Posted by Elroy on May 25, 2005, at 14:20:01
In reply to Million dollar answer! Everyone should read this., posted by Shawn. T. on July 12, 2002, at 1:52:55
Don't know if you are still accessing this reply link, but had some questions about your posting. First off, I cannot access your links as that is a subscriber site.
RE: "Also note that caffeine enhances cortisol release, which may explain why it is a common ingredient in many diet aids. "
That doesn't make any sense. Cortisol - excess cortisol - increases weight gain, it does not inhibit it. I believe that caffeine is added to those diet products for its supposed "thermogenic effect"... but over the long run the excess caffeine (especially if one was already a heavy coffee drinker) could end up having an adverse effect in raising cortisol to elevated levels.
Anyway, my main question has been to whether you feel that Remeron is still the best alternative around for lowering elevated cortisol levels and "re-setting" the HPA Axis.
I have seen a number of clinical studies that seem to indicate that:
http://www.pslgroup.com/dg/2030E2.htm
http://www.thieme.de/abstracts/pharmaco/abstracts2001/daten/187.html
http://www.docguide.com/news/content.nsf/news/8525697700573E1885256CFD004B4129
http://qualitycounts.com/fp/remeron.htm
http://content.karger.com/ProdukteDB/produkte.asp?Doi=68873Also, there is information out there that indicates that Prozac (and many other SSRIs) actually raise levels of cortisol significantly.
QUOTE:
Studies at the University of Colorado and Greenslopes Private Hospital in Brisbane, Australia, showed that Prozac (fluoxetine) increases both cortisol and ACTH levels.
Research at the Vanderbilt University School of Medicine in Nashville, Tennessee, also documented the cortisol-boosting effects of Prozac.
Laudenslager ML, Clarke AS. Antidepressant treatment during social challenge prior to 1 year of age affects immune and endocrine responses in adult macaques. Psychiatry Res. 2000 Jul 24;95(1):25-34.
Torpy DJ et al. Diurnal effects of fluoxetine and naloxone on the human hypothalamic-pituitary-adrenal axis. Clin Exp Pharmacol Physiol. 1997 June; 24 (6):421-3
Meltzer H et al. Fluoxetine, but not tricyclic antidepressants, potentiates the 5-hydroxytryptophan-mediated increase in plasma cortisol and prolactin secretion in subjects with major depression or with obsessive compulsive disorder. Neuropsychopharmacology. 1997 Jul; 17(1):1-11. END QUOTEI wonder if that might explain why SSRIs have such a tendency to cause weight gain in many people? If one had normal or high normal levels of cortisol prior to starting a regimen of an SSRI medication, the boosting of cortisol levels would then lead to the weight gain problem (elevated cortisol is not only notorious for frequently - though not always - causing weight gain, but also for causing the development of "Carb Craving").
But if that's the case, then why would Remeron cause weight gain, if it is in fact LOWERING cortisol and correcting an HPA Axis dysfunction? Is it a placebo effect?
Also:
http://www.thedoctorwillseeyounow.com/articles/behavior/depressn_5/
QUOTE: There is little doubt among scientists that glucocorticoids, the final products of the LHPA axis, have profound effects on mood and behavior.32 For example, those afflicted with Cushing's syndrome, a disease where excess cortisol (the "stress" hormone) is produced, have a high incidence of depression. Most interestingly, their depression disappears when cortisol levels return to normal with treatment. The precise mechanism by which glucocorticoids exert this influence on mood is not well understood. We do know that in depression the LHPA axis is very often hyperactive. We suspect that the mechanism likely involves interactions with brain neurotransmitters, since we know that the brain's central control of your mood is intimately associated with the actions of serotonin, norepinephrine and dopamine, the neurotransmitters affected by the most common antidepressant medications.... The LHPA overactivity observed with chronic unpredictable stress can be prevented by the daily chronic administration of either imipramine or desipramine, two tricyclic antidepressants.29 Both desipramine and imipramine (key ingredients in Norpramine® and Tofranil®) also reverse the stress induced downregulation of 5-HT1a in hippocampus, and the 5-HT2a upregulation in brain cortex. On the other hand, zimelidine (Zelmid®, an antidepressant formerly used in Europe) and fluoxetine (Prozac®), two specific serotonin reuptake inhibitors are unable to prevent the stress-induced elevation in corticosterone levels and correct LHPA overactivity... There is, in fact, some clinical evidence that the various depressive disorders might have differing physiological explanations. These differences may explain why some patients benefit from one antidepressant and not another. Continued persistence, for example, of high levels of stress hormones (hypercortisolemia) after antidepressant administration in depressed patients has been associated with relapse and poorer treatment outcome... An important therapeutic implication of this model is the prediction that agents which can reduce the stress response and/or decrease LHPA activation will be useful in the pharmacological treatment of anxiety, depression and, perhaps, suicidal behavior. In fact, patients with major depression, who are resistant to antidepressant treatment, have been reported to improve after receiving steroid suppression agents, like ketoconazole.37,45
These suppressor agents, unfortunately, have many side effects and are often difficult to tolerate... END QUOTEMy final question deals with the latter segment of that above quote.
