OddDuck's "odd" regimen

Tell us what you are using to treat your MS-- and how you are doing.

Postby Daunted » Wed Apr 20, 2005 6:03 am

OddDuck wrote:clinical depression if left untreated will also cause myelin degradation.


Deb,

Can you provide a reference for this claim?

To my knowledge clinical depression has absolutely no physical findings associated with it, by definition.

I'm quite curious,

D.
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Postby OddDuck » Wed Apr 20, 2005 10:02 am

Not really. Not just "one" reference that is. It was another one of those things that I "noticed" during my studies and "comparisons".

If you research in minute detail the physiological and biological things that happen to the human body during clinical depression (which will take some study under psychology and immunology - Dr. Fridolin Sulser has done some interesting studies, for one), and then you make a clinical biological comparison between the two, you come up with some interesting cross-overs.

I tested my knowledge on a couple of doctors. My former PCP knew what I meant when I mentioned that to him, also. I said once "besides, how can you tell if someone has MS or not? An affective disorder is so close that it's amazing." He said "Yeah, I know. The problem is, how do you determine which came first? The clinical affective disorder or MS?"

Remember now, too............I'm not talking about depression as we all think of it, i.e. in the definition as "I feel blue and down". This is "non-melancholic" clinical depression...........or non-melancholic clinical affective disorder. You wouldn't even necessarily know you have it.

Deb
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Postby OddDuck » Wed Apr 20, 2005 10:12 am

Ok..............here's why the MRI isn't the best thing (but the best we have right now) to diagnose MS.

Headaches cause UBOs (unidentified bright objects) on a brain MRI, depression (affective disorders) cause UBOs,.....uh........MS, PML, etc. cause UBOs..........

Ok......without being able to do a biopsy of the brain itself, how can anyone REALLY know exactly which thing is causing the UBOs. The UBOs all look the same (hence why you don't always get the same diagnosis from any two doctors reviewing the same MRI scans........it's purely subjective).

The ONLY thing that will additionally tell the doc if it might be MS are the other criteria (exclusion, LP CSF test, documentation of two separate "exacerbations", etc.) that help sway them to an MS diagnosis. The problem with the criteria for an MS diagnosis is that it keeps changing, because they still don't know much, because they can't really "see" exactly what IS causing the UBOs on the MRI. Not really! And MS "symptoms" can be mimicked by so many other conditions, that it's almost impossible to differentiate.

Besides, you always hear how often and closely related "depression" is with MS. They are talking about not just a person's "feeling", but the clinical and physiological picture behind it.

And even recently, on the NMSS website, (and it was posted here, also), they found that other disease was OFTEN being misdiagnosed as MS, too. The name escapes me right at this second, but I mentioned that in a thread somewhere.

Deb
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Postby Sharon » Wed Apr 20, 2005 10:33 am

Deb -

Thank goodness you are not saying goodbye!

I always pop-in to read the postings and was truly amazed that you were able to convert medical gibberish into something the rest of us could understand and relate to. You have succeeded in nurturing many of us. I am applauding you for your time and your interest. :D

Physical therapy, huh? I am also in PT (upon my request). My experience with the trial exercise program was so positive; I knew the exercise needed to be continued. I do get somewhat discouraged when a body part doesn't respond at first; but, I have found that talking to my brain and visualizing a movement does help. It is never to late to get those brain waves going on a different path! Good luck to you - hope you are able to "run" the stairs soon.

Sharon
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Postby OddDuck » Wed Apr 20, 2005 10:42 am

Sharon!

Hi, there! Gee..........thanks! I figured you guys would be happy to see me gone, I talk so much! :lol:

Anyway, to get back to just a "tickle" of how I came across (and why) I started making comparisons between what is happening in MS and "clinical" depression, here is just an example. Note the similarities in cytokine production, etc. And if you know me, I just kept on digging and making biological comparisons, until I finally said "Well, I'll be darned!" :lol: Oh, and in a certain percentage of people with non-melancholic affective disorder (depression), over time it eventually DOES revert to "melancholic". If you keep going, i.e. digging, believe me, you'll find so many similarities, you probably will get to the point where you can't tell which disease you are reading about! Weird, huh?

Eur Arch Psychiatry Clin Neurosci. 2001;251(2):90-7.

