149 replies to this topic

[kurdishfella]

 

 

 

 

 

 

 

 

 

 

''google ''antidepressants that inhibit crh'' etc

[kurdishfella]

prazosin and propranolol?https://www.ncbi.nlm...pubmed/21409840

 

tiagabine https://www.ncbi.nlm...pubmed/19346277

 

?paxil?escitalopram/citalopram??sertraline??

 

lorazepam?xanax etc , I  honestly don't find clonazepam/klonopin to have any anxiolytic relief at all  ,even taking 8mg at once I feel nothing from clonazepam.

 

Anticorticotropin

https://en.wikipedia...ticorticotropin

 

https://www.physiolo...1999.277.2.g391

 

Propylthiouracil (PTU)-induced hypothyroidism caused a significant reduction in CRH gene transcripts in the paraventricular nucleus of rats.

https://www.ncbi.nlm.../pubmed/8119200

 

pentobarbital

''Furthermore, blocking the neuroexcitant effects of CRH (using pentobarbital) abolished the alterations in CRF₁ binding and expression. These results indicate that CRF₁ regulation involves both occupancy of this receptor by its ligand, as well as “downstream” cellular activation and suggest that stress-induced perturbation of CRH–CRF₁ signaling may contribute to abnormal neuronal communication after some stressful situations.”

https://www.ncbi.nlm...les/PMC2930769/

 

Histone deacetylase 1 (HDAC1) participates in the down-regulation of corticotropin releasing hormone gene (crh) expression.
https://www.ncbi.nlm...pubmed/21463644 (Trichostatin A)

 

Edited by farshad, 14 September 2018 - 07:31 AM.

[kurdishfella]

-------READ-------

 

 

Substances That Decrease CRH

https://www.selfdecode.com/gene/crh/

 

Substances That Decrease CRHR1

https://www.selfdecode.com/gene/crhr1/

 

Im too lazy to go trough all the selfdecode drugs and see which ones inhibit CRH but here is a list I have made of all the drugs that lower CRH that I have posted on this thread:

(the ones in bold I recommend)

 

-Prochloraz (By using correlation analyses, it was found that the decrease in E2 plasma concentrations caused by PCZ was correlated with the down-regulation of CRH mRNA expression.)

-Pentobarbital (Furthermore, blocking the neuroexcitant effects of CRH (using pentobarbital) abolished the alterations in CRF1 binding and expression)
-Propylthiouracil (Propylthiouracil (PTU)-induced hypothyroidism caused a significant reduction in CRH gene transcripts in the paraventricular nucleus of male rats)
-Clomipramine (It was found that clomipramine lowers CRH mRNA expression in the PVN by 74%, regardless of stressor conditions)
-Pivagabine (pivagabine is now believed to act somehow via modulation of corticotropin-releasing factor (CRF).)
-Imipramine (As assessed by in situ hybridization, 8 wk of daily imipramine treatment (5 mg/kg, i.p.) in rats decreased corticotropin-releasing hormone (CRH) mRNA levels by 37% in the paraventricular nucleus (PVN) of the hypothalamus)
-Valproic acid (Moreover, CRF mRNA expression was decreased in the central nucleus of the amygdala (CeA) and paraventricular nucleus (PVN) of the hypothalamus.)
-Carbamazepine (Although CBZ has been shown to inhibit hypothalamic CRH secretion in vitro)
-Tiagabine (blockade induced a setpoint-shift of the stress hormone system toward lower levels as indicated by decreased plasma corticosterone concentrations and attenuated gene expression levels of corticotropin-releasing factor in the paraventricular nucleus of the hypothalamus)
-Xanax
-Diazepam
-Lorazepam
-Thorazine
-Haldol
-Clozapine
-Thioridazine

-Zyprexa

-Raclopride
 
Im leaning towards these: Clomipramine, Propylthiouracil, Carbamazepine or Valproic Acid. Any suggestion or ideas? Not sure how many people  keep up with this thread lol or care.

 

Maybe I will skip out on Propylthiouracil becuase: On this study using St John's wort https://www.ncbi.nlm...ubmed/11526469 ''it says: significantly decreased levels of corticotropin-releasing hormone (CRH) mRNA by 16-22% in the hypothalamic paraventricular nucleus (PVN)''

Same wording was used on the Propylthiouracil study: ''caused a significant reduction in CRH gene transcripts in the paraventricular nucleus''

So im assuming Propylthiouracil reduced CRH about the same as St John's wort.

