Rebranding psychiatry

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A lot of people with conditions that are defined in the DSM (Diagnostic and Statistical Manual of Mental Disorders) disagree with what their condition is called. In this post, I’m going to muse over changing the names of psychiatric disorders.

Manic Depression -> Bipolar Disorder -> Manic Depression

When the DSM-III was published, the DSM committee decided that the term “manic depression” had become overly stigmatized and abused. There was little to no change in the diagnostic features or description of the disorder (which has actually been fairly consistent for a very long time!), the only reason for changing the terminology was political. Many years later, I feel this has resulted in the term “bipolar” being just as stigmatized as “manic depression” ever was — except it’s even more abusable, since “bipolar” can be used as an adjective to describe many things, famously including the weather.

It should’ve been obvious that the stigma of manic depression didn’t originate from the term “manic depression” — and therefore not shocking that the same stigma followed, not the term that was used, but the people who live with the disorder. It was always the people, never the term. On top of that, I feel “manic depression” is more accurate as the term “bipolar disorder” doesn’t portray the common reality of mixed episodes and mixed mood presentation. “Bipolar” seems to imply a state of bistability, where two states representing opposite ends of one dimension (mania and depression) are cleanly and abruptly switched between; bipolar can be like this, but it is often messier.

Attention Deficit/Hyperactivity Disorder -> Executive Dysfunction Developmental Disorder

ADHD is a controversial term for some advocates and it’s understandable why. While attention and hyperactivity/impulsivity are characteristics that are used to diagnose the disorder, they’re downstream of the real difference experienced by people who live with the condition — which is developmental effects on executive functioning. Broadening the term to define it by its root cause would probably feel more accurate of the experience of living with the condition.

Inadvertently, if the diagnostic criteria were changed accordingly to reflect other developmental disorders of executive dysfunction, there may be groups of people who didn’t meet the criteria before who now do. This is something to be interested in, of course. Attention and hyperactivity/impulsivity could still be used as specifiers, and the developmental history aspects would probably still be required so that people with executive dysfunction of non-developmental origin aren’t accidentally included. Additionally, we know that autism is associated with some kinds of executive dysfunction and this change would probably blur the lines between them even more — but in reality, those lines are pretty blurry.

Autism Spectrum Disorder?

There is a lot of controversy over this one, and to be honest I don’t have all of the answers. I think “Asperger’s” was a term of limited utility because many studies could not find clear differences between “Asperger’s” and “High Functioning Autism” even though supposedly the Asperger’s group had no language delay and the HFA group did. Their outcomes, though, were the same. So it was decided that we would collapse autism into one diagnosis that represents a gradient or spectrum of features and levels of impact on the person’s life.

However, I actually agree with some advocates who say that this has proven obtrusive for people with high support needs as the common conception of autism drifts further and further from Rain Main to Sheldon Cooper. There are many people out there who no longer believe autism is a disability. I can’t fully reconcile myself with this stance when we’re talking about a nonverbal adult with an IQ of 40: this person’s life is much, much different than mine, and I genuinely want to help them in the most effective way I can. At this venture, I believe we need a term for people with high support needs. But, the options thus far have been problematic (for example, I do see the reasons why “high functioning” and “low functioning” are much too simplistic to capture meaningful differences).

In the end, the best I can come up with right now is to include Verbal IQ score as a specifier. It’s not perfect (we know IQ means something specific, and can’t be generalized to “intelligence”), but it’s one of the better indicators we reliably have of how disabled this person is, how many barriers they’re going to face to get treated fairly and with respect. And, it doesn’t create a competition where someone is more or less autistic than I am. We’re both autistic; it’s just that one of us has an IQ of 40 and that information isn’t trite. Despite the risks of increasing discrimination, I think we’ve seen with the bipolar fiasco that changing terms merely to avoid stigma (which is attached to people, not to terms) is not a good idea.

What does hyperactivity look like in adults?

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I had always thought I had ADHD inattentive type. However, when I recently asked my psychiatrist (out of curiosity) she chuckled and said that, in her clinical opinion, I have the combined type.

