The following is a presentation of some of what I learned so far (over the last thirty-some years of practicing psychiatry) about depression. My take on the topic differs substantially from the doctrine of mainstream psychiatry, which I believe is way off-target.
Asserting that the whole field of Psychiatry is off-target, especially over such a central topic, is a serious and contentious claim. I certainly don’t claim to be smarter than all (or almost any) of my colleagues, many of whom are very smart. Instead, I have developed a different point of view on the topic, based on my real-life clinical experience, that I believe is more accurate and productive. Of course, it is just one person’s experience, and — to quote the great Charles Barkley’s 2002 book title: “I may be wrong, but I doubt it.”
With this in mind, if you are still interested, please do continue reading.
(Thanks, I.D., for setting me straight on what is and isn’t pertinent to this discussion.)
Depression
Introduction
At the time of this writing, psychiatry has no objective diagnostic tools. Practitioners in the field do not have anything like a blood test or brain imaging technology to utilize in making diagnoses. (Moreover, when an available objective test is diagnostic of a patient’s mental condition, the case is automatically reassigned to another specialty, such as neurology, endocrinology, rheumatology, etc.).
Adult psychiatric diagnoses are made solely based on information provided by the patients (occasionally, additional information may be provided by a relative) and the clinician’s subjective impression. This data is compared to a diagnosis-specific bank of symptom-checklists. When the patient’s experience (and clinical observation) is believed to coincide with a minimum number of symptoms on a specific check-list, the patient’s condition is said to “meet criteria” for the associated diagnosis; the patient is then considered to suffer from that specific mental disorder, and it becomes their psychiatric diagnosis.
The symptom checklists for all recognized psychiatric disorders are presented in a book titled ‘The Diagnostic and Statistical Manual of Mental Disorders’ (commonly referred to as the DSM), published and periodically updated by the American Psychiatric Association. The DSM is designed to simplify the process of diagnosing mental disorders and circumvent contending with the overwhelming complexity of the mind. It is unquestionably primitive compared to today’s medical diagnostic standards, but it is better than not having a diagnostic system at all.
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In the most recent edition of the manual (DSM-5-TR, published in 2022), the diagnosis of ‘major-depression’ is based on a nine symptoms checklist: Two primary or “core” symptoms — depressed mood and anhedonia (defined as the “loss of interest and/or pleasure in all, or most, activities”) and seven “secondary” symptoms — sleep disturbance, change in appetite and weight, poor concentration, fatigue, psychomotor (i.e., physical/mental) slowing or agitation, loss of self-esteem, and suicidal thoughts.
To be diagnosed with major-depression a patient must experience a total of at least five of the nine symptoms, at least one of which must be a “core symptoms”, for at least two weeks representing a clear departure from the patient’s normal baseline state.
Obviously, the exclusive application of a nine-symptom checklist could not amount to even a cursory exploration of a person’s subjective experience of depression. To generate more meaningful insights, I approach the complaint of ‘depression’ as a non-specific statement used in reference to three different mental states: Grief, despair, and dispassion (or apathetic-dysphoria). The main feature of these three states is, of course, sadness, or a sad mood, which is often referred to as “depression.”
Grief, despair, and dispassion are distinct states with some overlapping features — think of a three-ring Venn diagram. In my experience, correctly identifying a person’s position in such a Venn diagram goes a long way toward understanding the specific meaning of their very non-specific complaint of “depression.”
In its early stages, psychiatry was keenly aware of the fact that patients presented with radically different kinds of “depression.” Historically, ‘grief’ and ‘despair’ were considered ‘reactive states,’ i.e., normal reactions to difficult life circumstances. Abnormal grief and despair were considered “neuroses.” The term ‘major-depression’, in comparison, was applied in reference to a relatively rare and invariably serious medical illness.
Over the last few decades, the importance of identifying the specific underpinnings of patients’ different depressive states appears to have been steadily eroding. As a result, both the general public and the psychiatric profession are increasingly likely to consider the fundamentally different depressive conditions as a single entity — a depression. Unwittingly, this has become a serious clinical and research problem because the line separating this generic “depression” from the diagnosis of ‘major-depression’ is difficult to define and easy to overlook.
In my experience, a substantial fraction, if not the majority, of the patients currently diagnosed with ‘major-depression’ actually suffer from ‘grief’ and/or ‘despair’. Treating these three states as a single condition has grave practical and theoretical consequences. Still, it has become common and acceptable, which renders Psychiatry’s approach to the phenomenon of depression in dire need of a major overhaul.
Let’s examine these three states in some detail:
Grief
The reaction to a significant loss — of an object (e.g., money), a function (e.g., the ability to walk), or a relationship (through a breakup or a death) normally triggers sadness. The sadness elicited by loss is unpleasant and is therefore typically regarded as an emotional pain. Grief is the suffering associated with the perceived pain of a loss. Grief can be defined as the meaning of loss. (For a detailed discussion of Pain and Suffering go to https://wp.me/P7aKBB-3w , for a detailed discussion of Meaning go to https://wp.me/P7aKBB-9X .)
Since loss is an unavoidable part of life, grief is inextricable from the human condition (a fact that all too often eludes mental health professionals and nonprofessionals alike, perhaps more than ever in today’s discomfort-intolerant climate).
Grief is experienced on an intensity continuum; obviously, the higher the intensity, the greater the hardship. Normally, the intensity of one’s grief is proportional to the magnitude of the loss triggering it (arguably, low-intensity grief may stay below the radar of consciousness, present but unrecognized and unacknowledged). Minimizing the magnitude of a loss is, therefore, tempting as a way to reduce the intensity of the associated grief.
(Therein lies the lure of denial: A short-lasting period of denial in the immediate aftermath of a loss may be an automatic, normal psychological defense. However, as an open-ended method of dealing with the reality of a loss, it simply doesn’t work. Persistent denial usually increases the hardship of coping with loss. Unacknowledged losses tend to linger subconsciously, contributing to a non-specific ‘bad-mood,’ ‘depressed mood,’ or just ‘depression.’ Because the process is subconscious the resulting ‘bad-mood’ is inexplicable which compounds the negative impact of denial.)
The presence of grief can elude conscious awareness in other ways. For example, imagine a business person who turned down an offer to join a startup venture that, a few years later, became a hugely successful, publicly traded company. It would be expected for this person to experience a negative emotional reaction in response to reminders of the wealth she could have had, had she made a different choice. Her negative emotional response is likely to be regret. Deconstructing regret reveals that one of its ingredients is (“past-based”) grief — the response to the loss of something that could have been had, given a different past.
Similarly, grief can be illusive when it is triggered by the perception of a loss stemming from imagining a different future. For example, a young couple trying to start a family will inevitably experience a negative emotional response every time they learn that their attempt to conceive has been unsuccessful. In part, they grieve the loss of the pregnancy and, ultimately, the child that they could have had in a readily imaginable future. In this case (“future-based”), grief is a hidden component of disappointment.
Grief (like everything else in existence) has a natural course that numerous theories attempt to delineate. The most recognized of these theories has been put forth by the psychiatrist Elizabeth Kübler-Ross in the late 1960s. Her model suggests that the normal course of grief includes five stages: Denial, bargaining, anger, depression, and acceptance. The grieving person moves through the stages, not necessarily in a strict linear order (i.e., the model recognizes that moving back and forth between stages and experiencing overlapping symptoms is normal) but overall progressing toward acceptance; the process concludes when firm acceptance is achieved.
According to Dr. Kübler-Ross, the first stage of grief is an automatic rejection of the reality of the loss, i.e., denial. Denial, in general, is a psychological defense mechanism deployed subconsciously to protect the ‘Self’ from the threat of overwhelming emotions, which, in the case of grief, are triggered in response to a loss. The initial denial must subside to allow progress through the other stages; hence, denial doesn’t work as a long-term strategy (as mentioned above).
Normally, denial is followed by the bargaining and anger stages. The eventual realization that both bargaining and anger are futile is followed by the depression stage (another example of the nonspecific and, therefore, confusing use of the word ‘depression’; I think that a ‘sadness stage’ would have been a more precise term). The intensity of the sadness normally decreases automatically over time and, eventually, is replaced by acceptance.
Acceptance, in my opinion, is not the final resolution stage of the grief process: Following acceptance, the process proceeds down one of two paths: The first path leads to inner-peace. The second path is taken when inner-peace is unattainable, leading from acceptance to surrender.
Obviously, of the two possible resolution points, inner-peace is the preferable option. Less obviously, but unquestionably, both points of resolution are preferable to the alternative — entrapment in an unresolved inner-conflict.
{Side note: The call to “never surrender” is infantile, at best (depending on the intent behind it; at worst, it may be evil). The mature/mindful stance aspires to attain the clarity necessary to differentiate situations that warrant a struggle from situations in which a struggle would be futile: In the former, surrender is a mistake; in the latter, surrender, while inevitably bitter, is unquestionably preferable to entering a struggle that is doomed to fail or has no clear end-point.}
Resolution of grief inevitably takes time: Shortening the duration of normal grief is difficult (if not impossible), and prolonging it is easy. Hence, the primary goal of grief management is to refrain from making it any worse than it has to be. (A discussion of this point as a general strategy can be found here: https://wp.me/P7aKBB-6u . )
A sure-bet way to worsen the course of grief is to consider and treat it as an illness, i.e., as ‘major-depression’. The treatment of grief as if it were a ‘major-depression’ is guaranteed to interfere with the normal progression toward acceptance and, at best, delay recovery from the loss.
Sometimes, the consequences of diagnosing normal grief as a depressive disorder are outright dreadful: The expectation of relief from the hardship of grief in response to medical treatment is unrealistic; it is, invariably, a setup for disappointment. The resulting worse mood, on the backdrop of a ‘major-depression’ diagnosis, justifies more intense treatment, potentially starting a cycle of worsening symptoms and increasingly aggressive efforts to treat them — a nightmarish scenario that happens in real life all too frequently.
Normal and Pathological Grief
Grief is a normal mental phenomenon, regardless of how unpleasant and difficult to bear it may be; moreover, the absence of grief in the face of significant loss may be a symptom of a mental disorder or a harbinger of future emotional problems. Nonetheless, grief can be pathological — a potentially serious mental-health problem requiring professional intervention.
Distinguishing normal grief from abnormal grief can be clinically challenging. The distinction can be made by assessing several factors (the assessment is inevitably subjective, but the right call is usually fairly obvious):
The first parameter is the grief’s intensity relative to the loss’s magnitude. For example, grief intense enough to cause persistent interference with occupational functioning in reaction to the loss of a pet, beloved as it may be, is suggestive of an abnormal grief reaction. A disproportionately intense grief reaction often points to unresolved grief over an earlier loss (or losses). Addressing this type of abnormal grief therapeutically hinges on identifying and, ideally, processing the earlier loss to promote acceptance (followed by inner-peace or surrender) of both the recent and the distant losses.
The second parameter is the presence of unrelenting emotions and/or thoughts that are clearly superfluous to the experienced loss — for example, intense guilt or a loss of self-worth in reaction to the passing of a grandparent. The persistence of such feelings and/or thoughts suggests unresolved issues embedded in the relationship. Therapeutically, these issues need to be identified, addressed, and resolved to facilitate progression through the stages of grief toward acceptance and, ultimately, peace or surrender.
Lastly, the pace of progress through the stages of the grief reaction is an important factor in the clinical assessment of grief. The normal pace of progress is largely defined culturally. Hence, an individual’s grief response that is markedly different from their culture’s norm is often a signal of a clinical problem that requires exploration and possibly treatment.
