Why is Netflix jumping aboard the stigma train?

Netflix Take Your Pills

Sigh.  This again?  I’ve written before about documentaries that portray psychiatric medications in a problematic way that tends to promote stigma (A Prescription For Murder and Stigma and the Pathologization of Normal).  Now Netflix has come out with Take Your Pills, which looks at the use of stimulant drugs like Adderall and Ritalin for mental performance enhancement.

I started watching this documentary and gave up in disgust.  But after I read a critique by Mental Health: Let’s Stamp Out the Stigma, I decided it was important to speak up about it, and to do that I thought it was important to give it another go and watch the whole thing.  While a somewhat more balance perspective was conveyed when I watched the film in its entirety, I was still left with a lot of concerns.

The documentary describes psychostimulants as a tool for cognitive enhancement, enabling people to get an academic or career edge, get higher grades, perform in a way they perceive as ideal (particularly in the tech and finance sectors), do more detail-oriented work, and control weight.  Medications like Adderall are described as enabling people to “get to perfect” or be “jolted back to life”.  One psychologist says that these medications prime people to to expect that a pill will give them what they want.  A researcher who was interviewed jumped on the bandwagon, saying he’d tried Ritalin once and it felt like “such an enhancement of my day; it was a good experience”, something it strikes me as irresponsible to say when being interviewed as an expert on the topic.

A university student said that her parents told her she should get a lockbox for her stimulant medication.  “It’s RX gold” she said, adding “I don’t think I know anyone who’s prescribed it who doesn’t sell a little on the side”, and “everybody takes Adderall.”  One male interviewed said that as a millennial who went to a great college and worked in finance, “it’s impossible to avoid stimulants”, and loopholes would be found and taken advantage of in order to obtain them.

Taking stimulants to be more productive was documented as early as the “pep pills” of the 1930’s.  ADHD was described as something that developed out of the marketing of stimulant medications as a way to improve children’s behaviour and grades.  The documentary explains that more children are diagnosed with ADHD in the United States than in any other country in the world, and the majority of them are medicated.  The implication was that ADHD was a mostly artificial condition created by drug companies’ marketing campaigns.  This is certainly not the first time I’ve seen this logical fallacy; misleading advertising does not invalidate the medical condition just because they falsely suggest that everyone suffers from it.

Serious side effects such as addiction are mentioned but the film doesn’t do a good job of contextualizing this as an individual risk vs benefit decision.  A political theorist interviewed suggested that stimulants blunt the human experience and creativity (I’ll just say that a PhD in one field does not qualify someone to speak as a subject expert on an unrelated field).  One student believed her stimulant medication made her more boring and angrier.  These examples provide a very limited context by which to judge the appropriateness of these medications.

A psychotherapist featured in the film said that “just like opiate painkillers are heroin in a pill, ADHD medicine is a very small dose of meth in a pill.”  A psychologist suggested that as a society we make a false distinction between licit amphetamines and illicit methamphetamine, and pointed out the chemical similarity of prescription amphetamines and illicit methamphetamine (which has an added methyl group consisting of 1 carbon and 3 hydrogen atoms).  To me this was an astonishing display of ignorance from someone whose doctorate in psychology doesn’t necessarily necessarily confer expertise in medicinal chemistry.  You know what also differs by a single methyl group?  The ethanol that you find at a liquor store and the poisonous methanol that’s in the antifreeze and can kill desperate alcoholics looking for a fix, including a former patient of mine.  Never mind a full 4-atom methyl group, think of what happens when you throw a few subatomic neutrons on an atom and create a radioactive isotope.  One need only look so far as Wikipedia, which points out that, “unlike amphetamine,  methamphetamine is directly neurotoxic to dopamine neurons in both lab animals and humans”; this statement is backed by 3 references from scientific journals.

I cheered a little inside my head when one student who was interviewed expressed concerns about people saying things like “everyone has a little ADHD”, as this delegitimizes the actual illness.  Another student with ADHD had chosen to go off of Adderall, even though his mother believed he likely wouldn’t have made it through high school without it.  It appeared from the documentary that those with a genuine medical need were actually the most reluctant to take medications.

In a study of college students without ADHD, using Adderall didn’t lead to objective improvements in cognitive performance, but participants did report a subjective sense of performance improvement.  A journalist interviewed in the film said that “what you have here is a dynamic of not only people using what is, you know, a dangerous drug… but you also find a bit of an arms race building up where if enough people see that their competition is doing it, they feel like they kind of have to do it too.”  The societal pressure  to always be competitive and outperform others is well worth exploring, but to me that got lost in the focus on stimulant medications.

