Depression Killing Neurons

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MattMVS7

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I heard that during depression, the stress hormones that are released kill the neurons themselves. In this video right here, it states that MRI imaging has shown that neurons become less active and can erode. I wish to know if the MRI imaging as explained in that video is proof that the stress hormones kill off the neurons during depression.

EDIT: I know that when it comes to depression, nothing is proven--there are only theories. But regardless of the fact that there's not proof, do those MRI imaging as stated in that video prove that depression erodes neurons anyway?

The people who performed those MRIs would have chosen depressed patients without any other neurodegenerative factors such as Alzheimer's (as that would obviously interfere with knowing if the neuron loss was from the depression or from something else). Which raises the question of what else could then be responsible for those neurons eroding besides the depression itself. Therefore, again, based on that, do those MRI imaging in the video of neurons eroding during depression prove that depression erodes neurons?

Here is the video I'm talking about:

http://www.thevisualmd.com/health_centers/neurological_health/depression/what_is_depression_video

2nd Edit: Now what about this. Is this proven during depression? That the release of cortisol from depression causes excess amounts of calcium to enter brain cells, which eventually leads to the production of free radicals, the reactive molecules that injure and kill cells. What arguments are there against this?
 
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Depression acts as a stressor, just like an external situation can. As a result, it prevents the production of brain derived neurotrophic factor, which is a hormone that protects neurons. Without this hormone, neurons die, particularly in the hippocampus. Psychotherapy and antidepressants both cause more BDNF to be produced, thereby protecting neurons.
 
In particular, depression is associated with hippocampal volume loss.
 
I know that when it comes to depression, nothing is proven--there are only theories. But regardless of the fact that there's not proof, do those MRI imaging as stated in that video prove that depression erodes neurons anyway?

The people who performed those MRIs would have chosen depressed patients without any other neurodegenerative factors such as Alzheimer's (as that would obviously interfere with knowing if the neuron loss was from the depression or from something else). Which raises the question of what else could then be responsible for those neurons eroding besides the depression itself. Therefore, again, based on that, do those MRI imaging in the video of neurons eroding during depression prove that depression erodes neurons?

Again, here's the video:

http://www.thevisualmd.com/health_centers/neurological_health/depression/what_is_depression_video
 
Please be careful in stating that antidepressants "cause more BDNF to be produced, thereby protecting neurons." No one really knows with certainty how antidepressants impact the brain. They seem to help relieve symptoms with some deep seated, "biological" depressions. However, other studies suggest that antidepressants can alter brain functioning and can promote brain changes that are detrimental to long term well-being, such as this one http://www.ncbi.nlm.nih.gov/pubmed/22536191
 
aagman01 said:
Please be careful in stating that antidepressants "cause more BDNF to be produced, thereby protecting neurons." No one really knows with certainty how antidepressants impact the brain. They seem to help relieve symptoms with some deep seated, "biological" depressions. However, other studies suggest that antidepressants can alter brain functioning and can promote brain changes that are detrimental to long term well-being, such as this one http://www.ncbi.nlm.nih.gov/pubmed/22536191
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That's not a study, it's an article with a hypothesis, using other people's research to back up their hypothesis. It's a minority opinion.

Not that that isn't important, and I'm always in favor of inclusion of an informed dissenter, but let's not pretend that there's equal weight of evidence on each side.
 
Well, one could argue that there is no known cause of depression, that antidepressants do not offer a thorough "cure" to the majority of folks who take them, and the evidence suggests that antidepressants can be unsafe and potentially hazardous for most individuals who take them, so perhaps you are right in that we shouldn't pretend "there's equal weight of evidence on each side."

