161 replies to this topic

[Flex]

I´m actually trying the bupleurum.
I got it on Monday and will take it today again.
 
I tend to wait a week or so before reporting the effects, bcause some, like Chinese skullcap, worked just the first 3-5- days then dimmished.
Untill now ~45min after usage I felt good, but it went negative and stabilized more or less to baseline,
but it seems to have a positive effect the next day after as well as today.
 
This one contains also Bupleurum, perhaps it could be interresting for You.
Seee the comments:
Planetary Herbals Bupleurum Calmative Compound, 550 mg
I have been trying everything under the sun to combat my extreme anxiety and depression. I was on Paxil for three years and it pretty much ruined my life. I was comatose and had zero motivation. I went from a person who worked out at least three hours a day to a fat, lazy slob who stopped showering. After It got bad my family/friends begged me to get off it and I did. The result was hell. I was so depressed and had so much anxiety I couldn't leave the house. I then started buying everything natural I could. I have tried: SAM-e, inositol, passion flower, ginseng, B-complex, Valerian root, EXPENSIVE/Gross kava kava root powder, omega-3,and L-Tryptophan... plus lots more I cant remember. None did anything positive and some like the kava and SAM-e made me really sick.
The very first day I took these was the same day I went through a horrible fight with my neighbor. Normally this would have stressed me out so much I wouldn't be able to sleep, but an hour after I took these I was able to sleep. Ever since I started taking these I have had substantially less anxiety. Normally I am a recluse but today I booked a weekend trip to the beach, something I haven't wanted to do for years. I feel like my self but not as cranky and high strung as I have been. I will say i am a strict vegan, I meditate daily and I workout a lot so this does all aid in feeling better but It wasn't enough.If you have tried other stuff with zero success you should consider this cause it does help.
Please note you must take these on an empty stomach. If you take these with food you really will only feel 20% better.
http://www.amazon.co...*=1&*entries*=0
 
Please consider to take the time to read into the following.
Because they could help perhaps My and Yours Depression/Mood diesease:
 
I found a researchpaper where they stated interresting conclusions about the decreased gene expression of  Glucocorticoids and thus rise in depression.
Its not only HDAC6 but also the gene methylation and other mechanisms
Unfortunaetly I cant remeber where I get the Full text even the link posted above doesnt work.

(Theres also a table, I will try to post it in the next days)
Anyway its:
Some rats have more
contact with their offspring, exhibiting high levels of pup
licking, grooming, and arched-back nursing (high LG-ABN),
whereas others exhibit these behaviors to a significantly
lesser degree (low LG-ABN). When the pups of high LGABN
rats were compared with the pups of low-LG-ABN rats,
the former group was observed to experience less anxiety as
adults and their HPA response to stress was lower (Liu et al.
1997; Caldji et al. 1998). When the pups born to low-LGABN
mothers were reared by high-LG-ABN mothers, their
development was reported to be similar to that of the pups
born to high-LG-ABN mothers. Likewise, pups born to high
LG-ABN mothers that were reared by low-LG-ABN mothers
exhibited development similar to that observed in the pups
born to low-LG-ABN mothers (Francis et al. 1999). These
findings suggest that the effects of maternal behavior on anxiety
are mediated by non-hereditary factors.
Since it became clear that epigenetic processes regulate genes
dynamically in adults, studies focused on the epigenetic
changes in genes critical to mood disorders that are induced
by stressful life events during different periods of life. The
majority of such studies targeted molecules involved in the
regulation of the HPA axis. Among the molecules studied
are the glucocorticoid receptor (GR) gene, which regulates
the HPA axis via negative feedback inhibition, and arginine
vasopressin (AVP) and corticotrophin releasing factor (CRF)
genes, which regulate the effect of stress on the HPA axis by
increasing the release of ACTH from the pituitary gland.
Glucocorticoid Receptor (GR) Gene
It has been reported that prenatal stress and early life stress
increase DNA methylation of the GR gene promoter, and decrease
GR expression in the hippocampus and hypothalamus
(Weaver et al. 2004, 2005; Mueller and Bale 2008) (Table 2).
In rat pups born to low-LG-ABN mothers and reared by high-
LG-ABN mothers, such change in GR methylation was not
observed. Interestingly, it was reported that administration of
an HDAC inhibitor, trichostatin A, increased GR levels in
the pups of low-LG-ABN mothers (Weaver et al. 2004). The
same group investigated the effects of systemic administration
of L-methionine (a methyl donor) in adult rats on methylation
of the GR gene and GR levels in the hippocampus, and
behavior in pups born to high- or low- LG-ABN mothers.
This intervention increased DNA methylation in GR promoter
and decreased GR levels in the hippocampus of the
pups born to high-LG-ABN mothers, and increased depression-
like behavior. A significant difference was not observed
between the pups of low-LG-ABN mothers that were administered
L-methionine and vehicle (Weaver et al. 2005) (Table
2). These findings are extremely important because they show
that epigenetic changes that occur early in life can be modified
in adulthood and therefore, changes in gene expression
engendered by negative factors via epigenetic mechanisms
may be reversed by treatment interventions in adulthood and
new treatments may be developed in this context.