I freely admit my own bias viewing this documentary, as I take Dexedrine (dextroamphetamine).  I first started taking it for significant psychomotor retardation (slowing of movement and thoughts) that I experienced as a symptom of depression.  When that resolved, I cut down on my Dexedrine dose, and my mood worsened.  I’ve tried a few more times since then to cut back the dose, and it’s become clear that it’s definitely having a beneficial effect on my mood.  My doctor is very comfortable keeping me at a dose of 10mg in the morning and 5mg at noon because it is obviously having a therapeutic benefit.  I don’t feel “high” from it and never have.  Dexedrine isn’t enough to fully compensate for the cognitive slowing and low energy I experience with depression, and my overall cognitive performance and energy level remain lower even while on Dexedrine than they are when my depression was previoulsy in remission.

So when Netflix portrays my medication as either a performance enhancer or a legal version of crystal meth, it does not sit well with me.  There is already so much stigma against mental illness and psychiatric medication, and this sort of messaging is not helpful.  There was a really valid point buried underneath the performance-enhancing pill-popping message, and it would be great to see a documentary that truly addresses the issue of societal hyper-competitiveness.  Unfortunately Netflix missed the mark


Judging a book by its cover

antique book

We live in a world that judges us on how we look.  Our body shape, our clothing, and any sign that we somehow deviate from what is “normal”, expected, or otherwise considered acceptable.  Mental illness is not always overtly obvious, but sometimes the effects of it are.  Hygiene may go out the window, and we emerge from our homes in dirty sweats and greasy hair.  Illness may slow us down or speed us up.  Eating disorders and other mental illnesses can affect our body shape, as can psychiatric medication.

I have a lithium-induced tremor, and I’ve been surprised by how often people comment on it. My tremor is worse with intentional movement than at rest, and this gets noticed often when I am paying for things in shops.  Clerks may come out with a condescending “take your time” or a concerned “are you ok?”  If I’m at a coffeeshop and carrying a wobbly mug to my seat, this will often elicit comments, either from staff or other customers.  I’m not sure why it’s anyone’s business, but it makes me feel very conspicuous.  I have a mostly invisible illness whose treatment has visible side effects.  I’m lucky that the antipsychotic that’s worked best for me (quetiapine) has a low potential to cause movement-related side effects like tardive akathisia.

Yet it’s hard sometimes to remember that I’m lucky.  One of my nursing jobs involves administering injections and teaching clients how to self-inject medications.  My hands are very much on display.  My tremor is worse with intentional movement than it is at rest, and I worry that clients will think I’m either nervous or incompetent.  I don’t really like either of those options.  I usually take propranolol before doing this kind of work to put a damper on the tremor, but if I’m tired/stressed/caffeinated the propranolol doesn’t do a whole heck of a lot.  I’ve seldom had clients comment, and if they do I brush it off as too much coffee, but the rest of the world seems to feel quite free to comment.

Another way I’m lucky is that I’ve never experienced a disordered relationship with eating.  I haven’t always been happy with my body, but it hasn’t impacted my relationship with food.  I’ve written before about illness, meds, and weight, but what comes to mind now as I’m writing this is questions about pregnancy.  My meds have caused the weight to pack on disproportionately on my lower abdomen.  The proportions have shifted around over time, but there was one particular summer that I was asked multiple times about my non-existent pregnancy.  I’m of the opinion that you should never ask a woman about being pregnant unless it looks like she’ll probably give birth tomorrow.  When others commented on my “pregnancy”, I felt like I had totally lost control over my body.  I felt really offended, less because of the very real psych med baby I was carrying around and more because others felt they had the right to talk about my body.

When I recently made the decision to add Botox to my depression treatment plan, a friend mentioned that they had thought about getting it cosmetically.  For some reason that made me feel icky.  And it’s not (at least I don’t think) so much that I would judge someone for getting a cosmetic procedure; it’s more that I don’t even care enough to wear makeup, and the thought of doing something to my body for cosmetic reasons seems utterly bizarre.  Maybe the issue is that I worry others will judge me for getting Botox.

This post has been a bit all over the place, but I guess my point is that we are judged.  No matter what we say, what we do, or what we look like, others will judge us.  We can’t stop it, much as we might wish to, so all that’s left is managing our own reactions.  And sometimes that’s much easier said than done.

Do antidepressants work? What a new meta-analysis says.


A recent paper published in the Lancet looked at how effective antidepressants are, and this has been reported on in the media.  Since media outlets don’t necessarily have strong research literacy, let’s take a look at what the paper itself has to say.  My earlier post on research literacy explains some of the terms I’ll be using here.

