult hippocampus might be linked to major depressive disorder (MDD). This hypothesis arose after it was discovered that antidepressant medications increased the synthesis of new neurons in the brain, and it was noted that the therapeutic effects of antidepressants occurred over a time span that approximates the time taken for the new neurons to become functional. Like antidepressants, exercise also increases the synthesis of new neurons in the adult brain: a 2-3-fold increase in hippocampal neurogenesis has been observed in rats with regular access to a running wheel when they are compared with control animals. We hypothesized, based on the adult-neurogenesis hypothesis of MDD, that exercise should alleviate the symptoms of MDD and that potential mechanisms should exist to explain this therapeutic effect. Accordingly, we evaluated studies that suggest that exercise is an effective treatment for MDD, and we explored potential mechanisms that could link adult neurogenesis, exercise and MDD. We conclude that there is evidence to support the hypothesis that exercise alleviates MDD and that several mechanisms exist that could mediate this effect through adult neurogenesis.
Publication Types:
* Review
Edited by nootropikamil, 20 July 2006 - 09:54 PM.
johnmk 20 Jul 2006
PS: I'd like to see psychiatrists prescribing cardiovascular exercise, treadmill use, etc. If the increase in BDNF is in the same league as SSRI drugs, and if we're reasonably sure that BDNF is the significant mechanism of anti-depressants, then I don't see how it couldn't be just as effective as any of these drugs.
doug123 20 Jul 2006
Psychiatrists do prescribe exercise....
Please use a reference to support your reasoning...
The increase in BDNF incurred from regular exercise I am 99.9% confident is more effective than any pill currently available and I am 100% sure there aren't side effects in populations such as dry mouth (20% of the tianeptine population), constipation (15% of the tianeptine population), dizziness (13% of the tianeptine population), drowsiness (10% of the tianeptine populaiton), postural hypo tension (3% of the tianeptine population), Insomnia and nightmares (20% of the tianeptine population).
You should try exercise.
johnmk 20 Jul 2006
I would like your opinions on this study. If you need to know more, I can get the full article and post extracts.
http://www.ncbi.nlm....n the forebrain
johnmk 20 Jul 2006
Please use a reference to support your reasoning...
Hi Adam,
My post discusses philosophy and not science. Just to clarify.
doug123 20 Jul 2006
After being extensively deceived by LifeMirage, I think it's best we start from the most skeptical and move from there.
So, to move us all in the positive forward direction, we should use the The scientific method to establish a basis from which to use compounds to extend or enhance the quality of our life.
Edited by nootropikamil, 13 August 2006 - 10:11 PM.
johnmk 21 Jul 2006
doug123 21 Jul 2006
Science is best defined as a careful, disciplined, logical search for knowledge about any and all aspects of the universe, obtained by examination of the best available evidence and always subject to correction and improvement upon discovery of better evidence. What's left is magic. And it doesn't work. -- James Randi
The scientific method is quite simple; this page is excellent!
An excerpt which I love:
The scientific method is the best way yet discovered for winnowing the truth from lies and delusion. The simple version looks something like this:
* 1. Observe some aspect of the universe.
* 2. Invent a tentative description, called a hypothesis, that is consistent with what you have observed.
* 3. Use the hypothesis to make predictions.
* 4. Test those predictions by experiments or further observations and modify the hypothesis in the light of your results.
* 5. Repeat steps 3 and 4 until there are no discrepancies between theory and experiment and/or observation.
When consistency is obtained the hypothesis becomes a theory and provides a coherent set of propositions which explain a class of phenomena. A theory is then a framework within which observations are explained and predictions are made.
Figure 1.1: Flow diagram describing the scientific method.
scottl 21 Jul 2006
To repeat myself has it occured to you that you are as vocal now as you were...say a year ago, only in the opposite direction?
Brainbox 21 Jul 2006
However, how to find a balance here in a world where obtaining sufficient funding for supplement research is rather difficult?
And regarding neurogenesis, if that were to be expected of any compound known to man today, wouldn't that be the ultimate subject to invest money in?