Psychiatric disorders and epigenetics.
http://www.ncbi.nlm....pubmed/22648875
 
Another very interresting one expalins by which mechanism Mifepristone works + the role of HDAC
:http://www.ncbi.nlm....pubmed/21367534
Glucocorticoid-induced p11 over-expression and chromatin remodeling..
In addition, chronic social defeat stress in mice causes a tran-
sient decrease, followed by a persistent increase, in levels of acet-
ylated histone H3 in the nucleus accumbens, an important limbic
brain region. Such an increase in H3 acetylation is associated with
decreased levels of histone deacetylase 2 (HDAC2). Similar effects
were observed in the nucleus accumbens of depressed humans
studied postmortem. Infusion of HDAC inhibitors into the nucleus
accumbens, which increases histone acetylation, exerts robust
antidepressant-like effects in the social defeat paradigm and other
behavioral assays. HDAC inhibitor [N-(2-aminophenyl)-4-[N-(pyri-
dine-3-ylmethoxy-carbonyl)aminomethyl]benzamide (MS-275)]
infusion also reverses the effects of chronic defeat stress on global
patterns of gene expression in the nucleus accumbens
[41]
. These
findings provide new insight into the underlying molecular mech-
anisms of depression and antidepressant action, and support the
antidepressant potential of HDAC inhibitors and perhaps other
agents that act at the level of chromatin structure.
 
A further article explains what epigenetic target is responsible for what :
Epigenetic Modulation Mechanisms in Psychiatric Disorders: Gene and Trigger and Erase and Re-write Hypothesis
http://www.rjpbcs.co...3_4(4)/[35].pdf
 
And this one could show which chinese herbs do alter epigenetic modifications
Histone modifications and traditional Chinese medicinals
http://www.ncbi.nlm....les/PMC3698099/

Edited by Flex, 05 November 2014 - 08:45 PM.

[Flex]

Could anybody tell me how to upload a PDF from my disc / harddrive to complete the above post ?

Seems that the uploading dont work anymore

Edited by Flex, 05 November 2014 - 09:23 PM.

[Joe Monroe]

interesting posts flex. Tell me how you feel after taking it a while. What else have you tried? anything that is helpful, Does anyone know any other reliable places to buy mifepristone online? 

 

Sorry not sure how to upload pdf from a hardrive 

 

 

[Flex]

Yes, I will report in a few days more detailed. Seems, that Caffeine interfere negatively with Bupleurum, even the next day.

The downs/pain are lower too, but Dan Shen is still one of the best ( in terms of naturaly reliving the pain).

Altough it doesnt have any longterm modulating effects exept perhaps 11ßDHS via GR inhibition ( at least according to what I´ve read).

It makes one a bit tired but helps in terms of anhedonia but not that much.

 

Another good one was Hordenine a selective MAO-B inhibitor (but short lived). You could also take Green oat / Neuravena or alternatively Rhodiola rosea extract.