Most cases of pathological grief manifest psychological rather than medical problems. Psychological problems need to be treated with psychological means, typically psychotherapy. Psychological disorders do not improve in response to medical treatments (i.e., to medications or any other biological treatment modality). The medical treatment of psychological disorders is futile (much like the medical treatment of normal grief, as discussed above ); at best, it is ineffective; at worst, it can cause serious medical and psychological complications.
To be clear, psychological disorders sometimes involve symptoms that may respond to medical treatment, temporary insomnia being the most common example. Indeed, in the right circumstances, symptomatic medical treatment can be helpful (e.g., a short-term use of a sleep-promoting medication). It is important, of course, to be clear that such a treatment is symptomatic and supportive care rather than a treatment for some underlying medical disorder. Otherwise, this treatment’s negative impact will likely exceed its benefit.
Rarely, grief may trigger a frank psychiatric disorder (both new onset and recurrence of earlier symptoms can happen). It should be suspected when an individual’s reaction to a loss is radically different from the expected, normal course of the grief reaction in the person’s culture. For example, an increasing, rather than decreasing, intensity of the grief over time, the onset of psychotic symptoms, or the onset of persistent suicidal thoughts.
The progression from reactive grief to a frank psychiatric illness (rare as it is) is usually encountered in vulnerable, predisposed individuals. That is, a personal or a family history of psychiatric disorders represent a potential risk factor, specifically, a (personal or family) history of major-depression, bipolar-illness, or a psychotic illness (some patients may not meet the diagnostic criteria for any other psychiatric disorder and may be diagnosed with ‘persistent complex bereavement disorder’, possibly a variant of ‘major-depression’). The treatment in these cases addresses the underlying psychiatric disorder (rather than the grief) and has a similar success rate.
Grief and Mindfulness
Mindful-grieving (or ‘Right-Grieving’, as a specific case of the Buddhist concept of ‘Right-Suffering’) means experiencing loss with acceptance, inner-peace, and gratitude. It begins with maintaining calm, regardless of how painful the loss is. (For a detailed discussion of Calm go to: https://wp.me/P7aKBB-nQ.)
Maintaining ‘calm’ in the face of loss is far from automatic: The instinctive response to a loss (or any pain) is to judge it as a negative or a ‘bad’ occurrence; the judgment invites a reaction and undermines ‘calm’; therefore, it is incompatible with Mindfulness. Mindful grieving then requires overcoming or transcending the innate tendency to judge our losses as ‘bad’ (without denying the hurt they elicit).
Mindfulness practitioners aspire to cultivate the ability to relate to Reality without judgment. From the nonjudgmental point of view, a loss is neither positive nor negative, not a good thing or a bad thing — just a thing, an event that has taken place in one’s Reality.
When Reality is observed without judgment, it appears flawless, i.e., perfect. The functional importance stems from the fact that whatever the mind perceives as ‘perfect,’ its acceptance is effortless and automatic. Conversely, that which is perceived as ‘flawed’ is rejected, and accepting it involves a struggle (the intensity of which is proportional to the magnitude of the perceived flaws). Cultivating a non-judgmental mind amounts to securing access to the point of view from which Reality is ‘perfect’ — including its undesired and painful aspects. The justification for making the effort required to cultivate a non-judgmental mind has a lot to do with maintaining calm, which, in turn, supports acceptance. The alternative — relating to painful experiences as ‘flawed,’ may be standard, even universal, but it initiates reactivity, ineffective struggle, and interferes with discovering acceptance.
(Side-bar: It is essential to be able to make the distinction between ‘Perfect’ and ‘Good’ to understand the point: The perception of Reality, or any part of it, as ‘Perfect’ is not saying that it is ‘good’ (which is a judgment, to be avoided). ‘Perfect’ (at least in this context) is not a qualitative assessment but means ‘not harboring flaws.’
Painful experiences, obviously, are undesired and thus automatically judged as ‘bad,’ which is easily equated with ‘flawed.’ In other words, painful experiences are instinctively construed as evidence of flaws in Reality (i.e., as evidence of something “gone wrong”). The negative judgment of painful experiences is essentially subjective. Painful occurrences are not objective evidence of flaws in Reality, they are just events that unfold with disregard for one’s preferences. To put it succinctly, not getting what you want, or getting what you don’t want, hurts, but it is not a breakdown of or a flaw in Reality.)
In addition to ‘calm,’ the mindful approach to loss and grief relies on compassion and tolerance, which are states of mind that support acceptance. (Side-note: Be reminded that from the Mindfulness perspective, the focus is on the cognitive facet of compassion and tolerance rather than their sentimental or emotional aspect.)
The centerpiece of compassion (by definition) is acceptance: Practices designed to cultivate interpersonal compassion aim to strengthen the ability to identify and remove conditions one’s mind places on a person as a stipulation for their acceptance (the general thinking behind withholding compassion is along the lines of “you are unacceptable as you are, because you cause me discomfort (or pain)” and “I will accept you when you become closer to the way I wish you to be”). Cultivating compassion then, with or without the practitioner’s realization, is cultivating acceptance. Arguably, the reason to cultivate compassion toward human (and other sentient) beings is to improve the mind’s ability to accept the Present it is in. (For more on this go to https://wp.me/P7aKBB-3C .)
Acceptance of a problematic person is no different from acceptance of a difficult situation. Like muscle strength acquired by practicing weight lifting and applied to tasks away from the gym, the strength of acceptance developed through cultivating compassion can be applied wherever needed, including the encounter with grief. In other words, a mind that possesses deep compassion will likely automatically deal with loss effectively, without a struggle, because its “acceptance muscle” is strong.
Tolerance is the willingness and ability to observe discomfort or pain without reacting to it; intolerance, conversely, invites reflexive reactions as a response to pain. Tolerance is relevant to the encounter with grief because it enables transcending the impetus to react reflexively to the pain associated with a loss.
Reflexive behavior is effective when confronted with survival threats, particularly when reaction speed is important. In all other circumstances, purely reactive conduct is, by definition, not mindful and, therefore, incompatible with an effective pursuit of happiness.
Grief is not a survival threat, regardless of how much it hurts. Intolerance of the pain of loss legitimizes responding to it reflexively — mindlessly, which is guaranteed to interfere with progress toward acceptance and, worse, is likely to create its own set of complications.
Overarchingly, acceptance (and thus, mindful grieving) is aided by the understanding that not all that hurts is (functionally) a pain (and vice versa, many sensations, e.g., tingling, numbness, loss of appetite, and shortness of breath are, functionally, forms of pain, even though they may not “hurt”).
Pain is a noxious signal designed to direct attention to a problem that requires it to be corrected. For example, stepping on a nail is supposed to elicit pain, the purpose of which is to direct attention to the injured foot and ultimately trigger a deliberate sequence of corrective responses e.g., applying pressure to stop a bleeding, cleaning, dressing, and monitoring the wound.
Grief — the hurt triggered by a loss, doesn’t function to bring attention to a problem for the purpose of correcting it — grief results from the realization that the problem cannot be corrected; we grieve in response to an irretrievable loss. Hence, grief does not have the same function as pain, although it hurts.
Consider, for example, a person waking up from an operation in which one of their limbs was surgically amputated: Registering their loss, this person is likely to feel hurt (sans any physical pain which, in our example, is completely blocked by analgesic medications). Their hurt is pure grief — the recognition of an irretrievable loss. The source of the hurt is the knowledge that there are no corrective actions to take, and the amputated limb is permanently lost. Since the problem cannot be fixed, the grief they feel cannot have the purpose of pain.
This then begs the question: What then is the purpose of grief? (Evolution does not support purposeless or nonsensical brain functions. Given that the capacity to grieve is a universal human trait, it must serve a purpose; doubtlessly, the purpose of grief could not be to bring attention to something (i.e., a fix) that does not exist.) One reasonable answer is that the wish to avoid the unpleasantness of grief may be a general motivation to act with a high degree of caution to reduce the likelihood of future losses (Thanks, DHR).
In addition, if one lets it, grief can elicit gratitude, which may be its primary purpose. Grief promotes gratitude by drawing attention to the value of what was lost: If a loss does not trigger grief, that which was lost has no value. Moreover, normally, the intensity (the depth and duration of the normal grief-reaction) is proportional to the magnitude of the value of the loss that triggered it — the greater the lost value, the more intense the grief.
By directing attention to the value once possessed, grief brings it into conscious awareness and invites appreciation, which, in turn, can elicit gratitude for it.
One of the psychological functions of gratitude is to support acceptance: Acceptance of a difficult circumstance is automatically made easier when something deserving of gratitude is identified in it. For example, when faced with the passing of a beloved person, it is common to try to focus on the cessation of their suffering or on the notion that “they are in a better place” — highlighting something in the loss that has a positive value, and thus rightly deserves gratitude, makes it easier to accept.
Linking grief to gratitude is not automatic; the instinct is to consider grief as a form of mental pain. However, since grief does not promote problem-solving, relating to it as if it were a pain (i.e., an impetus in the service of solving a problem) amounts to “wrong-grieving,” which contributes to frustration and hinders the healing process.
Grieving mindfully requires a deliberate effort, which, unquestionably, is worth investing in. Experiencing grief with calm, compassion, tolerance, and gratitude not only supports acceptance, it ultimately promotes inner peace and thus contributes to an effective pursuit of happiness.
Despair
Despair, which is also commonly, and nebulously, referred to as ‘depression,’ is a state of mind that emerges in response to entrapment (i.e., to the loss of freedom and, as such, it can be considered a unique form of grief). ‘Despair’ is inevitable when the loss of freedom is compounded by the loss of hope.
The immediate, instinctive response to entrapment is a fight-or-flight reflex — i.e., an automatic attempt to escape from the trap or overpower it. Past the reflexive response, flight-or-fight behavior is extended to the “next level” and appears like surrender-or-rage — the beginning of ‘despair.’ The futility of the attempts to resolve the entrapment undermines hope; when hope is lost, full ‘despair’ sets in.
This dynamic has been studied exhaustively in animal research over many decades, and is still conducted regularly, both in academic and in pharmaceutical-industry settings. It is broadly considered to offer an animal model for human ‘major-depression,’ which I consider a serious and costly mistake.
Studies examining this phenomenon fundamentally have the same design: The study animals are, in principle, well-cared for and have all their basic needs provided; obviously, they are entrapped and unable to escape. The acute adverse event they are subjected to is some form of “stress” (regrettably, a euphemism for torture). The specific “stress” varies in different experiments; typical “stressors” include non-lethal electrical shocks, sleep deprivation, repeated drowning, etc. The variables being studied include the duration of exposure to “stress” that is required to push the animals from the initial fight-or-flight level to the next level and the parameters of the required “stress” (the stress intensity, schedule, etc.).
Since this design is broadly considered to represent a model for human ‘major-depression’, this type of experiment is a core step in the early phase of antidepressants research-and-development. A molecule that appears to make the study animals less sensitive to the effects of the “stress” is considered to have a potential as an antidepressant, which justifies further investment in its exploration.
The animals’ response to the study conditions is entirely predictable: Initially, they display flight-or-fight behavior; after a while (which varies with the specific conditions), they enter one of three states: Some of the animals become passive; they show little or no reaction to the “stress,” or to anything else in their environment. They are said to enter a state of ‘learned-helplessness’, which is considered an animal model for human ‘major-depression’. The second state some of the animals display is a state of rage — they become frenzied, likely to attack targets in their environment without provocation or discrimination. The third state is a mixture of the first two: animals in the mixed state switch back and forth between ‘learned-helplessness’ and rage.
In my opinion, in as much as these studies may serve as a model for the human experience, these three states — ‘learned-helplessness’, rage, and the combination of both, are different manifestations of a single phenomenon — ‘Despair’.