With that said I am not against antidepressants per se, but rather against those who uncritically accept psychiatric drugs (or accept ideas or practices blindly, without any critical reflection). The criticisms against antidepressants, antipsychiotics, etc. certainly goes against what I learned in my training program for my phd. As someone completing a formal post-doc at the moment and starting a TT faculty position next fall, I think it is important that we all as psychologists or future psychologists critically examine our understanding and practices and not dismiss things because they go against what we may have learned in a class or a graduate program.
 
aagman01 said:
Well, one could argue that there is no known cause of depression, that antidepressants do not offer a thorough "cure" to the majority of folks who take them, and the evidence suggests that antidepressants can be unsafe and potentially hazardous for most individuals who take them, so perhaps you are right in that we shouldn't pretend "there's equal weight of evidence on each side."

With that said I am not against antidepressants per se, but rather against those who uncritically accept psychiatric drugs (or accept ideas or practices blindly, without any critical reflection). The criticisms against antidepressants, antipsychiotics, etc. certainly goes against what I learned in my training program for my phd. As someone completing a formal post-doc at the moment and starting a TT faculty position next fall, I think it is important that we all as psychologists or future psychologists critically examine our understanding and practices and not dismiss things because they go against what we may have learned in a class or a graduate program.
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Fair enough. I take issue primarily with the bolded words. There are many causes of depression, but no known one cause. There may be a common pathway that all causes of depression result in, though.

Nor is there evidence that medications are unsafe or hazardous for "most" people. Most would imply a majority, which evidence suggests is far from true. Maybe a significant minority, but recognition should be made of the significant risks of depression, the life impact and damage that that does, and that side effects from antidepressants (if they occur at all) are reversible once discontinued. An important distinction from extreme language like "hazardous," implying damage that cannot be undone. Even the evidence to support increased suicidality has No evidence to support actual suicide.
 
aagman01 said:
The criticisms against antidepressants, antipsychiotics, etc. certainly goes against what I learned in my training program for my phd. As someone completing a formal post-doc at the moment and starting a TT faculty position next fall, I think it is important that we all as psychologists or future psychologists critically examine our understanding and practices and not dismiss things because they go against what we may have learned in a class or a graduate program.
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Thats interesting. In my ph.d, the liottle we did learn about psychotropics was the names, what they were used for, what they should NOT be used for (ideally), and generally how terrible they were medically for the body.
 
Yeah, we read that article about how they're no better than placebo 50% of the time.
 
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cara susanna said:
Yeah, we read that article about how they're no better than placebo 50% of the time.
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Yeah, but 50% of the time, it works every time --

sex-panther.jpg
 
As much as I wish that people would initially try a non-pharmacological intervention to begin with before taking medication, I prefer that they at least try an antidepressant over nothing.

The whole black box warning situation (and the increase in suicide rates following the warning) was enough to convince me of the risk/benefit ratio of most antidepressants. Some of my patients have had such positive experiences on antidepressants that it is hard not to consider it as an option for others.

My primary complaint is how people just get on these medications from their PCP without any time limits. If it is the first episode of depression, it probably would make sense to stop taking the medication at some point after stabilization, as a good number of folks won't end up having another episode. I think some people stay on the antidepressants indefinitely for no good reason.
 
Pragma said:
As much as I wish that people would initially try a non-pharmacological intervention to begin with before taking medication, I prefer that they at least try an antidepressant over nothing.

The whole black box warning situation (and the increase in suicide rates following the warning) was enough to convince me of the risk/benefit ratio of most antidepressants. Some of my patients have had such positive experiences on antidepressants that it is hard not to consider it as an option for others.

My primary complaint is how people just get on these medications from their PCP without any time limits. If it is the first episode of depression, it probably would make sense to stop taking the medication at some point after stabilization, as a good number of folks won't end up having another episode. I think some people stay on the antidepressants indefinitely for no good reason.
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When someone with a MDE asks "do I have to take this forever," I mention common recommendations (APA) that first we get them feeling "normal," then we keep them normal for 6mos to 1 yr, then begin the process of trial tapering, slowly. But with the idea that it's up to them. Some people tell me "I don't want to chance ever going back to the way I was feeling," and so opt to stay on the medication for much longer, maybe indefinitely. That's their choice.
 