But for my case, Rhodiola wasnt that good because somehow I react bad on MAO-A inhibition and Rhodiola is MAO-A&B + it reduces some stress hormones.

From the Meds: I responded best to Nortrypline. Amitryptiline on the second place because this made me a bit ahpatic.

 

I would gladly know an Europe based source, since eurodrugstore doesnt seem to have any in stock.

Edited by Flex, 06 November 2014 - 05:56 PM.

[tunt01]

Flex/all:

 

I've read all the Szyf/Meaney papers and several others that have been spawned off their GR-hpa work.  I would suggest you give this paper a read:

 

Modulation of early stress-induced neurobiological changes: a review of behavioural and pharmacological interventions in animal models

 

I'm not sure if mifepristone is a silver bullet.  But I would also suggest looking at Telmisartan for attenuation of chronic stress.  Telmisartan is an exercise mimetic and seems to have preventative effects on a variety of hyper stress-induced outcomes like Alzheimers.

 

 

[Joe Monroe]

Flex/all:

 

I've read all the Szyf/Meaney papers and several others that have been spawned off their GR-hpa work.  I would suggest you give this paper a read:

 

Modulation of early stress-induced neurobiological changes: a review of behavioural and pharmacological interventions in animal models

 

I'm not sure if mifepristone is a silver bullet.  But I would also suggest looking at Telmisartan for attenuation of chronic stress.  Telmisartan is an exercise mimetic and seems to have preventative effects on a variety of hyper stress-induced outcomes like Alzheimers.

 

First link is talking about how early life stress has long lasting effects, I have read about that, possibly the same article previously. in fact there was a recent article I read about how trauma can actually be passed down from generation to generation. 

 

Are there any other studies with telmisartan, sounds interesting. All I really found regarding it was depression induced by telmisartan, lol.

[Flex]

I´ve found the following herbs/compounds to be potentional HDAC inhibitors ( if this makes any sense):

 

Zyflamend down-regulated the expression of all class I and II histone deacetylases where Chinese goldthread and baikal skullcap (two of its components) appear to be primarily responsible for these results.

http://www.biomedcen...1472-6882/14/68

 

http://www.hindawi.c...me/2013/821082/

And some further, but I´m actually too busy now to find them.

I dont know wheter they can pass the Blood brain barrier AND act as a HDAC in the Brain or whether there are other limitations & etc.

I would gladly hear from You some comments on this because I cant currently get much informations out of this.

 

I mean, it sounds too good to be true..

Edited by Flex, 09 November 2014 - 09:39 PM.

[Flex]

Seems that the links dont work.

Here again:

http://www.biomedcen...1472-6882/14/68

Heres the table:

http://www.biomedcen.../14/68/table/T2

Some other compounds

http://www.hindawi.c...me/2013/821082/

 

Edited by Flex, 11 November 2014 - 06:28 PM.

[Flex]

Flex/all:

 

I've read all the Szyf/Meaney papers and several others that have been spawned off their GR-hpa work.  I would suggest you give this paper a read:

 

Modulation of early stress-induced neurobiological changes: a review of behavioural and pharmacological interventions in animal models

 

I'm not sure if mifepristone is a silver bullet.  But I would also suggest looking at Telmisartan for attenuation of chronic stress.  Telmisartan is an exercise mimetic and seems to have preventative effects on a variety of hyper stress-induced outcomes like Alzheimers.

 

Hey nice one, Thank You !
 

I was the last days too busy to comment the effects of Coptidis.

Coptidis increased actually my latent amotivation, but also increased my emphaty, and pro-soical behavior.

I cant say for sure whether it has HDAC actions, since I´ve never used a definite one.

 

I´ve used it on last Friday, used 10mg Coluracetam on Sunday and ca. 1.2 gram Acetyl-carnitine on monday.

This in turn relievd my depressive thoughts which came up in the last time in a nice manner.

