Psychiatric Times.

Is Major Depression “Adaptive”? Clinical Data Say No

By Ronald Pies, MD | November 4, 2010

The poet Denise Levertov was no stranger to sorrow and loss. In her poem, “Stepping Westward,”¹she writes of the aging process, as both a burden and a gift. The poem begins,

What is green in me/darkens, muscadine . . .

Muscadine is a woody vine that produces a musk-scented purple grape, used to make wine. Levertov’s image is one of growing darkness, but also of emotional growth and maturation. With old age comes “the fruit of the vine”—wisdom and awareness. Levertov’s poem goes on to observe,

If I bear burdens/they begin to be remembered/as gifts . . .

We all know that sorrow can bring insight, if it is properly and deeply understood. This “gift” may also emerge from the pensive reflection of ordinary grief and bereavement. I begin with Levertov’s poetic images because I want to distinguish what Thomas à Kempis called “the proper sorrows of the soul” from what psychiatrists know as major depression. I would never argue against the claim that on some level, ordinary grief may be adaptive—in fact, in a series of articles, Dr Sidney Zisook and I have stated as much.^2,3

But when the same claim is made with regard to major depressive disorder (MDD), as in the so-called analytical (or adaptive) rumination hypothesis (ARH),^4-6 I am left shaking my head. In its simplest formulation, the ARH asserts that “. . . depression is nature’s way of telling you that you’ve got complex social problems that the mind is intent on solving” and that “depression is in fact an adaptation, a state of mind which brings real costs, but also brings real benefits.”⁴ In effect, the ARH asserts that the “analytical” and ruminative cognitive processes of the depressed person facilitate complex, social problem solving. A number of experimental manipulations are cited to support the ARH [eg, see Hertel and coworkers⁷], but few psychometric studies of clinically depressed patients (eg, meeting DSM-IV MDD criteria) are adduced as evidence. (Let’s leave aside the simplistic notion that depression arises from unresolved “social problems”—of course, this is sometimes so, but in many cases, interpersonal problems are the consequence of preexisting depression.⁸)

The basic claims of the ARH do not square with anything in my experience as a specialist in mood disorders for over 25 years, nor with the overwhelming majority of clinical studies of cognitive function in MDD, to be reviewed presently. But first, it is critical that we distinguish studies of clinical populations from experimental manipulations involving non-clinical test subjects—usually described as being “sad” or in a “depressed mood state”—who are asked to solve various artificial “problems” [eg, see Hertel and associates].⁷ These test subjects—eg, college student volunteers⁴—are usually “induced” to have very brief periods of depressed mood, using some experimental intervention. They have virtually nothing in common with the seriously depressed patients we treat, who have often been ill for weeks, months, or even years.

To be clear: I have many problems with the DSM-IV construct of MDD, such as its almost risible elasticity—MDD is a diagnosis that can be stretched around almost anyone with 2 weeks, or 2 years, of depressive symptoms.⁹ But when carefully applied to someone with a month or more of severe depression, 1 or more melancholic features, pronounced suffering, and substantial social-vocational incapacity, “MDD” describes a very real disease entity, with a suicide rate of about 4 in 100.¹⁰ The notion that such a condition is in any sense “adaptive” flies in the face of clinical experience, the reports of most severely depressed patients and, as I hope to show, most studies of cognitive and social function in depressed individuals.

As to “evolutionary” arguments for and against the ARH, I will leave those to authorities in the field of evolutionary biology,¹¹ although I am deeply skeptical of some recent claims regarding the benefits of “analytical rumination.”⁶My intention here, however, is to examine the published studies of cognitive function in patients with major depression and to pose the following questions:

1. Is there credible evidence showing that MDD (or clinically significant depression) enhances any specific types of cognitive skills or mental processes?
2. Is there credible evidence showing that rumination in MDD enhances any type of “problem-solving” skills?
3. Is there credible evidence showing that depressed individuals possess enhanced social or interpersonal skills, such that they might be at some kind of adaptive advantage?