nitemagi said:
When someone with a MDE asks "do I have to take this forever," I mention common recommendations (APA) that first we get them feeling "normal," then we keep them normal for 6mos to 1 yr, then begin the process of trial tapering, slowly. But with the idea that it's up to them. Some people tell me "I don't want to chance ever going back to the way I was feeling," and so opt to stay on the medication for much longer, maybe indefinitely. That's their choice.
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And what sort of dosage management goes with life time use of antidepressants?
 
nitemagi said:
When someone with a MDE asks "do I have to take this forever," I mention common recommendations (APA) that first we get them feeling "normal," then we keep them normal for 6mos to 1 yr, then begin the process of trial tapering, slowly. But with the idea that it's up to them. Some people tell me "I don't want to chance ever going back to the way I was feeling," and so opt to stay on the medication for much longer, maybe indefinitely. That's their choice.
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Possibly, but I think it could be the responsibility of the provider to suggest that this might not be in their best interests, and that alternatives are possible/available.
 
MBellows said:
And what sort of dosage management goes with life time use of antidepressants?
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Depends on the clinician. Many will maintain at whatever dose has been therapeutic, especially if there are no side effects.

This touches on what I believe is the true bias within many in psychology, and which I recognize I carry to a degree myself -- That the issue is not whether antidepressants work, but a philosophical bias against "chemicals," following an almost naturopathic philosophy of "I don't believe people should put stuff like that in their body," as if all "chemicals" = "poison." That bias then focuses on the data to support that philosophy, which there is data to support negatives to medications. But it comes at the de-emphasis often of positive data in favor of medication.

The bigger issues I take with this philosophical bend are that it leads to neglect of treatment for many that don't have access to anything other than medication, a demonization of medicine, and it perpetuates a false model that the human system (body/mind) is inherently self-healing and self-correcting (a philosophy perpetuated in many alternative healing models).

I believe that there may indeed be an evolutionary basis to depression, and that within that model it serves a purpose (garnering of support, conservation of resources - See Nesse), but that MDD or depression requiring treatment is outside the standard of normal and detrimental to functioning. /rant
 
AcronymAllergy said:
Possibly, but I think it could be the responsibility of the provider to suggest that this might not be in their best interests, and that alternatives are possible/available.
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Absolutely. It's to be offered in the beginning, and the quote is their response to that.
 
nitemagi said:
Depends on the clinician. Many will maintain at whatever dose has been therapeutic, especially if there are no side effects.

This touches on what I believe is the true bias within many in psychology, and which I recognize I carry to a degree myself -- That the issue is not whether antidepressants work, but a philosophical bias against "chemicals," following an almost naturopathic philosophy of "I don't believe people should put stuff like that in their body," as if all "chemicals" = "poison." That bias then focuses on the data to support that philosophy, which there is data to support negatives to medications. But it comes at the de-emphasis often of positive data in favor of medication.

The bigger issues I take with this philosophical bend are that it leads to neglect of treatment for many that don't have access to anything other than medication, a demonization of medicine, and it perpetuates a false model that the human system (body/mind) is inherently self-healing and self-correcting (a philosophy perpetuated in many alternative healing models).

I believe that there may indeed be an evolutionary basis to depression, and that within that model it serves a purpose (garnering of support, conservation of resources - See Nesse), but that MDD or depression requiring treatment is outside the standard of normal and detrimental to functioning. /rant
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Good point and I tend to agree with you. But at the same time, one could see the cognitive distortions in MDD never changing without some therapy, and could view this approach to prescribing as fostering an unnecessary dependency.

I also think some degree of parsimony in treatment is a valuable goal, particularly given the widespread problem of polypharmacy. If a mild MDD case could go away with diet changes and regular aerobic exercise, then why the lifetime of medication?

I do think some psychologists are too skeptical of pharmacological interventions, but I also see polypharmacy as a bigger problem at present.
 
Pragma said:
Good point and I tend to agree with you. But at the same time, one could see the cognitive distortions in MDD never changing without some therapy, and could view this approach to prescribing as fostering an unnecessary dependency.