But I´ve didnt used Coluracetam since May and Acetyl-carnitine since September, so I cant say for sure whether Coptidis had a enhancing effects over the days.

 

My pain in the chest was and is still overlaid through those effects.

So it wasnt again the right one but helped.

I will keep You updated on this because from my experience its possible that it fades away and a second usage doesnt work that strong anymore.

I´ve found in the meantime "again" some interresting articles.

Its about the different actions of GR alpha receptors and GR beta and the genetic causes in e.g. fatigue

( see table 2 at the bottom)

 

Familial/Sporadic Glucocorticoid Resistance

https://www.orpha.ne...dresistance.pdf

 

As well as the term, like above: Glucocorticoid Resistance

http://emedicine.med...925564-overview

 

I would gladly try Mifepristone, but the posted vendor doesnt have any in stock.

I would really appreciate if anyone would post an EU based vendor.

[tunt01]

 

I was the last days too busy to comment the effects of Coptidis.

Coptidis increased actually my latent amotivation, but also increased my emphaty, and pro-soical behavior.

I cant say for sure whether it has HDAC actions, since I´ve never used a definite one.

 

I´ve used it on last Friday, used 10mg Coluracetam on Sunday and ca. 1.2 gram Acetyl-carnitine on monday.

This in turn relievd my depressive thoughts which came up in the last time in a nice manner.

But I´ve didnt used Coluracetam since May and Acetyl-carnitine since September, so I cant say for sure whether Coptidis had a enhancing effects over the days.

 

My pain in the chest was and is still overlaid through those effects.

So it wasnt again the right one but helped.

I will keep You updated on this because from my experience its possible that it fades away and a second usage doesnt work that strong anymore.

I´ve found in the meantime "again" some interresting articles.

Its about the different actions of GR alpha receptors and GR beta and the genetic causes in e.g. fatigue

( see table 2 at the bottom)

 

Familial/Sporadic Glucocorticoid Resistance

https://www.orpha.ne...dresistance.pdf

 

As well as the term, like above: Glucocorticoid Resistance

http://emedicine.med...925564-overview

 

I would gladly try Mifepristone, but the posted vendor doesnt have any in stock.

I would really appreciate if anyone would post an EU based vendor.

 

 

Flex:

 

Thanks for the paper.  I read it.  It's interesting.  I'm not sure how they would distinguish between sporadic GR and a lack of sufficient GR due to environmental programming.  I've not thought enough about the differences in diagnosis, but the overall phenotype should be relatively similar.  Obviously, in the case of a rare mutation (familial glucocorticoid resistance) treatments like mifepristone will probably be a waste of time and the individual should probably focus on primary release of ACTH.  I guess sporadic GR would also not benefit from mifepristone.

 

Thanks for these links and also for mentioning Coptidis.  I've actually never heard of Coptidis, which was rather surprising to me.  I have a pretty lengthy file on all kinds of supplements related to Alzheimers, but this one was not in there.  Coptidis' protective behavior seems to be driven by groenlandicine, which acts as a peroxynitrite scavenger.  I've found rosmarinic acid, a constitute of rosemary, sage, and mint, to be a good source of peroxynitrite removal.  If you pubmed for rosmarinic with alzheimer or other related terms, you'll find some interesting papers.

 

I will have to look at it Coptidis more closely.

 

Thanks again for your contribution to the discussion Flex.

Edited by prophets, 21 November 2014 - 03:12 AM.

[Flex]

Edit

Edited by Flex, 23 November 2014 - 01:15 AM.

[Flex]

Hey OP, I´ve found this:

Fatigue: New Mouse Model in the Works

http://www.msdiscove...use-model-works

 

You could try a herb or compound that blocks IL-1ß and look whether there are any changes. Those compounds are actually common, like Magnolia or perhaps icariin but I´m unsure about the latter.

[HungryHippocampi]

Hey Guys, I have a good friend who was in the special forces and he and several of his buddies are suffering severe depression, suicidal thoughts, low affect, etc.  These guys were given Mefloquine for malaria when they were in the service.  Mefloquine is linked to "severe gastrointestinal and neuropsychiatric adverse effects, including cognitive disturbances, anxiety, depression, psychosis, and violence".