Full reference details for the paper:

  • Cipriani, A., et. al. (2018). Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis. The Lancet. doi:10.1016/S0140-6736(17)32802-7

A systematic review involves collecting a body of relevant literature on a topic using academic databases and search terms that are clearly specified, and then narrowing that down by applying certain criteria to find studies that are academically rigorous and fit with the research parameters being considered.  Typically, different investigators go through this process independently and then come to a consensus on which studies to include in the review.  The results are then evaluated to get a picture of the current state of the evidence.  A meta-analysis goes a step further by pooling the data from the various studies and then performing statistical analysis.

Inclusion criteria for this paper were:

  • randomized, double-blinded, controlled trials (either placebo-controlled or head-to-head trials of different antidepressants)
  • study participants were adults 18+
  • diagnosis of major depressive disorder
  • no more than 20% of participants in a study had bipolar disorder, treatment resistant depression, psychotic depression, or serious concurrent medical condition (while this might sound like a bad thing, when pooling numbers for a meta-analysis you want to make sure you’re comparing apples to apples)
  • evaluation of quality of evidence and risk of bias met specified academic standards

The outcome measures were response rate and acceptability (as measured by number of discontinuations due to side effects).  While ideally patients should be treated to full remission of symptoms, response rate is often used in research studies.  Response rate is defined as a 50% reduction in score on a standardized depression rating scale such as the Hamilton Depression Rating Scale (HAM-D).  For this meta-analysis they chose to evaluate outcomes at the 8-week point, and for the included studies that didn’t take ratings at 8 weeks this was imputed using statistical methods.


  • All 21 antidepressants considered were more effective than placebo in adults with major depressive disorder.
  • In head-to-head studies, agomelatine, amitriptyline, escitalopram, mirtazapine, paroxetine, venlafaxine, and vortioxetine were more effective than other antidepressants.
  • Fluoxetine, fluuvoxamine, reboxetine, and trazodone were the least efficacious drugs.
  • For acceptability, agomelatine, citalopram, escitalopram, fluoxetine, sertraline, and vortioxetine were the most tolerable.
  • The most discontinuations occurred with amitriptyline, clomipramine, duloxetine, fluvoxamine, reboxetine, trazodone, and venlafaxine.
  • Agomelatine was the only antidepressant with a lower dropout rate than placebo.

So, what does this paper not give information about, i.e. what conclusions are we not able to draw from it?

  • How effective these antidepressants are in terms of achieving full remission
  • Efficacy measures are only based on a 50% reduction in rating scale scores; there is no information about which particular clusters of symptoms are more or less likely to respond
  • What outcomes are beyond the 8-week point
  • Whether a specific antidepressant is or is not likely to be a) effective in a specific individual or b) more or less effective than any other antidepressant in that same individual
  • Whether a specific antidepressant is or is not likely to be tolerable for a specific individual
  • How often people experience side effects due to any of the antidepressants (it only looks at discontinuations due to side effects)
  • Whether any specific individual would or would not benefit from antidepressants at all
  • How well antidepressants work outside of the population considered in the review (i.e. under 18 years old or with treatment resistant depression, psychotic depression, or bipolar depression)

And what does all of this mean?  It’s important to keep in mind that a systematic review/meta-analysis such as this is only aiming to tell us very specific things.  The authors are deliberately comparing apples to apples so they can pool large groups of numbers and draw conclusions from that.  There’s a lot of real-world information that it doesn’t give us, but it’s worth keeping in mind that it makes no claims that it is.  The authors do not suggest that their findings can be extrapolated to answer any of the questions I’ve mentioned that the paper doesn’t give us information about.  What it does tell us is that antidepressants belong in our arsenal of available treatment strategies.  Anything more specific than that always needs to be a collaborative decision between the individual and their treatment team.


Image credit: matvevna on Pixabay

Travelling with depression as a carry-on

world map

Travelling has always been a passion of mine.  In the 10 years since I developed depression, my illness has certainly gotten its hands dirty interfering in my travel plans and hopping along for the ride.

In 2007, I had planned to do an organized tour across China, Mongolia, and Russia with a  couple of friends.  Around two months before our planned departure, I ended up in hospital with psychotic depression following a suicide attempt.  So much for that trip.  It was the one time I had ever purchased trip cancellation insurance, so I went ahead and made a claim, but the insurance company came up with an excuse to deny it.  I’ve never bothered purchasing cancellation insurance again.

In 2012, I was feeling quite a bit better after a 2-month hospitalization in late 2011, so I booked a 2-week trip to Russia for that summer.  As the trip neared, it was taking more and more effort to hold myself together.  Then the day before I left, things just fell apart.  I went ahead with the trip, thinking it would at least be a distraction, but my mood remained low, and I found myself just going through the motions and not enjoying anything.