These questions, of course, cannot address whether those who have endured an episode of severe MDD are or are not “wiser” for the experience, or whether they were able to find life-enhancing “meaning” or valuable perspectives in the course of their suffering. These are fundamentally philosophical and spiritual—not scientific—determinations. Finally, I will not address the controversial matter of antidepressant treatment, other than to note this: the claim that MDD is not “adaptive”—indeed, that it is pervasively maladaptive—is surely not to claim that all persons with MDD require, or benefit from, antidepressant treatment. Simply put, some do, and some probably do not.¹² In any case, the issue of pharmacotherapy would take us far afield.

Clinical studies of cognition in depression
Dr Charles DeBattista,¹³ in a recent review, concluded that “the types of executive deficits seen in depression include problems with planning, [as well as] initiating and completing goal-directed activities” and that such “executive dysfunction” tends to worsen in direct proportion to the severity of depression. Similarly, a review by French investigators concluded that “. . . executive deficits associated with frontal lobe dysfunction may be prominent in depression” and that “. . . unipolar depressed patients mainly exhibit cognitive inhibition deficits, problem-solving impairments, and planning deficits.”¹⁴ Furthermore, unipolar depressed patients tend to show “. . . difficulties in hypothesis testing with a loss of spontaneous and reactive cognitive flexibility,” attributable to dysfunction in the dorsolateral prefrontal cortex. (Ironically, proponents of the ARH suggest that prefrontal brain regions show enhanced activity in major depression, thus facilitating “analytical rumination”; in fact, the brain imaging evidence in MDD is complex and often conflicting, perhaps reflecting slightly differing subregions of the prefrontal cortex.¹⁵)

Cognitive problems may be especially pronounced in older depressed individuals, as Alexopoulos and colleagues¹⁶have shown. They note that “depressed patients often have disturbances in attention, speed of processing, and executive function even in the absence of dementing disorders.” Moreover, “. . . executive dysfunction and related cognitive abnormalities confer significant disability and add to adversity experienced by the depressed elderly person [italics added].”¹⁶ Collectively, these findings do not suggest any salient adaptive advantages in the cognitive state of most clinically depressed patients. Quite the contrary: as Alexopoulos and colleagues note, citing the work of Nezu and Ronan, problem-solving therapy for geriatric depression actually “. . . originated from the observation that depressed patients use inadequate or inappropriate approaches in addressing their problems. . . . [italics added]”.

Rumination: friend or foe?
There is little disagreement with the observation that clinically depressed patients tend to ruminate; ie, to focus repetitively on the same issue, problem, or thought (the term comes from the Latin ruminari , “to chew cud”). In general, the research literature points to the deleterious effects of depressive rumination. As Rimes and Watkins¹⁷ observe, citing the work of Nolen-Hoeksema¹⁸ and others,

Increasing evidence suggests that rumination plays a role in the maintenance of depression. . . . Experimental studies have found that in dysphoric participants, compared to [use of] distraction, rumination increases depressed mood, cognitive distortions and . . . impairs problem-solving skills . . .

These findings are consistent with those of Donaldson and Lam,¹⁹ who found that patients with major depression who were made to ruminate experienced a deterioration in their mood and gave poorer problem solutions. Similarly, Park and associates²⁰ found that experimentally induced rumination, as compared with distraction, increases depressed mood and negative memories in adolescents with a first episode of MDD.

Taken in total, these findings flatly contradict the central claim of the ARH; ie, that rumination is helpful and adaptive in addressing one’s problems, social or otherwise. But there is a complication we need to consider: rumination appears to be subdivided into analytical self-focus (ASF) and experiential self-focus (ESF). In essence, ASF involves thinking analytically ‘‘about’’ oneself and one’s symptoms; eg, “How did I get so depressed? Why do I feel so guilty?” In contrast, ESF involves a “here and now” focus on the direct experience of one’s thoughts, feelings, and sensations in the present moment; eg, “Right now, I’m feeling hurt and angry that John left me for someone else.”

