Posted by Elroy on June 22, 2005, at 20:10:28
In reply to Re: HPA Axis and Anti-Cortisol Therapy » KaraS, posted by Chairman_MAO on June 22, 2005, at 18:13:42
This is a 1997 study that was performed just a year after Remeron came out and before testing had been done on Remeron. I don't doubt that tianeptine might be effective in that regard, but am also aware of sveral studies with Remeron (initial links are general studies with later links involving cortisol / HPA Axis):
http://www.pslgroup.com/dg/994E.htm
http://www.pslgroup.com/dg/88A7E.htm
http://www.pslgroup.com/dg/BC202.htm
http://www.pslgroup.com/dg/150D62.htm
http://www.pslgroup.com/dg/1D25B6.htm
http://my.webmd.com/content/article/35/1728_59748
http://www.docguide.com/news/content.nsf/news/EC40CE41EC274B65852569BC006474FA
http://www2.eclinicalpsychiatrynews.com/scripts/om.dll/serve?action=searchDB&searchDBfor=art&artType=full&id=aqc010291124
http://www.docguide.com/news/content.nsf/news/8525697700573E1885256C670056CC80
http://www.docguide.com/news/content.nsf/news/8525697700573E1885256DB7007131E7
http://www.docguide.com/news/content.nsf/news/8525697700573E1885256DBF00474CA2
http://www.docguide.com/news/content.nsf/news/8525697700573E188525700E00608A93Here's where it gets real interesting:
http://www.pslgroup.com/dg/2030E2.htm
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10451911&dopt=Abstract
http://www.docguide.com/news/content.nsf/news/8525697700573E1885256CFD004B4129
http://qualitycounts.com/fp/remeron.htmAt least one study, reported in 2001 showed that tianeptine actually (starting at week 4) INCREASED cortisol levels in test rats... It also referes to yet another study where the same thing (elevated cortisol levels were found)...
QUOTE: Stress-Induced Activation of the Hypothalamic-Pituitary-Adrenal (HPA) Axis. Psychosocial stress induced a sustained activation of the HPA axis, as indicated by the nonadapting elevation of urinary cortisol excretion in the two stress groups (Table 2). No statistical differences between the Stress and Stress + Tianeptine group were found, except on week 4 yielding significantly HIGHER cortisol excretion (P < 0.02) in stressed animals treated with tianeptine. Despite the daily treatment of subordinate animals with tianeptine (Stress + Tianeptine), cortisol did not return to basal levels (Table 2). This finding is in line with one study in rats showing that stress-elicited elevations in plasma corticosterone were not reduced by tianeptine treatment (39). Other studies, however, demonstrated that tianeptine clearly reduces HPA response to stress (40). No effects on urinary cortisol excretion were observed in animals of the two control groups (Control; Control + Tianeptine). END QUOTE
I also noted the fact that it appears to "reduce HPA response to stress activity" (which is a far cry from "re-setting" the HPA Axis... if it did that the cortisol levels should return to normal and not remain elevated), but if one is experiencing effects of elevated cortisol above and beyond one's severe anxiety / depression then clearly more is needed...
Other sites have refered to tianeptine "countering the effects" of elevated cortisol. Again, quite different from actually reducing the cortisol and fully "re-setting" the HPA Axis (which should return cortisol secretions to normal).
Additionally, I believe that tianeptine is still not available in the US market (another disadvantage compared to Remeron).
And the bottom line is that neither of these show the benefits that have - so far - been noted in studies involving RU486 in a SHORT-TERM therapy mode. That protocol thereby avoided RU486's side effects (as when taken long term) but displayed some really significant results in re-setting the HPA Axis, resulting in lowered to normal cortisol levels and tremendous benefits with anxiety / depression situation.
FDA has supposedly "fast-tracked" RU486, so will be interesting to see just exactly what that ends up meaning....
That said, if Tianeptine was available on US market I personally would give a try if the Remeron doesn't do completely what I want it to! Have seen ancedotal instances of persons who have had very good AD effects from Tianeptine who had also tried Remeron and had just "so-so" effects.... unfortunately in none of those ancedotal stories did it mention the individual having elevated cortisol levels (they were taking it for anxiety and / or depression problems and made no mention of having certified high cortisol levels).
Elroy
X
X
X
> The best AD available for normalizing the HPA axis and reversing hippocampal atrophy due to excess cortisol is tianeptine.
>
> Prevention of stress-induced
> morphological and cognitive consequences
> by
> McEwen BS; Conrad CD; Kuroda Y;
> Frankfurt M; Magarinos AM; McKittrick C
> Laboratory of Neuroendocrinology,
> Rockefeller University,
> New York, NY 10021, USA.
> Eur Neuropsychopharmacol, 1997 Oct, 7 Suppl 3:, S323-8.
>
> ABSTRACT
>
> Atrophy and dysfunction of the human hippocampus is a feature of aging in some individuals, and this dysfunction predicts later dementia. There is reason to believe that adrenal glucocorticoids may contribute to these changes, since the elevations of glucocorticoids in Cushing's syndrome and during normal aging are associated with atrophy of the entire hippocampal formation in humans and are linked to deficits in short-term verbal memory. We have developed a model of stress-induced atrophy of the hippocampus of rats at the cellular level, and we have been investigating underlying mechanisms in search of agents that will block the atrophy. Repeated restraint stress in rats for 3 weeks causes changes in the hippocampal formation that include suppression of 5-HT1A receptor binding and atrophy of dendrites of CA3 pyramidal neurons, as well as impairment of initial learning of a radial arm maze task. Because serotonin is released by stressors and may play a role in the actions of stress on nerve cells, we investigated the actions of agents that facilitate or inhibit serotonin reuptake. Tianeptine is known to enhance serotonin uptake, and we compared it with fluoxetine, an inhibitor of 5-HT reuptake, as well as with desipramine. Tianeptine treatment (10 mg/kg/day) prevented the stress-induced atrophy of dendrites of CA3 pycamidal neurons, whereas neither fluoxetine (10 mg/kg/day) nor desipramine (10 mg/kg/day) had any effect. Tianeptine treatment also prevented the stress-induced impairment of radial maze learning. Because corticosterone- and stress-induced atrophy of CA3 dendrites is also blocked by phenytoin, an inhibitor of excitatory amino acid release and actions, these results suggest that serotonin released by stress or corticosterone may interact pre- or post-synaptically with glutamate released by stress or corticosterone, and that the final common path may involve interactive effects between serotonin and glutamate receptors on the dendrites of CA3 neurons innervated by mossy fibers from the dentate gyrus. We discuss the implications of these findings for treating cognitive impairments and the risk for dementia in the elderly.
poster:Elroy
thread:515432
URL: http://www.dr-bob.org/babble/20050622/msgs/517233.html