Different immune patterns in melancholic and non-melancholic major depression.

Rothermundt M, Arolt V, Fenker J, Gutbrodt H, Peters M, Kirchner H.

Institute of Immunology and Transfusion Medicine, University of Luebeck School of Medicine, Germany.

The search for immune patterns in major depression has thus far resulted in ambiguous findings, probably because patient samples are psychiatrically heterogeneous. We therefore focused on a detailed classification of subtypes of major depression, comparing patients with melancholic and non-melancholic major depression. Inpatients suffering from acute major depression were diagnosed and subclassified according to DSM IV criteria. Cell counts were determined by FACS analysis and morphology. Cytokine production (IL-2, IFN-gamma, IL-10) upon mitogen stimulation was measured by ELISA in a whole blood assay. Non-melancholic patients showed increased counts of leukocytes, lymphocytes and NK-cells in the acute stage of disease and after two and four weeks of treatment. Their lymphokine production was unchanged compared to that of healthy controls. Melancholic patients on the other hand demonstrated normal cell counts but a decreased production of IL-2, IFN-gamma and IL-10 during the acute stage of disease followed by a normalization with clinical improvement. Melancholic and non-melancholic patients showed different immune patterns. Classifying melancholic and non-melancholic patients is helpful towards the identification of immune characteristics typical for these diseases.

PMID: 11407444 [PubMed - indexed for MEDLINE]


EDIT: Does the red highlighted portion above sound familiar? A "little" like RRMS, maybe? Believe me, you keep going and it only gets more and more similar.
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Postby OddDuck » Wed Apr 20, 2005 10:50 am

Ok...........here's just another "tickle", and then I'm gonna stop. This only gives you a "small" idea of what I came across, etc.

Mol Psychiatry. 2005 Mar;10(3):309-22.

Transcriptional profiling reveals evidence for signaling and oligodendroglial abnormalities in the temporal cortex from patients with major depressive disorder.
Aston C, Jiang L, Sokolov BP.

Neuroscience Discovery Research, Wyeth Research, Princeton, NJ, USA.

Major depressive disorder is one of the most common and devastating psychiatric disorders. To identify candidate mechanisms for major depressive disorder, we compared gene expression in the temporal cortex from 12 patients with major depressive disorder and 14 matched controls using Affymetrix HgU95A microarrays. Significant expression changes were revealed in families of genes involved in neurodevelopment, signal transduction and cell communication. Among these, the expression of 17 genes related to oligodendrocyte function was significantly (P < 0.05, fold change > 1.4) decreased in patients with major depressive disorder. Eight of these 17 genes encode structural components of myelin (CNP, MAG, MAL, MOG, MOBP, PMP22, PLLP, PLP1). Five other genes encode enzymes involved in the synthesis of myelin constituents (ASPA, UGT8), or are essential in regulation of myelin formation (ENPP2, EDG2, TF, KLK6). One gene, that is, SOX10, encodes a transcription factor regulating other myelination-related genes. OLIG2 is a transcription factor present exclusively in oligodendrocytes and oligodendrocyte precursors. Another gene, ERBB3, is involved in oligodendrocyte differentiation. In addition to myelination-related genes, there were significant changes in multiple genes involved in axonal growth/synaptic function. These findings suggest that major depressive disorder may be associated with changes in cell communication and signal transduction mechanisms that contribute to abnormalities in oligodendroglia and synaptic function. Taken together with other studies, these findings indicate that major depressive disorder may share common oligodendroglial abnormalities with schizophrenia and bipolar disorder.

PMID: 15303102 [PubMed - in process]


If you keep researching, etc., you could add with that last sentence ".....share common oligodendroglial abnormalities with schizophrenia, bipolar disorder, AND MS."

See what I mean?

Deb
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Postby OddDuck » Wed Apr 20, 2005 10:56 am

Oh.........just ONE last thing.

If people remember, I've ranted a few times as to WHY the doggoned neuros do not as a NORM run ELISA and/or ELISPOT tests on MS patients to make comparisons with other diseases!

But none of them do. And none of them would answer me as to why they do not.

