Author's: Dr Y and Dr X. Names have been changed to protect anonymity.
Date: Febuary 11, 2016
Dr. Y
Depression a 5-Minute Seminar For Patients
Wouldn’t it be great if you could explain to your severely depressed patient exactly what causes major depression—in 5 seconds? For example, you might try one of these approaches:
1. Major depression is caused by a chemical imbalance in the brain
2. Major depression is caused by anger at others, turned inward against oneself
There—easy, right? The first “explanation,” of course, is a spinoff of the mythological “chemical imbalance theory of mental illness”—which was never a full-fledged theory propounded in the highest echelons of American psychiatry.1 The second statement was a psychoanalytic hypothesis that had some currency when I was in residency and for which there is some (mixed) empirical support.2 In my view, both “explanations” vastly oversimplify the complex causes of depression; indeed, they are both reductionistic. (Dr Glen Gabbard has pointed out that psychoanalytic interpretations may sometimes be as reductionistic as biological ones, ie, “Both [psychoanalysts] and their patients secretly are drawn to simple formulations that eschew complexity.”3)
But what if we abandon these 5-second oversimplifications, and spend, roughly, 5 minutes with our depressed patients, explaining what we know (and don’t know) about the etiology of major depression? In my experience, such a 5-minute discussion can be fit quite feasibly into a half-hour session. (Contrary to popular lore, the average psychiatric session is not a “15-minute med check”—it is probably closer to a 35-minute meeting.4). As a psychopharmacology consultant for over 25 years, I saw mostly patients with refractory mood disorders, usually referred by other psychiatrists.
What follows is an idealized dialogue—with annotations for the clinician—similar to the kind I would have when first evaluating a seriously depressed patient. It makes use of 2 metaphors or visual images that I found very useful, and which my patients seemed to appreciate—namely, the “funnel” and the “bridge.” I would often hand-draw these images and give the drawings to the patient, as a kind of transitional object-cum-educational device. Here’s roughly how the discussion would go with “Joe” (a composite patient), somewhat modified for teaching purposes.
Joe: You lost me, Doc! What do you mean, “internal environment”?
Dr Y: Well, Joe, you know that the brain is made up of billions of cells called neurons, right? We think that for many people with severe depression, the neurons in some parts of the brain may not be communicating properly with neurons in other brain regions—some brain “circuits” may be too active while others may not be active enough.6 That could be due to a problem with brain chemicals—neurotransmitters—released by the neurons, but it could also mean there’s a problem with the receptors for these chemicals—those little slots where the neurotransmitters land. The receptors might be too sensitive or not sensitive enough.
We also have evidence that growth of new brain cells and the little branches that connect them may be reduced in major depression.7 In children who suffer bouts of major depression, there may actually be a gradual loss of “grey matter”— basically, brain cells and their branching extensions.8 We don’t know exactly how antidepressants work, but they may boost brain cell growth and enhance the branching process.9
This takes some time, which may be why antidepressants take a few weeks to work. By the way, Joe, there are also lots of medical factors and conditions that can cause, or worsen, depression—like low thyroid function, some vitamin deficiencies, various drugs, and so on. That’s why we checked your labs earlier.
Joe: So far, this is all biology. So if depression is biological, can people get it from their parents?
Dr Y: It’s not like inheriting blue eyes or blond hair. But people probably do inherit the tendency toward depression. Your genes — the units of heredity — make proteins that are involved in thousands of biological processes. If your genes are not making the right proteins in your brain, that may increase your risk of depression.
With bipolar disorder — or manic-depressive illness — it’s pretty clear that there is a hereditary factor. For example, if one identical twin has bipolar disorder, the other has a 60% to 80% chance of developing it, too.10 The hereditary piece isn’t as strong in other types of depression, but . . .
Joe: Wait a minute, Doc! What about the other 20% to 40% in the bipolar twins? The ones who don’t inherit the depression? How do you explain that, if they’re identical twins?
Dr Y: So here is where we get into the “psychological” and “social” pieces of the puzzle. Even identical twins may have different psychological habits. We don’t know for sure if self-defeating, “negative” thoughts cause episodes of major depression, or whether they are the effect of a depressive bout. But for sure, the way a person views the world can have a profound effect on mood.
