The Bipolar Spectrum: 

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Subthreshold, Atypical, Midway Between…

Overview of the Bipolar Spectrum Concept

The bipolar spectrum encompasses a range of mood disorders that go beyond the traditional categories of bipolar and cyclothymic disorders, including milder and atypical presentations. This concept recognizes that individuals may exhibit varying shades and forms of mood disturbance that do not fit neatly into conventional diagnostic criteria. Understanding the bipolar spectrum is crucial for properly targeted treatment that addresses the unique cluster of symptoms within this spectrum.

For example, consider a person who experiences regularly cyclic episodes of severe depression lasting more than two weeks without any true manic or hypomanic episodes. This individual will not meet the criteria for Bipolar I, Bipolar II or Cyclothymia.  He will by default be diagnosed with Major Depression and “evidence-based” treatment algorithms will dictate he can be treated with antidepressants alone. He will be eligible to be among the subjects for a research protocol investigating a new antidepressant. The simplest way this view could be shown in error is as follows.

A bipolar diagnosis requires that there have been at least one manic or hypomanic episode, either previously or currently. Suppose we were able to look into the future of this individual and we see that twenty years from now he will have a manic episode. We would then know that the “correct” diagnosis is not Major Depression but Bipolar Disorder. Suppose however that in viewing his future he suffers an accidental death fifteen years from now but still would have had that manic episode had he lived. We would then persist in misdiagnosing him as not having Bipolar Disorder. This illustrates a fundamental flaw in the temporal component of how bipolar conditions are diagnosed. Since antidepressants alone frequently do not work properly to treat bipolar depression, evidence-based treatment of this patient is likely to fail. His presence (and that of many others like him) in research trials of antidepressants will negatively skew the results.

The other way the current diagnostic criteria for bipolar fail is a matter of degree. If someone has very mild and brief episodes of feeling cheerful or irritable that do not meet the criteria for even cyclothymia, his mild bipolar-ish characteristics will be overlooked. In other words, the sharp boundaries between psychiatric conditions seem rather artifactual. Indeed, they are an artifact, deliberately voted upon in the formative years of the psychiatric Diagnostic and Statistical Manual (DSM). It was felt at the time by the designers of the DSM that lacking sharp boundaries psychiatric diagnosis would be too confusing for the public and that it would depart from the categorical diagnostic structure of the rest of medicine.

In our hypothetical example, we might do better by expanding the way bipolar is defined. Arguably, “bipolarity” should be considered a human trait which turns into a diagnosis, and warrants treatment, only when it is sufficiently severe. It’s chief characteristic, implicit already in its name, is simply “Mood variability.” By acknowledging the diverse manifestations of mood disorders within the spectrum of “bipolarity”, professionals can better identify and support individuals who may benefit from targeted interventions. In our example, a psychopharmacologist viewing mood disorders through the lens of the spectrum concept will anticipate the likelihood that pure antidepressant is unlikely to be effective, regardless of current protocols.

Evolution of the Bipolar Spectrum Concept

The evolution of the bipolar spectrum concept has been influenced by historical shifts in diagnostic criteria and classification systems. Over time, researchers and clinicians have refined their understanding of mood disorders, leading to a broader recognition of the varying symptom patterns and severity levels that constitute the bipolar spectrum. Key research findings and clinical observations have played a significant role in shaping the concept of the bipolar spectrum and highlighting the need for a more nuanced approach to diagnosing and treating mood disorders.

One example of this evolution is the recognition of subthreshold presentations within the bipolar spectrum. Individuals who do not meet the full criteria for bipolar disorder but exhibit symptoms indicative of mood dysregulation may still benefit from interventions tailored to their specific needs. By embracing a more inclusive view of mood disorders, the concept of the bipolar spectrum continues to evolve, paving the way for improved identification and management of these complex conditions.

