Thursday, June 4, 2020

Comments by EFried

Showing 4 of 4 comments.

  • We have examined this study in detail, and published a commentary in the same Journal (Molecular Psychiatry) that comes to a very different conclusion than the authors.

    In sum, we simulated hippocampal volume data based on the sample and effect sizes reported by the authors. We find that the hippocampal volume differences are so small that knowing a person’s hippocampus size does not predict group membership much above chance (the discrimination accuracy is ~52.6%). While the volume is smaller in depressed patients than healthy participants, it certainly does not “robustly discriminate”. We also discuss why hippocampal volume may not be related to depression at all (for reasons such as lack of disease specificity and confounds), and even if it would be related, why it may not be reasonable to consider it a biomarker.

    You can find the commentary here:
    http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2015199a.html

    If you do not have access to the Journal, we have also uploaded a openly accessible version of the manuscript here:
    https://figshare.com/articles/Fried_amp_Kievit/1549680/5

    Eiko Fried

  • Some psychologists and psychiatrists historically understood “feeling lonely” as depressive symptom (similar to, for instance,”feeling helpless”), which is why the symptom is featured in a number of rating scales for depression (such as the CES-D by Radloff and colleagues). So it’s common to refer to it as “symptom” in these fields.

    However, we make the point in the paper that loneliness is *NOT* a passive and interchangeable depression symptom (in fact it’s one of the main points).

  • I just stumbled across this very nice summary of our paper, thanks for Mad In America for covering it.

    I am quite surprised by many of the reactions. We argue in the paper that bereavement is *not* a mental disorder (in most cases), quite contrary how our work is portrayed in the large majority of the comments above. We argue that it was likely a mistake that the DSM-5 got rid of the bereavement exclusion, and that many people are now misdiagnosed as depressed when they actually only have an absolutely normal response (grief / bereavement) to a terrible life event (spousal loss).

    E.g.
    “When will we stop describing natural sadness or even despair after losing loved one in any way shape or form as disease?”

    Yes, that’s an important point we make in the paper, actually, and has been an important reason for me to do this kind of work in the first place.

    Best
    Eiko Fried

  • “First off, I hope no one was actually surprised by this revelation.”
    By what exactly — the complex structure of the network? The fact that psychomotor agitation and psychomotor retardation are actually not negatively related (to us that was quite a surprise)? The fact that weight and appetite changes are highly related, but are not related whatsoever to any other symptoms in the network? I think some of these insights are newsworthy, no? 😉 We were also surprised that the DSM symptoms were not even a little bit more central in the emerging complex system than non-DSM symptoms. Again, nobody had looked at that before empirically, so we wanted to do it.

    ” It is the fact that it is considered NEW INFORMATION in the mental health field that is so distressing! I really appreciate your making this public so that others may recover from the misinformation they are flooded with on a daily basis.”

    I very much agree with you here Steve. The implicit notion of the common cause model is very common in large parts of psychiatry, but also parts of clinical psychology. That’s one of the main reasons I do this kind of work, and it’s not easy to publish network research, or research focused on specific symptoms, exactly for the reasons you mention — it violates the standard disease model. You’ve certainly heard of the NIMH’s RDoC initiative: their main paper (2010) states that “RDoC conceptualizes all mental disorders as brain disorders”.

    And Steve, when it comes to your constructive sentence “What an incoherent collection of blather! No actual mention of a human being or his/her experience in this paragraph or the article. […] Looks like the bi0-bio-bio model to me!”

    I believe you very much misunderstand the paper, and maybe want to give it a more detailed read. The network view understands human experiences (there you go) as causally interrelated, instead of being derived from a common cause. While this is intuitive and obvious, it is not how researchers in psychology and psychiatry usually model these experiences (i.e. symptoms) like sadness. If you want a shorter and less technical read, feel free to check out a piece The Psychologist published just an hour ago: http://thepsychologist.bps.org.uk/volume-29/january-2016/depression-more-sum-its-symptoms

    Best wishes
    Eiko Fried