Rimes and Watkins¹⁷studied these 2 types of rumination in 30 depressed participants (MDD by DSM-IV critiera) and 30 never-depressed volunteers. Participants were randomly allocated to “analytical” (high analysis) or “experiential” (low analysis) self-focused manipulations. The study found that in depressed participants, ASF increased ratings of feeling “worthless” and “incompetent.” The ESF condition resulted in no significant change in such judgments. (Neither mode of rumination had a significant effect in the nondepressed controls). The authors concluded that “. . . an analytical mode of self-focused rumination may be particularly maladaptive in depression.”¹⁷

Once again, no support for the ARH is provided. Indeed, in direct contradiction of the ARH, Watkins and colleagues²¹have shown that treating depressive rumination with cognitive-behavioral therapy “. . . appears to yield generalized improvement in depression and comorbidity.” If rumination were indeed adaptive and productive, we would expect the opposite result.

Social and interpersonal skills in depression
Does being clinically depressed somehow make one more empathic, or improve one’s ability to “read” the social cues of others? Might depression enhance social bonding in a way that could be “adaptive”—if not on an “evolutionary” time scale, at least in the here and now?

Some preliminary answers have emerged from studies of the ability to recognize facial expression. What does facial expression have to do with social and interpersonal skills? A good deal, according to Yoon and colleagues.²²They note that “biases in the processing of subtle facial expressions of positive affect may . . . contribute to the interpersonal difficulties that maintain [depression].” Put in more colloquial terms: if you can’t tell that someone is smiling at you, the two of you are not likely to hit it off. Indeed, in their study of subjects with MDD, Yoon and coworkers found that major depression interferes with “reading” subtle expressions of positive affect, such as the famous “Mona Lisa smile.” It is hard to see any adaptive advantage in this perceptual bias.

A core argument of the ARH is that unresolved “social problems” precede clinical depression, which is said to be an adaptive response to these problems. But as Segrin⁸ observes in his review,

Three different theoretical relationships between disrupted social skills and depression [have been] described . . . [namely] poor social skills as a cause of depression, depression as a cause of poor social skills, and poor social skills as a vulnerability factor in the development of depression. Currently, there is some evidence to support each of these conceptualizations.

Despite this ambiguity, there is little doubt that clinically depressed individuals show a variety of social and interpersonal deficits, including, according to Segrin,⁸

. . . inhibition in initiating new relationships and interactions with others; problems in expressing themselves clearly to others; inappropriately and excessively self-disclosing information, especially if it is negatively toned, to others; and sometimes being overly negative and perhaps even hostile around other people.

Once again, it is hard to imagine any short-term, adaptive advantage emerging from these widespread interpersonal difficulties in depression, much less an enhanced “evolutionary” advantage that would favor attracting a mate, engaging in sexual activity, reproducing, etc. But these are matters of debate for the evolutionary biologists.

Conclusion
I would wager that the great Renaissance artist Albrecht Durer understood clinical depression far better than some modern-day proponents of the ARH. In his 1514 depiction of “Melencolia I” (“Melancholy”—see Figure), Durer shows the pensive goddess sitting amidst an array of unused analytical tools and instruments, staring somberly into space. As one commentator observes,

. . . her fixed state is one of intent though fruitless searching. She is inactive not because she is too lazy to work but because work has become meaningless to her; her energy is paralyzed not by sleep but by thought.”23

A psychiatrist could hardly have described severe depression more accurately, or refuted the ARH more succinctly.

I do not doubt that for some patients with MDD, there are indeed “remembered gifts” that are appreciated on recovery from their depression. But this is not to say that MDD itself is “adaptive” during the course of the patient’s illness. Virtually all the evidence I have reviewed leads to precisely the opposite conclusion. Nonetheless, the final word has not been written on this controversy. It would be instructive to do a carefully designed, empirical study that examined the question of depression’s “upside” from the patient’s point of view—controlling for possible confounds, such as the type of depression; whether or not the patient is hospitalized; how much support the patient is receiving from significant others; when in the course of illness the patient is asked the question, etc.