(Sidebar: Therein lies the well-recognized (but generally poorly understood) link between anger and depression. This link is often encountered clinically and is a favorite topic in pop psychology (e.g., “depression is anger aimed inwardly”). It was nailed best by the comedian Steven Wright, who said, “Depression is nothing more than anger without enthusiasm”.)
The prevailing interpretation of these animal studies has a critical flaw — the assumption that the state of ‘learned helplessness’ is a model for human ‘major-depression’ is unfounded. It was proposed in the late 1960s and has not been challenged since. There is no scientific evidence for the claim that the state of ‘learned helplessness’ is related to ‘major-depression’ in any meaningful way. In my opinion, ‘learned-helplessness’ is a facet of the state of ‘despair’, which is a very different condition from the illness ‘major-depression’.
The difference between ‘major-depression’ and ‘despair’ is far from merely semantic — they are inherently different states, with different symptoms, psychological underpinnings, and, in all likelihood, different biochemical causes (which are yet to be delineated). Therefore, they would be expected to respond to different treatment approaches. Yet, the distinction between these two states is ignored.
I think that the following broadly accepted statists express this ignorance: The prevalence of ‘major-depression’ in the general population is currently estimated between 10-15% (in my opinion, this estimate is about tenfold greater than the actual prevalence of the bona-fide disorder but, for the sake of the present argument, let’s accepted this inflated estimate). The prevalence of ‘major-depression’ among patients with a severe chronic medical illness (any chronic medical illness, e.g., diabetes, heart disease, cancer, neurologic disorders, etc.) is estimated between 30-50% (i.e., 2-5 times higher than what may already be a very inflated estimation of the prevalence of the disorder in the general population). In addition, 85% of patients with ‘major-depression’ have at least one serious medical illness. (These numbers don’t make sense: the prevalence of two unrelated conditions — like diabetes and ‘major-depression’, occurring simultaneously is much lower than the prevalence of each one occurring on its own. For example, if 1 out of 10 people in a population has diabetes and 1 out of 10 people in this population has ‘major-depression,’ the probability of a person having both is 1 in 100.)
It is but guaranteed that the ‘major-depression’ that is presumably associated with a broad range of unrelated medical illnesses is not caused by some shared physiological mechanism. The most likely explanation for the staggeringly high rate of co-occurrence of ‘major-depression’ and serious medical illnesses is overdiagnosis of ‘major-depression’. More specifically — misdiagnosing ‘despair’ as ‘major-depression’.
Astonishingly, the typical conclusion mainstream psychiatry draws from these statistics is that patients with chronic medical conditions should be monitored more closely, i.e., diagnosed with ‘major-depression’ more aggressively!
Ignorance of the differences between these two states not only hinders progress in our understanding of ‘major-depression’, it also obscures the monumental role of ‘despair’ in the human condition, thus preventing the elucidation of effective ways of dealing with it.
‘Despair,’ as a natural occurrence, is largely (if not exclusively) a human phenomenon. In nature (as opposed to laboratory, zoo and other artificial conditions), a trapped animal dies before it has time to develop ‘despair’ (a trap, in this context, may be an external barrier, a broken limb, or a gastric ulcer — any set of inescapable negative conditions).
Things are very different when it comes to our species: Humanity’s ever-growing technological prowess and social structures (from the family unit to the State) make it routinely possible for individuals to live to a full life expectancy while trapped, even under physically and/or mentally “stressful” conditions.
(Sidebar: Arguably, the capacity to live a full lifespan in an inescapable trap is a uniquely defining human trait adjacent to another defining human trait — our interdependence.)
Chronic pain patients often live in what amounts to an entrapment in pain for years, sometimes decades; their living conditions are similar to the conditions in the animal studies described above. Not surprisingly, they exhibit some of the same outcomes: According to multiple studies, up to 85% (!) of chronic-pain patients develop ‘major-depression’. “Anger problems” and a mixture of anger and depression are also extremely common in this population. The professional literature thereof exemplifies the prevailing failure to distinguish between major-depression’ and ‘despair’: Patients in a state of ‘learned helplessness’ are misdiagnosed as suffering from ‘major-depression,’ patients in a state of rage are labeled as having an “anger problem”, and patients in the mixed state are commonly misdiagnosed with ‘agitated-depression’. In reality, most of this patient population is in an unrecognized state of ‘despair.’
The list of medical conditions that cause chronic pain (without posing a threat to survival, such as the various forms of arthritis, migraine, and other chronic headaches) is too long to tackle. Entrapment in mental pain is probably even more common, considering both the number of patients with chronic emotional pain secondary to mental disorders (such as pathologic grief untreated anxiety disorders) and individuals experiencing persistent emotional pain unrelated to a mental disorder (such as the pain of loneliness, regret, and a persistent sense of purposelessness).
Since entrapment in any pain — physical and/or mental, can result in ‘despair’, its prevalence is sure to be greater than the prevalence of bona fide ‘major-depression’ by orders of magnitude, yet, it is strangely ignored. Worse, as mentioned above, the leadership in the field pushes for increased vigilance and, by extension, increasing the rate of ‘major-depression’ diagnosis. The distinction between ‘despair’ and ‘major-depression’ is so lost that many mental-health professionals (at any level of expertise, from novice to expert) argue that it doesn’t exist at all or that if it does, it is inconsequential — a position of great detriment to both the science and the patients it aspires to serve.
In my experience, the current state of affairs is such that the vast majority of patients diagnosed with ‘major-depression’ actually suffer from ‘despair’. A person in a state of ‘despair’ seeking professional help is most likely to be misdiagnosed with ‘major-depression,’ followed by one of the other mood disorders — e.g., ‘agitated depression,’ ‘dysthymia,’ ‘non-specific depression’, ‘organic depression’, and, in the worst case scenario, ‘bipolar-depression’ (a minority is diagnosed with adjustment and personality-disorders; unfortunately, the specific diagnosis ultimately applied often reflects the clinician’s background and bias more than anything relevant to the patient’s condition).
‘Despair’ is not a binary, all-or-nothing phenomenon — it exists on a continuum, ranging from mild to overwhelming. Low-intensity ‘despair’ tends to manifest as a general dissatisfaction with life, disgruntlement, and non-specific “pissed-offness.” As it intensifies, it appears increasingly more as a state of demoralization, depression, frustration, and frank anger. Extreme ‘despair’ is paralyzing and is not compatible with normal functioning.
Interestingly, the state of ‘despair’ (and the conditions that lead to it) easily escapes conscious awareness, persisting without being recognized by the person in it and the people around them. The sadness (“learned-helplessness”) and/or anger that manifest ‘despair’ can not be ignored — like the visible tip of an iceberg. Most of the iceberg — the entrapment and the pain, can be submerged beneath the surface and easily overlooked.
This common characteristic of ‘despair’ is (at least partially) explained by the brain’s signal-processing routines: Signals with low (subthreshold) intensity can impact the mental process without registering in consciousness. I.e., low-intensity pain signals may escape conscious awareness but still impact the mental process. The accumulative effect of multiple subthreshold pain signals can add up and manifest with ‘despair’ even if the individual signals go completely or largely unnoticed. For example, a person may not pay attention to mild, chronic back pain or acknowledge the persistent emotional pain of disappointment in their career; yet, the combined effect of the two subthreshold but inescapable pains may result in a state of ‘despair.’
Signal-variability is also an important factor: Even intense (above threshold) signals can evade conscious awareness if they are constant (or constant/intermittent, i.e., starting and stopping at a constant frequency) like ‘white-noise’ that can be ignored regardless of its intensity, only to “pop-up” into conscious awareness once it changes, or stops (as anyone living near an airport or a train station knows first hand). In other words, a steady, unchanging chronic pain may be tuned out of consciousness, and at the same time, because it is steady and chronic — i.e., inescapable, it may lead to ‘despair.’
(Sidebar: (1) The distinction between physical and mental pain is somewhat misleading. Pain signals originating outside the brain (e.g., the toes, stomach, or scalp) register as physical pain, and pain signals originating inside the brain (e.g., anxiety, guilt, disappointment) register as emotional pain. In their essence (and function), both pain types are the same phenomenon, regardless of their point of origin. Hence, patients who suffer from chronic mental-pain are as susceptible to the same ‘despair’ related outcomes as chronic physical-pain patients.
(2) The earliest example of inescapable human mental-pain is typically encountered before we reach age 10, when we learn about mortality. Discovering that we, and everyone we care about, are guaranteed to die is universally unpleasant and stressful. Granted, we quickly develop ways of dealing with the awareness of our mortality; still, it is a form of mental pain from which there is no escape — once learned, this uncomfortable knowledge persists, and it never becomes more attractive than it initially is.
There are many other kinds of mental pains — self-doubts, disappointments, anxiety, isolation, rejection, injustice, shame, guilt, and purposelessness, to name some common examples; it is safe to say that everyone experiences, more-or-less, brief encounters with these pains. It is possible that most of us, perhaps all of us, struggle with one (or more) of these pains ongoingly, not necessarily indefinitely, but for periods long enough to qualify as entrapment and therefore breed ‘despair’.
(3) The conditions that potentially elicit ‘despair’ are inextricable from the human experience; this may be a part of the explanation of the peculiar high and rising prevalence of anger and “depression,” which are increasingly regarded as acceptable, normal mental states in modern society.
(4) By now, you may be beginning to suspect that my view of the current state of affairs in the field is somewhat critical. So, to be clear: My opinion is that the current level of clinical sophistication and the direction of research in mood-disorders are not, and should not be, acceptable. To put it mildly, the need for an overhaul of our approach is urgent. As I said at the top — I may be wrong, but I doubt it.)
More than three decades of practicing psychiatry left me with no doubt about the theoretical relevance and practical utility of the ‘despair’ model; I have seen it play out countless times. Here’s a typical example:
J. was a highly functioning adult with no history of psychiatric or substance abuse problems. He started experiencing diffuse joint pain, fatigue, and “brain fog.” These symptoms persisted, and after a couple of months, he brought it up for discussion with his primary care provider; his PCP ran some tests and, based on the results, referred him to a rheumatologist. The rheumatologist completed the workup and diagnosed J. with one of the autoimmune disorders (e.g., rheumatoid arthritis, systemic lupus erythematosus, fibromyalgia, etc.). Under the rheumatologist’s care, J. started a series of medication trials. It was a slow process, which tested J.’s patience. (It usually takes a few months to complete each of these trials. Things were particularly trying on a couple of occasions when his medical-insurance company refused to cover a medication he was prescribed until his doctor grovels long enough to their satisfaction).
After a little over a year of trying different medications, J. and his doctor decided which treatment was optimal, i.e., most effective with the fewest side-effects. J. followed the treatment recommendations closely; his symptoms improved significantly, and his condition was considered stable.
J. was appreciative and grateful for his doctor’s efforts, but he was less than thrilled with the situation overall: Although he was doing better, his symptoms did not resolve completely, and, in addition, he had to deal with some unpleasant side-effects. J. fully realized that none of this was unusual given the nature of his underlying disorder, but that didn’t help.
His residual symptoms were relatively mild, but occasionally, and most annoyingly — unpredictably, they intensified to a level that forced him to cancel plans. It was particularly difficult when he had to cancel plans that involved his wife or friends at the last minute. He hated the thought of disappointing people he cared about, which made him feel guilty and ashamed. So, he began to avoid making plans altogether, gradually leading to a significant drop in his overall activity level.