:(

Deb
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Postby Daunted » Wed Apr 20, 2005 2:17 pm

This research on depression is quite problematic and the details get a little too technical for this board, but let's just say that this is extremely preliminary. There are no objective findings to decide who has "depression" and who doesn't, for starters.

With MS you have lesions in the CNS (whether identified through MRI, neurological exam, or evoked potentials). There are no lesions in depression. In fact the definition of clinical depression is that a person has a normal medical evaluation, yet is depressed.

So, when a person with MS is depressed, it's pretty obvious why (lesions and their impact)- but clinical depression outside of MS is a multi-factorial, unreliable, ambigious entity so this kind of research is really not very solid and people shouldn't make too much of it.

For instance a study out today shows that therapy works just as well as antidepressants for people who have clinical depression- and I don't think talking to someone does anything to the myelin of a depressed person.

Having said all that it's of course quite conceivable that there are neurobiological reasons for some cases of depression (outside of MS), but I think your posts (and these articles) overstate the case for the relationship between depression and neurological disease. Of course, the article was funded by the Stanley Foundation, and that's their entire mission.
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Postby OddDuck » Wed Apr 20, 2005 3:06 pm

Yes, lesions do appear on MRIs associated with depression.

For the sake of just "speed" alone, here's a quick example. I know it refers to late-life depression, but still, the statement that depression does not show up as lesions on MRIs is totally incorrect:

Am J Geriatr Psychiatry 12:606-612, December 2004
© 2004 American Association for Geriatric Psychiatry

--------------------------------------------------------------------------------

Regular Article

A Volumetric Study of MRI Signal Hyperintensities in Late-Life Depression
Michael J. Firbank, Ph.D., Adrian J. Lloyd, M.D., Nicol Ferrier, Ph.D., and John T. O'Brien, D.M.
Received January 9, 2004; revised April 23, May 10, 2004; accepted May 13, 2004. From the Institute for Ageing and Health, University of Newcastle upon Tyne (MJF,JTO) and the School of Neurology, Neurobiology, and Psychiatry, University of Newcastle upon Tyne, UK (AJL,NF). Send correspondence to Michael Firbank, Institute for Ageing and Health, Wolfson Research Centre, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne, UK NE4 6BE. e-mail: m.j.firbank@ncl.ac.uk
©2004 American Association for Geriatric Psychiatry

Objective: An increase in white-matter lesions has been previously described in older subjects with depression. The authors investigated whether the regional location varied between depressed and normal subjects and determined the relationship of magnetic resonance (MR) signal hyperintensities to known clinical risk factors for vascular disease. Methods: Authors used automated image-processing software to determine volumes of signal hyperintensities from MR brain scans of older people with depression (N=29; mean age: 76 years) and normal subjects of similar age (N=32). Results: Overall, subjects with depression had a significantly greater frontal-lobe white-matter lesion volume than normal subjects (0.35% versus 0.22%). However, after excluding subjects with hypertension, diabetes, or ischemic heart disease (leaving 14 depressed and 15 normal subjects), we found even greater differences between groups, with a larger volume of MR signal hyperintensities in the frontal region of the depressed group, but no difference in the basal ganglia or parietal and occipital lobes. Conclusion: The results support the "vascular depression" hypothesis and suggest that those with depression but without traditional vascular risk factors may be much more susceptible to cerebrovascular disease than normal subjects. The mechanisms for this increased susceptibility remain to be determined.

Key Words: Depression • Neuroimaging • MRI • Cardiovascular Risk Factors
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Postby OddDuck » Wed Apr 20, 2005 3:08 pm

...In fact the definition of clinical depression is that a person has a normal medical evaluation, yet is depressed.


Except in non-melancholic depression, whereby a person has clinical depression, but does NOT present with the typical melancholia.
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Postby OddDuck » Wed Apr 20, 2005 3:12 pm

Again, just quickly, here's an example of a study in attempting to differentiate the different sub-types of depression:

Acta Psychiatr Scand. 2005 Feb;111(2):139-43. Related Articles, Links


Progressing a spectrum model for defining non-melancholic depression.

Parker G, Malhi G, Mitchell P, Wilhelm K, Austin MP, Crawford J, Hadzi-Pavlovic D.