For example, if someone turns you down for a date, and you tell yourself that you don’t deserve to be loved, or that you will never be loved, you will be setting yourself up for depressive feelings.11 If you constantly tell yourself that you must be perfect at everything you do, you are also setting yourself up for feeling depressed. Whether you will actually develop clinical depression probably depends on your genetic makeup and how resilient you are in the face of setbacks and stress—how well you “roll with the punches.”12
To complicate things, depression itself can generate a “negative filter,” so that everything looks grey and gloomy—which leads to more negative thoughts, in a kind of vicious circle. And then, of course, there are all the social experiences, good and bad, that happen to you from childhood on.
Joe: Like if you experience a trauma as a kid, or one of your parents die? Can that cause depression?
Dr Y: It’s always hard to know if one single thing “causes” a depressive bout. It is usually a combination of things, and it’s safer to call things “risk factors” rather than “causes.” Major stress early in life, such as child abuse or neglect, probably increases the risk of later depression.13 And there’s good evidence that parental separation — for example, when parents divorce — is a risk factor for depression.14 And just to round out the “social” component that goes into that funnel, there’s the issue of social support. Think about people with no friends or family to help them deal with the stresses and losses of life — it’s not surprising that a lack of social supports increases the risk of major depression.15
Joe: I get the “bio, psycho, social” thing, Doc. But I still have some trouble with the idea of taking the antidepressant. I mean, some of my friends —they say that I’m just using a crutch.
Dr Y: Well, Joe, there’s nothing wrong with a crutch if you’ve got a broken leg! But let me give you a different image to keep in mind. As I see it, medication is like a bridge between feeling terrible and feeling better. But you still have to walk across that bridge.
Joe: Meaning, I’ve got to do the work in therapy, maybe change the way I see things, change my mental habits?
Dr Y: That’s exactly right, Joe. And we have some evidence that medication and psychotherapy together work better or faster than one or the other alone16 and that each may work on different “pieces” of the depression. In my experience, medication is usually more helpful with low energy, poor concentration, poor appetite, and insomnia. Psychotherapy often helps more with low self-esteem, excessive guilt, or distorted ways of thinking.17 Almost always, I advise a combination of medication and therapy for severe major depression.
Conclusion
This sort of dialogue may not work for you in your practice, but some version of it might. Bumper sticker pseudo-explanations, whether biological or psychological, are a disservice to our patients, who deserve a basic discussion of causes and risk factors in major depression and other psychiatric illnesses. The good news is that, for many patients, the initial discussion needn’t take more than 5 minutes.18
Notes and References
1. See, eg, the 1978 statement by the Board of Trustees of the American Psychiatric Association: "Psychiatric disorders result from the complex interaction of physical, psychological, and social factors and treatment may be directed toward any or all three of these areas." American Psychiatric Association (1979).Position statement on active treatment. Am J Psychiatry. 136(5):753. http://www.psychiatry.org/File%20Library/Learn/Archives/Position-1978-Active-Treatment.pdf. Neither the DSM-III (1980) nor the DSM-IV (1994) asserted anything remotely resembling a “chemical imbalance theory” of mental disorders; the DSM-IV stated flatly, “. . . a diagnosis does not carry any necessary implications regarding the causes of the individual’s mental disorder or its associated impairments” (p. xxiii).
2. In his 1917 paper, Mourning and Melancholia, Freud advanced the hypothesis that depression (melancholia) arose following the loss of an ambivalently loved object, with anger subsequently directed against the internalized representation (introject) of the lost person. According to Prof. Roger P. Greenberg, PhD (co-author, with Prof. Seymour Fisher, of Freud Scientifically Reappraised, New York: Wiley; 1995), about 44% of self-report studies have supported Freud’s hypothesis; whereas 24% contradicted it and 32% were indeterminate. However, perceptual, projective and/or behavioral measures supported the anger turned inward idea in 72% of cases. Dr Greenberg concludes that “Overall . . . the evidence spanning several methodologies is reasonably supportive of Freud (R.P. Greenberg, personal communication, January 2016).
3. Gabbard GO. “Bound in a nutshell”: thoughts on complexity, reductionism, and “infinite space.” Int J Psychoanal. 2007;88:559-574.
4. Dr Mark Olfson, personal communication, January 2016. Dr Olfson has done extensive research on the provision of psychotherapy by psychiatrists; see, eg, Mojtabai R, Olfson M. National trends in psychotherapy by office-based psychiatrists. Arch Gen Psychiatry. 2008;65:962-970
5. A good general references is the article, What causes depression? http://www.health.harvard.edu/mind-and-mood/what-causes-depression.(Harvard Health Publications in collaboration with Michael Craig Miller, M.D). For a technical discussion of major depression subtypes and their relationship to stress, see: Gold PW, Machado-Vieira R, Pavlatou M. Clinical and biochemical manifestations of depression: relation to the neurobiology of stress. Neural Plast. 2015;2015:581976. The authors note that “Stress precipitates major depression and influences its severity, duration, and natural history.”
