In case you missed my psych 101 series, here’s the post on medications for sleep.
In case you missed my psych 101 series, here’s the post on medications for sleep.
In case you missed my psych meds 101 series, here’s the most on anti-anxiety meds.
In case you missed my psych meds 101 series, here’s the post on mood stabilizers.
In case you missed my psych meds 101 series, here’s the post on antipsychotics.
In case you missed my psych meds 101 series, here’s the post on antidepressants.
I have never had a problem with medications in general, and in my work as a nurse I’ve seen how much good they can do. Despite that, I’ve gone off the meds I take for depression a few times, and that’s what this post is about.
My first episode of depression was in 2007. I ended up hospitalized following a suicide attempt, and spent 2 months in hospital. I continued taking my meds for a few months and I then I had another suicide attempt, this time by overdosing on my psych meds. I didn’t do any significant damage, so I chose not to tell anybody at the time. I decided that to hell with it, if I was on meds and still feeling shitty, what was the point of continuing meds? Continuing on my deceptive theme, I didn’t want my treatment team to know I wasn’t taking meds, so I continued to pick them up regularly from the pharmacy. I ended up getting into full remission without meds, and I remained well for almost 4 years.
My plan all along was that if I started to have signs of getting worse, I would restart meds. When the depression started to hit me in 2011, I quickly recognized the red flags of poor sleep and low mood, and made an appointment to see my GP. I had to practically beg for meds, and he begrudgingly gave me 10mg of citalopram, although his preference was that I attend group therapy. 2 weeks later I ended up in hospital.
It took a year and a half to get fully well again, and I ended up on multiple weight gain-inducing meds (lithium, quetiapine, and mirtazapine). The weight gain was hard to adjust to, although I recognized it was probably a fair price to pay for being well. After 2 years in full remission, I decided I wanted to try going off the quetiapine, and my psychiatrist was agreeable. We tapered down the dose gradually, and at first it seemed like I was going ok, until suddenly it wasn’t. I got really slowed down, and ended up having to go back on the quetiapine as well as up my dose of lithium. Clearly I needed my full med cocktail.
It wasn’t too long afterwards that my workplace bullying debacle began. This culminated in me deciding to quit my job, and I became quite depressed again. My psychiatrist ‘s reaction was tremendously invalidating, so I stopped seeing him. I had recently begun seeing a new GP, and when I told her why I wasn’t seeing the psychiatrist any more, she came out with the same invalidating comments he did. I refused to see her again, so she booked me in to see another GP at the same clinic, who ended up being even worse. I couldn’t bear the thought of going to see another doctor, so I decided that with the meds I still had at home I would do a gradual taper and then stope them. It wasn’t that I wanted to stop taking meds, I just wasn’t willing to see another doctor. Not surprisingly, that strategy didn’t work out very well for me. I was barely sleeping despite taking everything over-the-counter I could think of.
It was when I decided that I needed to go back on meds that I found my current GP, who’s very reasonable and pragmatic. Even so, there have been a couple of times that I’ve thought screw it, there’s no point going in to get my meds reordered because I just feel like crap anyway.
My logical mind is very adamant that I need meds. Unfortunately, sometimes depression sneaks in and twists things around, and for me I don’t think that’s something that will ever go away no matter how pro-meds I am most of the time.
Have you gone off meds before? What was the experience like?
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In this post I’ll take a look at some of the available treatment guidelines for anxiety disorders. While psychotherapies are extremely important in the management of anxiety disorders, this post will focus only on anti-anxiety medications. The treatment guidelines I refer to come from the British Association for Psychopharmacology and the World Federation of Societies of Biological Psychiatry.
Benzodiazepines, while effective, are generally only recommended for short term use or where other treatments have failed, and there should be a careful consideration of the risks vs benefits for the specific individual.
It may take up to 12 weeks to achieve full response to antidepressant medication, but if there is no response at all after 4 weeks it is unlikely that particular medication will start to work with a longer duration of treatment.