Are you familiar with the clinical studies that have been done with RU486 as relates to lowering cortisol and "re-setting" the HPA Axis? The clinical studies that I have read have shown very rapid improvements with very short-term doses of RU486 (which has the benefit of avoiding the bad side effects associated with long term use of RU486).
This is an area of great interest to me as I have had severe anxiety (or what might be also refered to as "psychotic depression") for about a year now. Prior to that I had been trerated (for about 18 months) for very mild anxiety and had ongonig higher stress problems for probably 3 years prior to that.
I believe that the chronic stress/mild anxiety situation caused a continued level of hyperactivity stress on my HPA Axis caused an ever increasing secretion of cortisol... and (around last June) the HPA Axis (or LHPA Axis) simply went completely dysfunctional. In addition to the severe anxiety I had numerous physical symptoms come on within just a couple weeks of the onset of anxiety (so obviously there's a connection there of some type).
Elroy
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X> I think I give new meaning to psychosomatic addict insane :) This got me so interested I forgot to take my Remeron! People gaining weight on Remeron may be responding to its effects on cortisol, as I believe the following should illustrate nicely.
>
> By the way, I have reason to believe the following may be ways to tests for various diseases. I also believe that studies should be conducted on the substances which break down each of these substances. I am going to see if my local hospital can test me for cholesterol and its derivatives. I believe my levels should be normalized judging on how good I feel. My sister with fibromyalgia is also going to be getting tested, but she doesn't know it yet. Actually I'm going to convince my entire family.
> I have read that Remeron increases cholesterol levels, that very much makes sense to me(see my last link for a good diagram on all of this).
> Note that DHEA-S information can be found in the anxiety disorder study. You can also find out why benzodiazepines work!!! This has major implications for antidepressant mechanisms and the role of 5-HT2 receptors! Also note that caffeine inhances cortisol release, which may explain why it is a common ingredient in many diet aids. This also ties into why Phen-Fen is dangerous! If I could combine all of this with information on levels of intermediary breakdown substances, I could further explain all of these afflictions. Note that this explains who and who will not benefit from DHEA dietary supplements. This also seems to imply that someone with chronic fatigue syndrome should not take Remeron! I'll let you guys make some more logical connections with all of this; I'll add more as I come up with them. It is certainly a very well developed model of abnormalities in the HPA axis. I have reason to believe that schizophrenics do not have an altered HPA axis unless of course they have comorbid afflictions with one of the disorders listed.
>
> Anxiety Disorders: High cortisol, DHEA
>
> Depression: High cortisol and Low DHEA-S
>
> Chronic Fatigue: Low cortisol, DHEA, DHEA-S
>
> Depression: High cortisol and Low DHEA and/or DHEA-S
>
> Fibromyalgia: High cortisol and Low DHEA-S (and/or DHEA???), androgens
> =>A note on this... perhaps some chronically obese patients are unable to properly breakdown cholesterol? Perhaps anorexics break it down too easily? See the following. I would guess that patients with bulimia have lower levels of 17beta-estradiol than those with anorexia.
>
> Anorexia: High 3alpha, 5alpha-THP, DHEA, DHEA-S, cortisol and Low 17beta-estradiol, testosterone
>
> Bulimia: High 3alpha, 5alpha-THP, DHEA, DHEA-S, cortisol and Low 17beta-estradiol.
>
> AIDS w/ symptoms: HIV+ and High cortisol, testosterone, estrone and Low DHEA, DHEA-S, androgens (Advanced AIDS sees increased levels of estradiol)
>
> AIDS w/o symptoms: HIV+ and High cortisol, estrone, androgens and Low DHEA, DHEA-S (I believe these patients may exhibit low testosterone)
>
> Furthermore, individuals with low levels of DHEA and high levels of testosterone (DHEA is a precursor to testosterone and androgens) are at a higher risk to contract HIV.
>
> "Initiating protease inhibitor combination therapy was associated with an increase in DHEAS over 6 months (that is good!)"
>
> On anxiety disorders:
> http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=9223436
>
> On chronic fatigue:
> http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=9899382
> and
> http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=29938079
>
> On depression:
> http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=10889076
>
> On Fibromyalgia:
> http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=4982488
>
> On Anorexia & Bulimia:
> http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=16264486
>
> On AIDS:
> http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=29503255
> and
> http://www.naples.net/~nfn03605/dheaaids.htm
>
> See http://www.psychosomaticmedicine.org/content/vol61/issue5/images/large/G0465F1.jpeg
> For the link between cholesterol and DHEA.
>
> And finally DHEA-S levels linked to cardiovascular disease. This also helps to explain increased rates of major depressive episodes in the elderly.
> http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=19458812
poster:Elroy
thread:112093
URL: http://www.dr-bob.org/babble/20050521/msgs/502775.html