Part of my perception may come from that fact that, due to my mild cerebral palsy, I move at a much slower pace than other people — thereby masking some apparent “hyperactivity”. To complicate matters, I’m currently taking two antipsychotics (Thorazine/chlorpromazine and Zyprexa/olanzapine) both of which can cause side effects that are phenotypically similar to hyperactivity (this is called akathisia). But how much of that is the drug per se, and how much of it is my ADHD (which may, in turn, be worsened by the drug)?

I think there’s a broader misconception at play. We simply do not know how to identify hyperactivity in developmental adults.

The image of a hyperactive child is alive and well in our collective consciousness, but what happens to us when we grow up?

First off, let’s get some facts straight. In adults with ADHD, it’s more common to have symptoms of inattention (about 90% have these kinds of symptoms in a prominent way) while only about half of adults display clinically relevant hyperactivity or impulsivity1. By implication, we can assume that the population of adults with ADHD breaks down something like this: 10% have hyperactive type, 40% have combined type, and 50% have inattentive type. Those numbers may be a little off, but it’s a good place to start.

Yet, even though it is acknowledged that adults have hyperactivity and impulsivity, these symptoms are not well understood in adults — at least, they aren’t characterized as well as they are for children. And the presentation of these symptoms changes over the lifespan. It is thought by researchers that hyperactivity decays as the ADHD child becomes an adult, while inattention persists1.

Here are diagnostic criteria for hyperactivity and impulsivity in ADHD1:

Without a doubt these symptoms intentionally mirror those used for children, with some addendums (instead of running and climbing excessively, we just think about doing it — leading to “subjective feelings of restlessness”). Somehow, some adults with ADHD have internalized our externalizing behaviors. Instead of running from wall to wall like a four-year-old, I just feel this incredible tension in my body created by Not Moving. But it’s all inside my head. You can’t see it unless you look very closely.

I can see myself in this list of symptoms, nonetheless. I fidget, I stim, I stand when I’m supposed to remain seated, I feel restless constantly, I interrupt others when they are speaking, I feel a kind of somatic pain or intense pressure and frustration when I have to wait a long time for something that’s right in front of me.

But there is an element here that we are not capturing.

Inattention and hyperactivity stem from a common dysfunction of the executive systems.

We know from literature in children that hyperactivity/impulsivity and inattention are correlated. But, it’s not so clear what the relationship is, and it really gets at the core deficit we’re trying to get at with an ADHD diagnosis: poor executive functioning and self-regulation. I can’t focus my attention, so I pace around for hours, smoking cigarettes on the patio. I feel like I have to keep moving; I constantly have to be doing something, even if I’m doing nothing. I can’t relax. That isn’t good for a child, and it’s even less so for an adult. My body feels tense and worn, like a pair of old shoes.

It turns out, too, that ADHD in adults is associated with lower socio-economic status, lower levels of academic achievement, problems with relationships, and even poorer driving ability and more traffic violations1.

Not long ago children with ADHD were presupposed to exist in a liminal state: it was thought that ADHD was a disorder of childhood, and that it diminishes with developmental advancement. Yet research (including various brain anatomy, neuroimaging, and genetics studies) is showing that this is not the case1.

Ironically enough, it’s time to turn our attention to adults with ADHD. Although it does make some sense that classic symptoms of hyperactivity decline with age, I am interested in how hyperactivity later manifests in adults who no longer fit the typical, child-centered definition of hyperactivity.

Personally, I think inwardly-turned hyperactivity may be one of the driving forces behind high levels of depression and anxiety seen in adults with ADHD. Around half of adults with ADHD have had one or more major depressive episode, and around half of adults with ADHD have one or more clinical anxiety disorder2.

There’s also a fascinating overlap with bipolar disorder, which may be a blog post for another day!

Are you an adult with ADHD? Have you ever met criteria for hyperactive or combined type ADHD, either now or as a child? Share your experiences!