1st line: SSRI (selective serotonin reuptake inhibitor): citalopram, escitalopram, paroxetine, sertraline
Alternatives to SSRI: SNRI (serotonin and norepinephrine reuptake inhibitor: venlafaxine, duloxetine), pregabalin (high dose may be more effective); quetiapine may be effective as monotherapy at doses of 50-300mg/day
2nd line: agomelatine, quetiapine, some benzodiazepines (alprazolam, diazepam, lorazepam), imipramine (a tricyclic antidepressant or TCA), buspirone, hydroxyzine (a sedating antihistamine), trazodone
It may take up to 12 weeks for medication to fully take effect. When discontinuing medication after long-term treatment a lengthy gradual taper is recommended (over at least a 3 month period).
1st line: SSRI
Alternatives: some TCAs (clomipramine, desipramine, imipramine, lofepramine) venlafaxine, reboxetine, some benzodiazepines (alprazolam, clonazepam, diazepam, lorazepam), some anticonvulsants (gabapentin, sodium valproate)
Avoid: propranolol, buspirone and bupropion
It may take up to 12 weeks for medication to fully take effect.
1st line: SSRIs
Alternatives: venlafaxine, phenelzine, moclobemide, some benzodiazepines (bromazepam, clonazepam) and anticonvulsants (gabapentin, pregabalin), and olanzapine
Avoid: atenolol or buspirone in generalized social anxiety disorder; beta blockers can be effective for performance anxiety but not social anxiety disorder in general
1st line: SSRI (may need a high dose)
Add-on treatment: atypical antipsychotic, haloperidol, mirtazapine (may speed up response to citalopram)
What has your experience been like with anti-anxiety medication?
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The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial studied 2876 people with major depressive disorder to evaluate their response to depression treatment in a real-world setting. Unlike the randomized controlled trials that are often used to evaluate a drug’s efficacy, there were few exclusion criteria, the patient and their physician knew which drug they were taking, and patient choice was incorporated. Four sequential levels of treatment were established, and if a patient failed to achieve remission after 12-14 weeks, they would be moved to the next level. The target was full remission, unlike many other studies which measure response (i.e. a ≥50% reduction in symptom rating scale scores). Remission rates can be substantially lower than response rates, but are useful because there are better long-term outcomes for people who do achieve full remission.
Level 1 treatment consisted of citalopram, and 28% of patients achieved remission based on the Hamilton Rating Scale for Depression (HAM-D). Certain factors were identified, such as other comorbid mental illnesses, that were associated with lower or higher remission rates.
In level 2, patients were offered cognitive psychotherapy, a switch to another antidepressant (randomly selected), or the addition of another medication to augment the treatment. Among level 2 patients who switched to another medication, remission rates were 21.3% for bupropion, 17.6% for sertraline, 24.8% for venlafaxine. Rates were similar among those patients who switched to cognitive psychotherapy. Among the patients who received augmentation treatment, the remission rates were approximately 30% for both bupropion and buspirone. Augmentation with medication produced more rapid remission than augmentation with cognitive psychotherapy.
In level 3, patients who switched medication were randomly assigned to mirtazapine or nortriptyline, and patients who received an medication for augmentation were randomly assigned to lithium or the T3 form of thyroid hormone (liothyronine). Remission rates were 12.3% for mirtazapine, 19.8% for nortriptyline, 15.9% for lithium, and 24.7% for thyroid hormone.
In level 4, patients were randomly assigned to switch to either tranylcypromine (an MAOI antidepressant) or venlafaxine plus mirtazapine. Remission rates were 6.9% for tranylcypromine and 13.7% for venlafaxine plus mirtazapine.
Altogether, 67% of patients were able to achieve remission. The study found that people may still remit by 12 weeks even if there’s only a modest symptom reduction at 6 weeks. However, the more treatment steps that are required, the lower the chance of a patient achieving remission and the higher the chance of intolerable side effects and relapse.
Personally I found the take-home message from this study rather discouraging. During my last hospitalization I argued that my suicide attempt was supported by the STAR*D’s not so subtle hint that I was shit outta luck. I think it’s crucial that we find new kinds of treatment that will help that 33% of people who are treatment-resistant and just aren’t achieving remission with many currently available antidepressant medications. This study doesn’t consider all potential treatments; for example, atypical antipsychotics, ketamine, and ECT aren’ included, and psychotherapy plays a limited part. Still, we deserve better. A lot better.
For more info on the research terminology I’ve used in this post, see my post on research literacy.