6. Greicius MD, Flores BH, Menon V, et al. Resting-state functional connectivity in major depression: abnormally increased contributions from subgenual cingulate cortex and thalamus. Biol Psychiatry. 2007;62:429–437. The authors describe fMRI studies pointing to both over- and under-activity in specific limbic-cortical circuits, associated respectively with abnormal emotional and cognitive processes.
7. Ga?ecki P, Talarowska M, Anderson G, et al. Mechanisms underlying neurocognitive dysfunctions in recurrent major depression. Med Sci Monit. 2015;21:1535-1547. The authors argue that the biological underpinnings of depression have substantial overlap with those of neurodegenerative conditions, including reduced neurogenesis, increased apoptosis (programmed cell death), and immune-inflammatory processes.
8. Luby JL, Belden AC, Jackson JJ, et al. Early childhood depression and alterations in the trajectory of gray matter maturation in middle childhood and early adolescence. JAMA Psychiatry. JAMA Psychiatry. 2016;73:31-38.
9. Masi G, Brovedani P. The hippocampus, neurotrophic factors and depression: possible implications for the pharmacotherapy of depression.CNS Drugs. 2011;25:913-931. The authors note that “. . . Antidepressant treatment increases BDNF levels, stimulates neurogenesis and reverses the inhibitory effects of stress, but this effect is evident only after 3-4 weeks of administration . . .”
10. What Causes Depression? http://www.health.harvard.edu/mind-and-mood/what-causes-depression. For a thorough analysis of the genetics of bipolar disorder, see: Smoller JW, Finn CT. Family, twin, and adoption studies of bipolar disorder. Am J Med Genet C Semin Med Genet. 2003;123C:48-58.
11. For the classic presentation of cognitive issues in depression, see A Guide to Rational Living, by Albert Ellis PhD and Robert A. Harper PhD (Wilshire Books, 1975). There are many studies of cognitive therapies showing them to be effective in major depression, though whether “irrational” or “self-defeating” cognitions are causes or effects of depression—or both—is an area of some disagreement. Moreover, there is evidence that pharmacotherapy alone can reduce “dysfunctional attitudes” in major depression [Fava M, Bless E, Otto MW, et al. J Nerv Ment Dis. 1994;182:45-49]. Also, studies of psychotherapy efficacy are inherently complicated by the inability to “blind” subjects to the nature of the treatment; ie, cognitive-behavioral therapy trials cannot be double-blind [See Douglas Berger MD, PhD, http://www.japanpsychiatrist.com/Abstracts/Blinding_Bias.pdf]
12. Elisei S, Sciarma T, Verdolini N, et al. Resilience and depressive disorders. Psychiatr Danub. 2013;25:S263-S267. The authors note that, “The term resilience has been borrowed from physics where it is used to describe the ability of a material to withstand impact without cracking.” They cite evidence showing that “. . . Resilience has proven to be a protective factor against the development of psychiatric disorders such as depression.”
13. Seok JH, Lee KU, Kim W. Impact of early-life stress and resilience on patients with major depressive disorder. Yonsei Med J. 2012;53:1093-1098. The authors cite evidence that early life stressors like inter-parental violence, physical abuse and emotional abuse, might be a risk factor for developing depression.
16. Kendler KS, Neale MC, Kessler RC, et al. Childhood parental loss and adult psychopathology in women. A twin study perspective. Arch Gen Psychiatry. 1992;49:109-116. This study found that increased risk for major depression and generalized anxiety disorder was associated with parental separation but not parental death.
15. Aneshensel CS, Stone JD. Stress and depression. a test of the buffering model of social support. Arch Gen Psychiatry. 1982;39:1392-1396. This study concluded that a “lack of social support contributes to the creation of depressive symptoms.” Of course, significant depression may itself be a cause of social alienation, so the potential for a vicious circle of cause and effect must be considered.
16. Cuijpers P1, Sijbrandij M, Koole SL, et al. Adding psychotherapy to antidepressant medication in depression and anxiety disorders: a meta-analysis. World Psychiatry. 2014;13:56-67. This study found that combined treatment appears to be more effective than treatment with antidepressant medication alone in major depression. A recent review of 62 pivotal antidepressant trials (N = 13,802) and 115 published trials of psychotherapies concluded that “In the blinded trials, the combination of antidepressants and psychotherapy provided a slight advantage over antidepressants (p = 0.027) and psychotherapy (p = 0.022) alone.” (Khan et al. PLoS One. 2012;7:e41778.)