I’m not aware of such studies, whereas I have countless experiences hearing about the hellish suffering brought on by major depression. I remain open to the possibility that brief periods of mild depression may sometimes permit useful reflection on one’s problems, and perhaps even lead to some solutions. But in my experience, it is usually despite—not because of—serious depression that solutions to life’s problems are found. We owe our patients more than specious theories regarding the “upside” of their depression; we owe them safe, effective, and readily available treatment.¹²

Acknowledgments: I would like to express my appreciation to Drs Katharine Rimes and Rebecca Park for their helpful comments and references; and to Drs George Alexopoulos and Emily Becker-Weidman for providing their papers. I also want to acknowledge the seminal research of Dr Helen Mayberg in studying regional brain imaging in MDD. However, this commentary represents solely my own analysis and conclusions.

by Ronald Pies | January 27, 2011 1:22 PM EST

Thanks to Norton Clybourn for the thoughtful comments. The hypotheses he suggests, while speculative, seem much more plausible to me than the so-called "adaptive rumination hypothesis". Dr. Brian Johnson, my colleague at SUNY Upstate Medical University, recently wrote to suggest a similar hypothesis regarding why depression might be evolutionarily "conserved". I will append some of his comments and my response, below.--Ron Pies MD

excerpts from Brian Johnson MD:

Ron--PT just showed up, and I was excited to see what you wrote about the evolutionary advantage of depression...[ ] But I was disappointed that you did not cover the evolutionary theory that is being taught here at SUNY Upstate. Briefly, my buddies Doug Watt and Jaak Panksepp published the concept that humans are social for survival. If our ancestors were comfortable being alone, they were eaten by saber tooth tigers. In response, we started to get increasing symptoms of alarm as we became isolated; Panksepp's PANIC system. Eventually, instead of screaming for mother and drawing saber tooth tigers who wanted us for lunch, depression would ensue to enable us to conserve energy and wait to be found. This concept works great for approaching depression. I teach my medical students and residents to talk to patients, and use antidepressants to get them out of the shut down mode and back on the plane of anxiety. I attach the Watt/Panksepp paper and my book chapter from the Tom Schwartz textbook that builds off their concept...
Best regards,
Brian

Director of Addiction Psychiatry, SUNY Upstate Medical University
Purchase my book on addiction at www.gegensatzpress.com/zombies

Ref: Depression: An Evolutionarily Conserved Mechanism to Terminate Separation Distress? A Review of Aminergic, Peptidergic, and Neural
Network Perspectives. Douglas F. Watt (Cambridge, MA) & Jaak Panksepp (Pullman, WA) Neuropsychoanalysis, 2009, 11 (1)

Pies response to Dr. Johnson:
Hi, Brian--Thanks for the note re: my article in PT, and for the very stimulating chapter and article by Watt & Panksepp. There is a simple reason I didn't discuss your and their hypothesis: to paraphrase your illustrious namesake (and forbear?), Dr. Samuel Johnson, "Ignorance, sir, pure ignorance!"I was not aware of this work, and I certainly find the hypothesis put forth much more plausible and compelling than the "adaptive rumination hypothesis."

As you and Doug Watt et al note, we need much more evidence and study--which I think is hard, when it comes to positing evolutionary mechanisms. For example, what is the evolutionary "trade off" when an abandoned infant (monkey, human, etc.) no longer cries and wails for mom? On the one hand, he/she is less likely to attract attention from a predator--but is also less likely to attract attention from wayward or missing mom. It is also not clear to me why evolution would not favor a "shut up and quiet down" system, rather than one that would predispose, in humans, to self-loathing, intense guilt, accusatory auditory hallucinations (in psychotic depression) and suicide. However, I do think Watt & Panksepp begin to provide a plausible answer when they write, "...like any adaptive mechanism, this putative "shutdown" process can become disinhibited, hypertrophied, released from its normal control mechanisms, and subsequently recruited pathologically in the context of fairly minimal stresses or precipitants, yielding the diverse symptoms and variants of depressive illness...". This "adaptation run amok" hypothesis seems much more plausible than the [in my view] bogus notion that when people are experiencing a major depression, they are able to "ruminate" productively on their social problems!