So...

 

TOP CRH blockers..

1. Clomipramine

2. Carbamazepine

3. Valproic Acid

 

WTF even causes high CRH-CRHR1 signaling? Graves' disease, autoimmune disorder(autoimmune hypothalamic disease)/HPA Axis  disease, crh-secreting tumor(unless the tumor is in brain which mine wasn't cause I did an scan on my brain but not full body , anyway I don't think it would affect my anxiety) or hypermorphic mutation? Last one I think is my problem not 100% sure tho..

 

CRHR1 recepor can only be activated with CRH so it is not possible for me to have like too many CRHR1 receptors or my body somehow activates CRHR1 without CRH? I don't think so.

Edited by farshad, 14 September 2018 - 09:09 AM.

[kurdishfella]

Tiagabine  is also used   off-label in the treatment of anxiety disorders and panic disorder.

 

https://en.wikipedia.../wiki/Tiagabine

 

and also probably many Antithyroid agents etc reduce CRH.

 

 

Edited by farshad, 14 September 2018 - 09:27 AM.

[kurdishfella]

Regarding CRH-Secreting tumor : However, research has revealed that when high levels of corticotrophin-releasing hormone occur in tissues outside the brain, they can actually have a powerful inflammatory action.

[kurdishfella]

Also Note: most supplements I posted are way too weak to have any remarkable effect on reducing CRH that is why I didn't include them on the big post.

 

Dynorphins, Dipyrone, Zeranol & Indomethacin: Decreases reaction(CRH).

 

Thiamazole/Carbimazole?<  Perchlorate results in decreased expression of CRHR1 mRNA.

 

Promazine, Ketamine, Naloxone, Terbutaline, Vanadyl Sulfate, Risperidone, Prednisolone, Nicotine results in decreased expression of CRH mRNA.

 

Mifepristone, Manganese, Hu 211, Cycloheximide, Astemizole, Colchicine, Rimonabant, Naltrexone: decreased secretion of CRH.

 

Out of everything I have posted: Imipramine, Pivagabine,Tiagabine, Propylthiouracil, Clomipramine, Valproic acid & Carbamazepine seem the most promising.

 

Manganese & Vanadyl Sulfate (both supplements) I think are too weak. Who knows...  The other recent drugs above are just random category drugs.

 

Edited by farshad, 15 September 2018 - 05:44 AM.

[kurdishfella]

adenylate cyclase is an enzyme with key regulatory roles in essentially all cells.

 

DNA > mRNA > Protein(CRH cells)

 

I did a search on SelfDeCode and it turns out I have 6 mutations for regulating Protein expression...

 

https://www.selfdecode.com/gene/mc4r/

''The mutant version of the MC4R gene produces a protein receptor that doesn't activate as well - it is less sensitive to signals from the body that tell the body that it is already full.''

 

https://www.selfdeco...om/gene/mtnr1b/

''The activity of this receptor is mediated by pertussis toxin sensitive G proteins that inhibit adenylate cyclase activity.''

 

https://www.selfdecode.com/gene/chrm3/

''It also inhibits adenylate cyclase''

 

https://www.selfdeco...om/gene/gabbr2/

''Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase.''

 

https://www.selfdecode.com/gene/adrb1/

''Beta-adrenergic receptors mediate the catecholamine-induced activation of adenylate cyclase through the action of G proteins. ''

 

https://www.selfdecode.com/gene/fshr/

''The activity of this receptor is mediated by G proteins which activate adenylate cyclase.''

 

So this means due to all these mutations stacking up the adenylate cyclase which is supposed to regulate CRH is not being regulated.

 

I also have a mutation in my CRHR1 but not CRH or CRHR2. But CRHR1 can only be activated Via CRH right? So what would be causing high CRH to go trough CRHR1? Is it possible that due to the mutations not regulating the CRH protein cells and it somehow overactives CRHR1 which slowly made me more susceptible/prone to stress and the anxiety effect built up ? Is it possible due to the mutation in CRHR1 demands more CRH to be made? No idea or do I have a gene duplication in CRH/CRHR1?.. (doubt it)

I don't think I have a CRH-Secreting tumor either well atleast not in the brain tissues cause I did a brain scan but not full body anyhow outside of brain tissue it wouldn't affect me anyway.