17. These personal observations are somewhat supported by an early randomized, controlled study that compared the combination of amitriptyline and short-term interpersonal psychotherapy, either treatment alone, and a nonscheduled treatment control group in ambulatory acute, nonbipolar, nonpsychotic depressives [DiMascio et al. Arch Gen Psychiatry. 1979 Dec;36:1450-1456.]. The study found that amitriptyline had its effect mainly on “vegetative” symptoms, like sleep and appetite disturbance, often early in treatment. Psychotherapy had its effect mainly on mood, suicidal ideation, work, and interests, usually after 4 to 8 weeks. Recently, however, Roiser et al, in an elegantly synoptic paper, argue that “. . . both antidepressant drugs and psychological therapies modify negative [information processing] biases, providing a common mechanism for understanding treatments for depression.” [Roiser JP, Elliott R, Sahakian BJ. Neuropsychopharmacology. 2012;37:117-136]
18. The 5-minute approach is presented here as an alternative to a less thorough or simplistic explanation, such as attributing the patient’s depression to a “chemical imbalance.” It is not meant to replace longer, more sophisticated discussions that some patients may request or require, sometimes in an ongoing discussion over several sessions. And, of course, informed consent to treatment entails an ongoing discussion of risks and benefits.
Reply 1 From Dr X
Thank you for the article Dr Y. I think we all understand that proper informed consent is critical in any patient care situation. I would add a few things to what you have said to ensure the patient is clear. I have listed them below in order of Joe's questions:
Joe 1: You lost me, Doc! What do you mean, “internal environment”?
Dr X: But it’s very important to remember Joe that we did not do any tests at all of what I called your “internal environment”. This means that we do not know if your neurons are communicating properly, whether your circuits are active enough, whether there is a problem with your brain chemicals, or whether or not you have a problem with brain cell growth or any other such thing I just mentioned. In fact, we know so little about these things that we know very little about how to check to see if you do have a problem with any of the things I have just mentioned.
Joe 2: So far, this is all biology. So if depression is biological, can people get it from their parents?
Dr X: Joe, you just mixed up what depression is with what causes depression. When you said, “if depression is biological…”. When I was discussing the “internal environment” I was not talking about what depression is, I was talking about what causes depression. Depression is essentially a prolonged, debilitating, sad mood. This may or may not be caused by problems with your "internal environment". Remember Joe, we do not know if you have a problem with what I called your "internal environment".
Joe 4: Like if you experience a trauma as a kid, or one of your parents die? Can that cause depression?
Dr X: My apologies for confusing you about causes vs risk factors Joe. It is perfectly fine to talk about multiple causes of things; there is no need to talk about risk factors. Just as if you were to have had a heart attack, we might talk about genetic causes (your family history of heart disease), biological causes (high blood pressure), psychological causes (stress at work), and environmental causes (eating too much fat). There is nothing to be confused about here; life problems are often caused by many different things in combination with one another.
Joe 5: I get the “bio, psycho, social” thing, Doc. But I still have some trouble with the idea of taking the antidepressant. I mean, some of my friends—they say that I’m just using a crutch.
Dr X: But Joe, there is a difference in taking medication for a known biological abnormality like high blood pressure, and taking medication when we do not know if you have a biological problem with your internal environment. If you were to take drugs for your depression, you would be taking drugs to modify your brain chemistry when we do not know if you have a brain chemistry problem. This is why your friends might suggest that taking drugs in a case like yours is a crutch.
But let's be clear that many of us take drugs to help us feel better, perform better, work harder, etc. And we do this when we have no idea whether our brain chemistry is abnormal. For instance, when we have a coffee to wake up in the morning, or a cigarette to calm down, or a drink to relax after work, we are taking drugs to feel better. And we do this even when we have no idea whether our own biological state is abnormal.
But it is important to understand the side effects of the drugs we may be offering you and how likely they are to help you. Drug taking has a cost as well as a benefit. Now let’s talk about the cost of taking drugs for depression and exactly what we know about how helpful these drugs might be for you.……
Joe 6: Meaning, I’ve got to do the work in therapy, maybe change the way I see things, change my mental habits?
