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What to take to facilitate PTSD treatment? HDAC Inhibitor?

ptsd hdac trauma sodium butyrate

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#1 foreseason

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Posted 01 October 2014 - 09:56 AM


I'm currently in therapy to address and treat some PTSD issues. More accurately, I'm dealing with childhood traumas/developmental trauma disorder.

Regardless, I'm trying to figure out what I could take to enhance and facilitate this process. From my limited research it seems an HDAC Inhibitor is what I need. Any suggestions here? Would sodium butyrate make sense? I know depaakote is an option, but I'm not to eager to go that route.

How about other non-HDAC inhibitors?

Any input/suggestions would be greatly appreciated!

#2 foreseason

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Posted 03 October 2014 - 12:48 PM

Nothing at all?  I'd  have to imagine someone has some knowledge in this area. 



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#3 Nemo888

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Posted 03 October 2014 - 01:35 PM

Was an army medic and we sort of have our own collective wisdom.

Start with inositol 2-15 grams a day. Some other guys like niacin in the same scaled dosage range. Doesn't help everyone, but it does do wonders for some.

Phosphatidyl serine and CoQ10 are both good. The HPA can get all screwed up and cortisol and adrenaline become dysregulated. This will help, preferable if you catch it early/

 

Depending on the type of PTSD, and  a number of us think there are types, SSRI's could possibly be contraindicated. It all depends on your kynurenine(KYN) metabolism. If exercise helps and you have symptoms like joint inflammation and peripheral neuropathy it points towards the kyenurenic model. If that is the case stay away from SSRI's and tryptophan. You could erode parts of your hippocampus.  Take supplemental B6 injections and eat a healthy diet. If you also have concussive brain injuries a hormone panel is essential. Resting cortisol, LH, FSH, IGF, TEST, EST etc, Supplemental thymosins can be incredibly helpful in stopping the inflammatory loss of brain matter.

 

I really need to get an essay done on all this. Time is the issue. If there is enough interest I can get off my ass and write it all down eventually.


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#4 foreseason

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Posted 03 October 2014 - 07:50 PM

I appreciate the detailed response.  Lots of information. 

 

What would you recommend if I'm dealing with old, mainly childhood traumas.  Nothing very recent. 



#5 Nemo888

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Posted 04 October 2014 - 07:21 PM

I can't say what kind of changes the PTSD made to your physiology. If you have no other signs of inflammation it may not help much. These interventions are quite safe so ordering some online and giving yourself a month to try them and see how you feel is not too difficult to accomplish.

Expect to be pretty exhausted when you start digging and try and get extra rest. Reliving some shit can wreck you for a few days.

#6 blood

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Posted 05 October 2014 - 09:23 AM

Is there any human research or experience with HDAC inihibitors?
 
My own preference would be to look to drugs where there is at least *some* evidence of benefit (for PTSD) in humans...
 
Some of the SSRIs are FDA approved for PTSD. If you are looking for something a little more experimental, what about angiotensin receptor blockers (ARBs) such as telmisartan:
 

J Clin Psychiatry. 2012 Jun;73(6):849-55. doi: 10.4088/JCP.11m07316. Epub 2012 May 1.

The renin-angiotensin pathway in posttraumatic stress disorder: angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are associated with fewer traumatic stress symptoms.

Khoury NM1, Marvar PJ, Gillespie CF, Wingo A, Schwartz A, Bradley B, Kramer M, Ressler KJ.

Abstract

OBJECTIVE:
Posttraumatic stress disorder (PTSD) is a debilitating stress-related illness associated with trauma exposure. The peripheral and central mechanisms mediating stress response in PTSD are incompletely understood. Recent data suggest that the renin-angiotensin pathway, essential to cardiovascular regulation, is also involved in mediating stress and anxiety. In this study, the authors examined the relationship between active treatment with blood pressure medication, including angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), and PTSD symptom severity within a highly traumatized civilian medical population.

METHOD:
Cross-sectional, observational data were analyzed from a larger study; patients were recruited from Grady Memorial Hospital's outpatient population from 2006 to November 2010. Multivariable linear regression models were fit to statistically evaluate the independent association of being prescribed an ACE inhibitor or ARB with PTSD symptoms, using a subset of patients for whom medical information was available (n = 505). Categorical PTSD diagnosis was assessed using the modified PTSD Symptom Scale (PSS) based on DSM-IV criteria, and PTSD symptom severity (the primary outcome of interest) was measured using the PSS and Clinician Administered PTSD Scale.