References

  1. Wilens, T. E., Faraone, S. V., & Biederman, J. (2004). Attention-Deficit/Hyperactivity Disorder in Adults. JAMA, 292(5). https://doi.org/10.7326/acpjc-2016-165-2-010
  2. Sobanski, E. (2006). Psychiatric comorbidity in adults with attention-deficit/hyperactivity disorder (ADHD). European Archives of Psychiatry and Clinical Neuroscience, 256(SUPPL. 1), i26–i31. https://doi.org/10.1007/s00406-006-1004-4

After a suicide attempt

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Caution: this post contains explicit discussion of suicide

Two days ago (on September 10th) was World Suicide Prevention Day. Although it is important to address prevention of suicide attempts, the strongest predictor of a fatal (or “completed”) suicide is a history of previous, non-fatal suicide attempts. The risk factors for suicide attempts are more diverse and include: family history of suicide, early onset of bipolar disorder, extent of depressive symptoms, increasing severity of affective [mood] episodes, the presence of mixed affective [mood] states, rapid cycling, comorbid Axis I disorders, and abuse of alcohol or drugs1

Most suicide prevention effort focuses on people who are naive to psychiatric treatment and have reached a crisis point: people who don’t already have a psychiatric point of contact, and usually people who have never been treated in an inpatient setting before. In my experience, most people do not continue using crisis lines or similar services after they have been hospitalized once. Surmounting the fear and stigma around hospitalization itself is a primary reason crisis lines exist. Crisis lines are staffed by severely underqualified volunteers, who are usually following a script, and only have two action moves: call an ambulance, or tell you to go talk to someone else (sometimes your health insurance company). Yet, people find calling a crisis hotline less formidable than simply admitting themselves voluntarily.

But what about those of us with chronic illnesses, with volumes of psychiatric history, who have been admitted many times? This service is clearly not meant for me. If I spoke to a crisis line on what to me is an an average day, I might find myself being dragged to the ER and with an $800 ambulance fee to boot. There is no exception for chronicity. The stakes of a mistake are high, and the crisis line operator is equipped with a high school diploma.

There’s a gap between services for first-episode patients and services for profoundly disabled people who live in an institutional setting. After my close-to-fatal suicide attempt about two and a half years ago, I had to navigate what exactly life looks like after a serious suicide attempt. I consumed an amount of lithium equal to the 50% lethal dose in rats, and an antidepressant that is also a potent anti-emetic (anti-vomiting) drug. I knew I would absorb more of the lithium if I delayed the onset of (inevitable) severe vomiting.

I was hospitalized for only 16 days. The attending physician treating me thought I should go to a residential treatment program, but I was supposed to be at an academic conference and I begged to be realized in time to go. The head of the clinic evaluated the situation and decided to release me. I was discharged within hours of my flight to Europe. After the conference, I was enrolled in a partial hospitalization day program. The official length of the program was 8 weeks; I was probably enrolled for 4 months. My psychiatrist met with me nearly every day.

We tried a lot of medications, but for quite some time I was not permitted to take lithium. This was unfortunate, because lithium is probably the single most effective drug I take. I have cycled through almost every atypical antipsychotic: Seroquel, Abilify, Vraylar, Zyprexa, Saphris, Geodon… I’m sure I’ve forgotten something, it’s more than I can keep track of. I tried Depakote and Lamictal. Nothing has the same effect as lithium. Ironically, lithium also has a specific anti-suicide effect.

I continued to be suicidal throughout and beyond the partial program. I am lucky that my psychiatrist works well with me.

Chronic suicidality is probably more common than people realize. It doesn’t appear in the media. It’s taboo. You fear to acknowledge it exists somewhere. When we talk about improving mental health services, let’s give a little more attention to the people for whom posting a status update with the s-word in it is reason to panic and report it to Facebook headquarters.

