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Now if you add the additional neurons that are killed not just from the glucocorticoids, but also from a reduction of BDNF into my question above that you quoted, is it still hard to say in regards to depression in general? Is it a yes or a no (that it's still hard to say as to whether these brief moments of neuron loss from the glucocorticoids and reduction of BDNF will add up to a day's worth, a couple day's worth, or even a week's worth of shrinkage or that the medication will constantly make up and surpass all these moments of loss resulting in those feel-good areas of the brain gaining and not shrinking for the amounts of time I stated)?
Also, a yes or a no to this question I have here as well. Despite the fact that antidepressants stop the damage and gain back neurons, is it very rare for the brain to keep on shrinking from depression beyond the rate that the antidepressants are trying to gain? Is it also very rare for it to keep on shrinking from depression for the amounts of time I specified in the paragraph above even though the right antidepressants are being taken? |
[There is alot of thing here --but again there is no ---yes or no answers--- because small studies --clinical they know it takes 3-6 weeks to alter moods ---some studies have been done on long tern chronic depression ppl suffering over 2 yrs . Science shows evidence that people undergo neurogenesis all there lives ---the studies have been tested on new drugs and old drugs to wide array of results. Example prozac to some depression has been a miracle drug for some -- where showed after few weeks they started to enjoys doing this again and feeling joy. why it doesnt work for everyone leads to alot more studies. Personally i think stress is a huge factor and once it reduced can have a major impact on depression and feeling better ---but there is no time line i could give you---- because its not known again due to its complex nature.
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Here is a video illustrating how a "hidden" and misunderstood deficiency which can affect young people as well as older people commonly (up to 40%).
Vit B12 deficiency can cause shrinkage of the brain and spinal cord as it results in demyelination of nerve axons. http://www.youtube.com/watch?v=BvEiz...ature=youtu.be This is a long video, and does not go into some other features of supplementation. I have further information on this link: http://neurotalk.psychcentral.com/thread85103.html |
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Now in this link right here:
http://www.dailymail.co.uk/health/ar...ink-brain.html It says that when the GATA1 genes were turned on, the rodents acted depressed. In other words, depressive symptoms were instantaneous once those genes were turned on. Now during chronic depression, there are constant episodes that go on all day everyday where cortisol rushes to the hippocampus and the prefrontal cortex, over-exciting those neurons and eventually killing them (if these episodes were to continue) causing shrinkage in those brain regions. And that shrinkage will then cause more depression. Now for someone who is chronically depressed, can this person feel even more depressed just from one single or few of these episodes in which cortisol over-excites those neurons, or does it take time for the brain to eventually, over a long period of time, shrink from very many of these episodes in order for this person to feel even more depressed? In other words, does just one or few of these episodes result in instantaneous depression (like how there was instantaneous depression with the rodents when those genes were turned on)? Or, again, is it not instantaneous and takes time for the brain to shrink in order for more depression to occur in regards to the cortisol over-exciting those neurons? Again, I am just asking this question only in regards to cortisol over-exciting the neurons--not the genes or anything else regarding depression. |
[Hi Matt,
Remember we talked about neurogenesis occurs all thru life esp in the region of the hippocampus. Keeping that in mind our bodies are wired in away under stress to launch counter calming hormones so the hippocmpus doesnt get to hammered with cortisol. Sure there are moments under extreme stress rats may not find there way out of a maze --but once stress is reduced doesnt mean the damage is perm. To get to your point its something that occurs over time . |
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1.) So you're saying that for someone who is depressed, that there are no such moments where the glucocorticoids cause more depression instantly only in regards to them over-exciting the neurons and that, it's again, something that has to happen over time? 2.) Now if you add in the reduction of BDNF due to the glucocorticoids themselves (not due to the GATA1 genes or anything else) into my 1st question above, is it still something that has to happen over time and that more depression does not result instantly just from the glucocorticoids themselves over-exciting the neurons combined with reducing BDNF? 3.) So why is it that there are moments where someone who is depressed can have episodes where he/she feels more depressed instantly? It's again, not because the glucocorticoids themselves are over-exciting the neurons to death and reducing BDNF, is it? Is it because the GATA1 genes themselves instantly shut down BDNF and other genes responsible for neuron and synapse growth, causing this depressed person to feel even more depressed instantly? |
Now actually go ahead and forget those 3 questions in my previous post (don't answer them). Just answer this one question.
1.) For someone who is depressed, can there be temporary periods of more depression that can result only just from one or few instances where the glucocorticoids over-excite the neurons, or is it like you said, that more depression can only result from this over time (if these instances continue constantly over the course of a long period of time)? Again, this question is only in regards to the glucocorticoids over-exciting the neurons, nothing else that contributes to depression. |
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