Improving mitochondrial function may treat PTSD

haidut

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The study actually does not say that directly, but I am making the prediction based on other information I have learned over the years, and I am posting the studies that back it up.

Here is the study that talks about blood pressure drugs in the categories ACE and ARB help PTSD:

http://www.sciencedaily.com/releases/20 ... 093354.htm

Now, here is another study that says the drug losartan which is a known ACE/ARB boosts mitochondrial biogensis:
http://www.hopkinsmedicine.org/news/med ... ed_by_drug
http://www.ncbi.nlm.nih.gov/pubmed/12709417
http://www.ncbi.nlm.nih.gov/pubmed/20145991

So, based on Peat's writings on the link between bioenergetics and mental disorders, and other studies I have read I am suggesting that the positive effects of ACE/ARB drugs on PTSD are due to the mitochondrial rejuvenation effect of those drugs. Also, given that I like to point out natural alternatives with similar effects, taurine is a known ACE/ARB compound with known effects on both blood pressure and mitochondrial activity.

http://www.ncbi.nlm.nih.gov/pubmed/10949914
http://www.ncbi.nlm.nih.gov/pubmed/16025228
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994382/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136959/
http://www.sciencedirect.com/science/ar ... 3612715896
http://link.springer.com/chapter/10.100 ... 33504-9_13
http://abbs.oxfordjournals.org/content/ ... 9.abstract
http://wires.wiley.com/WileyCDA/WiresAr ... RNA65.html
http://www.ncbi.nlm.nih.gov/pubmed/12717106
http://journals.lww.com/cardiovascularp ... ced.4.aspx
http://jra.sagepub.com/content/early/20 ... 13481255v1


So, taurine could be useful for PTSD, well in line wit Peat's recommendations of its general usefulness.
 

Suikerbuik

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So, based on Peat's writings on the link between bioenergetics and mental disorders, and other studies I have read I am suggesting that the positive effects of ACE/ARB drugs on PTSD are due to the mitochondrial rejuvenation effect of those drugs.

http://www.ncbi.nlm.nih.gov/pubmed/19763608
The absence of AT(1A) protected multiple organs from oxidative damage and the alleviation of aging-like phenotype was associated with increased number of mitochondria and upregulation of the prosurvival gene sirtuin 3

ACE/ARBs and stress response:

http://www.ncbi.nlm.nih.gov/pubmed/15837532
The brain and the peripheral (hormonal) angiotensin II systems are stimulated during stress. Activation of brain angiotensin II AT(1) receptors is required for the stress-induced hormone secretion, including CRH, ACTH, corticoids and vasopressin, and for stimulation of the central sympathetic activity. Long-term peripheral administration of the angiotensin II AT(1) antagonist candesartan blocks not only peripheral but also brain AT(1) receptors, prevents the hormonal and sympathoadrenal response to isolation stress and prevents the formation of stress-induced gastric ulcers.
The mechanisms responsible for the prevention of stress-induced ulcers by the AT(1) receptor antagonist include protection from the stress-induced ischemia and inflammation (neutrophil infiltration and increase in ICAM-1 and TNF-alpha) in the gastric mucosa and a partial blockade of the stress-induced sympathoadrenal stimulation, while the protective effect of the glucocorticoid release during stress is maintained. AT(1) receptor antagonism prevents the stress-induced decrease in cortical CRH(1) and benzodiazepine binding and is anxiolytic. Blockade of brain angiotensin II AT(1) receptors offers a novel therapeutic opportunity for the treatment of anxiety and other stress-related disorders.

http://www.ncbi.nlm.nih.gov/pubmed/20827339
Taken together, these results show that olmesartan at low concentrations inhibits the CA secretion evoked by cholinergic stimulation (both nicotininc and muscarinic receptors) as well as by direct membrane depolarization from the rat adrenal medulla, but at high concentrations it rather potentiates the ACh-evoked CA secretion. It seems that olmesartan has a dual action, acting as both agonist and antagonist at nicotinic receptors of the isolated perfused rat adrenal medulla, which might be dependent on the concentration. It is also thought that this inhibitory effect of olmesartan may be mediated by blocking the influx of both Na(+) and Ca(2+) into the rat adrenomedullary chromaffin cells as well as by inhibiting the Ca(2+) release from the cytoplasmic calcium store, which is thought to be relevant to the AT(1) receptor blockade, in addition to its enhancement on the CA secreton.
 