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I can’t think of any other type of health condition that has as polarized a relationship with medication as mental illness. In some ways, to medicate or not to medicate has become a moral issue, with various involved parties taking a stance based on principle. Often this stance is very broad, making sweeping generalizations. I recently read and reviewed the book Lost Connections, which argues that all depression is situational and medications should not be used. Some people connect psychiatric medication use to violence, such as the incoming director of the National Rifle Association (NRA) who has suggested a link between school shootings and Ritalin (methylphenidate). I’ve seen Twitter comments blasting people who wrote about the positive effects they experienced from medication. We would never hear any of this kind of thing if we were talking about blood pressure medication, so why are there so many eager to shout from the rooftops when it comes to psychiatric meds?
My own view is certainly shaped by my professional training; I used to be a pharmacist, and now I’ve been practicing as a nurse for 13 years in mental health settings. I understand how medications produce the effects (both positive and negative) that they do, and have the research literacy to separate the BS from legitimate information. I look at medication as a tool, and any given medication may or may not work for any given individual, and may or may not be tolerated by that individual. I have seen medication be life-saving for people, and it certainly has made a huge difference in my own illness.
In general it seems like people tend to speak up, both online and in person, more often about things that go badly for them than things that go well. The same appears to be true with medication. I’m a bit fuzzy remembering the details, but not too long ago someone had written a post about antidepressant withdrawal, and someone else commented about how venlafaxine is a garbage drug that no one should take because of the withdrawal effects. I’m sure that individual’s experience was very negative, but it’s easy to see remarks like this about side effects and overgeneralize, making the assumption that they occur for all/most people taking the drug. Unfortunately we don’t yet have a way of predicting who will respond to or tolerate particular drugs (although I’m sure the science will get there as the role of pharmacogenomics expands), but to allow treatment decisions to be based on people’s negative comments online doesn’t seem particularly helpful.
I suspect that some of the time meds are demonized because of poor clinical practice by prescribers. If physicians aren’t responsive to the side effects people are having, ordering any necessary bloodwork, or prescribing drugs that are actually appropriate and effective for the condition being treated, those things don’t mean the drug itself is inherently bad. Instead, it means that the prescriber is being irresponsible. I can’t help but think of a blogger with bipolar disorder who was treated for many years with high-dose clonazepam, and then had it discontinued abruptly. In my mind that is shocking malpractice and a gross misuse of a medication that is not even indicated for treatment of bipolar disorder (but can be very useful when used carefully and appropriately).
It’s also problematic when doctors prescribe a medication and make it out to be a sort of panacea that will fix everything. We all know there’s a lot of different things involved in getting well, whether we’re on medication or not. Psychosocial stressors and underlying trauma aren’t going to disappear with a wave of the SSRI wand, and that’s fine, but doctors should be open with their patients about what medications will and will not do. If patients are coming in misinformed and expecting to pop a happy pill, the health professional has a responsibility to educate them about the nature of mental illness and its treatment.
As Shakespeare’s Hamlet might say:
To medicate, or not to medicate: that is the question:
Whether ‘tis nobler in the mind to suffer
The slings and arrows of outrageous fortune,
Or to take arms against a sea of troubles,
And by opposing end them?
Where do you stand when it comes to medications?
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In 2013 the International Society for Bipolar Disorders and the Canadian Network for Mood and Anxiety Treatments combed through the scientific literature and put together these guidelines for the pharmacological treatment of bipolar disorder. Treatments are classified as 1st, 2nd, or 3rd line based on the strength of existing evidence to support their effectiveness. Also included are treatments that are sometimes used in bipolar disorder but for whatever reason don’t necessarily have a research base to back them up.
No treatment guideline in the world is going to be able to say what treatment is going to work in a specific individual. However, they can provide a good idea of what has the best chance of working, and I think it’s always valuable to know what your options are.
Here are the recommendations for acute mania, acute depression, and maintenance treatment.
Not supported by evidence:
Not supported by evidence:
1st line: quetiapine
Not supported by evidence:
Antidepressants don’t always work well in bipolar disorder, and they can potentially do more harm than good. In case you’re interested, the International Society for Bipolar Disorder has a task force report on the use of antidepressants in bipolar disorder.
And there you have it, folks. Was there anything in the guidelines that surprised you? And for those with bipolar disorder, how does your treatment regimen compare to what’s in the guidelines?