 

One theory on causality:  http://www.ncbi.nlm....pubmed/23852388

 

 

The adverse effects of the drug are thought to result from the secondary consequences of hepatocellular injury; in fact, mefloquine is known to cause a transient, anicteric chemical hepatitis. However, the mechanism of mefloquine-associated liver damage and the associated neuropsychiatric and behavioral effects of the drug are not well understood. Mefloquine and other 8-amino-quinolines are the only antimalarial drugs that target the liver-stage malaria parasites, which selectively absorb vitamin A from the host. Vitamin A is also stored mainly in the liver, in potentially poisonous concentrations. These observations suggest that both the therapeutic effectiveness of mefloquine and its adverse effects are related to the ability of the 8-aminoquinolines to alter the metabolism of retinoids (vitamin A and its congeners). Several lines of evidence support the hypothesis that mefloquine neurotoxicity and other adverse effects reflect an endogenous form of hypervitaminosis A due to a process involving: mefloquine-induced dehydrogenase inhibition; the accumulation of retinoids in the liver; retinoid-induced hepatocellular damage; the spillage of stored retinoids into the circulation; and the transport of these compounds to the gut and brain in toxic concentrations. The retinoid hypothesis could be tested clinically by comparing cases of mefloquine toxicity and untreated controls in terms of retinoid profiles (retinol, retinyl esters, percent retinyl esters, and retinoic acid). Subject to such tests, retinoid profiling could provide an indicator for assessing mefloquine-associated adverse effects.

 

Role of Retinoid Signaling in the Brain: 

http://www.ncbi.nlm....pubmed/15882777

 

It seems like Mifepristone may be a viable treatment.  http://www.ncbi.nlm....pubmed/24346134

 

 

 

Clinical reports have highlighted a role for retinoids in the etiology of mood disorders. Although we had shown that recruitment of the nuclear receptor retinoic acid receptor-α (RAR-α) to corticotropin-releasing hormone (CRH) promoter is implicated in activation of the hypothalamus-pituitary-adrenal (HPA) axis, further insight into how retinoids modulate HPA axis activity is lacking. Here we show that all-trans retinoic acid (RA)-induced HPA activation involves impairments in glucocorticoid receptor (GR) negative feedback. RA was applied to rats chronically through intracerebroventricular injection. A 19-day RA exposure induced potent HPA axis activation and typical depression-like behavior. Dexamethasone failed to suppress basal corticosterone (CORT) secretion, which is indicative of a disturbed GR negative feedback. In the hypothalamic paraventricular nucleus, increased CRH⁺ and c-fos⁺ cells were found while a negative R-2⁺/ER⁺ correlation was present between the number of RAR-α⁺ and GR⁺ cells. This was paralleled by increased RAR-α and decreased GR protein expression in the hypothalamus. Additional in vitro studies confirmed that RA abolished GR-mediated glucocorticoid-induced suppression of CRH expression, indicating a negative cross-talk between RAR-α and GR signaling pathways. Finally, the above changes could be rapidly normalized by treatment with GR antagonist mifepristone. We conclude that in addition to the 'classic' RAR-α-mediated transcriptional control of CRH expression, disturbances in GR negative feedback constitute a novel pathway that underlies RA-induced HPA axis hyperactivity. The rapid normalization by mifepristone may be of potential clinical interest in this respect.

 

Mifepristone modulates seratonin transporter function  http://www.ncbi.nlm....pubmed/25206868

 

So my initial thoughts for my friend are to go get his retinoid levels tested at the VA, and talk to his doctor about Mifepristone.  Thoughts?

 

[Joe Monroe]

Hey Guys, I have a good friend who was in the special forces and he and several of his buddies are suffering severe depression, suicidal thoughts, low affect, etc.  These guys were given Mefloquine for malaria when they were in the service.  Mefloquine is linked to "severe gastrointestinal and neuropsychiatric adverse effects, including cognitive disturbances, anxiety, depression, psychosis, and violence".