I also think some degree of parsimony in treatment is a valuable goal, particularly given the widespread problem of polypharmacy. If a mild MDD case could go away with diet changes and regular aerobic exercise, then why the lifetime of medication?

I do think some psychologists are too skeptical of pharmacological interventions, but I also see polypharmacy as a bigger problem at present.
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All the reasons why we should be raising the bar on training, rather than lowering it for the purpose of more medications in the world.

Maybe therapy is absolutely necessary, but maybe not. The research on natural course of borderline PD seems to indicate that with time improvement can occur, likely through proper models in their environment over time. I do a lot of therapy in my practice, so I at least aim to speed up such processes rather than hope for the corrective nature of the world to do ALL the work. 🙂
 
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Maybe therapy is absolutely necessary, but maybe not. The research on natural course of borderline PD seems to indicate that with time improvement can occur, likely through proper models in their environment over time
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Yes, but therapy is necessary for managing BPD symptoms--especially given their high risk for suicide.
 
cara susanna said:
Yes, but therapy is necessary for managing BPD symptoms--especially given their high risk for suicide.
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Absolutely Necessary? Does the naturalistic data support that? More that the data of interventions shows improvement in particular symptoms (suicidality). Like the argument against medication - who warrants it then, vs. who could get by without it? Who doesn't require the cost, time investment of DBT (groups, individual)? Can you tell me who will respond to DBT- guaranteed, who will have bad responses to it (decompensate further when limits are set on them), who would DIE without it? Then how do we know it's "Necessary" for them.

I ask this somewhat tongue-in-cheek to stir discussion, knowing much of the answers (there's obviously a spectrum of BPD pt's, and the more severe impairment, risk, utilization of resources the more tx is warranted). And also to make a comparison to the arguments made about medications.
 
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It's hard to say since ethical research can't look at treatment vs. no treatment--it's always DBT vs. TAU. But not even just thinking about suicidality, more just quality of life. The whole idea of DBT is that people with BPD have a lot of suffering and DBT helps them decrease that by changing their responses and coping.
 
cara susanna said:
It's hard to say since ethical research can't look at treatment vs. no treatment--it's always DBT vs. TAU. But not even just thinking about suicidality, more just quality of life. The whole idea of DBT is that people with BPD have a lot of suffering and DBT helps them decrease that by changing their responses and coping.
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I recognize the utility, just challenging the definition of "necessary" in this context.
 
Fair enough, necessary isn't really the right word.
 
nitemagi said:
This touches on what I believe is the true bias within many in psychology, and which I recognize I carry to a degree myself -- That the issue is not whether antidepressants work, but a philosophical bias against "chemicals," following an almost naturopathic philosophy of "I don't believe people should put stuff like that in their body," as if all "chemicals" = "poison." That bias then focuses on the data to support that philosophy, which there is data to support negatives to medications. But it comes at the de-emphasis often of positive data in favor of medication.
Click to expand...

I completely understand your need to rant. I know some people who meds were horrible for but others who would probably either not be around today or wouldn't be able to hold a job down without the meds. Having a bias against chemicals isn't always the point, but rather the point is that people hold the opinion that the meds only mask certain symptoms without actually addressing the issues at hand. Then again many of the people who make that argument would probably be dismissive of a like argument from the psychoanalytical crowd that shares the same feelings about CBT/BT.

I'm simply curious about the economics of whether it's actually cheaper to pay for a set of therapy sessions or to pay for psychiatric visits for med management and to pay for the meds themselves over time.
 
I think numerous scholars are beginning to uncover many of the problems with drug research and outcome findings that support the use of many psychotropics. Namely, many of the studies in support of the drugs were flawed and many of the ways the research has been presented is highly dubious (e.g., ghost writers getting psychiatrists to sign off on the studies). Here is a book review of three fairly recent, critical books on the the drug industry and prescribing practices:

http://www.nybooks.com/articles/archives/2011/jun/23/epidemic-mental-illness-why/?pagination=false We read the Whitaker book with some local psychiatrists, and had some fascinating conversations...