Dr X: Well Joe, if you had just had a heart attack, we would be talking about your mental habits as well. But let’s be clear, it is not my place as a medical doctor to tell you whether you should take depression medication. That’s because my opinion would be, in part, an ideological belief about whether it is good for you to take drugs when there is no known biological abnormality. It is not my place to tell you what you should and should not believe about drug taking. That is up to you. My role is to help you as much as I can by explaining clearly to you what we do and do not know about your condition and what we do and do not know about the efficacy and side effects of medications for your condition. We call this informed consent. And, as long as you are clear about these things, you will be able to make your own informed judgment about whether to take drugs for the psychological troubles about which you have come to see me.
I hope that adds to the discussion here. Best,
Dr X.
Reply 1 From Dr Y
Dr Y
Hi, Dr. X, thanks for the thoughtful comments and suggestions!
First, let me say that many of the items you would like to add to a discussion with "Joe" would indeed be part of a comprehensive risk/benefit ("informed consent") discussion--which was really beyond the scope and intent of the present essay. That would certainly include a careful discussion of potential medication side effects; the risks and benefits of both medication and psychotherapy (yes--both have their risks!); and a discussion of all evidence-based alternatives, such as "bright light therapy", exercise, etc.
You clearly would like to emphasize to Joe that "we do not know if your neurons are communicating properly, whether your circuits are active enough..." etc. That's certainly true, except for those rare patients who may be part of a research study, using fMRI, PET scans, or other imaging studies. However, this state of "unknowing" is probably more the rule than the exception in general medical care--at least in family practice and primary care, and often in neurology, too. Let's take the example of the patient who presents to his family doctor with the complaint, "I get these terrible headaches on one side of my head. I get nauseous and see bright, flashing lights at the same time, and I'm really sensitive to light. These bouts last for a couple hours, then they go away." Most physicians will quickly recognize this as some form of migraine headache (in some cases, after ruling out, say, a brain tumor or other neurological problems). But while there are many neurochemical theories as to the causes and biological nature of "migraines", there is no way to say for sure that this particular patient's complaints are due to those putative abnormalities. Rather, we recognize the syndromal description of migraine headache; we see that the patient's symptoms conform to that phenotype; and we can confidently say to the patient, "I have a medication for you that I think will help" (e.g., sumatriptan).
The situation is essentially the same when "Joe" presents with the DSM-5 picture of severe, major depressive disorder (MDD); we can say (after ruling out various medical/neurological causes) that we can help Joe with psychotherapy, medication, etc. without having to demonstrate that his brain has such-and-such an abnormality. (Of course, we hope some day to be able to do so).
Re: your comment that "Depression is essentially a prolonged, debilitating, sad mood"-- here I think you are only partly correct. To be sure: we use the term "depression" in many senses; e.g., "I just broke up with my boyfriend, and I was so depressed for a whole week!" But this is not what I was describing in Joe's case, in which the back-story is one of recurrent, severe major depression. Severe MDD is much more than a prolonged, debilitating, sad mood, as I'm sure you know: it involves a pervasive impairment of energy, appetite, sleep, cognition, and psychomotor function, and we know this is often accompanied by neuroendrocrine abnormalities; e.g., in the case the melancholic subtype of MDD, there is evidence that the hypothalamic-pituitary-adrenal axis is often abnormally functioning [1].
Indeed, I believe that severe MDD is no less "biological" than hypertension, though MDD may have a more prominent psychological component. (Even hypertension is notoriously susceptible to changes in levels of anxiety, as with the well-known phenomenon of "white coat hypertension"). One of the problems with the bio-psychosocial model - which I didn't explore in my essay - is that it tends to reify the distinction between "biology" and "psychology". This is unfortunate, and contributes to the Cartesian duality that most psychiatrists seek to avoid.
As for your discussion of "causes" vs. "risk factors" - I think we need to be very cautious about calling anything a "cause" of depression, given that there are so many confounds and contributing factors. Put another way: while, in theory, I agree that we can speak about "multiple causes" of depression, I think it is very hard to demonstrate empirically, or experimentally, that "x" is causing the patient's depression. For example, the patient may attribute his depression to stress at work, while actually suffering from a brain tumor in his limbic system. We can say that both are "causes" of the depression, or we can say that each is a major risk factor for depression. The distinction may be academic, of course, since treatment would be directed at both the tumor and the stress at work.
Thanks again for your comments, Dr. X, and I will get back to you re: your other question!
Best regards,
Dr Y
1. Dinan TG, Scott LV. Anatomy of melancholia: focus on hypothalamic-pituitary-adrenal axis overactivity and the role of vasopressin. J Anat. 2005
Reply 2 from Dr X
Dear Dr. Y, thank you so much for responding to my comments. This forum provides us with a wonderful opportunity to debate issues and share ideas. Allow me to thank you publicly for what you are doing at the Journal to help us all discuss and debate these critical issues.