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haidut

haidut

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Suikerbuik said:
So, based on Peat's writings on the link between bioenergetics and mental disorders, and other studies I have read I am suggesting that the positive effects of ACE/ARB drugs on PTSD are due to the mitochondrial rejuvenation effect of those drugs.

http://www.ncbi.nlm.nih.gov/pubmed/19763608
The absence of AT(1A) protected multiple organs from oxidative damage and the alleviation of aging-like phenotype was associated with increased number of mitochondria and upregulation of the prosurvival gene sirtuin 3

ACE/ARBs and stress response:

http://www.ncbi.nlm.nih.gov/pubmed/15837532
The brain and the peripheral (hormonal) angiotensin II systems are stimulated during stress. Activation of brain angiotensin II AT(1) receptors is required for the stress-induced hormone secretion, including CRH, ACTH, corticoids and vasopressin, and for stimulation of the central sympathetic activity. Long-term peripheral administration of the angiotensin II AT(1) antagonist candesartan blocks not only peripheral but also brain AT(1) receptors, prevents the hormonal and sympathoadrenal response to isolation stress and prevents the formation of stress-induced gastric ulcers.
The mechanisms responsible for the prevention of stress-induced ulcers by the AT(1) receptor antagonist include protection from the stress-induced ischemia and inflammation (neutrophil infiltration and increase in ICAM-1 and TNF-alpha) in the gastric mucosa and a partial blockade of the stress-induced sympathoadrenal stimulation, while the protective effect of the glucocorticoid release during stress is maintained. AT(1) receptor antagonism prevents the stress-induced decrease in cortical CRH(1) and benzodiazepine binding and is anxiolytic. Blockade of brain angiotensin II AT(1) receptors offers a novel therapeutic opportunity for the treatment of anxiety and other stress-related disorders.

http://www.ncbi.nlm.nih.gov/pubmed/20827339
Taken together, these results show that olmesartan at low concentrations inhibits the CA secretion evoked by cholinergic stimulation (both nicotininc and muscarinic receptors) as well as by direct membrane depolarization from the rat adrenal medulla, but at high concentrations it rather potentiates the ACh-evoked CA secretion. It seems that olmesartan has a dual action, acting as both agonist and antagonist at nicotinic receptors of the isolated perfused rat adrenal medulla, which might be dependent on the concentration. It is also thought that this inhibitory effect of olmesartan may be mediated by blocking the influx of both Na(+) and Ca(2+) into the rat adrenomedullary chromaffin cells as well as by inhibiting the Ca(2+) release from the cytoplasmic calcium store, which is thought to be relevant to the AT(1) receptor blockade, in addition to its enhancement on the CA secreton.

Thanks, that's good info. So, is it fair to say drugs like candesartan would be good options for things like IBS that are known to be associated with both stress ulcers and the stress process itself?
 

Suikerbuik

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I would avoid the ARB-/ACE HCT (hydrochlorothiazide) drugs in any case. Anyway I don't know what candesartan might be wise for use in the long term. For short term it can really be useful for sure.
 

Mr Joe

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@haidut thank you for these articles. You've said in an other thread : "Last, traumatic memories may be a lot more difficult to erase once formed, which is not very good news for people with PTSD. " Would you think that improving mitochondial function could help erasing fear once memerized ? What would you suggest as a good approche for memorized fears ?
 

Hans

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@haidut thank you for these articles. You've said in an other thread : "Last, traumatic memories may be a lot more difficult to erase once formed, which is not very good news for people with PTSD. " Would you think that improving mitochondial function could help erasing fear once memerized ? What would you suggest as a good approche for memorized fears ?
5-HT2A, adrenergic and glutamate antagonists can help a lot against fear.

Magnesium might be very useful here as it reduces serotonin induced sensitization of 5-HT2A, antagonizes NMDA and angiotensin II and lowers noradrenaline and CRH.
 

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