Best regards, Ron

by norton clybourn | December 24, 2010 10:58 AM EST

I can see two ways that a depressive reaction could be adaptive:

The withdrawal and decrease in goal-directed bx could have originated as an adaptive response to physical illness or injury. An individual with melacholic symptoms behaves and feels much like an individual with a medical illness, and medical illness should always be ruled out first. In some medical conditions, a painful response to goal-directed bx could have been as adaptive as a painful response to moving a broken limb.

An extension of this response set can be useful in situations where the contingencies are highly unfavorable. Passive acceptance of learned helplessness is not adaptive, but neither is acceptance of unfavorable conditions. It makes sense to avoid such conditions, withdraw, and conserve energy.

In the most primitive forms of "thinking outside the box" of unfavorable contingencies, a trapped animal or one too low on the hierarchy to obtain sustenance may react with rage or attack a higher ranked individual. He may have little chance of defeating the stronger individual, but he has some chance, as opposed to certain starvation.

The response that is more adaptive for modern humans is to recognize that contingencies are unfavorable, stop trying to force oneself into going through the motions, and find new opportunities, or at least cognitively reframe the perception of reality. If the limbic system goes on strike for better conditions, it can be very beneficial to renegotiate terms.

As with the other unpleasant but vital experiences of pain or anxiety, chronic and severe levels of a melancholic reaction are harmful and counterproductive. But there is surely a reason that we have it in our repertoire.

by Ronald Pies | December 03, 2010 12:40 PM EST

Here is the reference I mentioned:

J Affect Disord. 2007 Jun;100(1-3):7-11. Epub 2007 Jan 16.

Pies R.

Tufts University School of Medicine, Boston, MA

Abstract

The construct of bipolar disorder, or bipolar spectrum disorders, has been a source of controversy in recent years. Some have argued that subtle variants within the putative bipolar spectrum are merely the creation of overzealous clinicians, perhaps encouraged by various special interest groups. In reality, the concept of a bipolar spectrum may be inferred from numerous classical sources, dating back to the 19th century and even into antiquity. The Greek philosopher Aristotle, usually considered the author of a work called Problemata, appears to have recognized some form of the bipolar spectrum, more than two millennia ago. This recognition continues throughout the 19th century, and into our own time. Such transcultural findings across many centuries have implications for the "objective" nature of psychiatric disease.

by Ronald Pies | December 03, 2010 12:03 PM EST

Well, my goodness! I appreciate Dr. Tan's taking the time and effort to respond so vigorously to my piece on the ARH and depression. Since medieval and Renaissance studies are dear to me, I'll try to respond with some further thoughts shortly. In the mean time, Dr. Tan might be interested in seeing my paper on Aristotle and bipolar disorder, which does deal with various degrees of temperament vs. clinical mood disorders. It's in Journal of Affective Disorders, and I'll try to post the reference later. --Best regards, Ron Pies

by Mong H Tan, PhD | December 02, 2010 4:03 PM EST

RE: Ditching the ARH (unequivocally): A (psychiatrist) rebel without cause!? -- Or, How the ARH could help illuminate, identify, and defuse ME (mind & emotion, including morality & ethics) distresses in clinical depression and adaptive remission (maladaptive socio-personal distresses idiosyncratic, subjective, major or otherwise, in current socio-psychology & neuropsychiatry, today & beyond)!?

