Now even though I'm on medication for my depression (which I believe is the right medication), will there be moments (instances) during my depression where the rate of neurogenesis decreases and the rate at which cortisol kills my neurons increases beyond the rate of neurogenesis, causing shrinkage for brief moments?

I think that is very strong theory that i do think there is strong evidence to indicate it.

Even despite the fact that the medication helps increase neurogenesis and prevents damage from cortisol?

Matt sorry im cosfused do you mean the hippocampus area ??--if so its showed it going back to pre-depression size once depression symptoms improved and hormone levels like cortisol went back to normal.

What I'm saying is that even though over time the neurons gain back through medication, will there be moments during depression where the glucocorticoids will kill the neurons more than the medication is helping gain new ones?

This question applies to neurons in the hippocampus and in the prefrontal cortex.

Hypothesis --goes back to the bdnf factor ---so i think it indicates if your under high level of stress but what been studied is treaments to reduce this bdnf factor--exercise,diet,relaxation ,learning new things it has to be a combo

But even though I'm on the right medication (because I feel that it is working a bit), I still experience this sort of chronic depression. So is this chronic depression killing more of my neurons than what the medication is gaining?

I know that you said before that I am gaining more than I am losing because the medication is stopping the damage as you said before right here in quotes:

"---Its the other way around your stopping the damage and there as been studies it can be reversed with meds and possibly other treaments. ---"

But it makes me wonder if there are moments during my depression where the glucocorticoids are killing more of my neurons than what is gaining through the medication due to the fact that my depression is still chronic.

Its possible for brief periods I think and it make sense from known theories ---have u had the cortisol levels checked ? 50% chronic depression ppl showed high levels

Have you ever talked to people or seen interviews with chronic depressed people who had it 20 or 30 yrs and mentally still sharp as a whip.

It's not that I'm afraid of losing my intelligence--I'm afraid of losing my pleasure. That even though there are those brief moments like you said where the rate at which the glucocorticoids kill the neurons responsible for pleasure becomes greater than the rate those neurons gain through the medication, that these brief moments will all add up to some loss (some shrinkage).

So will these brief moments all add up to some shrinkage over time (like a couple days, or even a week's worth of shrinkage or even longer), or will the medication constantly make up and surpass all these brief moments of neuron loss, resulting in those feel-good regions of the brain gaining neurons and not shrinking for a couple days or longer despite the fact that my depression is chronic and lasts all day everyday (although there are moments where I feel somewhat alright through these medications)?

Matt --neurogenesis is very popular subject right now being studied in science--so its hard to say.

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.

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

Mrs D---wow super great video and talk about eye opener !!! Thanks so much for this very informative post!!

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 .

I have 3 questions:

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.

yes i think it does result in more depression for a temporary period

3 more questions:

1.) Why and how does it result in temporary periods of greater depression?

2.) Now only just in terms of the glucocorticoids over-exciting the neurons responsible for pleasure, which is greater, the loss of pleasure that occurs only due to the glucocorticoids overworking those specific neurons responsible for pleasure, or the combined activity of the brain regions gained during depression in the limbic system--the combined activity gained of the brain regions that are responsible for making you depressed/controlling depressive thoughts (such as the hypothalamus) plus the brain regions that attempt to stop the glucocorticoids and gain back pleasure? I know that this is the same question as before, but it's different this time because before I was asking if the loss of pleasure in general due to depression was greater or less than the combined activity gained by those other brain regions. But this time, I am not asking this question in regards to a loss of pleasure in general due to depression, but I am now asking this question specifically in regards to a loss of pleasure due to depression only from the glucocorticoids overworking those neurons. So which would you assume is greater, the loss of pleasure only due to the glucocorticoids overworking those neurons, or the combined activity gained by those brain regions I mentioned above in the limbic system during depression?

3.) Regarding my 2nd question, are there ever moments where the loss of pleasure only due to the glucocorticoids overworking those neurons exceeds that of the combined activity gained by those brain regions I mentioned during depression?

Its therory --because there are so many neurochemical interactions that all come from stress. Depression is related to external stress and internal neurotransmitter problems in the brain. There is noway to give you a concrete answers to all your questions for two reasons because its all based on theroies and is very complex-- as I stated before. The technology is not there to study the brain activity in all these diffrent types of settings or enviroments a person goes thru with chronic depression.

So we don't even know if there are even very brief moments (like a few seconds or more or less) during depression where the loss of pleasure activity due to the glucocorticoids overworking those neurons exceeds that of the combined activity gained by those brain regions? You can't answer this question I just made here in this post just based on knowing how the brain works regardless of the fact that we don't have the technology?

I personally can assume even for short periods of times- I think sure there are many things that indicate loss of pleasure activity due to stress--but the 2nd part does it exceed the combined activity gained in those regions-- no i cant even guess at that part. I know that stress is toxic to brain and body-- so its crucial to get it under control for the general improved heath mentally and physcially.

What if I just narrow it down to the brain activity of just one brain region (like the amygdala as that is known to be hyperactive during depression as I showed you in that one video) or even just the hypothalamus instead of the combined activity of all those other brain regions to make it less complicated.

So just based on one brain region (either the amygdala or hypothalamus), it's still impossible to answer as to whether there are brief moments (like a second or more or less) where the amount of activity gained in just one specific brain region in the limbic system during depression (again, like the amygdala or the hypothalamus) is less than the amount of pleasure activity that is lost only due to the glucocorticoids overworking those pleasure neurons? What about when it comes to measuring neurotransmitter levels--does that give us an answer to these questions?

