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Depression - what's high, what's low (neurobiology summary)

depression neurobiology neurobiological correlates monoamine theory

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#1 agwoodliffe

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Posted 06 April 2014 - 12:08 AM


High: Arginine Vasopressin, Cortisol, Choline, Dynorphin (<- may be a consequence of high cortisol + Arginine Vasopressin)
Low: Monoamines (Serotonin, Dopamine, Norepinephrine), Neurotrophins (BDNF, NGF), Anandamide (may be related to low Omega 3), Inositol

Complex: Glutamate, GABA, Hormones (depending on gender), Immune system (opposing studies), Other neuropeptides ie. everything affected by 'prolyl endopeptidase' (conflicting studies)


Therefore, if you're taking a classic antidepressant, and you ain't getting a sufficient response, these other factors may be the reason why.

Supplements/substances which target these other factors are listed below:
High cortisol - Theanine, Ashwagandha, Rhodiola, DHEA (safe?), Mirtazapine (a medication which is perhaps the most potent)
High AVP - Alisma orientalis, Californian Poppy
Dynorphin - Amentoflavone (found in Ginkgo Biloba or St John's Wort [watch out for Serotonin Syndrome])
Choline - stay away from pro-choline supplements (Huperzine A, Citicholine, Alpha GPC)

Low neurotrophins - Theanine, Lion's Mane
Anandamide - Omega fatty acids, Cocoa, Maca (?)
Inostiol - Inositol

Fascinatingly, look at someone with antisocial personality disorder, or psychopathy, and you effectively have a reverse case scenario of all of the above.

Edited by agwoodliffe, 06 April 2014 - 12:23 AM.

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#2 protoject

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Posted 15 April 2014 - 04:11 PM

I'm surprised about the AVP (Arginine Vasopression), and why is it that there's higher production in the HPA but low expression in the SCN>?

 

Quick snippet from:

 

"Risk Factors in Depression

 edited by Keith S. Dobson, David J. A Dozois"

(below) 1.jpg, 2.jpg, 3.jpg, 4.jpg

 

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#3 YoungSchizo

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Posted 17 April 2014 - 11:55 PM

Boosting depression - causing mechanisms in brain increases resilience, surprisingly (new published article)

 

Abstract of the study/article which I do not have access to.


Edited by YoungSchizo, 17 April 2014 - 11:55 PM.


#4 YoungSchizo

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Posted 18 April 2014 - 12:01 AM

You also can battle high cortisol with Pregnenolone (much saver as DHAE, DHAE might give quite some side-effects because of it's direct action on Testosterone). Preg is also a good/great mood enhancer.



#5 hullcrush

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Posted 26 April 2014 - 06:38 PM

Inhibiting AVP is very easy. It's likely a small part of the depression cascade,  yet so integral to other homeostatic mechanisms that manipulation from a neuroscience perspective is difficult. Off the top of my head:

 

AVP is inhibited by caffeine, cortisol, progesterone, testosterone (but not after it aromatizes), fluid intake.

 



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#6 TerryFirmer

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Posted 23 January 2017 - 04:56 AM

One thing I don't understand about AVP: depression is often associated with sleep disorders. In the elderly nocturia is a common disruptor of sleep. Higher vasopressin should reduce nocturia, leading to better sleep and presumably better mood.

 

And, according to self-hacked, AVP is decreased by lying down which seems contradictory since at night you want to conserve water, surely? Further, BMAL1 which is needed to produce AVP is decreased by melatonin which is released at bedtime.

 

These 'facts' don't fit together. What am I missing here?







Also tagged with one or more of these keywords: depression, neurobiology, neurobiological, correlates, monoamine, theory

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