1) Despite the recent "fierce & in-depth"debates on the ARH in the Psychiatric Times (PT) -- especially debating from both the evodevo (evolutionary & developmental) perspectives of clinical depression -- Ronald Pies, MD (Editor-in-Chief Emeritus of PT) has managed and continued to cry foul on the subject matter: by renewing an attempt to trivialize, degrade, and deny the specific biomedicine-based evodevo psychological function and remedial adaptive mechanisms in our brain -- or the neuropsychiatric novelty of the ARH in clinical depression of ME (mind & emotion, including morality & ethics) distresses -- in the above Commentary article; and in it, he defiantly and boldly -- albeit unscientifically & uncritically & uncharacteristically -- asserts that:

I would wager that the great Renaissance artist Albrecht Durer understood clinical depression far better than some modern-day proponents of the ARH. In his 1514 depiction of "Melencolia I" ("Melancholy"-see Figure), Durer shows the pensive goddess sitting amidst an array of unused analytical tools and instruments, staring somberly into space. As one commentator observes,

". . . her fixed state is one of intent though fruitless searching. She is inactive not because she is too lazy to work but because work has become meaningless to her; her energy is paralyzed not by sleep but by thought."

And Pies further concludes (with edits for clarity in parenthesis) that "A psychiatrist could hardly have described severe depression more accurately, or refuted the ARH more succinctly [than that of the Durer's mastery portrayal of melancholy in his Melencolia I masterpiece above]."

2) On the contrary, I would beg to differ: I thought Pies has clearly misrepresented the ARH at issue; and been refuting it backwards into the "downside" medievalism of melancholy, or acedia, or ennui of the pre-Renaissance era; while disregarding an earlier (even more accurate) Aristotle's empathetic (albeit primordial or preliminary) observation, rumination, and consideration of depression (of ME interactive process) as an "upside" phenomenon of "from black melancholy to golden joy" ruminating or coping mechanism for melancholic remission, meditation, recovery, progression, and/or adaptation of melancholy; as one that Aristotle (384-322 BCE) might have had experienced and comprehended of his intimate subject matter of the Axial Age (1200-200 BCE) at his time!? -- Or, at a time (during the Axial Age) when several recorded world, major, and universal philosophies in humanism, intellectualism, spiritualism, ritualism, religionism, rationalism -- especially those aspirations, inspirations, & aesthetics in the art & literary creations, ruminations, recitations, intellectual & spiritual meditations, poetries, physics & metaphysics, etc -- had had all begun to flourish and establish independently, in and around the Mediterranean Sea, the Middle East, Asia, and South Asia: specifically in Greece, Mesopotamia, Egypt, Palestine, Judea, Babylonia, Persia, China, India, etc.

All these universal philosophies, observations, inspirations, and scholarships in and of our humanities during the Axial Age -- primarily originated, developed, & grew out of and from within each social, geographical & historical context; each humanity, creativity, & socio-psychology -- had had helped lay a fertile foundation for the later-day Renaissance (especially the European revivalisms in the arts, sciences, rationalism, realism, morality & ethics, etc) and the Reformation of religiosity (especially the European Christianity) to emerge, and flourish creatively, soon after the mostly repressive or regressive medievalism of the Middle Ages (circa 500-1450)!? -- Please also note that, prior to medievalism, the Middle Ages had had already begun to descend into feudalism and chaos of the then socioeconomic, political, and religious conflicts & wars, immediately following the fall of the Western Roman Empire (395-476)!

3) Whereas -- concerning specifically Pies' Renaissance art, socio-historical & psychiatric observations, and conclusion above -- I thought the Renaissance art commentator's "medieval diagnosis" of melancholy was clearly incomplete nor holistic: for its neglecting to empathetically outline a psychological profile of the goddess, at all; especially a profile that would be situated in and around her immediate and/or intimate social and historical context: scientific; religious; or in confusion of both contexts (please see more "confusion-depression, cause & effect" observations & consequences in commentary 4 below, in asterisk & italic) as one to be in whichever ME state of the "context in profile" that would be most likely to identify or implicate the probable sources or causes of her profound ME interactive depression, in question above!?