 

Here are my CRHR1 mutations but I have no idea what they mean:

 

https://www.selfdecode.com/gene/crhr1/

https://www.selfdeco...gene/crhr1-it1/ (gene duplication?) <-? Intronic RNAs constitute the major fraction of the non-coding RNA in mammalian cells)

https://www.selfdeco...mgc57346-crhr1/ (gene duplication?) <-? ADP-ribosylation factor)

 

Hm.....So I doubt I have gene duplication either , and no tumors either, and I don't think my body is making excess CRH mRNA. It is just my body is not enzyme (adenylate cyclase) is not regulating CRH protein expression..

 

it is possible to have low mRNA but high protein expression becuase a single mRNA molecule can stick around and be translated many times (which mine is becuase the enzyme is not regulating it!!!!!!!!)

 

Consider an enzyme: An mRNA molecule is translated to make a protein, which has enzymatic activity on some substrate, and can be regulated.

 

Expression is a readout for the translation of the mRNA into stable protein. 

 

constitutive protein activity - "Constitutive" activity means that the regulation of the enzyme's activity is gone, it's been mutated or something to allow it to always be active.

 

So the text in Bold I believe  is the issue, Are there any other things Im forgetting besides adenylate cyclase?

Becuase my DNA is fine then > mRNA is fine then when it is about to become protein the adenylate cyclase enzymes has to be active and able to regulate how much is becoming CRH protein...Now once it is an CRH protein I think the adenylate cyclase still can regulate it but the multiple mutation stacks are too many and the CRH becomes excess and now the CRHR1 mutations play a role and gets overactivated.

 

In that case Clomipramine I think wouldn't work? maybe possibly because it is reducing mRNA so less mRNA is being translated over and over, I would have to take something that inhibits CRH like Carbamazepine.

And the CRHR1 mutations no idea what they mean but Valproate decreases CRHR1 somehow.

Naltrexone is also an option.

Edited by farshad, 16 September 2018 - 07:33 AM.

[kurdishfella]

UGH! all these mutations.. I think im gonna lose my mind.. I dont know what is right and what is not.

 

effectors. Effectors are small molecules which modulate the enzyme activity.

 

https://www.selfdecode.com/gene/met/

''Acts as a receptor for Listeria internalin inlB, mediating entry of the pathogen into cells''

 

https://www.selfdecode.com/gene/erbb4/

''This gene encodes a protein that works as a cell surface receptor.'

 

https://www.selfdecode.com/gene/ikzf3/

''Plays an essential role in regulation of B-cell differentiation, proliferation and maturation to an effector state.''

 

https://www.selfdecode.com/gene/yap1/

''as a transcriptional regulator of this signaling pathway''

 

Forget it. Im just gonna focus on CRH-CRHR1 and High CRH protein expression or CRH mRNA being recycled (longer half-life too) and translated many times to CRH-Protein which activates CRHR1 or both combined...

 

https://www.selfdecode.com/gene/npsr1/

''Neuropeptide S (NPS) and its receptor NPSR1 act along the hypothalamic-pituitary-adrenal axis to modulate anxiety''... cytokine interleukin 8 (IL8), and the interleukin 6 receptor (IL6R) etc...!!!!!!

 

Forskolin-stimulates platelet adenylyl cyclase activity... could this reduce CRH?

''The relative amounts of heavy and light components

of forskolin-stimulated adenylate cyclase obtained in

sucrose gradient differential sedimentation were determined

as a function of time beginning 24 h after the

transfer into the heavy medium. The decrease of the

pre-existing light form could be represented by simple

first order kinetics with a half-time of 40 h. This result

suggests that the metabolic renewal of forskolin-stimulated

adenylate cyclase is comparable to that of most

plasma membrane proteins.''

 

Edited by farshad, 16 September 2018 - 10:00 AM.

[kurdishfella]

''On the other hand, cocaine-induced iCRH secretion was inhibited by GABA, a potent inhibitor of CRH secretion, dexamethasone, verapamil, a calcium channel blocker, tetrodotoxin, a sodium channel blocker, and carbamazepine, an antiepileptic and antidepressive agent.''

https://www.ncbi.nlm.../pubmed/2611679

 

CRH-inhibitors:

 

1. Clomipramine

2. Carbamazepine

3. Valproate

4. Verapamil

5. Indomethacin

6. Naloxone

7. Terbutaline

8. Prednisolone

9. Mifepristone

10. Naltrexone

11. Tiagabine

12. Imipramine

13. Pivagabine

14. Propylthiouracil

15. Xanax

16. Diazepam
17. Lorazepam(?)
18. Thorazine
19. Haldol
20. Clozapine
21. Thioridazine
22. Zyprexa
23. Raclopride

24. Promazine

25. Risperidone

Edited by farshad, 21 September 2018 - 08:44 AM.