References

  1. Hawton, K., Sutton, L., Haw, C., Sinclair, J., & Harriss, L. (2005). Suicide and Attempted Suicide in Bipolar Disorder: A Systematic Review of Risk Factors. The Journal of Clinical Psychiatry, 66(6), 693–704. https://doi.org/10.4088/JCP.v66n0604

Bipolar disorder and media consumption

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Recently, on Twitter, I confessed that I had not been able to complete reading NeuroTribes (a very interesting book, and also a lengthy one). The other person insisted that a PhD student should be able to read a book and accused me of lacking academic integrity — basically, that I am lazy and don’t deserve my PhD.

I’m here to say that attitude is inherently ableist. But to give the benefit of the doubt, perhaps most people don’t know that bipolar disorder actually can affect your ability to read. I learned to read early as a child — I was a prolific consumer of text, and I had a college reading level in elementary school (this is called hyperlexia). But after being medicated for bipolar disorder, my ability to sustain focus and momentum while reading a long document has been very limited.

Lithium is probably the biggest offender. It kind of affects how you see words on the page — like a pseudo-dyslexia, the words seem kind of blurry and distorted. It can be impossible to read full books. I can still read journal articles because they generally have a defined structure and an abstract. I can also read poetry, which I enjoy. I recommend seeking out these kinds of texts if reading is something you struggle with.

Most of all, I want you to know that this is common, you are not alone in having an acquired inability to read and you still deserve your career, whatever that may be. It’s not a matter of “intellectual thoroughness”; it’s part of a disability, and it’s more common than you think.

I also find it difficult to watch videos, TV, or movies. The information conveyed through video media covers many modalities — sound (music), speech, visuals, movement (spatial), and the overall plot you’re supposed to be following. Sitting for the length of a movie is hard, but it’s also just hard to follow so many things at once. My brain gets overwhelmed with too much information of different kinds to process (evidence of poor sensory integration, a symptom of autism). But it helps to reduce the overload by using captions (combining speech with visuals, thus reducing the number of information modalities) or watching something animated, which compresses the demands of visual and spatial information greatly.

Have you ever had trouble consuming media?

What strategies have you used?

Psychiatric disorders and discrimination by medical professionals

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There is much that could be written about the damage done by bad psychiatrists, but this post will specifically focus on non-psychiatric medical professionals: doctors, nurses, everyone involved with it.

Once I presented to the ER with a large abscess from a skin infection, and in great pain. I told the triage nurse that I had this abscess, and showed it to her (it was not subtle). She proceeded to look through my chart and started asking me about my bipolar disorder. I told her what she asked, and of course we got to “Are you planning to hurt yourself?” and I said no, because I wasn’t, I just really needed my abscess to be drained by a doctor.

Naturally, then, she put me in psychiatry and had a psychiatrist come speak to me. I told the psychiatrist what I told the nurse and showed him the abscess. He was horrified by it, and said he’d call my psychiatrist. After he spoke to her, he moved me to the medical area and gave his psychiatric stamp of approval. Finally, a medical doctor arrived and drained my abscess.

In retrospect, is it a big problem? I think it is. What if my condition were even more time-sensitive? They wasted significant time getting me a psych eval when I was not presenting with any major psychiatric symptoms, I just happen to have a chronic mental illness that I will have in my chart forever. What if I was having a heart attack? Would I have to get a psych eval because I’m bipolar?

If you have a label like “bipolar disorder type 1” they will always look for a psychiatric cause for your symptoms, even when the evidence doesn’t suggest it’s psychiatric (like, the huge abscess). They assume you are professionally crazy and anything you say is cause for suspicion, instead of an honest report of symptoms. Putting patients presenting with tangible physical illness in the psych area just because they have a diagnosis, but are not presenting with symptoms, is discrimination.

Anxiety and mania

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Recently, The Mighty published an article about the differences between anxiety and hypomania. However, I wanted to complicate the discussion by bringing up something that breaks the juxtaposition of anxiety and mania: primarily anxious mania, which is most likely a mixed episode associated with bipolar type 1.