And that's not happening (according to my limited observations), so.......
I remain sceptical.
doug123 21 Jul 2006
QUOTE[/b] (scottl)
<!--QuoteEBegin]
Drugs Aging. 2006;23(3):227-40. Links
A systematic review of the clinical and cost-effectiveness of memantine in patients with moderately severe to severe Alzheimer's disease.Kirby J, Green C, Loveman E, Clegg A, Picot J, Takeda A, Payne E.
Southampton Health Technology Assessments Centre (SHTAC), University of Southampton, Boldrewood, Southampton, UK.
Alzheimer's disease (AD) is the most common form of dementia and is characterised by a worsening of cognition, functional ability, and behaviour and mood. The objective of this study was to review the clinical and cost-effectiveness of memantine for the treatment of patients with moderately severe to severe AD. To achieve this, a systematic search and review of the clinical and cost effectiveness literature for memantine was undertaken. The literature search covered the period from the inception of MEDLINE, Cochrane Library, EMBASE and other electronic databases until July 2004. The search included randomised controlled trials (RCTs) and full economic evaluations that assessed the use of memantine in patients with moderately severe to severe AD.Two published RCTs were included in this review; in one of these trials the participants were already being treated with donepezil. The two RCTs showed benefit for patients receiving memantine compared with placebo on the outcome measures of the Alzheimer's Disease Cooperative Study Activities of Daily Living Inventory modified for severe dementia, the Clinician's Interview-Based Impression of Change Plus Caregiver Input, and the Severe Impairment Battery, and that memantine appeared to be slightly more effective in patients already receiving a stable dose of donepezil. Five cost-effectiveness studies were included in the review. Although these studies reported cost reductions and improved outcomes with memantine, the evaluations were based on a number of assumptions.In conclusion, memantine appears to be beneficial when assessed using functional and global measurements. However, the effect of memantine on cognitive scores and behaviour and mood outcomes is less clear. Cost-effectiveness is dependent upon assumptions surrounding clinical effect and context-specific cost data.
PMID: 16608378 [PubMed - in process]Cholinesterase inhibitors for Alzheimer's disease.Birks J.
University of Oxford, Department of Clinical Geratology, Radcliffe Infirmary, Woodstock Road, Oxford, UK, OX2 6HE. jacqueline.birks@geratol.ox.ac.uk
BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme acetylcholinesterase. The most that these drugs could achieve is to modify the manifestations of Alzheimer's disease. Cochrane reviews of each ChEI for Alzheimer's disease have been completed (Birks 2005, Birks 2005b and Loy 2005). Despite the evidence from the clinical studies and the intervening clinical experience the debate on whether ChEIs are effective continues. OBJECTIVES: To assess the effects of donepezil, galantamine and rivastigmine in people with mild, moderate or severe dementia due to Alzheimer's disease. SEARCH STRATEGY: The Cochrane Dementia and Cognitive Improvement Group's Specialized Register was searched using the terms 'donepezil', 'E2020' , 'Aricept' , galanthamin* galantamin* reminyl, rivastigmine, exelon, "ENA 713" and ENA-713 on 12 June 2005. This Register contains up-to-date records of all major health care databases and many ongoing trial databases. SELECTION CRITERIA: All unconfounded, blinded, randomized trials in which treatment with a ChEI was compared with placebo or another ChEI for patients with mild, moderate or severe dementia due to Alzheimer's disease. DATA COLLECTION AND ANALYSIS: Data were extracted by one reviewer (JSB), pooled where appropriate and possible, and the pooled treatment effects, or the risks and benefits of treatment estimated. MAIN RESULTS: The results of 13 randomized, double blind, placebo controlled trials demonstrate that treatment for periods of 6 months and one year, with donepezil, galantamine or rivastigmine at the recommended dose for people with mild, moderate or severe dementia due to Alzheimer's disease produced improvements in cognitive function, on average -2.7 points (95%CI -3.0 to -2.3), in the