Yatham, L.N., Kennedy, S.H., Parikh, S.V., Schaffer, A., Beaulieu, S., Alda, M., O’Donovan, C., MacQueen, G., McIntyre, R.S., Sharma, V., Ravindran, A., Young, L.T., Milev, R., Bond, D.J., Frey, B.N., Goldstein, B.I., Lafer, B., Birmaher, B., Ha, K., Nolen, W.A., & Berk, M. (2013). Canadian Network for Mood and Anxiety Treatments (CANMAT) and International Society for Bipolar Disorders (ISBD) collaborative update of CANMAD guidelines for the management of patients with bipolar disorder: Update 2013. Bipolar Disorders, 15, 1-44.
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In Lost Connections: Uncovering the Real Causes of Depression – and the Unexpected Solutions, Johann Hari takes a stand against the idea of biological causation of depression and anxiety. I expected going in that this book would annoy me, but at times it was just plain ridiculousness.
To start off, let me tell you the perspective I’m coming from. I support a biopsychosocial model that recognizes mental illness as complex and often multifactorial. Every individual’s illness stems from a unique combination of factors, and for a treatment plan to work best it needs to effectively target whatever contributing factors can be identified. Sometimes that’s meds, sometimes that’s psychotherapy, and more often than not it’s a combination of multiple different strategies. Meds aren’t a miracle cure but can get you well enough to do whatever it is you need to do to find true wellness. Ok, now that we’ve got that out of the way, let’s jump headfirst into the book.
Red flags were set off for me early on in the book when the author wrote that at age 18 he had an epiphany that he had the medical condition called depression, and from information in the media he knew that antidepressants were just what he needed to quickly make him all better. Initially he was convinced paroxetine made him feel even better than simply not depressed, and he spread the word to others that depression was solely about serotonin and antidepressants were the best thing since sliced bread. Years later, his therapist pointed out to him that it seemed like he was still depressed; the author responded that no, he couldn’t possibly be depressed because paroxetine was keeping his serotonin levels up; but then changed his mind and decided to stop meds. “It was only when I stopped taking the [SSRI] and I started having more pleasurable sex again that I remembered regular sex is one of the best natural antidepressants in the world.” I guess I’m just a little (or a lot) judgmental, but this dude seemed like he was energetically leaping onto the train to out-there-ville.
Next stop on that train is with researcher Irving Kirsch. Kirsch criticized the typical design of drug trials, i.e. randomized placebo-controlled trials (you can find more about that in my post on research literacy). He argued that to truly understand the effect of a drug there should be 3 arms to these kinds of studies: drug, placebo, and no-intervention, with the third arm capturing the number of people who get better with no treatment or placebo at all. This sounds all well and good except that it gives you zero new information about what the drug does. The people who would respond to no intervention are already captured in the placebo responders, so adding a do-nothing arm only gives you information about how much of the placebo effect is due to that sugar pill the researchers are giving the patients. Now that information may be useful in examining the placebo effect, but it doesn’t in any way change what a study shows about the effect of drug response over placebo.
Next stop on the train is holding up the old serotonin deficiency hypothesis for depression as evidence that the illness doesn’t have a biological basis. That hypothesis was originally developed to try to explain why drugs that blocked serotonin reuptake had an antidepressant effect, and at the time they didn’t have the scientific techniques available to test whether this was really accurate. It has since become clear that depression is not related to a deficit in the absolute amount of serotonin, but that doesn’t mean we should throw the baby out with the bathwater. Just because the overly simplistic early explanation was wrong doesn’t mean that neurotransmitters have nothing to do with depression period, and it doesn’t mean that antidepressants that affect neurotransmission won’t work. It’s like saying that because the flat earth hypothesis was wrong there must be no earth at all.
The author talked about bereavement being mislabelled as depression. A woman he interviewed said “So now if your baby dies and you go to the doctor the next day and you’re in extreme distress, you can be diagnosed immediately.” People have the right to be ignorant, but that doesn’t mean their ignorant comments should be thrown into a book as evidence. This idea that the DSM diagnostic criteria are a checklist and if you tick enough boxes you must be labelled with the disorder, well, it’s just not correct, which is why only highly trained clinicians are qualified to diagnose. Admittedly, some clinicians are too quick to jump to a diagnosis, but that’s very much a separate problem.