Over the next few months, J.’s rheumatologist became increasingly concerned about his mental well-being; eventually, she recommended a consultation with a psychiatrist (at that point, it had been a little over two years since he was first diagnosed; rightfully, rheumatologists usually don’t rush to suggest to their patients that their “problem may be in their head”). The rheumatologist contacted me with a request for “a psychiatric evaluation to rule out depression,” and a couple of days later, J.’s wife called my office to schedule an initial appointment.
J. showed up on time for the appointment, accompanied by his wife. He stated that the reason for seeing me was “depression” and acknowledged that his mood was “pretty lousy” most of the time “for months.” He firmly denied any thoughts of suicide. He endorsed a lack of energy, poor concentration, occasional insomnia (alternating with oversleeping), and some weight gain; since his appetite was not as good as it had been in the past, he attributed it to his reduced activity level. In addition, he was more easily frustrated, and he had lost some of his self-confidence. Overall, he wasn’t enjoying life like he used to.
J. was open to trying an antidepressant medication. He stated that he had been ambivalent about taking “psych meds,” but having discussed it with his rheumatologist, he accepted that it could well be the piece missing from his medical treatment.
His demeanor during the appointment was completely appropriate. He was somewhat distant and sometimes came across as a bit suspicious, but no more than I would have been in his place. His wife was pleasant, supportive, and concerned; she corroborated his account and didn’t add much information.
Clearly, J. endorsed more than enough symptoms to qualify for the diagnosis of ‘major-depression’ (although the possibility that some of his symptoms were secondary to his rheumatologic disorder and treatment side effects couldn’t be ruled out). My impression, however, was that he was in a state of moderate ‘despair.’ As I perceived it, his ‘despair’ was the result of his experience of living for more than two years trapped by residual symptoms and increasing social isolation, compounded by persistent side-effects and stress caused by the heartless bureaucracy of the insurance company he depended on. He seemed to have lost hope for a significant change for the better.
J. was reluctant to accept my opinion. He wasn’t receptive to the idea that his mental symptoms were a reaction to the circumstances he was in, in part because he thought it suggested a weakness of character and in part because he thought it would rule out an antidepressant trial (which, by then, he was more invested in that he may have realized).
Since we were not on the same page, J. had to make a decision about how he wanted to proceed. He had two options: One was to get a second opinion from another psychiatrist (with my full support). The other was to test the relevance of my impression by doing a ‘diagnostic trial.’
Testing the validity of the ‘despair’ hypothesis under such circumstances is relatively easy; all it takes is a short period of aggressive anti-pain treatment. Theoretically, to the extent that ‘despair’ is a consequence of entrapment, liberation — the discovery of a way out of the trap, should resolve it. Practically, acute, effective anti-pain treatment would be expected to transform the state of ‘despair’ when it is secondary to entrapment in chronic pain.
My clinical experience has been consistent with this expectation: Patients in ‘despair’ experience a dramatic improvement of their depressive symptoms in response to aggressive, short-term anti-pain treatment because it represents a way out of their entrapment. Finding freedom reignites hope, which automatically negates ‘despair’ (even without conscious awareness of any of the steps taking place). Chronic pain patients with depressive symptoms secondary to another condition — such as a bona fide ‘major depression’ or a personality disorder, of course, welcome relief from the pain, but they don’t respond to aggressive pain management with a significant improvement of their mental symptoms.
It is a broadly accepted principle in the treatment of ‘major-depression’, supported by a lot of research and clinical experience, that the clinical response to antidepressants begins to emerge no sooner than four to six weeks from the time the treatment starts (there are physiological reasons for this delay which are beyond the scope of this work). In other words, when depressive symptoms improve within less than four weeks of starting an antidepressant, the improvement is unlikely to be explained by the pharmacological effect of the treatment.
There are two likely explanations for a rapid improvement of ‘major-depression’ symptoms in response to an antidepressant (i.e., within significantly less than four weeks from the initiation of treatment): One is the placebo effect. The placebo effect is quite common and can be intense and dramatic; however, it is not sustained. The placebo response has a well-recognized course: it starts quickly — usually within a day or two from the initiation of the treatment, and lasts briefly — usually only for a few days. It rarely lasts for two weeks. The second explanation is misdiagnosis, i.e., that the condition that causes the depressive symptoms is not ‘major-depression’.
(Sidebar: (1) In my experience, in similar settings, the most effective medication for this diagnostic trial is methadone. Methadone is a tightly controlled opioid drug commonly used for the treatment of heroin addiction; it isn’t a light-weight drug. It is particularly useful in this setting because it is a potent anti-pain drug, but it does not cause a significant “high” (it is more sedating than it is euphorigenic). It is very useful diagnostically, i.e., when it is used briefly. It is controversial as a treatment for chronic pain, The long-term use of Methadone (and other opioids and opiates) is presently considered more problematic than it’s worth (for several reasons that are outside the scope of this work); the current recommendation is to avoid the long term use of these medications as much as possible. However, for most patients, a brief course of treatment with methadone for diagnostic purposes is safe and does not raise serious concerns.
(2) One of the latest medications approved by the FDA for treatments of ‘major-depression’ is a drug called Ketamine. It appears to work essentially instantaneously, like methadone. Much Ketamine as a treatment for depression (e.g., mechanism of action, long-term use guidelines, and the type of patient it is most appropriate for) is unknown and still being worked out. Historically, Ketamine has been (and still is) used for the treatment of severe pain, which I doubt is a coincidence.)
After we reviewed the relevant pros and cons, and with his wife’s support, J. chose to proceed with the ‘diagnostic-trial’. I gave him a prescription for methadone and instructed him to adjust his dose as needed to stop all or most of his pain but to keep it below a dose that made him sleepy or sedated. Lastly, before he and his wife left my office, we scheduled a follow-up appointment two weeks later. As a rule in this diagnostic trial, keeping the period between the two appointments close to two weeks is important. The reason is that a two-week period is too short for the pharmacologic effect of any antidepressant to emerge (other than Ketamine) and too long for a sustained placebo effect.
When J. and his wife returned, as scheduled, for our next appointment, J. was a changed man: He was cheerful, warm, and friendly. His wife, who was clearly delighted, kept saying, “I got my husband back.”
Interestingly, J. was less impressed with his own transformation than his wife and I were. This is not unusual in these cases; I think it reflects the patients’ lack of awareness of or detachment from how they come across while in ‘despair.’ When I presented my interpretation of his experience, J. related to it immediately. We were on the same page moving forward. We agreed on a gradual tapering schedule of the methadone over the following two weeks and scheduled regular meetings for psychotherapy.
As expected, J.’s pain returned after the methadone was discontinued, but his rekindled hope wasn’t lost — the firsthand discovery of a way out of his trap seemed to protect him from the recurrence of ‘despair.’ He was more energized which manifested with increased participation in physical therapy and a strong commitment to lifestyle changes (i.e., he stuck to a healthier diet and regular exercise). We started meeting regularly for psychotherapy; the topics we explored included the difference between pain, suffering, and misery (more on this here: https://wp.me/P7aKBB-3w), freedome (more on this here: https://wp.me/P7aKBB-7D ), focusing on doing the best he was able to do (more on this here: https://wp.me/P7aKBB-pa), and cultivating tolerance (more on this is pending). He also started a meditation practice. Over the next few months, his pain decreased, and his activity level increased.
Early on, we also came up with a plan whereby he could use methadone sparingly when he decided he absolutely had to. The parameters for using it were inflexible, and we agreed on the maximum amount he could use per month. As it turned out, he used much less of it than he had access to. As he said, the important thing was that having access to this medication added to his influence over his pain and, therefore, contributed to his sense of freedom. Overall, he continued to do well, and as he pointed out on more than one occasion — he wasn’t thrilled with the fact that he had a chronic autoimmune disorder, but the experience was not a waste. He felt that the lessons he learned were invaluable and broadly applicable to many areas of his life. I hope and believe that it improved his pursuit of happiness.
At some point along the way, I encouraged J. to try an antidepressant, which he did. He discontinued it after a couple of months because it didn’t seem to help (and it caused mild but annoying side effects). Nonetheless, I thought it was worth trying because, in my experience, antidepressants potentially can treat ‘despair.’
Even the animals in the “chronic stress” experiments described above respond to antidepressants: Typically, animals that receive a therapeutic dose of an antidepressant require longer exposure to and/or more intense “stress” to be brought to the ‘learned-helplessness’ state (hence these experiments are central in the preclinical phase of developing new antidepressant medications). There are no scientific estimates of the efficacy of antidepressants as a treatment for ‘despair’ because the research routinely ignores the distinction between ‘major-depression’ and ‘despair’. However, I have witnessed enough patients in ’despair’ derive benefit from the use of antidepressants to warrant recommending trying them in this setting (I generally recommend no more than two trials, using antidepressants from different classes, because if two trials fail, the yield positive results, it is extremely unlikely that further trials would be effective).
The rate of response to antidepressants (for both humans and animals in ‘despair’) is far from 100%. Still, any significant superiority of medical treatment over placebo raises a question: If that which is being treated is indeed a reactive, psychological problem, why does it respond to medical treatment at all?
The answer has to do with the analgesic (pain-reducing) effect of antidepressants — most if not all, antidepressants have a well-established anti-pain effect, independent of their presumed mood-elevating effect (antidepressants are part of the first-line treatment of chronic physical pain; several antidepressants are approved by the FDA for use as anti-pain medications, even in the absence of any depressive symptoms).
The point is that at least some of the time, the apparent mood-elevating effect of antidepressants is actually downstream from their pain-reducing effect.
The analgesic effect negates ‘despair’ because, consciously or subconsciously, it proves that there is a way out of one’s perceived entrapment and thus rekindles hope. It’s essentially the same effect of opioids (like methadone in J.’s case) and possibly ketamine, but it is much slower to kick in.
Any substance (elicit or prescribed) that reduces pain has the potential to act as an antidepressant. Even mild, non-prescription analgesics (e.g., acetaminophen or Tylenol) have been shown repeatedly to have a small but measurable positive effect on mood.
Studies demonstrating the mood-elevating effect of analgesics follow a similar, simple design: Participants are randomly assigned to one of two groups. Both groups answer an initial mood-assessment questionnaire after which the study-group members receive a dose of a mild anti-pain drug; the control-group members receive a placebo pill. The participants’ mood is reassessed a few hours later. Typically, the average mood in the study-group (the analgesic recipients) shows a small improvement in comparison to their initial rating; the average mood in the placebo-group remains unchanged.
The likely explanation for this phenomenon is that many of the participants in these studies suffer from mild, covert, background-pain. This pain is like “white-noise” i.e., a constant background signal, unrecognized until it stops. Even if the pain is not intense enough to register consciously, it has a negative impact on mood. Reduction of the pain reduces this negative impact, manifesting with an improved mood.
As I said earlier, chronic pain patients like J. illustrate the dynamics associated with ‘despair’ most vividly, but not exclusively. Chronic pain is only one of the settings in which ‘despair’ can be recognized. A somewhat less obvious (but not less common) illustration of ‘despair’ is displayed in the experience of patients with untreated anxiety-disorders; this is not surprising keeping in mind that anxiety is a pain, which means that patients with anxiety-disorders also struggle with chronic-pain, albeit mental rather than physical. (There is a unique facet to the association between anxiety and ‘despair,’ which I will return to in the following.)
The main difference in my approach to these two groups of patients is the specific medication used in their respective “diagnostic trials”: Anxiety is not particularly responsive to opioids; it is, however, remarkably responsive to a group of medications collectively known as ‘benzodiazepines’ (examples of benzodiazepines include Valium, Xanax, and Klonopin). I have seen countless patients who presented complaining of “depression” where, in fact, they were in ‘despair’ as a result of entrapment in the pain of anxiety. These patients’ “depression” typically resolved within a few days of treatment with an effective dose of one of the benzodiazepines, much like J.’s “depression” resolved within a few days of treatment with methadone.