In 2014, I had planned a trip to central Asia (Uzbekistan, Kazakstan, and Kyrgyzstan).  A few weeks before I left, a stressful event brought on a relapse of my depression.  I was very slowed down, both in movement and in thinking.  An increase in lithium helped, but I still wasn’t feeling great when I left for my trip.  I found myself having to schedule at least one or two nap breaks into each day, and sometimes I would just run out of gas and have to sit myself down wherever I could, even if that meant the floor or the sidewalk.

I think teleportation is the invention that I would most like to see happen in the near future.  I’ve never been all that keen on the actual in transit part of travelling; it’s uncomfortable and often a real pain in the ass.  But when I’m not feeling well, uncomfortable is definitely not a strong enough word to capture how yucky it is.  As I was at the airport waiting to leave on my recent vacation, I felt totally overwhelmed by external stimuli, which made me feel so dizzy I thought I was going to pass out.  I was desperate to drown out the onslaught of noises, so I blasted my music on my headphones as loud as my ears could tolerate.

seats in an airplane cabin

Being on the plane was also difficult.  I’m a fairly hippy girl and the girl next to me was even more endowed in that department, which meant that it was very hard to prevent our legs from touching.  Normally this would be no big deal, but as sensitive as I was feeling, this was just not working for me.  This translated into me trying as hard as I could to pour myself out of the seat and into the aisle.  Luckily on the flight home I had an empty seat between me and the next person over, but she was very antsy, and that in turn triggered me.

I am quite prone to motion sickness, and having barfed mare than once before on planes, I always take drugs for this.  Normally I take Gravol (dimenhydrinate), and it has the side benefit of sedating me at least a little bit.  But on this particular occasion I had run out of Gravol, so instead I took some promethazine that I’d picked up in India a couple years ago.  That’s not actually as dodgy as it sounds; it does prevent me from barfing, but doesn’t sedate me at all.  Damn it, should’ve brought Ativan!

I have to recognize that my early 20’s, a time when my body and mind were functioning optimally mental illness hadn’t yet reared its ugly head, and I could sleep almost anytime, anywhere…  well, those days are far, far behind me.  I need to drill it into my brain that I can’t function that way anymore, and it’s important to prepare myself better for experiences that used to come much more easily.  If nothing else, I’ve learned that Ativan needs to be a basic part of my sizeable travelling pharmacy (which I’ve written about before in How do you say antidepressant in Uzbek?).

Lithium is definitely the hardest medication for me to travel with.  I have to be very mindful of my hydration, and sun, heat, and alcohol all can have a major impact.  Particularly in countries where tap water isn’t necessarily the best idea, water intake requires effort and planning.  When it’s hot, I can’t be sure if I’m losing much lithium or mostly just water through sweating.  When I was in India, I had diarrhea most of the trip, and again, I knew I was losing fluids  but wasn’t sure how much salt I was losing as well.  When my lithium level gets too high I get a bad tremor, headaches, and nausea.  With no handy way of doing a quick lithium level check (besides a teleporter machine, I need a blood sugar-type monitor for lithium to be invented), I just have to guess.  When I was in India and again when I was in Mexico, I made the assumption based on my symptoms that my level was high and lowered my dose accordingly, which did seem to help.  I was able to find a few research studies that suggest there can be climate-based variations in lithium levels, but it doesn’t appear to be something that’s been studied very much.  It bugs me having to think about this.  It’s not that I have a problem with lithium per se; I just hate having to blindly approach the situation without the benefit of a lab or a doctor to problem-solve with.  At least my recent 1-week trip was short enough to be fairly manageable, but still, the frustration persists that I have to think about it at all.

Adding to my fluid balancing woes is that my body seems to have learned to automatically kick into travel mode, with my kidneys presumably trying to make life easier for me.  This has served me well when I’ve been on long train or bus rides with icky toilet options, as I can sometimes go up to 24 hours without urinating.  On the day I returned from my recent vacation, I went 12 hours without urinating despite drinking around 2L of water during  that time.  I don’t know if this is something that happens to other travellers, or perhaps I’m just a random oddity.

Speaking of oddities, it would be nice if solo travellers weren’t seen as going against social norms/expectations.  I’ll leave most of this rant for another post, but for now I’ll just say that when I’m not feeling very well and I’m treated like a weirdo because I’m on my own, it just plain sucks.  I wish I could bring my pet guinea pigs along to display as my companions, but they are non-stop poop factories, so it just wouldn’t be practical.

I’ve accumulated enough credit card points for a free flight to Europe, and I think I’m going to aim to do a trip this fall.  It would be the first time I’ve booked an international trip (other than a short beach getaway) knowing that I’m not feeling so great.  Given that I’m just working casual I don’t have to worry about booking off vacation time advance, so I can leave it until relatively last minute to make a decision.  I’ve seen from past experience that I can get by travelling when unwell, so it may be a good idea to push myself to do something that I might actually end up enjoying  Stay tuned.