 

One theory on causality:  http://www.ncbi.nlm....pubmed/23852388

 

 

The adverse effects of the drug are thought to result from the secondary consequences of hepatocellular injury; in fact, mefloquine is known to cause a transient, anicteric chemical hepatitis. However, the mechanism of mefloquine-associated liver damage and the associated neuropsychiatric and behavioral effects of the drug are not well understood. Mefloquine and other 8-amino-quinolines are the only antimalarial drugs that target the liver-stage malaria parasites, which selectively absorb vitamin A from the host. Vitamin A is also stored mainly in the liver, in potentially poisonous concentrations. These observations suggest that both the therapeutic effectiveness of mefloquine and its adverse effects are related to the ability of the 8-aminoquinolines to alter the metabolism of retinoids (vitamin A and its congeners). Several lines of evidence support the hypothesis that mefloquine neurotoxicity and other adverse effects reflect an endogenous form of hypervitaminosis A due to a process involving: mefloquine-induced dehydrogenase inhibition; the accumulation of retinoids in the liver; retinoid-induced hepatocellular damage; the spillage of stored retinoids into the circulation; and the transport of these compounds to the gut and brain in toxic concentrations. The retinoid hypothesis could be tested clinically by comparing cases of mefloquine toxicity and untreated controls in terms of retinoid profiles (retinol, retinyl esters, percent retinyl esters, and retinoic acid). Subject to such tests, retinoid profiling could provide an indicator for assessing mefloquine-associated adverse effects.

 

Role of Retinoid Signaling in the Brain: 

http://www.ncbi.nlm....pubmed/15882777

 

It seems like Mifepristone may be a viable treatment.  http://www.ncbi.nlm....pubmed/24346134

 

 

 

Clinical reports have highlighted a role for retinoids in the etiology of mood disorders. Although we had shown that recruitment of the nuclear receptor retinoic acid receptor-α (RAR-α) to corticotropin-releasing hormone (CRH) promoter is implicated in activation of the hypothalamus-pituitary-adrenal (HPA) axis, further insight into how retinoids modulate HPA axis activity is lacking. Here we show that all-trans retinoic acid (RA)-induced HPA activation involves impairments in glucocorticoid receptor (GR) negative feedback. RA was applied to rats chronically through intracerebroventricular injection. A 19-day RA exposure induced potent HPA axis activation and typical depression-like behavior. Dexamethasone failed to suppress basal corticosterone (CORT) secretion, which is indicative of a disturbed GR negative feedback. In the hypothalamic paraventricular nucleus, increased CRH⁺ and c-fos⁺ cells were found while a negative R-2⁺/ER⁺ correlation was present between the number of RAR-α⁺ and GR⁺ cells. This was paralleled by increased RAR-α and decreased GR protein expression in the hypothalamus. Additional in vitro studies confirmed that RA abolished GR-mediated glucocorticoid-induced suppression of CRH expression, indicating a negative cross-talk between RAR-α and GR signaling pathways. Finally, the above changes could be rapidly normalized by treatment with GR antagonist mifepristone. We conclude that in addition to the 'classic' RAR-α-mediated transcriptional control of CRH expression, disturbances in GR negative feedback constitute a novel pathway that underlies RA-induced HPA axis hyperactivity. The rapid normalization by mifepristone may be of potential clinical interest in this respect.

 

Mifepristone modulates seratonin transporter function  http://www.ncbi.nlm....pubmed/25206868

 

So my initial thoughts for my friend are to go get his retinoid levels tested at the VA, and talk to his doctor about Mifepristone.  Thoughts?

As much as it would be nice to just go and get mifepristone prescribed... right now it's only used as an abortion pill,  I think your best bet is to buy mifepristone overseas somewhere like a few others have previously posted doing so... I have been meaning to do this, but I just have been really lazy about working and and just have had too much bills to pay. 