Nor was the commentator's observation more insightful than those of the modern neuropsychiatric evaluation and definition of the socio-personal ME identity and maladaptive depression: a ME crisis (major or otherwise) in mal-calculus or in "confusion-depression" state of one's own socio-personal identity, function, and/or adaptation or life-work coping issues (religious, scientific, or otherwise) etc; and a psychologically introspecting/ruminating or self-understanding, self-defining, self-affirming and self-healing process, that is located in the VLPFC -- [the prefrontal cerebral cortex that may include the nucleus accumbens: a neural circuitry nexus, which plays an important role in the ME senses & responses to one's own feelings of, in, & for pleasure; fear; reward; addiction; and/or depression, as well as rumination] -- in our brain, as theorized and observed by the ARH at issue!

Thus, by modern ARH clinical standards and qualifications, the "melancholic goddess" above, could have had been more in-depth -- both psychologically & empathetically -- diagnosed of her seemingly more "acute & underlying" ME distresses or causes of depression, as follows (with critical, crucial & probable causes of depression cited in parenthesis):

". . . her fixed state is one of intent though fruitless searching -- [or more accurately by the ARH examination: staring in emptiness, without any reflective mindfulness or purposes in thought, at all]. She is inactive not because she is too lazy to work but because work has become meaningless to her; her energy is paralyzed not by sleep but by thought [of her paralyzing emptiness & meaninglessness in life and/or in work purposes, at all & thereof]."

4) As such, the ARH shall enable the goddess to better understand, analyze, introspect, or ruminate her own acute "depressed or fixed state" or her "emptiness" in ennui, acedia, or both (a common psycho-phenomenon of ME distresses in the medieval times); or the nature of her "meaninglessness" in life-work-perceptivity in and of herself: a subjective ME state that has indeed rendered her paralyzed with thoughtlessness or mindlessness; as well as deprived her of any ME drives of self-motivation, self-mindfulness or meaningfulness, self-worth; or any other self-defined life-purposes and/or work issues, etc at all!

With the understanding of the ARH -- primarily that of a self-rumination ME mechanisms in the VLPFC of our brain (with or without professional aid of talk therapy or CBT; medication; or in combination of both) -- the "Renaissance goddess" -- who might have had contracted a "medievalism-affective syndrome" of melancholy -- would now be able to start ruminating "positively & deeply" into her life-memories: experiences, moods, social and personal issues, work purposes, beliefs, aspirations (religious or not) etc; so as to begin to introspect, reevaluate, renegotiate, readjust, and readapt to her soon to be self-revived life and work definitions and purposes, etc; so as to resolve, re-motivate, reinvigorate, and reestablish herself as the Renaissance goddess, so as to get up and out of her currently (major or otherwise) ennui or depressive state -- meaningfully and mindfully: in a renewed sense of self-worth, and/or a real sense of the "Renaissance divinity" or creativity (intellectual & spiritual; religious or not) in the "upside" humanism of self-understanding: self-respect and expression; creativity in the arts and sciences; life and work purposes; aspirations; enlightenment; integrity; liberty; equality and pursuit of happiness, etc beyond the "downside" subscription of depression, as often defined and confined by the socio-historically "regressive and/or repressive" medievalism!? -- *Or, beyond the 20th-century folly and haunting of neo-Darwinism as the armchair evolutionist scientism, or the more recent foray of "new atheism" -- [please see Richard Dawkins' 2006 book "The God Delusion"] -- as One neo-atheism that has had been oversubscribed and touted by mostly today's "evolutionary pinheaded" neo-Darwinists and neo-atheists, who would uncharacteristically, unscientifically, cross-disciplinarily, selectively, and arbitrarily define, transgress, and corrupt their own incomprehension and insensibility of our humanities of "science & religion" issues; and would further (irrationally & uncritically) confuse and convict these 2 human "innate but separate" and parallel "intellectual & spiritual" life and ME issues among themselves (in perpetuity) by their now oversubscribed and hyped of the "Darwinism vs. Creationism" or "intellectualism vs. spiritualism" or "naturalism vs. supernaturalism" or "scientism vs. religionism" fallacy: the One domineering and malignant neo-Darwinist fallacy -- [or the One inexorably pseudoscientific, pseudo-genetic, & the One axiomatically anti-theistic "neo-atheism without cause" nor reason; nor discerning their own armchair (not pew) evolutionist-atheist ethos or their evolutionist academic pathos; nor respecting any secularist or agnostic conscience or jurisprudence; nor considering any consequences of their viciously anti-socio-personal ME identity, belief, faith, or religiosity; specifically their willful transgressions & corruptions of the "confusion-depression, cause & effect" consequences, at all; of their armchair evolutionist-atheist fallacy] -- and the One fallacy that has had caused grave anguish, duress, and distresses (in silence) in mostly religious laypeople, worldwide; especially since the days of their first "most faithful & dogmatic" Darwinist: the great "grand evolutionary biologist"-turned-armchair evolutionist and sophist, Thomas Huxley of the 19th-century England (please see link in commentary 1 above)!