MBellows said:
I completely understand your need to rant. I know some people who meds were horrible for but others who would probably either not be around today or wouldn't be able to hold a job down without the meds. Having a bias against chemicals isn't always the point, but rather the point is that people hold the opinion that the meds only mask certain symptoms without actually addressing the issues at hand. Then again many of the people who make that argument would probably be dismissive of a like argument from the psychoanalytical crowd that shares the same feelings about CBT/BT.

I'm simply curious about the economics of whether it's actually cheaper to pay for a set of therapy sessions or to pay for psychiatric visits for med management and to pay for the meds themselves over time.
Click to expand...
 
aagman01 said:
I think numerous scholars are beginning to uncover many of the problems with drug research and outcome findings that support the use of many psychotropics. Namely, many of the studies in support of the drugs were flawed and many of the ways the research has been presented is highly dubious (e.g., ghost writers getting psychiatrists to sign off on the studies). Here is a book review of three fairly recent, critical books on the the drug industry and prescribing practices:

http://www.nybooks.com/articles/archives/2011/jun/23/epidemic-mental-illness-why/?pagination=false We read the Whitaker book with some local psychiatrists, and had some fascinating conversations...
Click to expand...

Sounds like a really interesting book club group you had there!
 
Now could someone answer my question in my opening post as to whether those MRI imaging in the video is proof or not even though there are only theories about depression and that nothing is proven? I wish to know if those MRI imaging in the video is proof anyway.
 
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You had your own answer in your original posting. Theories of depression are only that, theories. Imaging studies can reveal similar patterns that occur with depressed patients, but similar studies can also detect similar patterns in non-depressed patients or patients with other issues going on. Sorry, but there is no detectable markers or mechanism for depression or other psychiatric problems....
 
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aagman01 said:
Sorry, but there is no detectable markers or mechanism for depression or other psychiatric problems....
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I think NIMH would strongly disagree.
 
aagman01 said:
Really, please cite one article from NIMH that states a genetic marker or other approach to detecting depression (outside of diagnosis). On an interesting note, how do folks think the NIMH decision regarding DSM-V will impact research funding in the coming years? http://www.psychologytoday.com/blog/side-effects/201305/the-nimh-withdraws-support-dsm-5
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Perhaps you misunderstand my statement (though I'm sure people will have some references on psychobiology of depression). You stated that "there is no detectable markers or mechanism for depression or other psychiatric problems." Unless you're going to try to say that there can be psychological phenomenon that aren't brain based, one would have to assume that there are mechanisms at work, these things of course being measurable, whether we have the current knowledge and technology to measure them are a different story, and it seems that NIMH has put its power behind finding out more about those markers.

Had you said that there are currently no known markers or mechanisms for depression, I would have spent more time researching before making my statement. Frankly, I don't know about any known markers but I can with 100% certitude say that they exist, but that it's likely that we will find multiple different markers and mechanisms that facilitate what we call "depression."
 
Now what about this. Is this proven during depression? That the release of cortisol from depression causes excess amounts of calcium to enter brain cells, which eventually leads to the production of free radicals, the reactive molecules that injure and kill cells. What arguments are there against this?
 
MattMVS7 said:
Now what about this. Is this proven during depression? That the release of cortisol from depression causes excess amounts of calcium to enter brain cells, which eventually leads to the production of free radicals, the reactive molecules that injure and kill cells. What arguments are there against this?
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Weren't you told that you shouldn't use SDN forum to get information about a personal medical condition? You then started 4 threads about this same topic.
 
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I mean, are there arguments against the free radicals killing the brain cells?
 
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MattMVS7 said:
I mean, are there arguments against the free radicals killing the brain cells?
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I'm sure there have been many brain cells lost due radicals being on the loose.
 
I have 2 more questions:

1.) When depression makes excess calcium enter the brain cells in the hippocampus which releases the free radicals, do the vast majority of these free radicals kill mostly the cells in the hippocampus, or do they not kill mostly the cells in the hippocampus, but go on instead to kill different cells in different parts of the brain?

2.) Are there arguments against depression causing the release of free radicals due to the calcium entering the brain cells?
 