Many patients develop ‘despair’ as a result of entrapment in other emotional pains, such as self-doubt, guilt, shame, purposelessness, etc. (A complete list of human emotional pains and their management principles will be presented elsewhere in this work). Since there are no medications that stop any of these pains, there is no diagnostic test to validate the ‘despair’ hypothesis for these patients. Nonetheless, their ‘despair’ follows the same course: it resolves when the patient discovers a way out from their trap — with the acquisition of mental freedom. Freedom in this context amounts to gaining influence over one’s mental position relative to their emotional pain, i.e., the ability to increase their distance from it.
Three general processes support freedom from emotional pain: Firstly, this freedom can be acquired as a part of normal maturation, particularly when relevant, corrective experiences support it. Secondly, freedom from entrapment in emotional pain can be gained through a sincere spiritual practice. I think that any kind of spiritual practice can be effective as long as it rejects fanaticism (which is a form of entrapment) and highlights inner discipline. And thirdly — psychotherapy: Mental freedom from emotional pain can be said to be the overarching, ultimate goal of psychotherapy.
(Last sidebar! (in this section): Opioids and benzodiazepines are very different types of medications, yet they share several key features. For example:
1. Both are indicated for the treatment of severe pain (albeit of different types).
2. Both are remarkably effective, with a very rapid onset of action (hence, both have the potential to alleviate ‘despair’ quickly).
3. Both are remarkably safe (essentially harmless when used within the therapeutic parameters).
4. The long-term use of both is associated with the risk of tolerance and dependence; discontinuing their use can cause a rebound of the pain they are prescribed to treat.
5. Both are associated with very unpleasant withdrawal symptoms if their long-term use is stopped abruptly (i.e., “cold turkey”).
6. Both can be abused.
7. In both cases, their misuse, abuse, and dependence are exceedingly rare when prescribed appropriately; both have been vilified by the medical profession and the general media (to the point that their utilization is avoided irrationally, at times even when there is no alternative treatment that is remotely as effective).
The psychological and social dynamics behind these similarities are fascinating but, to my knowledge, understudied. Exploring them is undoubtedly well beyond the scope of this work.)
Normal and Pathologic Despair
‘Despair’ can be normal in the face of entrapment when there is no hope for escape. However, it is not inevitable, even in the face of extreme hardship, as illustrated by the lives of Nelson Mandela, Stephen Hawking, and the current Dalai Lama, to name a few examples. The ability to transcend ‘despair’ should not be considered superhuman (as, doubtlessly, they would be quick to confirm). Countless anonymous, ordinary people throughout human history have dealt with tremendous adversity without succumbing to despair — it requires a high level of psychological maturity and/or unshakeable spiritual balance, but not superpowers.
‘Despair,’ however, can be pathological, resulting from either a biological or psychological dysfunction. Biological ‘despair’ is uncommon, probably manifesting a breakdown of the brain’s hope-generating apparatus (that is yet to be delineated). In my clinical experience, patients suffering from ‘despair’ secondary to an organic cause present with a psychotic-like conviction that they are doomed to experience a painful future from which they have no way to escape (a similar presentation can occur in the context of severe ‘major-depression,’ often referred to as ‘psychotic depression,’ an example of ‘despair’ and ‘major-depression’ overlapping).
Pathological despair secondary to psychological dysfunction, i.e., reactive ‘despair’ (or ‘despair’ that results from “wrong thinking”), is much more common. The underlying psychological problems associated with ‘despair’ range in severity from mere immaturity to adjustment and personality disorders. The common thread is the patients’ attachment to an unrealistic point of view from which they appear (to themselves) trapped with no hope of escaping. For example, the conviction that one is inherently unlovable and, thus, trapped in a life of loneliness and isolation, or the conviction that one is inherently not good enough (e.g., not smart enough, not attractive enough) and is thus doomed to fail. Such convictions invite ‘despair’ and, as they become self-fulfilling prophecies, anchor it.
Psychological ‘despair’ can also emerge from an intense discomfort with uncertainty. Uncertainty is a prerequisite for hope — where there is uncertainty, there is hope (and conversely, where there is certainty, there is no hope). But uncertainty also contributes to anxiety, which is, of course, uncomfortable. Therefore, the belief that one can know in advance how things will turn out is soothing. Hence, the illusion of predicting the future has a seductive appeal, the intensity of which is proportional to the intensity of the anxiety caused by uncertainty (it largely explains the stability of professional fortune-tellers throughout human history).
The notion of certainty has an anxiety-reducing effect even when the predicted outcome is negative (e.g., “I know I’m not going to get the promotion; I am always looked over”). Seeking relief from anxiety through the illusion of certainty is a veiled setup for hopelessness. Applying it repeatedly carries the risk of habituation, ultimately supporting a state of ‘despair.’ Consequently, ‘despair’ is a prevalent complication of disorders in which anxiety is a prominent feature (frank anxiety disorders such as generalized anxiety disorder, panic disorder, social anxiety disorder, OCD, and phobic disorders, as well as adjustment and personality disorders).
Anxiety disorders then contribute to ‘despair’ in two ways: One is through entrapment in chronic mental pain, and the other is by negating hope as a result of discomfort with uncertainty. (For more on Anxiety go to https://wp.me/P7aKBB-zU .) Anxiety disorders are notoriously under-recognized by both the patients suffering from them and their health-care providers. The majority of patients who suffer from anxiety disorders seek help for depression, not for anxiety — because they are in a state of ‘despair.’ Most are misdiagnosed with ‘major-depression’ and prescribed an antidepressant. Many improve — even though the diagnosis of major-depression is wrong. The explanation of the positive response to treatment despite the underlying misdiagnosis, is that antidepressants treat anxiety at least as effectively as they treat depressive symptoms; arguably, antidepressants are more effective treating anxiety than depression (indeed, most FDA approved antidepressants are also FDA approved as a first line treatment for anxiety disorders).
It is only natural for both patients and treatment-providers to conclude that the improvement in the patient’s mood following a course of treatment with a medication known as an antidepressant confirms the diagnosis of ‘major-depression’. Typically, neither the patient nor the treatment-provider have a reason, or an incentive, to explore the validity of this assumptive conclusion. Consequently, the reality — the role of ‘despair’ and the fact that the improvement in mood is an indirect effect — secondary to the relief from the chronic pain of anxiety, remain obscured; at the same time, the wrong diagnosis and wrong understanding of the response to treatment are confirmed. Urg.
Modern psychiatry is largely oblivious to the phenomenon of ‘despair’ which, of course, guarantees failure to distinguish it from ‘major-depression’. Ignoring the distinction between these two states is no different from ignoring the distinction between conditions that share some superficial features, such as dyspepsia (heart-burn) and angina (the chest pain associated with coronary artery disease), or Parkinson’s disease and essential tremor. The consequences of this ignorance to both the research and clinical practice are incalculable.
Despair and Mindfulness
Psychological ‘despair’ can be managed with psychological means, i.e., psychotherapy and/or a spiritual practice, both of which can be supported by the practice of mindfulness. The mindfulness-based approach to ‘despair’ hinges on the same two concepts reviewed in the management of grief: tolerance and compassion.
The specific relevance of tolerance to the management of ‘despair’ stems from the critical difference between reactivity and (deliberate) activity. By definition, reactive, reflexive behaviors circumvent thoughtful assessment and analysis. It offers the advantage of speed at the expense of sophistication, which is best suited for encounters with survival threats, where speed can make all the difference. Reflexive reactivity is not only ineffective in the pursuit of happiness, it carries the risk of making matters worse. Ineffective actions (and, worse, actions that have a negative impact) contributes to self-doubt and anxiety. Persistent futility of one’s actions eventually yields a sense of entrapment and, thus, ‘despair’.
According to a fundamental principle of mindfulness, observing, contemplating, and refraining from action is preferable until the behavior that constitutes ‘right action’ is clear. Refraining from reflexive, quick reactions in the face of discomfort or pain until the ‘right action’ becomes clear requires tolerance.
In other words, tolerance enables resisting the impulse to react in favor of taking the ‘right-action’. Right actions — by definition, increase one’s influence over their position in a given situation (that is what makes them right). The degree with which one is able to influence their position (i.e., the ability to move in a chosen direction) is the degree of freedom they possess, and the degree of their immunity from ‘despair’.
The specific relevance of compassion to ‘despair’ also stems from the fact that compassion protects freedom. Here’s the breakdown of the logic behind this claim:
- The experience of freedom (and of entrapment) is inseparable from awareness of Time. Both freedom and entrapment have a meaning only when they are linked to some length of time (it is not a coincidence that a prison sentence is referred to as “doing time” or “serving time”). A wrong attitude toward Time (or any one of its components: past, present, and future) typically results in getting (mentally) stuck, or trapped, in it, which is synonymous with the loss of freedom.
- The right-attitude toward Time can be deconstructed to forgiveness of the past, acceptance of the present, and hope for the future. Lacking these traits results in the experience of getting stuck: Lacking forgiveness results in an inability to get distance from past trauma. Lacking acceptance of the present makes moving forward a non-option. Lacking hope for the future directly contributes to despair, as discussed earlier.
Compassion is defined as a state of mind composed of forgiveness, acceptance, and hope. (A detailed discussion of Compassion can be found here: https://wp.me/P7aKBB-3C .) That is, cultivating compassion is cultivating forgiveness of the past, acceptance of the present and hope for the future, which is to say that cultivating compassion is cultivating the right-attitude about Time. - Cultivating compassion then negates the risk of getting mentally trapped in Time which offers protection from ‘despair’ (with or without the practitioner’s awareness of the mechanism at work).
Major-Depression
The term ‘major-depression’ is applied indiscriminately to various conditions hallmarked by sadness, both in clinical and general settings. In my professional experience, most of the patients diagnosed with ‘major-depression’ are actually in a state of ‘despair’ and/or ‘grief’(either of which may, or may not, be pathological). Only a small fraction suffer from the relatively rare and serious medical illness that the term ‘major-depression’ denotes.
The terminology we have come to use discussing ‘depression’ is confusing, both generally and professionally. The term ‘major-depression’ is an abysmal medical term for a number of reasons: Firstly, the word ‘depression lacks specificity; ‘depression’ describes a very broad range of human experiences — it is used in reference to a trivial emotional reaction (e.g., “Jill was depressed when the Lakers lost the series”), a perfectly normal but unpleasant emotional state (e.g., “We were all depressed when dad died”), a psychological disorder (as in ‘adjustment disorder with depressed mood’), and a serious medical/psychiatric condition associated with disturbingly high morbidity and mortality rates — the bona-fide diagnosis of ‘major-depression’.
Secondly, ‘major-depression’ implies the existence of a ‘minor-depression’ which, clinically, is a very murky issue. As a diagnosis, ‘minor-depression’ is even more poorly defined than ‘major-depression’ and (thankfully) it is rarely used in practice or in the psychiatric literature. (‘Minor-depression’ is often said to be synonymous with a condition known as ‘dysthymia’. However, since dysthymia is defined as a chronic condition {to qualify for the diagnosis of dysthymia a patient must experience symptoms for at least two years} and ‘major-depression’ is an acute condition {to qualify for the diagnosis of ‘major-depression’ a patient must experience symptoms for at least two weeks} I find it difficult to justify considering them to be the a minor and a major expression of the same phenomenon.)