In the DSM-IV, bereavement was listed as an exclusion criteria for diagnosing a major depressive episode; this was done in an attempt to avoid bereavement from being mistaken as depressiom. The author raised concerns that maybe depression wasn’t so sound an entity if a normal experience mimicked the symptoms. But then he does a 180 and questions the removal of that bereavement exclusion in the DSM-5 and the addition of only a “vague footnote”. That “vague footnote” is actually part of diagnostic criterion C for a depressive episode, and says: “Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural disaster, a serious medical illness or disability) may include the feelings of intense sadness, rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion A, which may resemble a depressive episode. Although such symptoms may be understandable or considered appropriate to the loss, the presence of a major depressive episode in addition to the normal response to a significant loss should also be carefully considered. This decision inevitably requires the exercise of clinical judgment based on the individual’s history and the cultural norms for the expression of distress in the context of loss.” So yeah, no day-after-death diagnosis.
The author announced that based on his information gathering (and no training whatsoever in psychiatry/psychology) he has identified 9 causes of depression. He adds that depression is a form of grief over these various forms of disconnection. The identified causes are:
Part II of the book, “Reconnection: A new kind of antidepressant”, looks at ways in which people can reestablish those needed connections. This starts off with what to me seemed to be a rather rambling story about an apartment block in Berlin slated for demolition. An older woman had posted a note saying she was going to kill herself because she’d be losing her housing and she had no other options (there’s no indication that this was a woman with any history of mental illness). This sparked community activism that positively impacted all of those involved. And lo and behold, the woman’s suicidal thinking disappeared – so that’s what I must have been missing those times I tried to kill myself! It made me think of a line from a medical historian interviewed in the documentary The Age of Anxiety: “If your problem can be corrected by a new boyfriend or a cheque for $5000, you probably don’t have a psychiatric disorder.”
The author came to the conclusion from this and other examples that “if you want to stop being depressed, don’t be you. Don’t be yourself. Don’t fixate on how you’re worth it. It’s thinking about you, you, you that’s helped to make you feel so lousy. Don’t be you. Be us. Be we. Be part of the group. Make the group worth it… So part of overcoming our depression and anxiety—the first step, and one of the most crucial—is coming together.”
The author says that “work is essential”, which made me wonder why he has his head up his privileged ass. He talked to a woman who was anxious because of her negative work situation, then she joined with her husband and others in creating a cooperative bike repair business and things were hunky dory. The author describes this “recipe for mental health” as “Elect Your Boss”. So that’s what we’re all doing wrong…
Hari wrote that if he could speak to his younger self, he would say: “You are not suffering from a chemical imbalance in your brain. You are suffering from a social and spiritual imbalance in how we live. Much more than you’ve been told up to now, it’s not serotonin; it’s society. It’s not your brain; it’s your pain… Because you are being told depression and anxiety are misfirings of brain chemicals, you will stop looking for answers in your life and your psyche and your environment and how you might change them. You will become sealed off in a serotonin story.” I suspect there may be some funky paint fumes going on up in that serotonin story.
If this had been a book about general dissatisfaction and unhappiness in society at large, I would be writing a very different review right now. I suspect that Hillary Clinton and some of the other well known people who have commented positively on the book may have been looking at it from that perspective. If the book had talked about some people having mental illness that is heavily influenced by social/environmental factors, or the need to take social/environmental factors into account in approaching the treatment for mental illness, then I would have far more positive things to say. But that’s not the case. He is saying that mental illness is not biologically caused and medication is not a valid treatment for depression. Full stop. I think that’s just as bad as the purely biomedical stance that he criticizes. Such a reductionistic approach really isn’t useful to anybody, and is insulting to those of us living with the complexity of mental illness.
So what can I conclude personally from this book? Apparently to get better I’m supposed to engage in local activism, participate in a community garden, start a co-op, hang out in nature, and get laid. Forget meds, give me a little penis therapy instead. Why would anyone be suicidal when they could bond over community activism? Of the various disconnects that he believes cause depression, I had a whopping none of them for my first two depressive episodes. Screw pain, I was generally happy and optimistic, and had no childhood trauma, a supportive social circle, a job I liked, a strong preference for the value of travelling the world rather than accumulating possessions, a home in an urban oasis right with a forest just steps away… and yet there I was, depressed, psychotic, suicidal. Meds are certainly not the only tool in my toolbox, but without them, I probably wouldn’t be alive today. So rather than go postal on the author’s ass for presuming to tell me what’s going on with my illness, I’ll just wave as he goes by on the train to out-there-ville. Enjoy the ride!