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Distinguishing Features of Bipolar Spectrum Conditions

There is a set of distinct symptoms and responses that should be thought of as “soft signs” or markers of an underlying bipolar spectrum condition when an individual does not meet the criteria for a full bipolar diagnosis. Some or all may be present; the more there are, the more likely a significant degree of bipolarity and the more likely that good treatment response will not be found simply with antidepressants. These include:

  1. Mood variability
    1. Episodes may last anywhere from many within a single day to swings that are months in length
    2. Episodes may be anywhere from highly regular (literally “cyclic”) to irregular and apparently random in duration, severity and/or frequency
  2. Correlation to biological cycles, sometimes very tightly, but often loosely
    1. Menstrual (Premenstrual Dysphoric Disorder)
    2. Seasonal (Seasonal Affective Disorder: winter depression, less frequently summer depression, transitional depression—that is briefly in the spring or fall)
    3. Pregnancy/Delivery
  3. Medication Response/Reaction
    1. Often do well on mild mood stabilizers, e.g., lamotrigine (which has antidepressant properties)
    2. May be among that subset of people diagnosed only with Major Depression who respond adequately to an antidepressant only if it is augmented by a “booster”—and these boosters all happen to be mood stabilizers used to treat bipolar disorder. The one exception is Wellbutrin (bupropion) which is treated as a “booster” but is actually an antidepressant targeting a different combination of neurotransmitter systems. Indeed, it makes more sense to think of these individuals as having not “pure” unipolar depression but rather some degree of admixture of unipolar and bipolar features and that is why low-dose so-called “boosters”  work: They are treating the smaller bipolar component.
    3. Bipolar type reactions to antidepressants, either:
      1. paradoxical (e.g., worsened depression, suicidal thoughts and impulses), or 
      2. hyperactivating (e.g., hyperthymia, hypomania, mania, agitated dysphoria).
    4. Tachyphylaxis—i.e., antidepressant “poop out,” often serially with sequential antidepressants. The tachyphylaxis may set in slowly after many years of success, albeit with gradually increasing doses, or it may be relatively rapid, with any one antidepressant providing no more than a few months of remission.
  4. Creativity and Intelligence
    1. Unusual ability and interest in creative pursuits weighted by domain, roughly: poetry, literary writing, music, mathematics
    2. Three or more advanced degrees
    3. Three or more languages
    4. Strong analogic abilities
    5. Mental speed (which is largely captured by “G,” that which IQ tests measure)
  5. Overlapping (“comorbid”) conditions
    1. ADHD
    2. Anxiety, especially OCD
    3. ASD (Autism Spectrum Disorder)

With respect to “boosters” (Point 3.b. above) it makes more sense to think of responding individuals as having not “pure” unipolar depression but rather some admixture of unipolar and bipolar features, and that is why low-dose so-called “boosters” work: They are treating the smaller bipolar component. The terms “booster” or “augmentation” contain no explanatory principle—they merely label an observed phenomenon. The bipolar spectrum perspective provides a rationale for this and the other phenomena listed above. The fact that these tend to cluster together reinforces the perspective that they are part of a single underlying condition.

Note that the very fact of boosters, FDA approved for that purpose, introduces a distortion in the development and testing of antidepressants. Suppose a new antidepressant has a 30% success rate (however defined). This rate will have been determined in trials with subjects who meet the criteria for depression, do not meet the criteria for bipolar, and who are on no other antidepressants. Some 70% therefore will not respond. However, some significant fraction of those non-responders will respond to that same antidepressant in combination with a mood stabilizer and not to a mood stabilizer alone, either. If one understands these responders as not having simple unipolar depression—their qualifying diagnosis—but rather bipolar spectrum, and if they were therefore excluded from the trials, the success rate of the antidepressant would have been much higher. In other words, the concept of bipolar spectrum provides a way of explaining why some proportion of people do not respond.

There is another important implication. Since the first antidepressant discovered in the early 1950s, the baseline success rate of antidepressants in formal trials has scarcely budged, hovering at around 50%, 30% if side effects are considered. What has mostly improved is the reduction of side effects. This is a striking lack of progress. At least part of the problem may lie in what we are discussing—the inclusion of too many people whose actual condition more or less insures they will not respond.