Image credits:

Christine Roy on Unsplash

ty_yang on Pixabay

Psych meds 101: Sleep meds

pills beside a glass of water

This is the last in the psych meds 101 series; I’ve previously posted about antidepressants, antipsychotics, mood stabilizers, and anti-anxiety meds, drawing on my perspective as a mental health nurse, former pharmacist, and person with depression.

While some of these meds are used  primarily for sleep, many have other uses as well.  The choice of medication for any given person will be based on their diagnosis among other factors, and sleep aids may no longer be necessary once the underlying mental illness is well controlled.


I covered these in more detail in my previous post on anti-anxiety meds.  The choice of benzo will depend on whether you want it more for getting to sleep or staying asleep (i.e. shorter or longer acting).  I’ve found clonazepam, which is long-acting, to be helpful in the past when I was having problems with waking up early.

Oxazepam and temazepam do not have the same degree of anti-anxiety effect as other benzos, but they are useful for sleep because their half-lives match up pretty well with a night of sleep.  They are also are cleanly metabolized, meaning they don’t leave any active metabolites sticking around that can cause a hangover-type effect.  The key thing to be aware of when using benzos for sleep is that if you use them regularly you will develop a tolerance and they’ll become less effective.


The so-called Z-drugs include zopiclone and zolpidem.  Their main therapeutic use is for sleep.  Like benzos, they act on GABA receptors (GABA is a calming neurotransmitter), but they act at a different site and cause different changes in the receptor.  As a result, they are less likely to result in dependence, tolerance, or withdrawal symptoms.  I’ve had moderate success taking zopiclone in the past, but I’ve needed 15mg rather than the most common dose of 7.5mg.


Histamine does a number of things in the body, but in the brain it promotes wakefulness.  Blocking H1 histamine receptors results in a sedative effect.  Most over-the-counter sleep medications include diphenhydramine, which is the drug found in Benadryl to treat allergies.  A downside of H-1 histamine blockers is that they can cause weight gain when used long-term.

A lot of the prescription medications that may be used for sleep block H1 receptors in addition to whatever their primary therapeutic purpose might be.  Trazodone is an antidepressant that’s used more often for sleep than as an antidepressant.  It’s used for sleep generally at doses of 50-150mg, and needs to be taken at higher doses for an antidepressant effect.  Tricyclic antidepressants like amitriptyline are quite sedating, as is mirtazapine.  Interestingly enough, mirtazapine is most sedating at lower doses, and at higher doses becomes more activating.  For me the sweet spot seems to be at 30mg.  Antipsychotics that affect H1 receptors may also be used for sleep, such as methotrimeprazine and quetiapine.  Quetiapine extended release can be useful if early morning awakening is a problem.


Gabapentin is an option but not necessarily the most effective one.  It would tend to be most appropriate for someone who would also benefit from its other therapeutic effects, e.g. for neuropathic pain or anxiety.


Prazosin isn’t a sleep medication per se; however, for people with PTSD it can help tone down nightmares and thus improve sleep.  It blocks alpha-1 adrenergic receptors, slowing down some of the sympathetic nervous system fight-or-flight-related activity.


Melatonin is a hormone that is naturally produced by the pineal gland in the brain, and it’s involved in regulating the Circadian rhythm, i.e. sleep-wake cycle.  For some people melatonin supplements work well, such as people whose circadian rhythm gets disrupted by things like shift work.  For other people, taking melatonin doesn’t do much of anything; I happen to fall into this category.  Ramelteon is a drug that stimulates the same receptors as melatonin does, but I’ve never actually seen it used; melatonin is cheaper and more readily available.

Valerian root

This is a herbal product that may have some sort of activity at GABA receptors, although it’s not clear what exactly this is.  There isn’t a lot of evidence to back up its effectiveness, but it’s worth being aware of as a non-drug option.  I’ve tried it and personally didn’t find it helpful.


There are a variety of other non-drug options that are worth giving consideration to.  Tryptophan is an amino acid that is a precursor for serotonin production.  It’s the substance in turkey that’s associated with drowsiness, and can be taken as a supplement to promote sleep.  Herbal teas, particularly those containing chamomile, may be helpful.  There are also certain substances that it may be be best to avoid; caffeine is an obvious one, but perhaps not so obvious is alcohol.  Alcohol may help you get to sleep, but it decreases sleep quality and makes it more likely you will wake up during the night.  Sleep hygiene is very important, but I’ll address that in another post.