 

Well Merry Christmas everyone

[perplex]

At the risk of deviating from mifrepistone focus,

 

According to the literature i've come across Tianeptine seems like the best candidate for stress-induced HPA-dysregulation. Although I haven't experimented with it myself (yet) reports make it seem quite promising especially for non-cush high cort.

 

http://www.ncbi.nlm..../pubmed/1660816

http://www.ncbi.nlm....pubmed/12445834

http://www.tianeptin...hpa-stress.html

 

anyone with thought or first hand experience?

 

Edited by perplex, 20 January 2015 - 05:46 AM.

[Flex]

Tianeptine was nice for ~2 hours, but gets back to baseline.

In addition to that, my case differs a bit in contrast to others.

[Joe Monroe]

It's hard to find this mifepristone for a reasonable price... I have found a few but wanting 100+ dollars for just one. I was reading ... in india apparently you can get mifepristone for about 5 dollars .. Over the counter on top of that. If only I knew someone in india, or I'm not sure how to go about this. I'm trying to find someone in india that I'd be able to trust and buy from them and send it to me? What do you guys think? I'm sure there's some sites that people use to find jobs, I've ran across a few, but most seem to be online work, like creating websites or scripts for software etc.. 

[Flex]

Apparently: forexworld12 hes from India, on Longecity since ~September and is good with area1255 (if it helps anyhow)

http://www.longecity...ncrease-libido/

[Joe Monroe]

Apparently: forexworld12 hes from India, on Longecity since ~September and is good with area1255 (if it helps anyhow)

http://www.longecity...ncrease-libido/

hey thanks for that! I messaged him 

[tunt01]

mifepristone is also a progesterone receptor agonist in addition to its cortisol action.  does anyone know the long-term implications of using a progesterone receptor agonist?

Edited by prophets, 24 February 2015 - 02:22 PM.

[tunt01]

I had tons of lab work done showing all of my hormone levels, including cortisol, at the very bottom of the "normal" range, and it's still not well established when to prescribe low dose cortisol in chronic fatigue cases.

 

I'm a bit confused as to how you resolved that mifepristone was a good answer for your situation given that it is predominantly used for hypercortisolism and you describe yourself as suffering from low (hypo) cortisol levels.

 

Thanks for any feedback and congrats on your success w/ this ordeal.

[Joe Monroe]

 

I had tons of lab work done showing all of my hormone levels, including cortisol, at the very bottom of the "normal" range, and it's still not well established when to prescribe low dose cortisol in chronic fatigue cases.

 

I'm a bit confused as to how you resolved that mifepristone was a good answer for your situation given that it is predominantly used for hypercortisolism and you describe yourself as suffering from low (hypo) cortisol levels.

 

Thanks for any feedback and congrats on your success w/ this ordeal.

 

 

Mifepristone corrects hpa axis dysfuntional signaling, meaning that it can help with hypo OR hypercortisol

[YoungSchizo]

 

Mifepristone corrects hpa axis dysfuntional signaling, meaning that it can help with hypo OR hypercortisol

 

 

Did you have success contacting the guy from India?

[tunt01]

 

 

Mifepristone corrects hpa axis dysfuntional signaling, meaning that it can help with hypo OR hypercortisol

 

 

Based on what data exactly?

[Joe Monroe]

 

 

 

Mifepristone corrects hpa axis dysfuntional signaling, meaning that it can help with hypo OR hypercortisol

 

 

Based on what data exactly?

 

Well if you read through this thread (which I suggest you should there's a plethora of information regarding mfepristone) at all you would already have your answer but I'll link one of the studies again.. http://journals.plos...al.pcbi.1000273

[Joe Monroe]

 

 

Mifepristone corrects hpa axis dysfuntional signaling, meaning that it can help with hypo OR hypercortisol

 

 

Did you have success contacting the guy from India?

 

 

I actually did but found somewhere else that seemed more promising, I'll let everyone know how it goes. 

[Joe Monroe]

hey you guys figured I'd give an update... so i got the mifepristone, actually got quite a bit for pretty inexpensive. The site I used was http://www.ec21.com/you can actually find all kinds of stuff on there. There's plenty of sellers of this and many are verified. 