Gene Networks

The first psychiatric diagnosis to have its sharp, artifactual, boundaries broken down was Autism which is now known as Autism Spectrum Disorder (AUD). After many years of observation, it became evident that autism appears in many different forms and in continuous gradations of severity. There remains in the current diagnosis of AUD a residue of simple categorization in the idea that there is sharp delineation between having any degree or type of autism and not having it at all. This remaining boundary is arbitrary and almost certainly does not exist in nature. Nonetheless, the change to the diagnosis of ASD is much closer to a description of reality. All that remains is to understand that the severity of autistic traits among people blends seamlessly into characteristics so mild that we consider them “normal” and give such traits no special name. 

The next condition that will break out of its artificially categorical structure will almost undoubtedly be Bipolar Disorder. However, the reality is that almost all diagnoses in psychiatry are spectra. The reason for this is straightforward: We already know that most all psychiatric conditions have a heavily genetic underpinning, and that this underpinning consists not of a single or a few genes—that in black and white fashion are either inherited or aren’t—but of interactive gene networks consisting of many hundreds of genes with normal or disorder-inducing variants. It is statistically impossible for anyone (ever) to have either all of the gene variants that produce a disorder or none of them. Everyone has a unique combination of some; some people have more and some have less. Furthermore, the networks for any two allied conditions such as unipolar depression and bipolar depression share both many genes and many symptoms. This inevitably creates a spectrum not just from normality to the condition in gradations of severity but between the two conditions in a spectrum of proportions.

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The major common distinguishing features of conditions on the bipolar spectrum is the variable nature of mood disturbance, encompassing episodes of any or all of depression, mania, hypomania, irritability, dysphoria, elation, grandiosity which may be subtle. While sharply delineated bipolar and cyclothymic disorders have more narrowly-defined diagnostic criteria, the bipolar spectrum acknowledges the continuity of mood symptoms along a spectrum of severity. Individuals within the bipolar spectrum may exhibit overlapping symptoms with traditional unipolar, bipolar and cyclothymic disorders but may not neatly fit into one specific category.

For instance, consider a patient who experiences recurrent episodes of depression interspersed with periods of normality (“euthymia”). This fluctuating pattern of mood disturbance falls within the realm of the bipolar spectrum, highlighting the complexity and variability of mood disorders beyond traditional diagnostic boundaries. By recognizing the continuum model of mood disorders, clinicians can better appreciate the diverse ways in which individuals may manifest symptoms and are more likely to identify effective treatment.

Clinical Implications of Episodic Recurrence of Depression

The recurrence of depression within the bipolar spectrum has significant clinical implications for treatment planning and management. Individuals who experience episodic in contrast to persistent depression respond best to interventions tailored to address the specific challenges associated with their unique symptom pattern. The frequency, intensity and duration of depressive episodes all play a crucial role in determining the positioning of individuals within the bipolar spectrum and in the selection of appropriate therapeutic approaches and pharmacologic interventions. For example, while antidepressants alone are often ineffective or problematic for such individuals; and while lamotrigine has rarely shown adequate effectiveness in the treatment of narrowly-defined bipolar conditions; clinical experience shows that lamotrigine is very frequently effective in bipolar spectrum depression.

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Overdiagnosis and Vagueness in the Bipolar Spectrum Concept

To mitigate the risk of overdiagnosis, and clarify diagnostic boundaries within the bipolar spectrum, strategies focusing on thorough evaluation, and such diagnostic precision as is possible, are essential, looking at details and characteristics that fall outside of standard, symptom-based diagnostic criteria. These include all of the soft signs listed above. By addressing concerns about overdiagnosis and vagueness, clinicians can improve treatment accuracy and provide targeted care for individuals within the bipolar spectrum. The challenge of being more precise lies in the very nature of spectrums—in reality they lack precise boundaries. It was this inherent “fuzziness” that led diagnosticians in the 1950s to impose a set of boundaries not found in nature, hoping to create less confusion. Arguably, doing so has actually created more confusion.

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