midrange of the 70 point ADAS-Cog Scale. Study clinicians blind to other measures rated global clinical state more positively in treated patients. Benefits of treatment were also seen on measures of activities of daily living and behaviour. None of these treatment effects are large.There is nothing to suggest the effects are less for patients with severe dementia or mild dementia, although there is very little evidence for other than mild to moderate dementia.More patients leave ChEI treatment groups, approximately 29 %, on account of adverse events than leave the placebo groups (18%).There is evidence of more adverse events in total in the patients treated with a ChEI than with placebo. Although many types of adverse event were reported, nausea, vomiting, diarrhoea, were significantly more frequent in the ChEI groups than in placebo.There are four studies, all supported by one of the pharmaceutical companies, in which two ChEIs were compared, two studies of donepezil compared with galantamine, and two of donepezil compared with rivastigmine. In three studies the patients were not blinded to treatment, only the fourth, DON vs RIV/Bullock is double blind. Two of the studies provide little evidence, they are of 12 weeks duration, which is barely long enough to complete the drug titration. There is no evidence from DON vs GAL/Wilcock of a treatment difference between donepezil and galantamine at 52 weeks for cognition, activities of daily living, the numbers who leave the trial before the end of treatment, the number who suffer any adverse event, or any specific adverse event.There is no evidence from DON vs RIV/Bullock of a difference between donepezil and rivastigmine for cognitive function, activities of daily living and behavioural disturbance at two years. Fewer patients suffer adverse events on donepezil than rivastigmine. AUTHORS' CONCLUSIONS: The three cholinesterase inhibitors are efficacious for mild to moderate Alzheimer's disease. It is not possible to identify those who will respond to treatment prior to treatment. There is no evidence that treatment with a ChEI is not cost effective. Despite the slight variations in the mode of action of the three cholinesterase inhibitors there is no evidence of any differences between them with respect to efficacy. There appears to be less adverse effects associated with donepezil compared with rivastigmine. It may be that galantamine and rivastigmine match donepezil in tolerability if a careful and gradual titration routine over more than three months is used. Titration with donepezil is more straightforward and the lower dose may be worth consideration.
PMID: 16437532 [PubMed - indexed for MEDLINE]
See you around.
Edited by nootropikamil, 21 July 2006 - 11:42 PM.scottl 21 Jul 2006
Adam,
1. It is unfortunately true that there are....far too many people on these boards looking for a fast biochemical fix where there is none. For any part I have played in that e.g. I posted that thread on avant that started the....Breverman stuff me aculpa. I have written an article on the opposite way of dealing with things which is applicable to more (here FYI:
http://www.mindandmu...eID=38&artID=30
and tried to remind people of this. Having said that
2. There are people who have benefited from nootropics....It apparently made a huge difference...you can search the board...forget who it was....though they have not done much for me aside from neurostim and biotests...whatever it was called. But people have benfited. I believe Lynx was one.
Soo while they ain't a panacea, I do believe they can be of benefit. I've a supply of tianeptine I've had for ages. There was no point in trying it till I had everything else in order i.e. while I was still being stressed. I've adressed everying else and will probably try it in the next few months.
Anyway I beleive they are not the panacea you made them out to be a year ago, nor as useless as many would believe. But you gotta have your metaphorical house in order first, and they are very individual and may or may not do anything for ya.doug123 21 Jul 2006
I think that many people are interested in this stuff as a hobby (literally taking pills!) These days, there are so many pills to choose from, I think it's a good idea to be as choosy as possible; especially since most of us don't have a limitless budget.