The author describes how her anxiety leaves her “immobilized”. This can actually happen in mania, too — but usually not in hypomania. Hypomania is often very productive. Full mania is no longer productive — it’s frantic, potentially confused, and may be characterized by manic stupor. Emil Kraepelin used this term to describe a flight of ideas and elevated mood (not necessarily happy, but revved-up) combined with psychomotor slowness or immobility. I’ve been in this state, and I experienced it subjectively as intense feelings of anxiety paralyzing my every move. This might also be referred to nowadays as catatonia, and something similar can occur in severe depressive states; however, the catatonia that coincides with mania is likely excited catatonia (characterized by purposeless movements rather than being completely still).

Hypomania isn’t rare, exotic, or exciting to me. It’s just part of my life, and I take advantage of it when it comes around — which it will, no matter what. But, to me, full mania is to be avoided. Anxiety is also a daily part of my life, but the anxiety and paranoia I experience during a manic episode is even more excruciating than it usually is. Juxtaposing them as discrete, separate states can only take you so far in understanding what mania is and how it affects people.

One bipolar person’s drug regimen

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Currently, I take 8 medications for psychiatric reasons. I’ve also been on many others — including most of the atypical antipsychotics, several anticonvulsants, antidepressants, and more. These are my current drugs ranked in terms of how essential they are (if, for example, I could only get some of them, perhaps due to a catastrophe):

  1. Lithium — Big Pharma has yet to come up with something better. It could never be patented, it wasn’t paid for by anybody. It actually works. And it’s all-natural. But also, it sucks. Nature is brutal.
  2. Haldol — Indispensable, though I might be switching to Thorazine in the near future. I don’t picture myself living without an antipsychotic again. Typicals seem to work better for me than atypicals did, though I’ve notably NOT tried Risperdal (even though it’s a good fit for my symptoms) or clozapine. Both were considered, though.
  3. Ativan (lorazepam) — My symptoms tend to cluster around anxiety, insomnia, and irritability — maybe paranoia — all things helped by benzodiazepines. If it were not so problematic, I might have ranked it #2. It’s the best immediate symptom relief I can get aside from maybe sublingual Zyprexa (olanzapine).
  4. Adderall — I would never actually achieve anything in life without Adderall. That said, my need to do something with my life is inherently superseded by my need to be alive, which is why it ranks #4.
  5. Lamotrigine (Lamictal) — An anticonvulsant medication. It seems to be doing something, because I become depressed without it. Though I’m not exactly sure what it’s doing.
  6. Gabapentin — I’m supposed to be using it for anxiety to offset my lorazepam use. It’s also useful for severe headaches. I still feel the pain, but I kind of don’t care, like the pain just doesn’t command my attention.
  7. Clonidine — It’s a blood pressure med, but I’m using it for insomnia. I cycle through medications for insomnia because they all lose their effectiveness eventually. I haven’t been on clonidine before so I don’t know how long it will be useful for. Other drugs I’ve used for sleep: Trazodone, Remeron, Ativan, Seroquel (and other atypical antipsychotics)…
  8. Diphenhydramine (Benadryl) — An OTC drug! The original antihistamine. I take it as 50mg softgels (two of them, which is slightly more than the bottle indicates — consult your doctor). Sometimes works for sleep, not super reliable and fades quickly. Useful if I have a cold or flu because Sudafed is not the best choice for my wiring. Also potentially protective against Haldol-induced side effects. So overall, something I take regularly, but not every day.

Anyone want to share their regimen?

Theories about stimming

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Whatever you want to call them — stims, repetitive behaviors, stereotypies — the terms are more-or-less interchangeable, but it remains that they are of importance in how we think about autism. The repetitive behavior/restricted interests domain is essential to an autism diagnosis. Autistic people, when asked, mostly seem to believe this is an important part of autism. Strangely, very few people have undertaken empirical research to validate (or challenge) common ideas about the nature of stimming.

For those who don’t know: what is stimming? There’s actually some variation in what people consider stims, but I think most people would agree that it includes rhythmic, repetitive movements of the body such as rocking, hand flapping, and pacing. Many people include vocalizations such as grunting or whistling. Based on the conventional description of some autistic children having a fascination with parts of objects (like the wheels on a toy car), I feel manipulation of items such as fidget toys and spinners should be counted as well.