School of Psychiatry, University of New South Wales, and Mood Disorders Unit, Black Dog Institute, Sydney, Australia. g.parker@unsw.edu.au

OBJECTIVE: To further develop a 'spectrum model' for non-melancholic disorders that encompasses underlying personality styles and clinical patterning. METHOD: In a sample of patients with non-melancholic depression, we studied four personality constructs influencing risk to depression, assessing associational strength and specificity between personality scores and symptom and coping response patterns. RESULTS: Analyses refined four personality dimensions (anxious worrying, irritability, social inhibition, and self-centredness) for testing the model. For all dimensions, personality style was specifically linked with a mirroring 'coping' response. Quantification of specific links allowed development of a spectrum model for the non-melancholic depressive disorders in which underpinning personality style showed some specific links with the clinical 'pattern' of symptoms and coping repertoires. CONCLUSION: The model has the capacity to assist clinical assessment, identify aetiological personality influences and allow specific treatment effects for the heterogeneous non-melancholic depressive disorders to be determined.

PMID: 15667433 [PubMed - in process]


I'm probably not coming up with the best examples, but there is PLENTY of research into this going back to the 80s. I'm just grabbing things on the fly.
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Postby OddDuck » Wed Apr 20, 2005 3:21 pm

Ok........getting a little farther off track, but still just as proof that affective disorders (of which depression is one) can and most often DO show lesions on MRIs, here is just an excerpt from one publication (there are many, though).

http://www.nimh.nih.gov/publicat/bipolarresfact.cfm

....Structural Imaging

NIMH has supported considerable research with the new technology of magnetic resonance imaging (MRI) to examine the structure of brain tissue in various mental disorders, including bipolar disorder. The first such studies have appeared only within the past 10 years, with the pace of progress accelerating steadily since that time. The goal of this research is to discover the ways in which specific areas of the brain in people with bipolar disorder may differ from healthy individuals.

One of the most consistent findings to date has been the appearance of specific abnormalities, or lesions, in the white matter of the brain in patients with bipolar disorder.8 White matter consists of groups of nerve cell fibers surrounded by fatty sheaths that appear white in color. These sheaths help the transmission of electrical signals within the brain. While the white matter abnormalities appear in many parts of the brain in individuals with bipolar disorder, they tend to be concentrated in areas that are responsible for emotional processing. These brain changes increase in frequency with age both in people with bipolar disorder and individuals with no mental illness, but they appear more often than expected in young patients with bipolar disorder. This finding suggests that the white matter abnormalities seen with MRI are related to the presence of the disorder. However, some patients with bipolar disorder do not show the white matter changes, and conversely, some entirely healthy individuals have the lesions. Also, it is not yet clear whether these changes contribute to the onset of the disorder, or are in some way a result of becoming ill. While these MRI abnormalities likely indicate one type of malfunction in the brain circuits involved in bipolar disorder, more research is clearly needed to understand their significance and their utility for early diagnosis and treatment. ...


Now..........is there a "practice" in the medical community yet for diagnosing affective disorders via the help of MRIs? No, not yet.

But can or do affective disorders, including depression show "lesions" on MRIs, and/or are they "connected" with myelin and oligodendrocyte dysfunction? Yes.

If you do searches and more reading, you'll find LOTS of these findings.

That's all I'm saying.

EDIT: Oh, and not to forget my original posts above whereby affective disorders affect immune function. The similarities and cross-overs are astounding, biologically speaking.

Again, a person can suffer from "clinical" depression without actually "feeling" depressed. There is the label of "depression", and then there is "clinical depression". Not to mention non-melancholic, and melancholic. Mixing up the two terms and/or medical conditions as one and the same is a mistake.
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Postby Daunted » Wed Apr 20, 2005 7:01 pm

OddDuck wrote:Again, a person can suffer from "clinical" depression without actually "feeling" depressed. There is the label of "depression", and then there is "clinical depression". Not to mention non-melancholic, and melancholic. Mixing up the two terms and/or medical conditions as one and the same is a mistake.


Deb, I respect your research efforts, but the efforts to identify a "physical" disease of depression separate from the psychologica/emotional category are really primitive so far.

And a study out a couple of weeks ago shows that for those with depression, Cognitive-Behavioral therapy is as effective as antidepressants. I don't believe that thinking happy thoughts and talking to a counselor would cure brain lesions.