Thirdly, and most gravely — the “thing” that is depressed in ‘major-depression’ is obviously the patients’ mood, that is, the term implies that the condition is defined by a depressed mood. In other words, the term ‘major-depression’ implies that the condition is fundamentally a disorder of sadness. This notion is so ingrained in our thinking (professionally and generally) that pointing to it may seem redundant. However, this broadly accepted notion has never been scientifically proven, or even tested in any meaningful way. It is completely arbitrary, driven by a subjective perception of the appearance of some patients who may, or may not, actually suffer from the disorder. It is entirely possible (and happens to be my opinion) that sadness is not a central feature of ‘major-depression’ at all (and that the axiomatic notion that it is reflects how far off-target our approach to the condition is).
In my view, the primary brain function at the core of bona fide ‘major-depression’ is the ability to care. In other words: ‘Major-depression’ is fundamentally a disorder of caring and passion.
Caring and passion (which are synonymous — caring about something is the same as having passion for it) refer to the intensity of the emotional experience in general, not to any specific emotional experience.
Caring (or passion) qualifies both positive and negative emotions: It captures the intensity of both the attraction triggered by positive emotions (e.g., love, wonder, and gratitude) and the repulsion triggered by negative emotions (e.g., hatred, disgust, and feeling threatened). In other words, the more we care about something, the more intensely we are moved toward or away from it.
(Sidenote: Caring in association with positive emotions is obvious and does not require an explanation. In case caring in association with negative emotions is less obvious, here’s a real-time example of it: As you may be able to sense, I am quite passionate about this topic — I care about it a great deal (to a point that I worry my level of caring may get in the way of the message). My caring is linked to an assortment of negative emotions: I am appalled and frustrated by the state of affairs in my profession. It pains me to witness the avoidable suffering we cause through our ignorance, and shames me to think I may have contributed to it.)
The loss of the ability to care is, in a sense, immobilizing, as it negates both the attraction and the repulsion that are normally triggered by the emotional response. Sadness may accompany some cases of ‘major-depression’, but it is a distant, secondary feature, not a central characteristic of the disorder (indeed, sadness is not a required symptom for the formal diagnosis of ‘major-depression’, as discussed below).
The consequences of the misplaced focus on sadness as a central feature of ‘major-depression’ are incalculable: It caused a blurring of the distinction between ‘major-depression’, ‘grief’, and ‘despair’, which is a major factor in the meteoric rise in the prevalence of ‘major-depression’ seen over the last few decades; it is impeding research, derailing clinical efforts, and legitimizing the mislabeling a broad range of normal human experience as a disease.
The formal, DSM guided, diagnostic approach to ‘major-depression’ is actually in line with the fact that it is not a disorder hallmarked by sadness: The DSM recognizes that sadness is not a required symptom for the diagnosis of ‘major-depression’ (although, unfortunately, it falls short of stating it clearly) and, consequently, it requires the presence of only one of the two ‘core symptoms’: Either “a profoundly depressed mood” or anhedonia for the diagnosis of ‘major-depression’ — not necessarily both. The DSM gives anhedonia the same diagnostic weight as depressed mood. It defines anhedonia as the “loss of interest and/or pleasure in all, or most, activities” — essentially, it is an impaired ability to care, or to experience passion. In other words, even according to the DSM, a patient can suffer from ‘major-depression’ without experiencing a depressed mood!
Over my years of practicing psychiatry I have seen countless patients whose primary complaint was “depressed mood”, or just “depression”. The vast majority suffered from ‘grief’ and/or ‘despair’. Invariably they struggled with sadness and often with other negative emotions. But, typically, their capacity to care was intact, which actually added to their suffering.
In comparison, the relatively rare patients who suffered from a bona-fide ‘major-depression’ were not particularly sad; usually they were impassive, describing their mood as “bland”, or “dreary”. Their primary problem was (usually, an acute) loss of the ability to experience any emotion with normal intensity.
Conversely, I have never seen a patient with bona-fide ‘major-depression’ whose ability to care about life, or experience passion for it was intact.
Patients with ‘major-depression’ always suffer from anhedonia. They describe it as an odd, overpowering apathy. It strangely forces detachment from aspects of life that, intellectually, patients recognize as the most important. When sadness is part of the presentation of a patient with ‘major-depression’ it is down-stream from, or a result of, this apathy.
It is difficult to overstate the importance of the normal capacity to care. In addition to experiencing it as a mobilizing force, as mentioned above, ‘caring’ is linked to ‘interest’ — we are automatically interested in that which we care about, and therefore, to ‘attention’ — we automatically pay attention to the things that interest us. Conversely, not caring about something renders that thing uninteresting and therefore, it doesn’t receive attention.
Hence, the impaired capacity to care at the core of ‘major-depression’ is inseparable from impairment in the capacity to sustain interest and attention. Interest and attention are required for normal functioning. An impairment of these critical brian functions is guaranteed to have a detrimental impact on functioning in every role — academic, profession, interpersonal etc..
Therein lies the explanation for the global functional impairment associated with bona fide ‘major-depression’ — it is a consequence of the impaired capacity to care, manifested as a loss of the ability to maintain interest and pay attention. In comparison, sadness (and other types of a ‘bad-mood’) doesn’t really explain the functional incapacitation caused by ‘major-depression’. Sadness can be very unpleasant, but it does not necessarily impair functioning.
As discussed elsewhere, information in consciousness can be organized categorically into three compartments: Self, Other, and Process; each of these compartments is subdivided into past, present, and future. Since pathological loss of ‘caring’ that defines ‘major-depression’ can impact every facet of consciousness, ‘major-depression’ can manifest with loss of caring about any process and every relationship in the patient’s life — including the relationship with the ‘Self’.
Loss of caring about the ‘Self’ explains some of the characteristics of the disorder, from neglect of personal hygiene to increased propensity for accidents. In the extreme it may manifest with a loss of interest in sustenance which may become life threatening; sadness, in comparison, does not explain these features of the disorder.
Loss of ‘caring’ about one’s future readily translates into lack of motivation and, ultimately, hopelessness, which are remarkably common features of the disorder. In extreme cases, patients’ hopelessness can reach delusional intensity — a non-negotiable conviction (i.e., a sense of “knowing with certainty”) that they are doomed to experience as much or more pain in the future as they are experiencing in the present (delusions, defined as nonnegotiable beliefs held despite irrefutable contradictory evidence, are a symptom of psychosis; hence depressed patients experiencing delusional hopelessness are said to suffer from “psychotic major-depression”, the most severe form of the disease). Delusional hopelessness can make an extremely difficult condition utterly insufferable. It can raise the appeal of death as an end to one’s suffering and consistently, ‘psychotic major-depression’ is associated with a high risk of suicide.
In addition, the mental cascade that begins with caring (i.e., caring → interest → attention) is critical to the sense of connection between a mind and anything in the environment in which it exists. Simply put, events, or data, that don’t qualify as deserving attention are excluded from consciousness. Obviously, information that is not present in consciousness is not available to connect with.
Therein lies the unique toll of ‘major-depression’: By impairing the ability to connect it results in an oppressive sense of isolation, which is a major factor in the unbearability of the disorder. The fear of isolation is a primal fear; it is much more difficult to endure than sadness. Sadness is an unpleasant feeling we’d prefer to avoid, but it is not nearly as terrifying as isolation. Ultimately, it is this forced isolation that gives ‘major-depression’ its distinctive nightmarish quality.
Clinical Considerations in ‘Major-Depression’
Unlike ‘grief’ and ‘despair’, which may be either normal or pathological, ‘major-depression’ is always a pathology: ‘Major-depression’ is a serious illness that affects the brain.
While theories are in abundance, the cause(s) of ‘major-depression’ is(are) presently unknown. The consensus is that it is a biological (rather than a psychological) condition, a notion supported by many studies that indicate a role for inheritable/genetic factors in the disease formation. For example, family studies show that first-degree relatives of patients have a two – to threefold increased lifetime risk of developing the disorder in comparison with the general population, and twin studies that show that the disorder has a 40-50% heritability rate.
Further evidence of the biological underpinnings of ‘major-depression’ is provided by a large body of research and vast clinical experience indicating that ‘major-depression’ responds to a variety of biological treatments. The actual rate with which ‘major-depression’ responds to medical treatment is a matter of controversy; clearly, it is far from 100%. Overdiagnosis, which unfortunately is very common, inevitably significantly reduces the observed rate of response to medical treatment. Still, ‘major-depression’ appears to respond to biological treatment modalities at a significantly higher rate than to placebo.
The most commonly used biological treatment of ‘major-depression’ pharmacological, i.e., antidepressant medications. The number of FDA approved antidepressants has been growing steadily since they were discovered, in the late 1950’s. Antidepressants are organized into classes, according to their presumed mechanism of action (i.e., the biochemical processes they influence). Interestingly, even though medications from different classes are believed to employ very different mechanisms of action, no single antidepressant has ever been shown to have superior efficacy over the rest. Antidepressants classes differ in their side-effect profiles but, to date, all “head to head” studies comparing the efficacy of different antidepressants indicate that they are all equally effective. An individual patient may respond preferentially to a specific agent, but in population studies all antidepressants appear to be equally effective.
Other biologic modalities with demonstrable efficacy and FDA approval for clinical use in the treatment of ‘major-depression’ include Transcranial Magnetic Stimulation (TMS) and electroconvulsive therapy (ECT). The role of non-biological treatments (i.e., psychotherapy, exercise, meditation) in the treatment of bona-fide ‘major-depression’ is, at best, secondary (more on this in the following).
The characteristics of bona-fide ‘major-depression’ are well established: It is an acute, episodic, disabling, and recurring illness. Permit me to relucidate:
– The acuity of ‘major-depression’ means that it has a rapid onset. The period separating patients’ functioning at their normal baseline from the time at which they experience the full-blown symptoms the disease is measured in days or weeks, not months or years. The acuity of the disorder is addressed in the DSM by stating that the diagnosis of ‘major-depression’ can be made on the basis of as brief as a two-week period of persistent symptoms, representing a sharp departure from the patient’s baseline.
– The episodic nature of the condition means that patients do not experience symptoms before an episode begins and after it resolves, whereby most patients return to their pre-illness state and level of functioning. More often than not, consistent with the biological underpinnings of the disorder, episodes are not reactive, i.e., episodes tend to be unforeseeable, presenting “out of the blue” rather than as a response to an identifiable loss or stress (episodes may be reactive, i.e., precipitated by a stressful event in the patient’s life, but that is the exception, not the rule).
Episodes of ‘major-depression’ are generally self-limiting — most cases resolve with or without treatment. Nonetheless, treatment is valuable because it can reduce the severity of the symptoms and/or shorten an episode’s duration. In other words, effective treatment can diminish patients’ suffering and contain the damage to their lives; moreover, given that suicidality is one of the symptoms of the disease, effective treatment may reduce the risk of premature deaths.
– The disabling nature of the disorder is referenced in the DSM’s by making it a diagnostic requirement that “symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning”. Indeed, bona-fide ‘major-depression’ is not a subtle condition. Episodes of ’major-depression’ invariably involve significant functional impairment, if not complete disability.
– Because it is a recurring disorder, most patients experience more than a single episode in their lifetime. Experiencing an episode of ‘major-depression’ is the primary risk factor for encountering future episodes.
The average duration of an acute episode, and the average duration of the period between episodes are a matter of some controversy. Generating clear parameters for the typical durations of an episode and inter-episodic period is hampered by numerous factors, primarily the lack of definitive diagnostic capability and the consequential a high rate of misdiagnosis; other factors that may influence the duration of the phases of the illness and thus make assessing them more difficult include the utilization of treatment, level and impact of situational stress, availability of a support system, and the coexistence of other medical, psychological, and psychiatric disorders (including substance abuse). In my clinical experience the average duration of an episode of ‘major-depression’ is 6-9 months, and the average duration of the period between episodes is around five years. The duration of an episode can be shortened with treatment; the inter-episodic phase may be prolonged in some cases by prophylactic treatment.