RESULTS:
A significant association was determined between presence of an ACE inhibitor/ARB medication and decreased PTSD symptoms (mean PSS score 11.4 vs 14.9 for individuals prescribed vs not prescribed ACE inhibitors/ARBs, respectively [P = .014]). After adjustment for covariates, ACE inhibitor/ARB treatment remained significantly associated with decreased PTSD symptoms (P = .044). Notably, other blood pressure medications, including β-blockers, calcium channel blockers, and diuretics, were not significantly associated with reduced PTSD symptoms.

CONCLUSIONS:
These data provide the first clinical evidence supporting a role for the renin-angiotensin system in the regulation of stress response in patients diagnosed with PTSD. Further studies should examine whether available medications targeting this pathway should be considered for future treatment and potential protection against PTSD symptoms.

© Copyright 2012 Physicians Postgraduate Press, Inc.


Yes, this research is observational, but it's better than nothing... and ARBs have been thoroughly investigated in people (for hypertension) & so their safety profile is known...

Here is a nice summary of some related research (animal model research, looking for a mechanism that might explain the observational findings, above):
 

Common Hypertension Treatment May Reduce PTSD Symptoms

June, 2014

There are currently only two FDA-approved medications for the treatment of posttraumatic stress disorder (PTSD) in the United States. Both of these medications are serotonin uptake inhibitors. Despite the availability of these medications, many people diagnosed with PTSD remain symptomatic, highlighting the need for new medications for PTSD treatment.

The renin-angiotensin system has long been of interest to psychiatry. Some of the first drugs targeting this system were the angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), commonly prescribed treatments for high blood pressure.

In the 1990's, multicenter studies evaluating ACE inhibitors suggested that they improved quality of life as well as other medical outcomes, but these medications did not prove to be sufficiently effective for the treatment of psychiatric disorders to become established treatments.

Recently, however, investigators at Emory University observed that individuals diagnosed with PTSD, and who happened to also be treated with ARBs or ACE inhibitors, exhibited fewer PTSD-like symptoms.

This led the researchers to investigate the underlying mechanisms using an animal model of PTSD in order to expand upon this clinical finding.

Dr. Paul Marvar, first author and Assistant Professor at The George Washington University, explains their findings, "Our current preclinical results show that the ARB losartan, given acutely or chronically to mice, enhances the extinction of fear memory, a process that is disrupted in individuals with PTSD. Overall these data provide further support that this class of medications may have beneficial effects on fear memory in PTSD patients."

Fear extinction is a process by which a memory associated with fear is gradually 'overwritten' in the brain by a new memory with no such association. For example, exposure therapy is a form of fear extinction, whereby repeatedly exposing a patient in a safe manner to a feared object or situation slowly reduces or eliminates their fear. A medication that could potentially enhance the extinction of fear would be welcome to the millions of individuals who continue to suffer with symptoms of PTSD...


Edited by blood, 05 October 2014 - 09:50 AM.

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#7 penisbreath

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Posted 05 October 2014 - 04:03 PM

I find 7,8-Dihydroxyflavone really good for removing that chronic sense of fear; it's like you're mentally still aware of the anxiety, but it seems far easier to confront phobic situations. 



#8 Flex

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Posted 10 November 2014 - 05:42 PM

I´ve found this:

 

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/

 

But I dont know whether those compounds 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.


Edited by Flex, 10 November 2014 - 05:55 PM.


#9 me-i-am

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Posted 26 August 2015 - 08:03 AM

 

I really need to get an essay done on all this. Time is the issue. If there is enough interest I can get off my ass and write it all down eventually.

 

 

Any luck in getting this written down....? Having dealt with long term chronic PTSD I would be interested in knowing as much as I can....



#10 gamesguru

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Posted 26 August 2015 - 07:38 PM

Many genes aggravated in PTSD play a role in normal depression and anxiety, eg. TPH1&2 and SLC6A4 or 5-HTTLPR, FKBP5, SERT, and BDNF.

 

Consider supplements for normal depression, eg. bacopa, turmeric, green tea, zinc, magnesium (pepitas or hemp protein or sprouted grain bread), chromium (broccoli), and lithium (spring or mineral water).

I'm extra curious if Bacopa helps.  It affects SERT and TRP2, and BDNF.