My initial response was based mostly on the premise that you may have misled Joe in to thinking that he did have a biological abnormality of his brain. I felt you were somewhat unclear with Joe about what you knew to be the case and invited him to think that his depression was, at least in part, a biological abnormality of his brain.
On reading your response, I think we can now clearly characterize our two positions. It seems to me that you think depression is partly biological, partly psychological and partly social. Is that fair? If so, it makes sense that you would invite Joe to think of his depression as partly biological in nature.
My position is that depression is psychological with possible biological, psychological, and social causes. So, I would not encourage Joe to think that his depression is biological. I would make it clear to Joe that when we say he has depression, we are not saying that he has a biological abnormality. I just want to add that to characterize this view as "my position" is a bit unfair. I'm not taking a position on what depression might be here - I do not have a theory about what depression is. I am using the concept of depression as it is correctly used. That is, as it is defined in the dictionary, used on ordinary English conversation, defined in DSM, etc. So the notion that depression is psychological is not really "my position", it is part of the definition of depression that we all learn and use as a normal part of the learning and use of the English language.
So, my view leads Joe to think that we do not know if he has a biological abnormality and yours leads him to think he does. Is that fair?
It seems also that when you talk about the bio-psychosocial model, you are talking about a conceptual model of what depression is - a theory about the nature of depression. That is, that depression is partly biological, partly psychological and partly social. Is that right?
When I talk about the bio-psychosocial model, I am not talking about the nature of depression. I am merely talking about a causal model of depression - that is, a model of what the causes of depression might be. Just like if I were to talk about the bio-psychosocial model of heart disease, this would not invoke a metaphysical theory about the nature of heart disease to me. This would merely be a model of the possible types of causes of heart disease.
It seems to me that this is consistent with your criticism of the bio-psychosocial model as Dualistic - that is that it encourages us to think about humans as made up of two distinct entities, a biological entity and a psychological entity (by the way, I think that is correct, I do not think of humans that way either).
I would not criticize the bio-psychosocial model in this way because it is not a conceptual model about the nature of depression to me. It is merely a model of what causes things to happen. So for me, there is no real philosophical problem with the bio-psychosocial model - it is not a model about the nature of something. Hence, I can apply the model to depression with little trouble. For example, depression is a psychological problem (specifically a mood problem) with possible biological causes (e.g., brain abnormalities), possible psychological causes (e.g., faulty attributional styles), and possible social causes (e.g., death of a parent at a young age).
I thought you might appreciate a brilliant and enlightening discussion of Cartesian Dualism given by Professor Peter Hacker. It discusses Cartesian Dualism in a way that I think you might find useful. The link is:
https://www.youtube.com/watch?v=SaJcQ6Zk364&feature=youtu.be
In closing, I would just like to thank you so much for engaging this discussion. I feel you are doing a great service to the academic community by having this discussion in a forum that others can read and evaluate. The opportunity to share ideas and points of view in this way is, I believe, a new and important opportunity for academic professionals. So thank you very much for what you have done here.
Dr X
Reply 2 From Dr Y
Hi, X - Thank you for the kind words regarding my contributions here; and thanks, as well, for your thoughtful questions and comments. A detailed discussion of the "Biopsychosocial Model" (BPSM) would require several pages [see ref. 1], and a good deal of philosophizing over that perennial conundrum of "mind/body" relationships.
My personal view is summarized in the rather arcane but accurate philosophical formulation, "Ontological monism, explanatory dualism"--or rather, "explanatory pluralism." Based on the work of the philosopher Baruch Spinoza, and the modern-day philosopher, Donald Davidson, I believe that there is only one "substance" of which humans are composed--not "mind" or "body", but a single, undifferentiated organismic "stuff." We can describe this substance in "physical" or "mental" terms, and, indeed, we cannot "explain" our experience as conscious beings in purely biological terms - we need a language of mentality and psychology [2,3]. This is why, as an explanatory model, I still use the BPSM, even though it tends to reify and separate "biological" from "psychosocial" causation.
All that philosophizing aside, I am reasonably comfortable with your formulation:
"Depression is a psychological problem (specifically a mood problem) with possible biological causes (e.g., brain abnormalities), possible psychological causes (e.g., faulty attributional styles), and possible social causes (e.g., death of a parent at a young age)."
I would simply add that major depression is often experienced in the physical/somatic realm; e.g., as loss of appetite, poor sleep, decreased energy and libido, etc.