[kurdishfella]

  26. dexamethasone

Edited by farshad, 22 September 2018 - 08:22 AM.

[kurdishfella]

Excess CRH-CRHR1 signaling causes high serotonin release which in turn makes your mouth produce a lot of saliva becuase of stress.

Edited by farshad, 22 September 2018 - 10:01 AM.

[kurdishfella]

BUMP. no1 knows any other meds/drugs that inhibit CRH that I haven't mentioned yet? So far the top 3 seem to be:

1. Carbamazepine

2. Valproate

3. Clomipramine

 

options also:  Indometacin, Verapamil, Terbutaline,Prednisolone,Naltrexone,Tiagabine,Imipramine ,dexamethasone , Raclopride and Pivagabine,

 

(edit) whoa: ''a slight inhibitory effect of cimetidine on CRH mRNA expression in the PVN.''

''Cimetidine, sold under the brand name Tagamet among others, is a histamine H₂ receptor antagonist that inhibits stomach acid production.^[2][8][9] It is available over-the-counter and is mainly used in the treatment of heartburn and peptic ulcers.''

Edited by farshad, 23 September 2018 - 10:07 PM.

[kurdishfella]

''Tianeptine also reduces levels of CRH mRNA in the dorsal and ventral bed nucleus of the stria terminalis and in the central amygdala ( central nucleus of the amygdala) in both naı¨venaı¨ve and chronic mild stressed rats''

 

https://www.research...ss-exposed_rats

 

''Noradrenaline and glycine decreased the spontaneous release of CRH from the hypothalamus but neither of these substances affected hypothalamic CRH content''

https://www.ncbi.nlm...les/PMC1353568/

Edited by farshad, 01 October 2018 - 06:47 PM.

[kurdishfella]

or due to excess production of hypothalamus CRH (Corticotropin releasing hormone) (tertiary hypercortisolism/hypercorticism). 

[kurdishfella]

The antidepressant agomelatine inhibits stress-mediated changes in amino acid efflux in the rat hippocampus and amygdala.

https://www.ncbi.nlm...ubmed/22647752?

[kurdishfella]

Rhodiola Rosea and Schisandra have a noticable effect on CRH

 

Withania also.

 

https://www.ncbi.nlm...les/PMC4727095/

 

Phosphatidylserine too.

 

Xiao Yao San lowers CRH and possibly CRHR1.

 

https://www.ncbi.nlm...les/PMC4109698/

 

Tulsi (Holy basil) reduced cortisol by reducing CRHR1 receptor density.

 

https://www.ncbi.nlm...pubmed/26899341

https://www.ncbi.nlm...les/PMC5855364/

[kurdishfella]

treatment with fluoxetine (Prozac) prevents the increased CRH expression in the amygdala, and decreased CRHR1 expression in the hippocampus in male Wistar rat.

[MankindRising]

Probiotic Lactobacillus casei strain Shirota relieves stress‐associated symptoms by modulating the gut–brain interaction in human and animal models

https://onlinelibrar....1111/nmo.12804

 

Academic stress‐induced increases in salivary cortisol levels and the incidence rate of physical symptoms were significantly suppressed in the LcS group compared with the placebo group. In rats pretreated with LcS, WAS‐induced increases in plasma corticosterone were significantly suppressed, and the number of CRF‐expressing cells in the PVN was reduced. Intragastric administration of LcS stimulated gastric vagal afferent activity in a dose‐dependent manner.

 

FYI: that is Yakult, an easily obtainable probiotic.

[kurdishfella]

0. chronic lithium treatment decrease CRHR1 mrna in the amygdala(where in the amygdala tho?)

'Lithium administration decreased CRF(1) mRNA expression in both the amygdala and frontal cortex'' https://www.ncbi.nlm...pubmed/12606697

1. Chronic dosage of XiaoYaoSan decrease CRHR1 binding in the (basal?) amygdala

Results. Chronic pretreatment with Xiaoyaosan or antalarmin significantly reversed elevated anxiety-like behavior and the upregulated level of CRF1R and BDNF in the amygdala of stressed rats. pCREB did not differ significantly among the groups. https://www.hindawi....m/2016/1238426/

https://www.amazon.c...B001MAVEV6?th=1

 