While ideally we wouldn’t need to take drugs to help us sleep, the reality of mental illness is that most of us will have problems with sleep at one time or another.  Given how hugely damaging poor sleep is to mental health, I’ll take drugs over insomnia hands down.  As with any kind of medications, knowledge is power, and knowing our options puts us in a position to make the best decision in our own specific circumstances.


Photo credit: pina messina on Unsplash

Book review: Birth of a new Brain – Healing from Postpartum Bipolar Disorder

Birth of a New Brain book cover

Birth of a New Brain – Healing from Postpartum Bipolar Disorder chronicles author Dyane Harwood’s journey with postpartum onset bipolar disorder.  The story’s rich, vivid descriptions draw the reader along on the intense roller coaster ride of the author’s illness experience.  Many elements of her story will be hauntingly familiar to those whose lives have been touched in some way by bipolar disorder, including mood symptoms whose true nature only became apparent with hindsight and well-meaning attempts to get off medication that result in disaster.

Mental illness was a part of Dyane’s life from the beginning, as her father had bipolar disorder.  When she first began to struggle with her own mental health, she was diagnosed with depression.  Glimmers of hypomania made occasional brief appearances, but as is so often the case with hypomania the symptoms were only recognizable as such upon later reflection.

Depression is the most recognized postpartum mental health problem, while postpartum hypomania may not raise red flags.  As Dyane began to recognize that her thoughts were problematic, she became concerned, as many mentally ill new mothers might, that disclosing the true nature of her thoughts would result in her being designated an unfit mother.

It was after the birth of her second daughter that mania openly reared its head, resulting in a diagnosis of bipolar disorder with the specifier of “postpartum onset”.  Dyane described the surreal experience of hypergraphia, an uncommon symptoms involving excessive writing, including the juggling act of franticly writing while at the same time tandem breastfeeding her infant and toddler.

Dyane was hospitalized multiple times for her illness, and she recounted the sorts of challenges that are all too commonly faced by those with mental illness.  On one occasion she was handcuffed by police and taken to hospital in the back of a police car.  She was reported to Child Protective Services by one hospital psychiatrist, and when she reacted angrily she was placed in a seclusion room.  Being on locked wards that prevented from going outside and kept her cut off from internet and cell phone use had a detrimental effect on her recovery, and her hospitalizations worsened her anxiety and raised concerns about post-traumatic stress.  Mental health services could certainly benefit from incorporating this type of feedback.

Birth of a New Brain captures the frustration and desperation of treatment-resistant mental illness.  Dyane was trialled on numerous medications that triggered horrible side effects rather than a therapeutic benefit.  One particularly harrowing experience was with the antidepressant amitriptyline; taking a single dose led to intense suicidal thoughts requiring hospitalization.  Electroconvulsive therapy (ECT) was helpful, but she struggled with the considerable logistical and financial barriers that often go along with outpatient ECT.  For therapies like ECT to be at their most effective, it is important that mental health services work to minimize these sorts of barriers.

Over the years Dyane went off medications multiple times.  Despite giving it careful thought, consulting books by credible sources, and incorporating alternative strategies, her illness relapsed.  Finally she found success with an MAOI antidepressant, an option that has strong evidence of efficacy but is seldom considered due to the need for dietary restrictions. Once she was finally stabilized on an effective medication combination, she accepted that for her the reality was that medication would be an essential part of her wellness.  The book also describes a host of holistic strategies that Dyane incorporates as key elements of her treatment plan.

Birth of a New Brain offers hope to those struggling with mood disorders, and raises awareness about the little-known postpartum onset specifier for bipolar disorder.  By the end of the book the reader is left feeling as though Dyane is a dear friend who has bravely shared all and held nothing back.  While mental illness plays a starring role in the story, as Dyane concludes her final chapter, “I’m so much more than bipolar.  And so are you.”  Her book reminds us that no matter how hard the illness journey may be, recovery is possible.

Birth of a New Brain – Healing from Postpartum Bipolar Disorder

Foreword by the perinatal psychiatrist and acclaimed author Dr. Carol Henshaw. Available on Amazon in paperback & Kindle versions!

You can also find Dyane Harwood on her blog, Birth of a New Brain, and on Twitter @DyaneHarwood.


You can find my other book reviews in my blog index,

Psych meds 101: Anti-anxiety meds

anxiety written in Scrabble tiles

This is part of a psych meds 101 series written from my perspective as mental health nurse, ex-pharmacist, and psych med users.  Previous posts have covered antidepressants, antipsychotics, and mood stabilizers, and an upcoming post will touch on sleep meds.  Much of this post will focus on the benzodiazepine class of medications, but I’ll also cover other meds used for anxiety.


