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Oct 5 2014 10:13pm
Quote (Balla @ Oct 5 2014 09:20pm)
Basically
that's why I gave some insight into depression in general lol


the farther i get in my studies the more i understand your posts :lol:

This post was edited by Clicquot on Oct 5 2014 10:13pm
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Oct 5 2014 10:14pm
Quote (N3rd @ Oct 6 2014 12:12am)
Is whey protein a waste of money? If I can consume say 40-50 g protein without it per day? I weigh 175 pounds. If you think it would be beneficial, would you recommend MTS weigh? Supposedly it is the best tasting protein on the market.


Not a waste
very cheap and effective way to get solid protein in
You need more than that for your weight for optimal muscle building
somewhere around 1.7g/kg is a good goal to shoot for
the brand literally doesn't matter, I just go for the cheapest. If I had more money I'd def go for strictly the best tasting

Quote (Clicquot @ Oct 6 2014 12:13am)
the farther i get in my studies the more i understand your posts  :lol:


Nice lol. What are you studying?

This post was edited by Balla on Oct 5 2014 10:14pm
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Oct 5 2014 10:15pm
Quote (Balla @ Oct 6 2014 12:14am)
Not a waste
very cheap and effective way to get solid protein in
You need more than that for your weight for optimal muscle building
somewhere around 1.7g/kg is a good goal to shoot for
the brand literally doesn't matter, I just go for the cheapest. If I had more money I'd def go for strictly the best tasting


So as far as some whey protein amino spiking, that is bs?
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Oct 5 2014 10:19pm
Quote (N3rd @ Oct 5 2014 10:46pm)
So if I just take an anti inflammatory, such as advil, my depression will lesson?


SSRIs don't work due to increasing serotonin, they work after 3-4 weeks due to enhancing neurogenesis, synaptogensis, and overall neuronal survival and neurite outgrowth.

Scientists think SSRIs might promote synaptogenesis and neurogenesis but there isn't full proof that it does.
Unless something came out this year saying otherwise.

And to state "It typically begins due to some type of low grade systemic inflammation or stress." I assume is talking about Atypical Depression and none of the other forms, correct?
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Oct 7 2014 04:49pm
Quote (S3th @ Oct 6 2014 12:19am)
SSRIs don't work due to increasing serotonin, they work after 3-4 weeks due to enhancing neurogenesis, synaptogensis, and overall neuronal survival and neurite outgrowth.

Scientists think SSRIs might promote synaptogenesis and neurogenesis but there isn't full proof that it does.
Unless something came out this year saying otherwise.

And to state "It typically begins due to some type of low grade systemic inflammation or stress." I assume is talking about Atypical Depression and none of the other forms, correct?


Well, SSRIs increase both BDNF & TrkB expression.. that's obvious, as serotonin will bind to a variety of receptors, in particular Gs & Gq ones will cause CREB expression through distinct pathways (cAMP vs Ca2+). Moreover, there's been several reports indicating long term usage of antidepressants upregulate the functioning of the cAMP-PKA-CREB pathway in both the hippocampus and neocortex.
BDNF signaling causes those changes I outlined. They've also shown SSRIs covalently modify histone proteins, altering chromatin packaging and overall gene expression.. which persists after treatment stops.

There's also been a study, here: http://www.ncbi.nlm.nih.gov/pubmed/12907793?dopt=Abstract&holding=npg -- that demonstrates inhibition of neurogenesis prevents the behavioral amelioration of SSRIs, adding more veracity to the theory.
Many studies have corroborated the findings of SSRI induced increase in overall neurogenesis, neuronal precursor cell proliferation, and BDNF expression.

They've also shown that SSRI use causes a shift in the expression of miR16, which increases levels of S100Beta.. this is mostly an astrocytic specific neurotrophic factor, increasing glial cell proliferation and influencing neurite outgrowth/cell shape, and protects astrocytes. This brings me to the tripartite synapse then, involving astrocytes in antidepressant action, typically overlooked. For instance, SSRIs stimulate astrocytes to to produce neurotrophic factors and protect from glial cell loss that occurs via depression & stress. There's also some studies showing SSRIs signal via 5HT2A & B receptors on astrocytes to increase FGF and EGF production, both of which are growth factors.. and they also favor an ERK pathway, which is robustly involved in mood and neurogenesis.

I mean, there's really not much extrapolation that needs to be done to see this.. too much mechanistic insight. The only thing missing is actually administering the drug for a prolonged period of time then examing the brains and noting the structular changes altogether, which simply hasn't been tested.. but there's enough insight from other studies to say that as all the related and necessary pieces for that to occur has been tested.

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Posts: 30,461
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Oct 8 2014 02:07pm
Quote (Balla @ Oct 7 2014 06:49pm)
Well, SSRIs increase both BDNF & TrkB expression.. that's obvious, as serotonin will bind to a variety of receptors, in particular Gs & Gq ones will cause CREB expression through distinct pathways (cAMP vs Ca2+). Moreover, there's been several reports indicating long term usage of antidepressants upregulate the functioning of the cAMP-PKA-CREB pathway in both the hippocampus and neocortex.
BDNF signaling causes those changes I outlined. They've also shown SSRIs covalently modify histone proteins, altering chromatin packaging and overall gene expression.. which persists after treatment stops.

There's also been a study, here: http://www.ncbi.nlm.nih.gov/pubmed/12907793?dopt=Abstract&holding=npg -- that demonstrates inhibition of neurogenesis prevents the behavioral amelioration of SSRIs, adding more veracity to the theory.
Many studies have corroborated the findings of SSRI induced increase in overall neurogenesis, neuronal precursor cell proliferation, and BDNF expression.

They've also shown that SSRI use causes a shift in the expression of miR16, which increases levels of S100Beta.. this is mostly an astrocytic specific neurotrophic factor, increasing glial cell proliferation and influencing neurite outgrowth/cell shape, and protects astrocytes. This brings me to the tripartite synapse then, involving astrocytes in antidepressant action, typically overlooked. For instance, SSRIs stimulate astrocytes to to produce neurotrophic factors and protect from glial cell loss that occurs via depression & stress. There's also some studies showing SSRIs signal via 5HT2A & B receptors on astrocytes to increase FGF and EGF production, both of which are growth factors.. and they also favor an ERK pathway, which is robustly involved in mood and neurogenesis.

I mean, there's really not much extrapolation that needs to be done to see this.. too much mechanistic insight. The only thing missing is actually administering the drug for a prolonged period of time then examing the brains and noting the structular changes altogether, which simply hasn't been tested.. but there's enough insight from other studies to say that as all the related and necessary pieces for that to occur has been tested.


While on this subject though, I found these quite interesting:

"Signaling pathways underlying the pathophysiology and treatment of depression: novel mechanisms for rapid-acting agents"
http://www.cell.com/trends/neurosciences/fulltext/S0166-2236%2811%2900191-3

"Antidepressants and Changes in Concentration of Endocannabinoids and N-Acylethanolamines in Rat Brain Structures"
http://link.springer.com/article/10.1007/s12640-014-9465-0/fulltext.html

"Potential Molecular and Cellular Mechanism of Psychotropic Drugs"
http://synapse.koreamed.org/DOIx.php?id=10.9758/cpn.2014.12.2.94
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