Also, depression is only diagnosed from symptoms, e.g., feeling depressed, not sleeping well, etc. There is no such thing as an asymptomatic mental disorder.

The type of studies you have posted have been critiqued at length in the literature.

Other than that, I'll just let this drop, as it is too complex to discuss at length here.

But interesting stuff, an evolving field, but too primitive to draw any conclusions at all, yet.
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Postby OddDuck » Thu Apr 21, 2005 4:05 am

Ah.............so YOU are a believer that affective disorders are ALL just in someone's "head", i.e. arising from their "mood" and conscious thought processes. Without the involvement of adrenal or hormones, too, I bet. No such thing as the HPA axis or serotonin, dopamine or norepinephrine being out of whack? Probably not, as those things are all "physical" causes. Well, I'm sure you will find many who will differ with you completely - especially WOMEN! HAH!

I wouldn't exactly say neuropsychiatry is primitive whatsoever. And studies supported by the NIMH I would believe hold considerable weight.

But, I agree with you. Time to drop it.

(But note...........out of total respect for YOU, I never asked YOU to "prove" where you read the studies YOU read and came to your conclusions, nor asked YOU to provide references and post them. In otherwords, I never intimated YOU as being a liar when you simply spoke of the "recent study" you just talked about, did I?)

As the movie says............analyze that! :wink:

Take care,

Deb

Ok.........I think I'll leave you with this:

EDIT:
And a study out a couple of weeks ago shows that for those with depression, Cognitive-Behavioral therapy is as effective as antidepressants.


Not always! :wink: Therefore, wouldn't that study then be implying that anti-depressant medications are nothing more than "sugar pills"? Well, I beg to differ with THAT study! Oh, and by the way.........advise an MS patient with cognitive problems to "think happy thoughts" and they'll get much better. Then run for cover and/or DUCK! :lol:

I don't believe that thinking happy thoughts and talking to a counselor would cure brain lesions.


Exactly my point! Nor would I think that those same things would always cure clinical depression!

Also, depression is only diagnosed from symptoms, e.g., feeling depressed, not sleeping well, etc.


hmmmmmmmmm......that's funny, I myself was diagnosed with "clinical" depression based on a "chemical imbalance" WAY back in the 80s. It had nothing to do with my "mood" or behavior, which was fine, and there was NO evidence of "mental disorder" when fully examined by psychologists. It was a complete "physical" dysfunction diagnosis, not mental in the least. Of course, they NOW wanted to say it was MS instead back then. Based on the exact same symptoms, too! ALL of which were "physical", not "mental". Now how in the world could medical professionals get those two conditions mixed up? hmmmmmmmmmmmm............... funny how MS researchers in numerous countries are finding in MANY instances how anti-depressants (which DO work for many types of depression) ALSO appear to provide immune system regulation AND neuronal protection in MS (as I provided above). hmmmmmmmmm............ confusing indeed!

There is no such thing as an asymptomatic mental disorder.


Are you SURE about that? I thought it was too "primitive" to reach any firm conclusions at this point? Actually, your statement is probably correct (although, the field of neuropsychiatry are obviously and apparently finding that that's not always true). The term "mental disorder" again implies that any type of depression is simply all in someone's "mind", and could not POSSIBLY arise from anything physical (which such belief would also include side-effects from medications. Depression caused by a drug side-effect is "physical".) Actually, Daunted, I'm astounded! So, you would rapidly advise a "client" who came to you with "depression" that it was "all in their head", and could not POSSIBLY be caused by anything physical or any physical imbalance whatsoever? You sure you're not a "neuro"? :wink:

But.............you're right. Whichever "side" of the equation you are expressing you believe in. It's hard to tell, actually. :?

Have a good one!! All the best!
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Postby OddDuck » Thu Apr 21, 2005 5:20 am

Hey, Daunted..........this might interest you (on the side).

At the University of Michigan Behavorial Science Center (MHRI), they have been doing some really interesting work there since the 1960s.