Benzos bind to GABA-A receptors on neurons to boost the activity of the neurotransmitter GABA, which exerts a calming effect on the brain.  GABA counteracts the excitatory neurotransmitter glutamate.  Besides being used for anxiety, benzos are used for acute management of seizures and alcohol withdrawal.  Very rapid- and short-acting benzos like midazolam may be used for procedural sedation.  Despite their downsides, benzodiazepines (benzos for short) work for anxiety.  They work very well, and they work quickly.  And  that’s what makes them so darn problematic.

Duration of action

Drugs within the benzodiazepine class differ considerably in their half-lives, i.e. the time it takes for the body to clear half of the medication.  Half-lives are also affected by a given individual’s ability to metabolize the drug.  The half-life of lorazepam (aka Ativan) can range from 8-24 hours, and clonazepam’s half-life is 19-60 hours.  Time of onset tends to be between 20-60 minutes after administration.


Taking benzos regularly for an extended period will lead to tolerance.  Full stop.  How long it takes and the extent to which it happens may vary from person to person, but over time the same benzo dose will produce less of a therapeutic effect.  A general rule of thumb is that benzos work best the less you take them.  Ideally, this might look like finding another medication for sustained use and using a benzo as needed (prn) for breakthrough anxiety symptoms.  Of course, we don’t live in an ideal world and for some people benzos are the only thing that helps them get through the days.  Still, it’s the kind of thing you want to know about going in rather than finding out after you’ve already been on regular benzos for a year.


That brings me to my next point: withdrawal.  Withdrawal can range from nasty (increased heart rate and blood pressure, cramps, anxiety, insomnia, impaired memory and consciousness) to downright dangerous (high fever, seizures, psychosis).  Withdrawal results from physiological dependence, where essentially your body chemistry changes to adapt to the regular presence of the drug.  We might think of addiction as involving both a physiological and a psychological dependence, but whether you consider yourself addicted or not if you have been on long-term high-dose benzos and you stop cold turkey, you will have withdrawal.  Getting off of benzos requires a gradual tapering down of the dose, and even then it can be a really tough experience.  That brings me back to my earlier point; it’s good to know going in that benzos work best the less you use them, if that’s something that’s feasible for you.


Antidepressants that promote serotonin neurotransmission can help to settle down the amygdala, part of the primitive caveman brain that is associated with anxiety, fear, and panic.  SSRIs (selective serotonin reuptake inhibitors) or SNRIs (serotonin and norepinephrine reuptake inhibitors) are commonly used.  Older antidepressants from the TCA (tricyclic antidepressant) or MAOI (monoamine oxidase inhibitor) classes may also be used and are quite effective, but they are more likely to cause side effects.  Typically higher doses are required than for the treatment of depression, and it can take longer to see a therapeutic effect because of the complex signalling loops that are involved.  In OCD, it can take up to 10 weeks for SSRIs to be effective.  It can be a frustrating waiting game, and benzos can certainly be useful in getting through this.


This acts on 5HT1a serotonin receptors to suppress neuron firing in a portion of the brainstem known as the dorsal raphe nucleus.  It may take a few weeks to become effective.  It’s an older drug that’s not used all that commonly, but a psychiatrist that I used to work with often prescribed it and found it to be quite effective without a lot of side effects.  It’s not addictive and not sedating, so it’s a pretty low-risk medication to try out.

Gabapentin, pregabalin

These anti-seizure medications act on the transporter that moves calcium ions in and out of neurons.  This helps control the release of the excitatory neurotransmitter glutamate in the amygdala.  While these are not among the anti-seizure medications that have demonstrated mood stabilizing activity, they can be useful for anxiety.  They’re not addictive, although some people experience discontinuation symptoms if they’re taken off too quickly.  Both gabapentin and pregabalin are dosed three times a day.  Gabapentin has a wide dosing range, so it may take some tweaking to get the right dose.

Atypical antipsychotics

Atypical antipsychotics may also be useful.  It’s not entirely clear how they exert this effect, but it may be related to changes in norepinephrine and serotonin signalling via interaction with alpha-2 adrenergic receptors.  Quetiapine is commonly used for anxiety, and risperidone has demonstrated effectiveness in obsessive compulsive disorder.  Atypicals may be used as an add-on treatment for longer-term management or for prn (as needed) use.  Generally lower doses are required than for management of psychosis.


Clonidine acts on alpha-2 adrenergic receptors.  While it has shown some effectiveness, this doesn’t tend to be sustained, and it’s not considered a first-line treatment option.

Beta blockers

Beta blockers like propranolol can settle down some of the body’s fight-or-flight response, and can be useful for “performance anxiety”.  It tends to target the physical effects of anxiety rather than the mental experience.