I think nootropics have helped me too...but that could be because I wanted to convince myself they work. I got to a point with the pills I was taking such that they started to hurt my performance in school due to the psychosis. I thought every professor and TA had some kind of conspriacy against me...I ended up dropping out. I am trying to convince myself to go back to school...it's hard going back.eternaltraveler 21 Jul 2006
i never found any significant benefit from any nootropics. Drugs like aricep may be a different matter, but my brain works just fine now, so why risk screwing it up.eternaltraveler 21 Jul 2006
The side effects from tianeptine are QUITE terrible and occur in WAY too many patients for MDs to prescribe without getting a million calls...geez....20% of patients experience dry mouth, 15% constipation, dizziness 13%, drowsiness 10%, postural hypo tension 3%, Insomnia and nightmares 20%! It's no wonder this drug never caught on!
compared to other drugs that treat depression/anxiety the side effects of tianeptine may be superior, and so if you really have one of the conditions its indicated for it may be of use. Of course this doesn't address your original point of whether or not it induces neurogenisis in healthy subjects.scottl 21 Jul 2006
Those side effects are...in no way out of the ordinary of many drugs that are being prescribed (you really have no idea), and keep in mind for myself and I think many/most of the people on the board we are only talking about a cycle or two or the stuff, not long term treatment.ikaros 22 Jul 2006
I was prescribed tianeptine for OCD and so far I can report that it has had a beneficial effect on my mood and reduced anxiety levels to a very low level. What's more is that it seems that my ability to cope with stressful events is greatly improved and having OCD, you'll have a lot of them. A problem with OCD is that you can't shut your mind down, all you can do is think if you want to feel normal and think about complex problems all the time. It's like being stuck on somekind of fixed path. I do not know if this is a proof of neuroplasticity(which shoold be the brain's ability to adapt to new experiences and in a more abstract sense, keep the inside in objective harmony with the outside), but I can note that my overall ability to be objective (without falling into a pit of obsessing) to life's events has improved.doug123 13 Aug 2006
I was prescribed tianeptine for OCD and so far I can report that it has had a beneficial effect on my mood and reduced anxiety levels to a very low level. What's more is that it seems that my ability to cope with stressful events is greatly improved and having OCD, you'll have a lot of them. A problem with OCD is that you can't shut your mind down, all you can do is think if you want to feel normal and think about complex problems all the time. It's like being stuck on somekind of fixed path. I do not know if this is a proof of neuroplasticity(which shoold be the brain's ability to adapt to new experiences and in a more abstract sense, keep the inside in objective harmony with the outside), but I can note that my overall ability to be objective (without falling into a pit of obsessing) to life's events has improved.
If it works for you, that is great. Did you experience any of the negative side effects and had you tried anything else before? I am curious if maybe some of this data may be exaggerated..,
What country are you in? This drug seems to have a particularly unfavorable side effect profile and it seems there are now better options available in medicine -- I think I understand why this drug never made it into the US pharmacopeia. over 1/3-1/5 of your patients experience dry mouth, 1/4-1/5 experience constipation, 1/5 experience dizziness/syncope, 1/6 experience drowsiness, 1/11 experience postural hypotension, and 1/5 experience Insomnia and nightmares -- uh, doc, is there something else I can try? I guess it could be prescribed if better studied and tolerated agents fail to work.Side effects
Tianeptine was both studied for short-term (3 month) and long-term treatment (12 months) and equally well tolerated. The studies encompassed 1,300 to nearly 3,000 patients each.
Side effects are as follows (Amitriptyline vs Tianeptine):
dry mouth (38 vs 20%)
constipation (19 vs 15%)
dizziness/syncope (23 vs 13%)
drowsiness (17 vs 10%)
postural hypotension (8 vs 3%)
Insomnia and nightmares occur more often in tianeptine than in amitriptyline recipients (7 vs 20%)ikaros 13 Aug 2006
Nootropikamil, compared to the SSRIs tianeptine is an innocent child. I did experience one side-effect which is usually common to serotonergic antidepressants and it was slight muscle cramps, but those weren't anything serious and went away in 5 days. By the way because I was diagnosed OCD, I have tried all SSRIs out there and I can say most of them are packed with side-effects and not just with side-effects you listed for tianeptine, but much worse kind of side-effects, (on fluvoxamine) for me the worst was a hypomanic episode which lasted 2 months (my doc rushed to diagnose me as a bipolar, but it was actually the med). I've been on tianeptine for over a month now and I still can't find anything bad about it, maybe slight energy rush time to time, but who whines about that, helps me pull more work and at the university I manage to get more studying done also.