I hope you will forgive a hiatus in my further replies, as I am now focusing on a pending writing project. (I will get back to you on your other query re: rates of neurobiological abnormalities in depression vs. controls - this is proving hard to pin down!).
I hope to watch that video at some point, and again, I thank you for your congenial correspondence.
Best regards,
Dr Y
1. Novack DH, Cameron O, Epel E, et al. Psychosomatic medicine: the scientific foundation of the biopsychosocial model. Acad Psychiatry. 2007 Sep-Oct;31(5):388-401.
2. Pies R. Mind-language in the age of the brain: is “mental illness” a useful term? J Psychiatr Pract 2015; 21: 79-83. [PubMed]
3. Pies R. BJPsych Bull. 2015 Oct;39(5):264. doi: 10.1192/pb.39.5.264. Can psychiatry and neurology 'simply' merge? [full PDF available online].
Reply 3 from Dr X
Thanks again for your response Y.
I apologize if I did not make myself clear in my last post. In part, I was suggesting the opposite of what you said in your response:
“A detailed discussion of the "Biopsychosocial Model" (BPSM) would require several pages [see ref. 1], and a good deal of philosophizing over that perennial conundrum of "mind/body" relationships.”
I was suggesting that philosophizing over the nature of the mind and body would not be required if you were to view the bio-psychosocial model as a causal model of depression. To my mind, philosophical questions to do with the mind-body problem are not only irrelevant here but also potentially confusing to patients and psychiatrists alike.
As I suggested earlier, the discussion with Joe mislead him just because it encouraged him to engage in unnecessary considerations about THE NATURE of depression (not the causes of depression as I was suggesting). My point in discussing the case of heart disease was to demonstrate this. There is no need for philosophizing about the nature of a heart attack when we suggest to our patients that heart attacks may be caused, in part, by psychological problems (stress at work), biological problems (hypertension) and social problems (sedentary occupations).
The same is true for depression. As long as we say to Joe that he has a psychological problem (depression) that may be caused, in part, by psychological problems (attribution style), physical problems (chemical imbalance) and social problems (death of a loved one), we have no philosophical problem.
The same can be said for the difference between the symptoms of depression and THE NATURE of depression. When you said above that:
“I would simply add that major depression is often experienced in the physical/somatic realm; e.g., as loss of appetite, poor sleep, decreased energy and libido, etc.”
it seems to me that you were suggesting that the symptoms of major depression have something to do with THE NATURE of depression. When you say patients are “experiencing depression in the physical realm” it sounds like you might be trying to propose a theory about what depression is. That is, that you are suggesting that depression is partly physical. I think this is a mistake. There is a much more clear and less philosophically confusing way to approach the issue. We just need to recognize that the idea that patients experience depression in the physical realm is recognition of the fact that depression has associated physical symptoms. To recognize that psychological problems have physical symptoms is not a deep philosophical mystery; it is just an everyday observation that psychological problems can cause physical problems. When a physician confides in a patient that prolonged anxiety and stress at work can cause heart disease, they are suggesting to their patient that a psychological problem can cause a physical problem. This goes on every day in clinical practice without the slightest need for philosophical reflection.
To conclude, it is my view that Joe was mislead in this case because he was invited to believe that depression is, in part, physical. This practice is, I believe, both mistaken and common. Had depression been characterized to Joe as a psychological problem with possible physical, psychological and situational causes, there would be no grounds for confusion at all1. Just as there are no grounds for confusion when we say that heart disease may be, in part, caused by psychological problems.
To my mind, Kant, Spinoza, and all the others do nothing but deepen the confusion. I think psychiatry would be much better off if it would concentrate on identifying and treating the causes and symptoms of psychological problems, rather than engaging in questionably coherent debates between philosophers about THE NATURE of psychological problems.
Thank you again for the opportunity to discuss these issues. If you have other more pressing commitments, please feel free not to respond.
Dr. X
1. The fact that we do not know the “internal environment” causes of depression in the vast majority of cases of depression is an empirical problem waiting to be solved. As you said in a previous post, this is nothing but the ordinary case of not knowing, in some cases, the causes of a patient’s migraines. I have been suggesting that we get in to trouble here when we imply to patients that we do know the “internal environment” causes of their depression when we do not.
Reply 3 From Dr Y
Hi, X,
Thanks for your further reflections. I suspect that we are getting into areas of philosophy, linguistics, and metaphysics that are probably outside the interest of most patients and even many clinicians -- but as an amateur philosopher myself, I'm happy to address at least one of your concerns; i.e., the issue of "the causes of X" vs. "the Nature of X."