Regrettably, the disorder’s well recognized characteristics are all too often ignored (understandably by laypersons, inexcusably by researchers and clinicians). For example, the diagnosis of ‘major-depression’ is frequently made with disregard to both the acuity and the severity that define the condition: The diagnosis is routinely given to patients that clearly suffer from insidious and chronic mental disorders (as opposed to acute and episodic). That is, patients are routinely diagnosed with ‘major-depression’ in spite of the fact that they have been struggling with the same symptoms for years (often beginning in adolescence or earlier). Moreover, it is not uncommon that the diagnosis is made without observable, or even reported, change in the patient’s level of functioning. Doubtlessly, most of these patients suffer from something, but ‘major-depression’ it is not.
Granted, psychiatry recognizes a chronic form of major-depression and a chronic depressive disorder referred to as ‘dysthymia’ which (as mentioned above) is a depressive disorder that persists for a minimum of two years, with less severe and/or fewer symptoms than ‘major-depression’. However, chronic depressive disorders are quite rare (the estimated lifetime prevalence of chronic ‘major-depression’ is around 3%; the estimated lifetime prevalence of dysthymia is around 1%). Chronic major-depression and dysthymia are not only rare, they are also diagnostically elusive — they are very difficult to distinguish from some of the personality disorders, substance abuse disorders, persistent ‘grief’ and/or ‘despair’ and the general dissatisfaction that stems from an ineffective pursuit of happiness.
Complicating matters further, over the last 3-4 decades psychiatry has become increasingly enamored with a condition referred to as ‘Treatment Resistant Depression’ (TRD). The definition of TRD, and the ways in which it differs from chronic ‘major-depression’ are, at best, loosely established. According to many experts (both in academia and in the pharmaceutical industry) ‘major-depression’ should be considered ‘treatment-resistant’ after two medication treatment trials prove ineffective (for what it’s worth, the two failed trials need to utilize antidepressants from different classes, and both need to be considered “adequate”, which means that the antidepressants utilized is prescribed at a therapeutic dose for a period of at least 4 weeks).
As I see it, this definition of TRD blatantly goes against reason and common sense: The most likely explanation (consistent with Occam’s-razor principle) for lack of response to two antidepressant trials is that the condition being treated is not ‘major-depression’. Declaring it ‘major-depression’ that is ‘treatment-resistant’ after two (or any number of) failed medications trials seems, at best, arrogantly out of touch with the reality of the field’s diagnostic and therapeutic limitations (oh, the irony of psychiatrists operating out-of-touch with reality).
(Sidebar/pet peeves: (1) The typical terminology in the medical literature, especially when discussing TRD, refers to patients as “failing to respond to treatments”, which I find outrageous. Obviously, it is the treatment that fails patients, not the other way around. This common use of language may be innocuous; alternatively, it may be (as I fear it is) an expression of professional arrogance and an inexcusable deflection of professional responsibility in favor of blaming the patient. I hope that, in the foreseeable future, the notion of “patients failing treatment” will become unacceptable and obsolete.
(2) Since there are no objective diagnostic tools for psychiatric disorders, a high rate of diagnostic error, both false-positive and false-negative, is unavoidable. (Calculating the actual rate of misdiagnosis of major-depression is a difficult and uninviting area of research; it is unquestionably high. Estimates of an error rate around 50% seem realistic if not conservative). The fact that a significant percentage of the patients diagnosed with major depression do not suffer from the illness should automatically elicit considerable skepticism about the concept of ‘treatment resistance’. But this is not the case: Psychiatry appears to embrace it enthusiastically, devoting increasing attention and other resources to it, both in research and in clinical practice. I am sure that, to some extent, this is driven by sincere scientific curiosity and genuine concern for patients’ well being. Yet, I am equally convinced that other, less benign, factors — such as professional arrogance, blind followership, and (primarily on the side of the pharmaceutical industry) profit-generation are also in the mix.)
‘Major-Depression’ from a Psychological Perspective
The fact that ‘major-depression’ is a biological disorder does not mean that psychological considerations are irrelevant to it. On the contrary — the relevance of psychological issues is apparent at all stages of the illness, including the conditions leading up to an episode, the duration of an episode, and the duration of time separating recurrent episodes. Moreover, episodes of ‘major-depression’ almost always have psychological consequences.
The reaction to situational (i.e., environmental) factors plays a significant role in many medical disorders, particularly in genetically predisposed individuals. For example, behavioral factors (e.g., dietary habits, the use of tobacco products, and a sedentary life-style) clearly can play a role in the onset and course of medical conditions such as type II diabetes, some cancers, and coronary artery disease.
In the case of ‘major-depression’, situations in which ‘caring’ leads to suffering may represent a psychological environment that can contribute to the precipitation of a depressive episode — in individuals that are biologically predisposed to developing the disease. The same experience (i.e., caring leading to suffering) can be traumatic, even emotionally scarring, but it is unlikely to lead to an episode of bona fide ‘major-depression’ in individuals that are not genetically predisposed for the disease.
Experiences in which one’s ‘caring’ contributes to their suffering are the rule in the human condition, not the exception, because ‘caring’ and ‘suffering’ are connected: The more one cares about some ‘thing’, the more they are likely to suffer as a result of an undesired outcome involving that ‘thing’. Conversely, not-caring offers a degree of immunity from suffering when things go wrong.
[Sidebar: Etymology reveals a connection between ‘caring’ and suffering: The origin of the word ‘passion’ (which, as stated above, is synonymous with ‘caring’) is the Latin word ‘passiō’, which means suffering. The word ‘passion’ can be used interchangeably with the word ‘suffering’, for example — ‘the passion of Christ’ which means ‘the suffering of Christ’.]
Sentient beings instinctively try to avoid experiences that cause pain. The experience of ‘caring’ is not exempt from this rule (even if ‘caring’ is an exclusively human trait): ‘Caring’ may trigger an automatic avoidance reflex if it is perceived as a potential cause of pain and suffering.
According to a well established principle of behavioral-psychology, the frequency of any behavior is likely to increase if it is rewarded. Reduction (or avoidance altogether) of pain and suffering is a powerful reward. It is likely to promote the repetition of a behavior associated with it — such as retraction of caring (even if the association is made subconsciously). With enough repetition, any behavior may become ingrained — a habit. Putting this together — when reducing one’s ‘caring’ is rewarded by (even the perception of) lessening their pain, it is likely to be repeated; with enough repetition, avoidance of ‘caring’ can become habitual, or a second nature.
One can actively invest in avoiding ‘caring’ (or ‘passion’) by devaluing it. ‘Caring’ can be devalued by portraying it as irrelevant, and/or as a weakness. This is the dynamic behind the peculiarly common labeling of ‘caring’ as childish, naive, or a feminine (and therefore, weak) trait, and the similarly peculiar opposite, where ‘not-caring’ is praised and regarded as evidence of “growing-up”, “getting-real”, or “manning-up”.
A repetitious, systematic reduction of the role that ‘passion’ and ‘caring’ are permitted to have in one’s mental process can have grave, if hidden, consequences: Conditioned avoidance of ‘caring’ can amount to the acquisition of anhedonia; it may play a role in the course of ‘major-depression’ in a genetically predisposed individuals, and mimic it in individuals that are not predisposed for the disorder.
Consider the following as an illustration of such a conditioning process: Imagine a college freshman who just learned that she failed the final exam in one of her core courses. Understandably, failing the final exam, particularly in an important class, hurts. She is likely to associate the intensity of her pain with the level of her caring — the more she cares (about the exam, the course, or even about her education in general), the more it hurts. Therefore, she may try to reduce her caring — as a way to reduce her pain. She can do this simply by repeating to herself that she ‘doesn’t care’, or ‘shouldn’t care’, about failing the exam, about the class, and even about her education in general. She may also repeat to herself that she is no longer a child — after all, she’s in college now, and therefore she shouldn’t care as much as she used to when she was a child, in highschool or earlier. This line of thinking is very likely to be encouraged by well-meaning, supportive figures in her life: It’s easy to imagine her being told by caring friends and relatives that she “cares too much” or that (to feel better) she “shouldn’t care so much”.
Failing the exam may trigger ‘grief’ (e.g., over loss of status, confidence, or aspirations) and/or ‘despair’ (e.g., as a result of feeling trapped in self doubt, disappointment, or in failure in general). Her ‘grief’ or ‘despair’ may be considered within the normal boundaries or outside of it, i.e., manifesting psychological pathology. However, if she happens to be genetically predisposed to ‘major-depression’, her perception of normal ‘caring’ as a liability, followed by repeated attempts to extract it from her mental process may be enough to trigger her first acute episode of the disorder.
On Caring
(As I said earlier, it is difficult to overstate the importance of ‘caring’; nonetheless, I’ll give it a shot:) The capacity to care is at the foundations of feeling attracted and repulsed, sustaining interest, focusing attention, and establishing connections which are critical human mental functions. Moreover, caring, or passion, is required in order to pursue happiness effectively.
‘Caring’ is related to pain and suffering — the more one cares, the more they are prone to suffer, and vice versa — withholding caring does offer some protection from suffering. Hence, the notion that by reducing ‘caring’ one reduces their vulnerability is luring. However, examination of this strategy readily reveals its futility: ‘Caring’ is always an asset — even when it hurts. The cost of withholding ‘caring’ is much greater than its potential benefit; it can covertly lead to an erosion of passion about any aspect of life — from peripheral hobbies to the most important, central relationships. Ultimately, a conditioned loss of normal ‘caring’ can result in an acquired state of ‘despair’ (in biologically predisposed individuals it can contribute to the expression of acute and chronic depressive disorders). More generally, loss of passion negates the effective pursuit of happiness.
Acquired loss of ‘passion’ (or ‘caring’) is a serious affliction of modern society and, given that it happens covertly, it is probably much more common than realized. It is likely responsible for a suspected silent-epidemic of low-grade depression (more accurately, ‘despair’) and a contributing factor to a variety of modern day public-health crises (e.g., the epidemics of obesity, substance abuse, and overdose deaths).
The practice of mindfulness can protect the normal capacity to care in various ways, for example, through cultivating tolerance and compassion, as discussed above. Another way in which mindfulness can protect the normal capacity to sustain passion is by highlighting the distinction between caring and ‘matterness’: ‘Caring’ mindfully is founded on the awareness that one’s level of ‘caring’ about something does not reflect how much that thing matters.
It is a simple, but elusive, fact: Your level of ‘caring’ or ‘passion’ about some ‘thing’ is simply not the same as how much that ‘thing’ matters. The automatic, thus mindless, tendency is to conclude that “that which I care about obviously matters”; moreover “the more I care about it, the more it matters”. It simply is not so: Your level of ‘caring’ does not reflect the objective ‘matterness’ of that which you care about; it only reflects how much it matters to you, at that moment.
It is remarkably easy to overlook this basic fact of life. It is normal to care about things that don’t matter, and not to care about things that do.
To illustrate this, let’s revisit our imaginary student: The moment she learned that she failed the exam her level of ‘caring’ about it is acutely exposed — clearly, she cares a lot. However, at that moment it is impossible to say how much failing the exam actually matters — it may turn out to not matter at, only to be forgotten before the end of the next term, or it may matter greatly; it may change the course of her life, possibly for the better or for the worse (using unrestricted imagination, it may even change the course of humanity for better or worse). As a matter of fact, how much it (or anything) matters is, inevitably, a speculation. How much each of us ‘cares’ (about any ‘thing’) is obvious to us at any given moment; a definitive assessment of the ‘matterness’ quality of the same thing is simply outside of the reaches of our consciousness. Hence, they are not the same feature. The effective pursuit of happiness hinges on realization that what you care about does not necessarily matter as much as you care about it.