You can find my other book reviews in my blog index.
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.
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.
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:
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.
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.
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 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.
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.
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.
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.
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.
You can find my other book reviews in my blog index,
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.
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.
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 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 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……
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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.
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?
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This is the 3rd in a series of primers on how psychiatric meds work. The previous posts were on antidepressants and antipsychotics, and upcoming are anti-anxiety meds and sleep meds. These are based on my professional knowledge as a mental health nurse and former pharmacist as well as my own experiencing taking these medications (although with a diagnosis of major depressive disorder I’ve never taken any of the anticonvulsant mood stabilizers).
Mood stabilizers work in a number of different ways to control signalling between nerve cells. They are used to treat and prevent both mania and depression, although some drugs are more effective for one than the other. They fall into 3 broad categories: lithium, anticonvulsants, and atypical antipsychotics.
Lithium has been around for many years. It works via a number of different mechanisms, including regulating genetic expression of various neuron-related factors, and boosting activity of the calming neurotransmitter GABA. GABA counterbalances the excitatory neurotransmitter glutamate. Lithium is effective for both mania and depression, and has been shown to decrease the risk of suicide.
Lithium is a type of salt, so blood levels are affected by kidney function and hydration status. In the past, some people developed kidney damage from long-term lithium use, but that is rare now as we have a better understanding of what levels are safe. People taking lithium need periodic bloodwork to check their lithium and creatinine levels (an indicator of kidney function). Target levels are 0.6-1.2 mmol/L, with higher levels being needed in acute mania. It takes 5 days after a dose change for blood levels to restabilize.
Lithium can potentially cause a lot of side effects: nausea/vomiting/diarrhea, tremor, weight gain, hair loss, acne, frequent thirst, frequent urination, hypothyroidism, and effects on the heart. And if that wasn’t enough, lithium toxicity (levels over 1.5) can cause confusion or even seizures and coma. Yikes. Except lithium works very well, and some people may have no side effects at all.
Lithium has definitely been effective for me. I’m using it for depression, so I aim for levels between 0.65-0.8 depending on how I’m doing. I have side effects, but for me the benefit outweighs the negatives. I have a tremor, which is worse when I’m fatigued or if I’ve had to increase my dose. Taking propranolol (a beta-blocker) helps with this. I’ve gained weight on meds, but I’m on 2 other meds that cause weight gain so it’s hard to tell what’s causing what.
These medications were initially developed as anti-seizure medications, but have since come to be used as mood stabilizers. They affect signalling between nerve cells by acting at voltage-sensitive ion channels that allow sodium/calcium to flow in and out of neurons, and they also boost GABA neurotransmission.
These are essentially the same molecule, but divalproex can be formulated into an enteric-coated tablet that decreases stomach upset. Valproic acid is effective for mania, but it is less clear how effective it is for bipolar depression. Dosing is targeted to reach a blood level of 350-700 µmol/L.
Side effects include nausea, sedation, weight gain, hair loss, tremor, negative effects on the liver, cessation of menstrual periods, and polycystic ovarian syndrome. It is also teratogenic (causes harm to a developing fetus). I talk more about this in my post on mental illness and childbearing.
Carbamazepine is most clearly effective for mania. It affects the liver’s cytochrome P450 system, leading to interactions with a number of different medications. It can also decrease the reliability of oral contraceptives.
Side effects include gastrointestinal upset, sedation, dizziness, impaired coordination, and negative effects on the liver, white blood cells, and platelets.
Lamotrigine is not effective for bipolar mania, and works best for the prevention of bipolar depression. It interacts with both valproic acid and carbamazepine, requiring adjustments in dose. It must be initiated slowly to decrease the risk of Stevens-Johnson syndrome, a type of severe rash.
Other side effects include dizziness, headache, double vision, drowsiness, impaired coordination, nausea, and weight gain.
There are other anticonvulsants that have been tried in bipolar disorder but don’t necessarily have strong evidence to support their use. These include levatiracetam and topiramate. Gabapentin does not appear to be effective.