This isn’t an exhaustive list by any means.  There are some other medications including mood stabilizers that may be used, and treatment of choice varies depending on the particular diagnosis.  In the recent DSM-5 PTSD has been moved out of the anxiety disorders category, so I haven’t touched on that at all here.

Next up in the psych meds 101 series will be sleep meds zzzzz……


Photo credit: Wokandapix on Pixabay

Pill Popper RN

horde of flying tablets and capsules

The title is a kind of weak ripoff from the Seinfeld-ian Pimple Popper MD, but still, it’s fairly apt.  I have major depressive disorder, and I take a boatload of pills.  Because my memory isn’t that great and I don’t want to forget to take them, I have them all laid out on a shelf in my bookcase.  If anyone comes into my living room chances are they’ll notice the mini pharmacy I’ve got going on, but I am so beyond caring about what people think about that.

In this post I’m going to break down the various things I’m putting into my body to try and stay afloat with my depression.  Medications will never be all of the picture, but for me they are an important part of my treatment plan.

Mirtazapine 30mg and venlafaxine 300mg: These are my two antidepressants.  I have always responded better to antidepressants with more activity related to norepinephrine than serotonin, so these two fit the bill.  The combo is sometimes referred to as “California rocket fuel” because of its potency.  Mirtazapine is actually most sedating at lower doses, so I’ve settled on the middle of the road 30mg dose because I didn’t sleep as well on higher doses.

Lithium 1200mg: I don’t have bipolar disorder, but lithium has actually been recognized for a long time as an effective augmentation strategy in major depressive disorder.  If I start feeling worse one of the first things my doctor and I consider is increasing my lithium, since I tend to respond fairly quickly to dose increases.  When my serum levels get higher, though, I tend to have increased problems with tremor and coordination, turning me into a complete klutz, complete with wipeouts on the sidewalk and falling down stairs.

Quetiapine 600mg: Atypical antipsychotics are also effective for treatment augmentation in depression.  Of the ones I have tried, quetiapine has been most effective for me.  It helps with my mood and is very reliable for getting to sleep.

Dextroamphetamine 15mg: I first tried dextroamphetamine a year and a half ago when I was really slowed down in both movement and thinking.  It helped, but I wasn’t keen on taking “speed” any longer than needed, so I only took it for about a month.  I restarted it earlier this year when I got really slowed down again.  It helped, but when I tried to decrease the dose my mood dropped.  Research has shown that it tends to be effective as an antidepressant augmentation strategy for only a couple of months or so, and then the effect tends to wear off; however, I’ve tried several times to decrease the dose and it makes me feel worse.  My doctor has a good attitude about it, and has no problem with me taking it on an ongoing basis when it’s clearly working.

Propranolol 10mg prn (as needed): Lithium gives me an intention tremor, which occurs with intentional movement as opposed to a resting tremor.  It’s worse if my lithium level is higher or if I’m worn out, and probably the dextroamphetamine doesn’t help either.  Propranolol helps keep it in check, and I tend to use it mostly for days that I’m working, since patients generally aren’t reassured about getting an injection if the nurse drawing it up has shaky hands.

nurse administering intramuscular injection

Lorazepam 0.5-1mg prn: Anxiety is generally not a prominent feature of my illness, so I’ve never needed to use lorazepam (Ativan) on a regular basis.  I find for me it’s most effective to get a bit of a numbing effect when I’m going into particularly stressful situations.  Since I use it so seldom, I’m able to get away with a small dose.

Min-Ovral: I have spent much of my adult life on birth control, but decided a couple of years ago to take a break.  When I got depressed last year, my hormones went crazy.  I was getting my period every 3 weeks and PMS was having a big impact on my mood.  Now I’m back on birth control and my hormones are steady and happy.  The estrogen in the Min-Ovral may also give my neurotransmitters a bit of a boost.

Omega-3 fatty acid plus vitamin D supplement: There have been research studies that have shown that omega-3’s have some beneficial effect on depression.  Vitamin D may also play a role in depression, and since I live on the Wet Coast of Canada where it rains for a good chunk of the year supplementation seems like a good way to go.

Multivitamin/mineral/antioxidant supplement: Besides helping my overall health, the goal with this is to have some effect on decreasing oxidative stress, which may play a role in depression.

L-methyfolate and vitamin B12 supplementation: I get these in an intramuscular injection every 2 weeks from my naturopath.  Both play a role in the methylation cycle that’s involved in neurotransmitter synthesis, and L-methylfolate in particular has been shown to be useful in depression.

So that’s me, Pill Popper RN.  What’s in your medicine cabinet?


Photo credits:

Qimono on Pixabay

huntlh on Pixabay