Losing sight of the distinction, i.e., operating under the misguided assumption that if you ‘care’ about a thing, it must matter, to a degree that mirrors your caring about it, charges ‘caring’ with risk. Conversely, awareness of the distinction between ‘caring’ and ‘matterness’ diffuses the risk of ‘caring’ and makes it safer.
(A detailed discussion of this important topic — the distinction between ‘caring’ and ‘matterness’, is currently pending.)
The Psychological Consequences of Major-Depression
An encounter with a serious and/or disabling medical condition — such as a heart attack, cancer, or ‘major-depression’, usually elicits a significant psychological reaction. Common examples of reactive/psychological symptoms associated with serious health problems include loss of self confidence, a heightened sense of vulnerability/fragility, anxiety, anger, and behavioral avoidance (particularly of situations that, consciously or subconsciously, are regarded as risk factors for the initial illness). It is important to identify reactive symptoms for what they are — a psychological response to a serious medical illness, and, when indicated, treat them accordingly i.e., with psychotherapy.
Obviously, when the medical issue is ‘major-depression’, it is particularly challenging to separate the primary (medical) symptoms from the secondary (psychological) symptoms. Since the reactive/psychological symptoms tend to persist long after the resolution of the primary problem (be it cardiac, a malignancy, or ‘major-depression’) it is easy to misconstrue the reaction to the illness as evidence of a treatment resistant ‘major-depression’.
Since reactive/psychological symptoms do not respond to medical treatment, attempts to treat these symptoms with medications (or other biological modalities) are invariably futile. Frustratingly, the predictable lack of response to medical treatment easily becomes a self-fulfilling fallacy — the persistent (reactive) depressive symptoms may readily be interpreted as evidence that confirm the (wrong) diagnosis of treatment-resistant ‘major-depression’.
Sometimes this triggers a sequence of increasingly aggressive, pointless, treatment trials. These trials are not only ineffective, they often involve significant adverse-effects. In the worst case scenario the distinction between symptoms and side-effects is lost, which can lead to a tragic, unrecognized outcome: Over the years I have seen more than a few patients disabled by what they considered as symptoms of a depressive disorder (most commonly lethargy, over-sleeping, poor concentration, and loss of libido) only to discover, following the discontinuation of treatment, that their “symptoms” were actually side effects of an unnecessary treatment.
The psychological consequences of ‘major-depression’ can also manifest at the patients’ relationships level. ‘Major-depression’ is associated with an increased rate of divorce. This is not surprising given the illness’ core symptoms: It is easy to misinterpret the reduced caring, dispassion, loss of interest, and disconnectedness that manifest the disorder as a relationship commentary. These symptoms are usually confusing to both the patient and their partner and, obviously, have the potential to damage their relationship. Conversely, the realization that the diminished capacity for caring and the various consequences thereof are symptoms of a medical disorder can go a long way toward protecting patients’ relationships. Couples-therapy therefore has a definitive role in the comprehensive treatment of ‘major-depression’.
Additionally, the prevalence of ‘major-depression’ reportedly increases following a divorce. Of course, bona-fide ‘major-depression’ can follow a significant loss. However, in my opinion, most of the patients diagnosed with ‘major-depression’ following a divorce are misdiagnosed. In reality, most suffer from ’grief’. Responding to a significant loss with ‘grief’ is normal (albeit invariably unpleasant); yet, a ‘grief’ reaction can be pathological and may require professional intervention. Statistically, the likelihood that persistent sadness (i.e., depression) following a divorce represents a psychological disorder (most commonly, an adjustment disorder with depressed mood) is much greater than the likelihood of it representing a medical disorder, such as major-depression’.
Mindfulness and ‘Major-Depression’
The mindful approach to major-depression, in principle, is the same as the mindful approach to any serious illness. ‘Major-depression’, however, may present additional challenges — because it is a brain disorder.
Medical problems that impact the brian directly, i.e., all psychiatric and most neurological disorders, carry unique threats, for a couple of reasons: Firstly, because the human brain[glossary] is the “storage place” of the ‘Self’ (in the form of memories, knowledge, aspirations, and values) threats to the integrity of the brain therefore threaten the integrity of the ’self’, a threat unparalleled by the compromise of any other organ.
Secondly, brian disorders threaten the quality of the brain’s ultimate product — the [glossary]choice. This is of the utmost importance not only because the ‘Self’ is defined by the choices its brain generates but, moreover, because the ‘choice’ is the only instrument with which we can influence our environment (the choice is the point of interface between a consciousness and the reality in which it operates). As such, good (high quality) choices support pursuing one’s causes, particularly, the pursuit of happiness, and poor (low-quality) choices undermine it.
In a way, the practice of mindfulness is ultimately in the service of promoting the quality of the practitioner’s choices. The earlier discussions of the mindfulness approach to ‘grief’ and ‘despair’ are also relevant to the maintenance of mindfulness in the face of ‘major-depression’ (as are most of the practices reviewed in the Practice section of this work, particularly the practices of refraining from making matters worse (https://wp.me/P7aKBB-6u), optimize doing the best one can do (https://wp.me/P7aKBB-Ci), and generating high quality choices (https://wp.me/P7aKBB-6h).
It may be especially difficult to practice and maintain mindfulness when facing a condition that impacts the brian’s normal level of functioning, including ‘grief’, ‘despair’ and ‘major-depression’. Managing to do it can be especially rewarding.
Bipolar Depression
I am compelled to address ‘bipolar-depression’ in this section because according to modern psychiatry’s definition, the course of bipolar-illness involves episodes of ‘major-depression’: ‘Major-depression’ episodes are in the context of bipolar-illness are referred to as episodes of ‘bipolar-depression’ (which than spawned the term ‘unipolar-depression’ in reference to “ordinary” ‘major-depression’, in distinction from ‘bipolar-depression’ — making the lame terminology that governs the field even more nebulous). In my opinion the so-called ‘bipolar-depression’ is an inherently different condition from ‘unipolar-depression’ (i.e., ‘major-depression’). Since, as I see it, “bipolar-depression” is not truly a depressive disorder, the following discussion is going to be (relatively) brief.
To my knowledge, the notion that ‘major-depression’ (i.e., ‘unipolar-depression’) is the same condition as ‘bipolar-depression’ has no scientific foundation (in line with the other unproven assumptions mentioned earlier). It is an arcane, arbitrary claim — more of an axiomatic “truth” passed down generations of psychiatrists than a fact supported by research generated evidence. It is based on the similar appearance of some features of both conditions and is akin to considering gastric cancer as the same illness as anorexia nervosa, because both can cause reduced food intake and extreme weight loss.
Bipolar-disorder is a poorly understood (and poorly defined), serious, usually disabling, episodic, lifelong illness. The diagnosis of bipolar illness is riddled with an extremely high rate of error: conservative estimates of the rate of misdiagnosis of bipolar illness are around 40%; both false-positive and false-negative misdiagnoses are very common.
The disorder has a broad, varied clinical presentation; our current diagnosis of bipolar-illness is probably a mixture of known and yet-to-be-identified psychiatric conditions. Attempting to address the broad variety of presentations of the disorder systematically, psychiatry designated a number of bipolar illness subtypes, or variants. These include types 1 and 2 (and 3, according to some), mixed, cyclothymic, schizoaffective, rapidly-cycling, and (an ultra-questionable) ultra-rapidly-cycling variants. The validity of some of these subtypes remains a matter of debate.
A number of psychiatric disorders, recognized as unrelated to ‘bipolar-illness’, can cause symptoms that are similar to the symptoms observed in the course of bipolar illness. Examples of psychiatric disorders that can mimic ‘bipolar-illness’ include some anxiety disorders (especially when compounded by depression {most likely to be ‘despair’} giving the course of the illness a “bipolar” appearance), personality disorders (most notably borderline and narcissistic personality disorders), attention deficit hyperactivity disorder (ADHD) and, of course, ‘major-depression’.
The bottom-line is that our understanding of ‘bipolar -illness’ is rudimentary at best, and is still very much a work in progress.
In my opinion (which to be clear, in case you haven’t noticed, is different from the mainstream psychiatric view) ‘bipolar illness’ is not a mood-disorder. As I see it, the primary brain malfunction caused by the disease is the ability to assess and sustain a realistic sense of self-worth. In other words, I think of bipolar-illness more as a disorder of humility than a disorder of mood. As such, I consider the mood symptoms commonly observed in the course of the illness secondary to pathological instability (with extreme highs and lows) of the patient’s sense of self-worth: The pathologically inflated sense of self-worth induces an extremely elevated mood state, and the opposite — the pathological sense of worthlessness, induces anhedonia and an extremely depressed mood.
As the name implies, ‘bipolar disorder’ (particularly, types I and 2) is hallmarked by two “poles”, or phases: A manic, or “high”, phase and a depressed, or “low” phase. A defining symptom of the ‘manic phase’ is referred to as ‘grandiosity’ (“inflated self-esteem”, in the DSM), which appears like a pathologic loss of normal humility. The association between this grandiosity and other symptoms of mania — most notably elevated mood, or euphoria, and an irrational inclination to engage in high-risk behaviors (“excessive involvement in activities that have a high potential for painful consequences e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments”, per the DSM) makes sense. Why wouldn’t one be euphoric and eager to take high risks if they are convinced that they are special, precious, and invulnerable?
The opposite phase, or “pole”, of the illness is hallmarked by a pathologic sense of worthlessness. The sense of worthlessness is, understandably, saddening (i.e., depressing) and leads to avoidant behaviors and anhedonia, mimicking the symptoms of ‘major-depression’.
The view that ‘bipolar-depression’ and ‘unipolar-depression’ are inherently different conditions is supported by the radically different ways they respond to treatment. Presently, antidepressants are the mainstay treatment for ‘major (unipolar)-depression’. Clearly, many patients with ‘unipolar-depression’ derive significant benefits from antidepressants therapy (the dire need for more effective treatments notwithstanding). In comparison, it is well established that antidepressants are completely ineffective as a treatment for “bipolar-depression”. Worse, it is generally accepted that antidepressants can be harmful to patients with bipolar-illness(!). It is broadly accepted that antidepressants introduce a risk of acutely worsening a bipolar depressive episode (by eliciting manic symptoms in some patients, in what is referred to as a “phase switch”). Moreover, some evidence suggests that significant exposure to antidepressants may worsen the long-term (life-time) course of ‘bipolar-illness’.
I have, like any experienced clinician, seen an occasional patient with ‘bipolar-illness’ benefiting from treatment with antidepressants. In my opinion, these relatively rare cases have two explanations: Either the bipolar-illness diagnosis is wrong and the patient actually suffers from an antidepressant-responsive disorder, or, if the bipolar diagnosis is accurate, the patient suffers from a second, co-existing disorder that is antidepressant responsive, most commonly, a comorbid anxiety disorder.
Be that as it may, the current practice guidelines are to avoid the use of antidepressants in the treatment of patients diagnosed with bipolar-disorder, or minimize their use if avoiding it altogether is not an option.
To reiterate, the controversy is not about the lack of antidepressants’ efficacy as a treatment for ‘bipolar-depression’ — that is broadly accepted. The debate centers on the potential harm the use of antidepressants exposes patients with bipolar illness to. The radically different responses to the same treatment suggests that “bipolar-depression” is not the same condition as “unipolar-depression”. Since in my view it is not a ‘depression’ at all I will not discuss it any further in this section.