Wheee!

Of course, then we’re get into restricted interests territory. Restricted interests and repetitive behaviors are counted in the same “domain” in the DSM, along with sensory atypicalities. In my view, they blend into each other, forming a continuum — but more on that later.

If you asked me, I’d say there’s a lot we don’t know about this topic. A lot of people have beliefs, for sure, but there’s little to no real evidence. At least, not the kind of evidence you can cite.

Most of the knowledge that’s out there comes from the beliefs of autistic community members. Dr. Steven Kapp (who is, coincidentally, a friend) did a qualitative analysis of 31 autistic people’s opinions on stimming.1 Nobody said they disliked their stimming; most people said they found it calming. The study thusly found that stimming most likely serves a regulatory function, and identified three factors that autistic people said caused their stimming behavior: overwhelming environment/sensory overload, noisy thoughts, and uncontainable emotion.

It’s interesting to me that nobody in this study mentioned under-stimulation of sensory input.1 They seemed more to believe that stimulation in excess of a certain individual or situational threshold was the primary cause, and in this case the “stimulation” could be an internal stimuli (a thought or an emotion).

It’s such a simple theory that it seems baffling that nobody has really tested it. Why is that important? Well… sometimes, as humans, things aren’t what we expect them to be. I know a lot of people will react negatively to that sentiment, but I’m autistic too, so it really is an everyone thing. A lot of psychology (ex, cognitive psychology) is actually not self-evident, and may be counter-intuitive. For example, people are not particularly good at judging how they best learn. People overestimate the benefit of massed rehearsal (cramming for an exam) because they feel like it helps them remember more than spaced rehearsal (studying every night), even after seeing evidence that spaced rehearsal results in better task performance.2

Don’t get me wrong, metacognitive insight is valuable — it’s my own greatest weapon! — but it helps to have evidence to back it up. (Likewise, it helps to have qualitative information to back up empirical results.) So why don’t we have studies about this?

Massed practice is inferior to spaced practice, even though you think it’s not.

One study that has been done (although, again, not an empirical study) used Bayesian statistical principles to think about the mechanisms of cognition in autism.3 They concluded that autism features atypical accuracy of predictions — or, more precisely, that they did not use as much prior knowledge in their perception, leading to potentially more accurate perceptions of the world. However, this makes ambiguity and uncertainty very difficult to deal with. The authors use this framework to understand stimming as a means of reducing the uncertainty in the environment, and thereby reducing the sense of alarm or sensory overload experienced by that person.

As I mentioned, repetitive behaviors blend together with restricted interests. Something I’ve become interested in is the role of perseverative or repetitive thoughts and its relation to the role of repetitive behaviors. I explored this idea a little bit in my first paper,4 but I have yet to truly investigate my thoughts on the matter as much as I would like. Here’s my underlying theory: autistic children, as children, have both repetitive behaviors and repetitive thoughts. Normally, these two processes inhibit each other. This seems to corroborate well with the accounts of “noisy thoughts” being a precursor for stimming behaviors to control them.1 However, when children with normative verbal ability become older, they stop doing repetitive behaviors — leading to increased repetitive thoughts, which my study found could be a risk factor for developing depression.4 This might explain, at least in part, why rates of depression are highest in autistic adults with more normative verbal ability. And it lines up quite well with what the autistic people in Kapp’s study said: they identified others’ tolerance of their stims as a matter of acceptance vs. devaluation.1

Do you have any theories?