2. Holy Basil block CRHR1 receptor(pituitary hypothalamus?)

https://www.gaiaherb...Holy-Basil-Leaf

Thus, O. sanctum(holy basil) was found to be effective in the management of stress effects, and anti-stress activity could be due to inhibition of cortisol release, blocking CRHR1 receptor. https://www.ncbi.nlm...pubmed/26899341

3. Tianeptine reduce CRH mRNA in the Central nucleus of the amygdala. Not good enough, we need something that decrease CRHR1 binding there.

https://www.ncbi.nlm...les/PMC2701287/

https://mitolab.com/...-ml-30ml-100ml/

 

4.  Prozac decreased CRHR1 expression in the hippocampus 

https://www.research...ssness_paradigm

 

5. CRF1 receptor binding was decreased in both the basolateral amygdala and cortex by Valproic acid.

 

So from this I can gather. Valproate/valproic acid (XR) mix + Prozac + Holy Basil(if holy basil does decrease CRHR1 receptor activity in the pituitary) + and something that decrases CRHR1 binding in the central amygdala, for now tianeptine will do I guess until I find something else, possibly wont even need to. And also locus ceruleusand has CRHR1 receptors... But I hope the combination I put up will be enough...

 

Why these places? well they are involved in social defeat you can read more social defeat here: https://en.wikipedia...i/Social_defeat

''Social defeat is a source of chronic stress in animals and humans, capable of causing significant changes in behaviour, brainfunctioning, physiology, neurotransmitter and hormone levels, and health (Bjorkqvist, 2001; Rohde, 2001; Allen & Badcock, 2003).''

''Research also implicates that the referred behavioral effects are moderated by neuroendocrine phenomena involving serotonin, dopamine, epinephrine, norepinephrine, and in the hypothalamic-pituitary-adrenal axis, locus ceruleusand limbic systems (Bjorkqvist, 2001; Rygula et alli, 2005; Selten & Cantor-Graae, 2005; Marinia et alli, 2006; Huhman, 2006).''
''Anatomical connections between brain areas such as the amygdala, hippocampus, prefrontal cortex and hypothalamus facilitate activation of the HPA axis'' 

 

Edited by farshad, 20 November 2018 - 05:18 AM.

[kurdishfella]

https://en.wikipedia...onvulsant#Drugs

possibly many interact with crhr1 

 

also clomipramine doesen't work, reducing crh in the pvn is useless. you have to target cortex,hippocampus, basal and central amygdala & hypothalamus (pituitary). these places have crhr1 receptors you wanna either decrease crh or crhr1 binding/activity/mRNA etc etc  in these specific places.

Edited by farshad, 25 November 2018 - 12:33 PM.

[kurdishfella]

Escitalopram also decreased hippocampal CRF/CRH transcript.

 

Administration of Citalopram increases estrogen and progesterone production, but it does not alter gene expression of Fev, TPH2, SERT or 5HT1A in the dorsal raphe nucleus. Rather, it decreases CRH innervation in the raphe.

 

Fluoxetine inhibits corticotropin-releasing factor (CRF)-induced behavioural responses in rats.

 

the SSRI paroxetine appears to return CRF/CRH levels effectively to normal while adjusting the animals increased receptor sensitivity to more normal levels, as well. in addition, the medication produces an overall reduction of undesirable fearful and anxious behaviour.

 

The effects of the selective serotonin reuptake-inhibitor fluvoxamine on body weight in Zucker rats are mediated by corticotropin-releasing hormone.

 

OBX-induced increases in CRF concentrations in the hypothalamus and bed nucleus of the stria terminalis were specifically and significantly decreased by sertraline. OBX-induced increases in TRH concentrations in the hypothalamus were reversed by sertraline. The concentration of SRIF was significantly reduced by OBX in the anterior caudate and the piriform cortex, but sertraline reversed these changes only in the anterior caudate.

Edited by farshad, 04 December 2018 - 10:32 PM.

[kurdishfella]

Hypomethylation and hyperacetylation is associated with increased CRHR1 expression.

Hypoxia too. (Lactic acid)

Edited by farshad, 10 December 2018 - 06:53 PM.