Stress hormones are clearly involved with dep---we go back to CRF extremly important with dep its good for short term bad when chronic. Cortisol is released by the adrenal glands is controlled by 2 stress hormones that come from the hypothalamus it tell the pituitary what to do with the crf--the pitiuatary responds with ACTH --this is how its regulated normally. The problem is when to much stress happens this system shows it stops normal function. There is current research being studied currently with to much stress and the breakdown of this system. i stated all this to show you Matt science cant answers this even when your trying to simplify to a certain region.

So even though science has gained a lot of knowledge about the brain, just based off of what science already knows and methods (such as measuring neurotransmitter levels) and experiments that can be carried out, regardless of the fact that we don't have the technology, science still can't answer the question of whether there can be brief moments where the loss of pleasure activity only due to the glucocorticoids overworking those pleasure neurons can be greater than the combined activity gained of (these specific brain regions) during depression: either one of the regions that make you depressed plus either one of the regions that automatically attempt to gain back pleasure while the glucocorticoids are still overworking those pleasure neurons? Again, you don't have to explain--just a simple "yes, science can answer this," or "no, science can't answer this" is good.

No---science cant answer this

Correct me if I'm wrong on this, but when the hypothalamus atrophies during chronic depression, the activity that it gains during chronic depression is soon lost (due to the fact that the hypothalamus is failing--it is losing activity because it is overworking and the activity that it gains is soon lost). And I'm wondering if there are brief moments (1 second or more or less) where this loss of gained activity can be less than the loss of pleasure activity (the loss of pleasure activity being greater) due to the glucocorticoids overworking the pleasure neurons during chronic depression. So are there such moments, or again, science hasn't advanced that far to even answer this question?

I get where you been going with this all along--- but science I cant find anything in research that would answer or indicates this ---at this time.

Science can't even indicate if there can be brief moments (or even longer or prolonged periods) where the loss of gained activity in the failing hypothalamus during chronic depression can be greater or less than the loss of pleasure activity only due to the glucocorticoids overworking those pleasure neurons? Again, as before, just a simple answer like "yes, science can answer this," or "no, science can't answer this." Again, this question is in regards to the hypothalamus overworking and failing (losing activity and losing activity that it gains) as a result during chronic depression.

no science cant answer this

Does the hypothalamus overwork and lose activity (fail) as a result of it overworking during chronic depression? Again, you don't have to explain anything--just a yes or a no is fine.

Sorry Matt ----its not as simple as yes or no --can't be answered this way.

Some abonormalties of hypothalmus are found in depression.

Like I said yesterday about the CRF hypothesis was seen in 50% of people with depression.

AS far as your 2 ? goes-------- I agree personally I think there is strong evidence suggest a person can feel worse or even more depressed until the stress/cortisol level is contolled

2 more questions (please answer each one):

1.) If it does lose activity, then there will be moments where some of the activity that it gains during chronic major depression is lost (resulting in little gain) and I'm wondering if there are moments where that little gain can be greater or less than the loss of pleasure activity during depression. Or can science not answer this question either. Again, just a "yes, science can answer this question," or "no, science can't answer this question" is fine.

2.) Now for someone who has chronic major depression, can there be brief moments where he/she will feel temporarily worse (more depressed) only just from one or few instances where the glucocorticoids overwork the neurons? Again, this question is only in regards to the glucocorticoids overworking the neurons, nothing else that contributes to depression.

Edit: I think I already asked this question before, but go ahead and answer it anyway with a yes or a no.

I see that you edited your post to "2 ?" meaning that you have answered my 2nd question in my previous post (the 2nd question in my post already after yours). But could you answer that 1st question in that post as well with a "yes, science can answer this," or "no science can't answer this." It's just that I'm having an obsessive thought over this which is why I am asking.

as far as your ? for #1 -- my reply is science cant answer this

In regards to my 1st question in my above post that you just answered, are you absolutely sure that there is no scientific knowledge, methods, or technology, etc. that can answer whether that little gain (gain that is lost in the failing hypothalamus during chronic major depression resulting in that little gain that I mentioned in my 1st question above) if there are brief moments (like a second or more or less) or even longer moments where that little gain is greater or less than the loss of pleasure activity only due to the glucocorticods overworking the neurons? Again, you can just reply with "yes, there is scientific knowledge, methods, and technology, etc. that can answer this," or "no, there is no scientific knowledge, methods, and technology, etc. that can answer this."

Im sorry Matt but ----there is no scientific knowledge, methods, and technology, that can answer this ?---or at least nothing I have found.

Now for someone who has chronic major depression, even if there are moments where he/she feels alright, the glucocorticods are still overworking and killing the neurons even during those moments of feeling alright.

Now even while the glucocorticoids are still overworking the neurons even during moments where a chronically majorly depressed person feels alright, can there be moments where when he/she then feels extremely little depressed (which would then result in the hypothalamus gaining a rate of extremely little activity since the hypothalamus gains activity during depression), that there will be moments (like a second or more or less or even for longer) where this extremely little rate of activity gained by the hypothalamus is less than (or could it even be greater than) the current rate of loss of pleasure activity due to the glucocorticoids overworking the neurons from the very moment that this person felt alright coupled with the fact that this person's hypothalamus is failing and that this extremely little rate of activity gained becomes even less due to the failure of the hypothalamus?

Again, just answer with "yes, science can answer this," or "no, science can't answer this." And also correct me if I'm wrong on all of this.