References

  1. Kapp, S. K., Steward, R., Crane, L., Elliott, D., Elphick, C., Pellicano, E., & Russell, G. (2019). ‘People should be allowed to do what they like’: Autistic adults’ views and experiences of stimming. Autism, 23(7), 1782–1792. https://doi.org/10.1177/1362361319829628
  2. Logan, J. M., Castel, A. D., Haber, S., & Viehman, E. J. (2012). Metacognition and the spacing effect: The role of repetition, feedback, and instruction on judgments of learning for massed and spaced rehearsal. Metacognition and Learning, 7(3), 175–195. https://doi.org/10.1007/s11409-012-9090-3
  3. Pellicano, E., & Burr, D. (2012). When the world becomes “too real”: A Bayesian explanation of autistic perception. Trends in Cognitive Sciences, 16(10), 504–510. https://doi.org/10.1016/j.tics.2012.08.009
  4. Keenan, E. G., Gotham, K., & Lerner, M. D. (2017). Hooked on a feeling: Repetitive cognition and internalizing symptomatology in relation to autism spectrum symptomatology. Autism, 2012, 136236131770960. https://doi.org/10.1177/1362361317709603

I’m lucky to have my bipolar disorder

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There are times that I’ve felt cursed by having ultra-rapid-cycling, somewhat-atypically-presenting bipolar 1 disorder. My mood episodes are short (sometimes as short as one day, although usually lasting a few days to a week) and they can be very intense. I also suffer from mixed episodes, which are agonizingly painful to experience, and at times I have had profound suicidality that has led to multiple suicide attempts — one of which left me in a coma for three days and nearly claimed my life. Doctors said I wasn’t going to make it. But I did.

During the worst of times I’ve wished to have “classic” bipolar disorder instead of my bipolar disorder. In truth, “classic” features may be relatively rare; but it conjures the idea of long, bleak depressions punctuated by shorter, but still somewhat long, grandiose and euphoric manias. Separate and distinct periods of each, usually lasting for months at a time, with bouts of clean euthymia (wellness) in between.

I haven’t really experienced prolonged euthymia, instead merely catching glimpses of it over the course of my continuous ups and downs. My manias are “dirty” and dysphoric, tainted with depressive themes. My hypomanias are very productive; but if my mood spikes too high, my thoughts become dark and gruesome. If I were to jump off a building, it would be to kill myself, not because I believed I could fly.

And I’m also a researcher. Without a doubt, my research in the area of bipolar disorder draws upon my insights as a bipolar person. If I had “classic” bipolar disorder, the research I have done (some of it relying theoretically upon data collection of my own personal changes in mood) would not have been possible. Because I’m an ultra-rapid-cycler, I was able to capture long-term patterns that might take many years to become evident in “classic” bipolar disorder. I believe the same patterns exist in both, but when moods last for months at a time, it is harder to see those patterns.

My ability to detect patterns has served me well in life (including in my professional career) and to some extent, my bipolar disorder trained me to do it. Predicting my own mood was not only possible, thanks to the accelerated timeframe, but essential to my ability to cope with them. Part of the devastation of mixed episodes came with the loss of my ability to predict with reasonable accuracy when moods would peak or change and in what direction. Even so, I learned new patterns and slowly became able to tell what a “mixed episode” felt like, and whether I was experiencing one. This was not something I could do at first.

Insight into the emotions, cognitions, and memory issues that come along with my bipolar disorder developed over time, starting at an early age (as I first developed symptoms around the age of 10). In turn, this level of insight has allowed me to hypothesize connections no other researcher has yet seen. I understand firsthand how bipolar disorder intersects with changes in thinking and memory.

I have the opportunity to discern cause and effect in relation to changes in my mood much more easily than someone with “classic” bipolar disorder, thanks to the immediacy of any reactions. Upon hearing from my psychiatrist that nitrates in beef jerky were causally linked to mania, I took note of my own reactions. I had known for quite some time that beef jerky had a stimulant-like effect on me, but I was surprised to learn it did not have this effect on everyone. (Too bad!) I experience this stimulant-like effect almost instantly, while I’m still eating. The temporal proximity of the cause and the effect makes them easier to distinguish.

My bipolar disorder is a blessing and a curse. I have struggled immensely to control it, but I wouldn’t trade it for “classic” bipolar disorder or no bipolar disorder at all. The knowledge and abilities I have gained as a result of my battle with bipolar disorder — my bipolar disorder, not someone else’s — have actually, truly been indispensable to my life and my career. Plus, that excessively productive hypomania is pretty good too.