[kurdishfella]

xanax similar to valproate

 

Both acute and chronic alprazolam administration was found to decrease CRF concentrations within the locus coeruleus. Furthermore, chronic alprazolam decreased basal activity of the hypothalamic–pituitary–adrenal axis, CRF mRNA expression in the central nucleus of the amygdala, and CRF1 mRNA expression and receptor binding in the basolateral amygdala. In marked contrast, urocortin mRNA expression in the Edinger-Westphal nucleus and CRF2A receptor binding in the lateral septum and ventromedial hypothalamus were increased. Similar findings of an inverse relationship between the CRF1 and CRF2A receptor systems have been reported in an anxiety model based on adverse early-life experience, suggesting the intriguing possibility that CRF neuronal systems may be comprised of two separate, but interrelated, subdivisions that can be coordinately and inversely regulated by stress, anxiety, or anxiolytic drugs

[kurdishfella]

Pre-perfusion with sub-therapeutic concentration lamotrigine  inhibited CRF1-induced serotonin reduction without affecting CRF2-induced serotonin release, LTG  inhibits CRF1-receptor-mediated serotonergic transmission.

 

[kurdishfella]

http://science.scien...t/333/6051/1903

Glutamatergic and Dopaminergic Neurons Mediate Anxiogenic and Anxiolytic Effects of CRHR1

 

 

too much crhr1 activation increases anxiety but too little also increases anxiety due to lowered dopamine in one part of the brain, so it is about having an balance.

Edited by farshad, 25 January 2019 - 08:52 PM.

[kurdishfella]

my theory is if you have too much crhr1 activation in the hippocampus you cannot exhibit self-control to stress. the hippocampus regulates how well you handle stress if you should react or not. Together with too much crhr1 in the basal amygdala which means you see more things as stress-inducing and which will dysregulated everything. Too little crhr1 you end up with too little dopamine in certain areas needed to overcome fear.

[kurdishfella]

CRHR1Polymorphisms

[kurdishfella]

Can CRHR1 activators help depression by increasing serotonin and possibly have an anti-anxiety effect by increasing dopamine? (hippocampus,amygdala), just a little activation but not too much becuase it would be counterproductive. Together with a FAAH - inhibitor mechanism or magl inhibitor just incase so the anxiety / depression wont be too much cause of the CRHR1 activation. 

 

 

too much CRHR1 activation:

 

Hippocampus > Basal amygdala > Central amygdala > repeat

Edited by farshad, 10 February 2019 - 07:38 PM.

[kurdishfella]

lexapro decreased CRF transcript in the hippocampal DG

 

olanzapine inhibits stimulated CRH release from the hippocampus

 

Xiaoyaosan Results. Chronic pretreatment with Xiaoyaosan or antalarmin significantly reversed elevated anxiety-like behavior and the upregulated level of CRF1R (others?) and BDNF in the amygdala of stressed rats. 

https://www.hindawi....m/2016/1238426/

 

valproic acid and lithium https://www.ncbi.nlm...pubmed/12606697

and https://www.ncbi.nlm...pubmed/11331142

 

Edited by farshad, 15 February 2019 - 05:14 PM.

[kurdishfella]

the researchers at Stanford found that the larger the amygdala—and the stronger its connections with other regions of the brain responsible for perception and the regulation of emotion—the greater the amount of anxiety a child was experiencing. the amygdala is an evolutionarily primitive part of the brain located deep in the temporal lobe. It comprises several subregions associated with different aspects of perceiving, learning, and regulating emotions. Studies of laboratory animals placed in an environment causing chronic stress have determined that the animals' amygdalae grew additional synapses and that this synaptic connectivity resulted in chronic anxiety. The Stanford researchers acknowledge that some anxiety is an important emotional and biological reaction to both 'eustress' (good stress) and 'distress' (bad stress) at all stages of life. However, sustained anxiety can lead to disabling conditions such as phobia, post-traumatic stress disorder(PTSD) and generalized anxiety disorder. Studies of adults suffering from anxiety disorders have shown that they also possess enlarged, highly connected amygdalae. The basolateral amygdala is the specific region that was larger in children with higher anxiety. This is an evolutionarily older and ‘primal’ subregion which processes emotion-related sensory information and communicates it to the more cerebral neocortex which is an evolutionarily newer part of the brain. "The basolateral amygdala had stronger functional connections with multiple areas of the neocortex in children with higher anxiety levels,"

 

https://www.psycholo...redicts-anxiety

 

https://www.psychiat...polar-disorder/

 

btw regarding lexapro and hippocampal the DG stands for: https://en.wikipedia...i/Dentate_gyrus (only one part of the hippocampus) vs olanzapine whole hippocampus but not basal level. And lithium is Lithium carbonate in high dosages same with valproic high doses. 

Edited by farshad, 25 February 2019 - 11:21 PM.