 

PTSD & Exercise: What every exercise professional should know

Low-to-moderate intensity exercise can elevate BDNF and SERT mRNA levels, mood, reduce anxiety, and act as an overall stress-buffer.

 

Glucocorticoid Receptor and FKBP5 Expression Is Altered Following Exposure to Chronic Stress: Modulation by Antidepressant Treatment

Probably due to linkage with BDNF-mediated antidepression (which would suggest exercise/tea/bacopa/curcumin as equally effective antidepressive treatments), though the hen-and-egg question or a dog chasing his tail is what leaps to mind

While glucocorticoid receptors have a key role in HPA axis regulation, they have widespread activity by regulating the transcription of several genes that may also have a role in mood disorders, such as the neurotrophin BDNF. We have recently shown that GR-deficient mice (GR+/), a genetic model of predisposition to depression (Ridder et al, 2005), show altered modulation of BDNF expression in response to an acute stress (Molteni et al, 2010) and impaired adult hippocampal neurogenesis, which is further reduced after stress exposure

 

Dietary Modulation of Uptake Transporters

For the first time, it was reported that green tea and coffee acted as modulators of serotonin uptake

 

 

Additional resources:

Association of posttraumatic stress disorder with reduced in vivo norepinephrine transporter availability in the locus coeruleus

The PTSD group had significantly lower NET availability

 

Postmortem locus coeruleus neuron count in three American veterans with probable or possible war-related PTSD

All three veterans with probable or possible WR-PTSD were found to have substantially lower LC neuronal counts compared to four comparison subjects (three nonpsychiatric veterans and one veteran with alcohol dependence and delirium tremens). To the authors' knowledge, this case series is the first report of LC neuronal counts in patients with PTSD or any other DSM-IV-TR anxiety disorder. Previous postmortem brain tissue studies of Alzheimer's Disease (AD) demonstrated an upregulation of NE biosynthetic capacity in surviving LC neurons. The finding reported is consistent with the similar upregulation of NE biosynthetic capacity of surviving LC neurons in veterans who developed WR-PTSD. Especially if replicated, this finding in WR-PTSD may provide further explanation of the dramatic effectiveness of propranolol and prazosin for the secondary prevention and treatment of PTSD, respectively.

 

Amygdala, Medial Prefrontal Cortex, and Hippocampal Function in PTSD

Neuroimaging research reviewed in this article reveals heightened amygdala responsivity in PTSD during symp- tomatic states and during the processing of trauma-unrelated affective information. Importantly, amygdala responsivity is positively associated with symptom severity in PTSD. In contrast, medial prefrontal cortex appears to be volumetrically smaller and is hyporesponsive during symp- tomatic states and the performance of emotional cognitive tasks in PTSD. Medial prefrontal cortex responsivity is inversely associated with PTSD symptom severity. Lastly, the reviewed research suggests diminished volumes, neuronal integrity, and functional integrity of the hippocampus in PTSD.

 

http://pennstatehers...d=33&gid=000130


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#11 Junk Master

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Posted 26 August 2015 - 10:04 PM

If it's really bad I'd think about trying NSi-189 if you can find a reputable source.  It seems some people respond immediately.



#12 Flex

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Posted 27 August 2015 - 12:43 PM

If it's really bad I'd think about trying NSi-189 if you can find a reputable source.  It seems some people respond immediately.

 

the hengda company was indenpendly tested by the user tolerant but You can find reputable sorces also elsewhere. Just ask on reddit.
 



#13 me-i-am

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Posted 31 August 2015 - 03:24 PM

My PTSD comes from childhood trauma as well and is Chronic PTSD which basically means, its much worse then normal PTSD. Unfortunately it effects everyone differently. For me the main issues are energy levels, anxiety and memory (I had huge gaps in my long term memory almost to the point of amnesia). So far Bacopa and oddly Piracetam seemed to have helped a bit with regaining some of that long term memory. It's quite nice to access to memories again!

 

I am still grappling with whats the best way to eliminate anxiety and trying some of the info here in this thread:  /54028-treating-anxiety-safely-effectively/

 



#14 sentics

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Posted 30 November 2018 - 11:05 AM

what about Valproic acid/Valproate?

 

https://www.ncbi.nlm...pubmed/22992332


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#15 MankindRising

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Posted 01 December 2018 - 01:57 PM

what about Valproic acid/Valproate?

 

https://www.ncbi.nlm...pubmed/22992332

Its pure toxic. In fact its used in animal models to mimic social deficits in autism, stay far far away from that...







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