Here's a synopsis. You might find their studies quite interesting.

http://www.med.umich.edu/mhri/

....About MHRI

While fundamental research takes place in multiple settings in the Department of Psychiatry, the single greatest concentration of basic work takes place at the Mental Health Research Institute, which is co-directed by Drs. Huda Akil and Stanley Watson. MHRI is a nationally and internationally recognized research institute. It is also an interdisciplinary unit that has a broad-based program of basic research on the etiology and treatment of mental illness. Since its founding in 1955, the Institute has grown from three scientists to more than 20 who are active in both the basic and applied studies of the brain and behavior. The faculty of MHRI is composed of a mix of PhD's, MD's, and MD/PhD's. They hold their tenure or tenure-track appointments in a range of departments including Psychiatry, Biochemistry, Pharmacology, Psychology, Genetics, Neurology/Internal Medicine and Radiology.

Research at MHRI revolves around four central themes:

a) Basic Mechanisms of Signaling and Neurotransmission;

b) Developmental Neurobiology;

c) Basic Mechanisms of Stress and Emotion and their Relation to Mood Disorders;

and d) Cognition, Neuroimaging and Psychosis.

In addition, MHRI has recently established a Microarray Laboratory to pursue studies on gene profiling of relevance to both animal and human studies.

*********************

Here is further information regarding Dr. James Miller that also tells the history of the MHRI:

http://projects.isss.org/James_Grier_Mi ... _A_Swanson

“….Beginning in 1953, the Committee on the Behavioral Sciences planned to create an Institute of Behavioral Science and Miller, as its chairman, began to raise funds to construct a building and endow the program. Dr. Raymond W. Waggoner, chairman of the Department of Psychiatry at the University of Michigan, learned of this activity and invited Miller, together with a group of his senior colleagues, to move to Ann Arbor. He obtained from the Michigan Legislature a commitment to construct the sort of building that had been envisioned for Chicago and to provide a continuing appropriation of sufficient size to operate the planned institute. Chancellor Lawrence Kimpton of the University of Chicago and President Harlan Hatcher of the University of Michigan agreed that a move to Ann Arbor was the optimal solution for the situation.

On July 1, 1955, Miller arrived as director of the new Michigan institute, accompanied by Ralph W. Gerard and Anatol Rapoport. Later, Robert I. Crane and Richard L. Meiser joined them from Chicago.

The Institute was established in the Department of Psychiatry of the University of Michigan School of Medicine. Dr. Raymond W. Waggoner, chairman of the department, had initiated all the necessary administrative and financial actions required to make this possible. President Harlan Hatcher asked that the new Michigan program be named the Mental Health Research Institute rather than the Institute of Behavioral Science because he thought that that name would make it easier to secure financing. It was always understood, however, that the Institute was to carry on behavioral science research in a systems framework like that begun at the University of Chicago.

In the Institute's basic research, special emphasis was placed on the evaluation of cross-level hypotheses, a then novel sort of investigation. Quantitative laboratory measurements of comparable phenomena were made across multiple levels of biological and social systems. The first such research ever carried out was the Information Input Overload study made by an interdisciplinary group of scientists with Miller as principal investigator. This study of comparable input-output effects and adjustment processes, at the levels of the cell, organ, organism, group, and organization, was published in 1960 [8]. In 1982 Professor Daniel Bell of Harvard University, in his book The Social Sciences Since the Second World War, listed such research as one of 62 basic innovations in social science between the years 1900 and 1965 [9].

Other cross-level experiments on different systems hypotheses were conducted by Anatol Rapoport and other investigators at the Institute in the 1950s and 1960s.

Miller was director of the Mental Health Research Institute from 1955 to 1967. Shortly after his arrival he refused the invitation of Dr. Robert Oppenheimer to join the staff of the Institute for Advanced Studies at Princeton because he wished to remain to lead the development of the Mental Health Research Institute. During his years there, the program advanced and expanded in many directions. It increased in size to about 100 scientists in approximately 20 disciplines of the mathematical, physical, biological, social, medical, and engineering sciences. Among the numerous areas given special attention were neuropsychopharmacology, brain biochemistry, and physiological basis of memory, schizophrenia, game theory, and conflict resolution. ....


This might help reconcile for you how mental disorders can and do cross-over into biological and physical disorders. They do some interesting work at the U of M in this area. You, especially, might find it fascinating. I know I did.

It's not "primitive" science at all. :)

Best always,

Deb
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