Since you put "Nature" in all caps, you clearly want to stress the distinction between "causes" of major depression and its "Nature." I am not at all persuaded that these are fundamentally distinct concepts.
If you recall Aristotle's seminal writing on "causation", it was his contention that an understanding of a thing's "Nature" must entail an understanding of its causes. He therefore argued that to understand the "Nature" of X, we need to understand the four types of causes that account for X; i.e., "material", "formal", "efficient" and "final" causes. Specifically, "The formal cause [of X] embodies the essential nature (all essential attributes)" of X.
As a fan of "ordinary language" philosophy (e.g., the later Wittgenstein), I believe that in our ordinary language, we usually include "causes" in our discussion of "the Nature" of something. Thus, if we ask "What is the nature of cancer?" we are likely to reply, "Well, cancer involves the excessive and uncontrolled growth of abnormal cells." But it is reasonable to say, as well, "Cancer is caused by the excessive and uncontrolled growth of abnormal cells."
So, too, with discussions of depression. And I think it is perfectly reasonable and consistent with both science and ordinary language to say, "Depression is partly physical" (or "biological"). I don't think this is in any way misleading.
In practical terms, though, X, I suspect that you and I, sitting with a depressed patient, would both be comfortable saying to Joe, "Depression has associated physical symptoms." Frankly, Joe doesn't care much about Aristotle or the causes vs. nature distinction. Joe just wants to get out of my office, and feel better as soon as possible! Thanks for the interesting discussion, X, and I think I'll leave it to our readers to comment further on this thread.
Best regards,
Y
Reply 4 from Dr X
Thanks again Y for your timely response. I agree, we should let the readers decide now. I’m sure we both have other pressing engagements.
But just to be sure the readers are clear, when I was talking about the NATURE OF something, I was simply talking about what it is. I wanted to distinguish between:
1) The cause of something (e.g., smoking)
2) The symptoms of something (e.g., fatigue)
3) What that thing is (e.g., lung cancer)
I am arguing as Wittgenstein would that there is a clear distinction in ordinary language between these things. I am also suggesting that if we do not maintain ordinary language distinctions between concepts such as this there is great potential for misunderstanding and confusion. Wittgenstein wrote:
“Our investigation is a grammatical one. Such an investigation sheds light on our problem by clearing misunderstandings away. Misunderstandings concerning the use of words….”
So just to be clear about the cancer example, when I speak about the nature of cancer, I am speaking about nothing more than what cancer is. You think it is perfectly reasonable, when asked what cancer is, to say: “Cancer is caused by….”, I do not. I think that is a conflation of the causes of something with what it is – in Wittgenstein’s terms, it violates the rules for the use of the concept of cause.
In the example above, if we commit ourselves to the idea that causes of something tell us, in part, what it is, then we would have to accept that lung cancer is, in part, smoking. But this is, of course, wrong.
I completely agree with you that Joe should not be drawn in to discussions about Aristotle or any other philosopher for that matter. But I do not believe that Joe is not capable of making the ordinary language distinctions between what something is, what causes it, and what the symptoms of it are. I would just like to offer an alternative explanation to Joe as a more conceptually clear, accurate, and simpler way to communicate with him about his situation:
“Joe, you have depression. Depression IS a psychological problem. It is a mood problem. We think mood problems may be, in part, CAUSED BY brain abnormalities, but research is not yet at the stage in which we can be clear about what these abnormalities might be or how to test for them. So we have not tested you for any such abnormality and we do not know if you have a brain abnormality. You also have a number of SYMPTOMS OF depression including problems sleeping, withdrawal from friends, loss of appetite, etc. The following are some ways in which we could help you…..”
This conversation with Joe has a number of advantages over the original 5-minute conversation that you suggested. It does not conflate the cause of depression with what it is, does not conflate the symptoms of depression with what it is, does not invite Joe to think that we know he has a brain abnormality, is much shorter than 5-minutes, and does not require the use of debatable analogies or contentious theories about the nature of depression.
I should just say that the video I attached earlier in this thread is of a talk given by a man widely regarded to be the world’s leading Wittgenstein scholar, Professor Peter Hacker. He is talking to a gathering of scholars about conceptual errors that are currently being made in FMRI and MRI research. I’m sure if you are a supporter of the ordinary language view, you will find it very exciting (as I did when I first came across it).
All the best Y and thank you so much for this. I’m deeply impressed with your commitment and the efforts you took to debate this issue with me. With respect,
Dr. X