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Matt, I'm not sure if this is a homework assignment or something (if so, your professor should probably be fired) but the reason you aren't getting answers is because the questions you are asking are flawed. They are being framed in a weird way and it seems you are looking for absolute answers to extremely nuanced questions where there simply aren't any and I'm not sure even the authors of the research articles on this very topic could provide the answers you are looking for.

These are new areas and it is very dangerous to look at a handful of articles on the "Cutting edge" and interpret them absolutely. Maybe calcium enters the hippocampus causing release of free radicals that destroy brain cells as you explain above. Maybe in a month we discover its not calcium that causes them to be released. Maybe we discover its not getting into the hippocampus. Maybe the free radicals being released are "harmless" free radicals. Maybe we discover that what we thought was "damage" in the brains of depressed individuals is actually adaptive and something else is responsible for all the problems that go along with depression. I can't tell you an "argument" against the theory you posit. I can tell you that the body of literature supporting is not even remotely close to providing adequate support that the entire chain of events you cite is actually happening, or that it even matters if it does.

You are looking for simple answers to very complicated questions that I'm quite confident the leading neuroscientists in the world would not be able to provide a definitive answer to. This is why science is exciting - if you want the answer, join a lab (I'm guessing you're an undergrad?) and help us find one🙂
 
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This is where it talks about what I've been explaining. Under the bolded title "Glutamate, calcium, and apoptosis," it talks about the calcium releasing the free radicals that damage the cells during depression. The article also states in conclusion that there is no current evidence (at the time) that neuron death occurs during depression. But in that video I posted, it stated that MRI imaging has shown depression erodes neurons which is why I asked if this is now proof that depression causes neuron loss and was wondering if depression causes the release of free radicals which kill the cells and if the excess calcium itself excites the cells to death.

Here is the article:

http://www.sci.sdsu.edu/classes/psychology/psy860/readings/leesapolsky.pdf
 
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Well that one can be answered.

No, it isn't proof. At best we're looking at "Evidence that is loosely consistent with the possibility that existing theories could potentially have some validity". No single finding is proof of anything, let alone something this complicated.
 
Now for someone who is uneducated (like myself) and unaware of just how complicated depression is, it would only be expected that I would add 2 things together (the article and that video) and view that as proof that depression causes neuron loss. But for someone who is educated and aware of how complicated depression is, he/she would view that as not being proof and that it, again, being much more complicated than that.

So right now, for someone as myself, it's embedded in my simple mind that this is proof that depression causes neuron loss. So perhaps if you could complicate this simplistic view of mine (explain just how complicated depression is in regards to the validity of the subject of depression causing neuron loss as well as the alternate possibilities that could be causing this neuron loss explained in that video besides the depression itself). If you can explain all of this to me, it will give me a better understanding of how this is not proof that depression causes neuron loss.
 
Neuron loss due to other causes could result in depression. Even if you associate the two, you have no evidence of a casual relationship.

As for what else can cause neuronal loss, well, a lot of things. And even if it's free radicals, a lot of things can result in those (such as environmental toxins).
 
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Also, what about the glia cells. Does the excess release of cortisol from depression cause excess calcium to be produced which kills the glia cells, which then causes a loss of neuronal synapses? Or is that not proven either? And what arguments are there against this?
 
Eh? How would killing glial cells result in a loss of synapses?
 
MattMVS7 said:
Because don't the glia cells aid in the growth of neuronal synapses by providing nutrients and such?
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Perhaps it is a good idea to end this thread and let MattV do his own homework or school work :laugh:
 
I heard that glial cells are the brain's functional other half as stated in the last sentence of this article and provide nutrients and such to the neurons and I'm wondering if, again, that the excess release of cortisol from depression causes excess calcium to be produced which kills the glia cells, which then causes a loss of neuron function and synapses. Or again, is it not proven that depression kills the glial cells and that there are arguments against this?

Here is the article

http://blogs.scientificamerican.com...is-the-ratio-of-glia-to-neurons-in-the-brain/
 
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