 

.. as much as I had hoped this would help, for me personally it didn't. Now let me just say that MOST drugs I try I have an adverse reaction to so.. I think people should try it for themselves... because I know it has the potential to be therapeutic as it seems to have helped "compute this" and there's studies supporting it's positive effects, but for me it mostly just made my sleep off and just put me in a bad mood. I still have plenty left over. 

While I'm pretty disappointed I'll keep looking for an answer... 

 

Right now I'm really looking into bacterial/ viral, specifically "l form bacteria" as to the cause of this state of being... I dunno right now that's what's giving me hope, so trying a new route.  Anyway, hope everyone is well, if anyone has more questions about it feel free to ask anything. I'll keep following this thread. We're in this together. 

[tunt01]

 

.. as much as I had hoped this would help, for me personally it didn't. Now let me just say that MOST drugs I try I have an adverse reaction to so.. I think people should try it for themselves... because I know it has the potential to be therapeutic as it seems to have helped "compute this" and there's studies supporting it's positive effects, but for me it mostly just made my sleep off and just put me in a bad mood. I still have plenty left over. 

While I'm pretty disappointed I'll keep looking for an answer... 

 

Thanks for the update.  I have to say, I don't think it's very surprising that it didn't work.  This drug is meant for people who are hypercortisolism in nature.  I think a lot of COMPUTE's benefit came from the progesterone antagonistic effects, not just the cortisol/GR reset capability.

[YimYam]

Hi guys,

Prophets, as you know from reading my latest thread my issues are quite bizarre.

I very clearly have HPA dysregulation of some kind, but due to severe cognitive issues trying to investigate treatments and find the etiology of my issues along with being able to accurately measure how positively or negatively a drug is affecting me is nigh on impossible; my brain is just completely inactive and unable to quantify my symptoms due to them constantly changing in severerity. So the bottom line is I need a cognitive lift before I can start self experimenting and investigating treatments for my HPA dysregulation.

I really don't want to hijack this amazing thread so if anyone is able to offer some advice for cognitive treatment as a first port of call I'd be ever so grateful. So far I have bought some NSI-189 and plan to buy some Tianeptine sulphate for my cognition but also read here it could help a bit with HPA.

What I would like to know is if they would have an effect on my cognition if my HPA axis is constantly activated or would I have to control my HPA axis first? (Best to provide an answer in my thread, if you have one of of course.. ) Thankyou and keep up the good work on this thread guys.

My thread: http://www.longecity...gaba-gone-gaga/

[tunt01]

I very clearly have HPA dysregulation of some kind,
 

 

Based on what data?  Stop self-rationalizing a medical condition.

 

 

but due to severe cognitive issues trying to investigate treatments and find the etiology of my issues along with being able to accurately measure how positively or negatively a drug is affecting me is nigh on impossible; 

 

 

This obviously depends on the drug.  If you take an ACE inhibitor or an ARB and see your blood pressure drop 10 points, then obviously you can see the effect on some level.  If you have such a severe cognitive impairment and you can't even tell whether or not a drug is making your cognition worse or better, then I would say nothing useful is happening (likely) and the only effect will be bad (probably).

 

my brain is just completely inactive and unable to quantify my symptoms due to them constantly changing in severerity. So the bottom line is I need a cognitive lift before I can start self experimenting and investigating treatments for my HPA dysregulation.

 

 

This can mean so many things.  "brain is inactive" and "constantly changing symptoms" is impossible for anyone to seriously give you advice about, especially in the context of an Internet messaging forum.  How do we know it's not a mitochondrial disease?  How do we know if it's not chronic fatigue syndrome?  How do we know if it's not poisoning (lead, mercury, etc.)?  I suggest you see a neurologist.  

 

Reaching for very experimental drugs (NSI-189) in some hopeful attempt to try anything because it sounds like it might work is dangerous and can possibly make the situation worse.

Edited by prophets, 01 April 2015 - 04:38 PM.