5) Nowadays, although each case of clinical depression of ME issues, may be idiosyncratic in nature -- in each individual's causal and remedial ME interactive processes and progresses -- there will be aplenty cases that may inattentively and regressively progress into depression or paralysis by those melancholic symptoms, as vividly and as expressively portrayed in and around the Renaissance goddess above! Furthermore, especially at any point in time and space, worldwide, anyone could or would easily contract or encounter, whatever or however, any unexpected or extraordinary life or work upheavals, challenges, or change: especially those unprepared change or misfortunes that may incur in, whichever or whatever, adverse socioeconomic, political, religious, and/or personal health issues and circumstances; especially those "dynamic but contradictory" issues of the many interpersonal life-work-health-mentality concerns; or the universal "up & down" socioeconomic mobility or freedom issues, that were all too prevalent during the medieval times, recurrent thru the modern times, and now these socio-personal ME interactive issues are increasingly becoming widespread; easily influenced and affected by the Internet and globalization -- and now rampant recession -- of our diverse socioeconomic, political and religious issues and consequences; for good or ill: It seems to be causing a great variety of the never-ending or recurring (universally since antiquity) cases of the socio-personal (albeit idiosyncratic) ME interactive, issue-affective depressions, worldwide; today and beyond (please see my seminal book "Gods, Genes, Conscience" Part II Unraveling Our Mind and Gods: The Psychodynamics of Drives, Cognition, Memory, Consciousness, Conscience, and Survival of the Humankind; especially Chapter 13: Afflictions and Remedies of Mind; linked below)!?

While to be evaluated under the strict "patient-psychiatrist confidentiality" rules and conduct, these modern observations and treatments of the ME depressive symptoms are the clinical data that the ARH shall be looking at -- at both the social and the personal affective dimensions and psychodynamics -- and help depressed patients (with or without medication) so as to understand, illuminate, ruminate, readdress, and remedy their own ME symptoms and/or causes of depression, in each of themselves (as those observations bold-phased of the probable depressive symptoms & ME adaptation history above) -- and not those data and presentations (as argued by Pies above) that are clearly irrelevant; and were found to be running scientifically counter to the modern ARH of the ME depression-adaptive rumination processes, evaluation, and qualifications; and/or to the evodevo neuropsychiatry definitions, as examined and discussed above; as well as deftly debated elsewhere before (please see commentary 1 above)!?

Best wishes, Mong 12/2/10usct3:03p; practical science-philosophy critic; author "Decoding Scientism" and "Consciousness & the Subconscious" (works in progress since July 2007), Gods, Genes, Conscience (iUniverse; 2006) and Gods, Genes, Conscience: Global Dialogues Now (blogging avidly since 2006).

References
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Is Major Depression “Adaptive”? Clinical Data Say No

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