The mechanism by which atypical antipsychotics have a mood stabilizing effect is not entirely clear, but may be related to their action at the 5HT2a serotonin receptor and resultant effects on glutamate, dopamine, norepinephrine, and serotonin signalling. They are useful for both bipolar mania and depression. Examples include lurasidone, aripiprazole, quetiapine, and olanzapine (which can be combined with the SSRI antidepressant fluoxetine for bipolar depression).
For more detail on atypical antipsychotics, please have a look at my post Psych Meds 101: Antipsychotics.
There are two key problems with antidepressants in bipolar disorder: they don’t work particularly well, and there is a risk of triggering mania. The International Society for Bipolar Disorder task force on antidepressant use found that evidence for antidepressant use is limited and weak, and as a result they could not broadly endorse the use of antidepressants in bipolar disorder. An exception is fluoxetine, which is effective when used in tandem with olanzapine.
For more on antidepressants, you can read my post Psych Meds 101: Antidepressants
I hope that this has all made sense and shone some new light on mood stabilizers. If you have any questions please feel free to shoot them my way!
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Welcome to the second post of my psych meds 101 series on how psychiatric medications work, this time focusing on antipsychotics. In these posts I’m bringing together my knowledge as a mental health nurse, ex-pharmacist, and gal with depression who’s tried a boatload of meds, and hopefully putting out something that will make it easier to understand the nuts and bolts underlying the meds that so many of us take. Knowledge is power, after all.
**note: I will exclusively use generic drug names, since brand names vary from country to country
Needless to say the primary use of antipsychotic medications is in the treatment of psychosis. There are a number of other uses, though, and the atypicals (I’ll get to that soon) are more versatile than the older drugs. Atypical antipsychotics have an important role to play as mood stabilizers in bipolar disorder and to augment antidepressant regimens in major depressive disorder. They may also be used for anxiety, and quetiapine is a common example of this. Sedating antipsychotics such as quetiapine and methotrimeprazine may be used for sleep. Haloperidol, a typical antipsychotic, is used in the treatment of delirium, a rapid-onset disturbance in cognition and orientation.
Antipsychotics work by blocking D2 dopamine receptors. This impacts four major dopamine pathways in the brain, producing the therapeutic effect as well as side effects:
There are two broad classes of antipsychotics: the “typicals” (older) and “atypicals“. The key difference between these classes is that atypicals also block 5HT2a serotonin receptors. This actually boosts dopamine signalling in the pathways other than the mesolimbic, which decreases the risk of side effects related to those 3 pathways. Additionally, the effect on 5HT2a receptors contributes to a therapeutic effect on mood. Another difference is that the atypicals are thought to move more rapidly on and off the D2 receptors, which is thought to allow for the full therapeutic effect without as much potential for side effects (this effect is referred to as “hit-and-run”).
To complicate matters, most antipsychotics aren’t very “clean”, in that they affect a number of other receptors aside from D2 and 5HT2a. And that means side effects.
While there is no way to predict which specific person is going to experience which particular side effects, in general medication side effect profiles are based on the types of receptors they interact with.
Extrapyramidal symptoms (EPS) occur most commonly with typical antipsychotics. These are named for an area of the brain that is part of the nigrostriatal dopamine-signalling. Excessively blocking dopamine in this region produces movement-related side effects, including tremor, rigidity, and akathisia (restlessness). Anticholinergic medications such as benztropine can help to reverse these symptoms, due to an inverse relationship between the neurotransmitters acetylcholine and dopamine in this part of the brain.
Tardive dyskinesia (TD) is a slow onset, potentially reversible involuntary movement disorder that may affect the mouth, hands, and trunk. It is caused by enduring changes in dopamine receptors in the basal ganglia as a result of long-term use of high-potency typical antipsychotics. The risk of TD with atypicals is very low, and clozapine may actually improve TD symptoms.
This is a fancy name for causing apathy and related symptoms similar to negative symptoms of schizophrenia. This can result from blocking dopamine receptors in the mesocortical pathway, and primarily occurs with typical antipsychotics.
Dopamine blockade in the tongue-twisting tuberoinfundibular pathway can increase levels of the hormone prolactin, which can result in some distressing side effects. It can affect both sex drive and sexual function, and can also cause gynecomastia (development of breast tissue in men). In general atypicals are less likely to cause this, although risperidone tends to carry a higher risk than other atypicals.
The atypicals win out over the typicals in many senses, but a major downside is that they do carry a risk for metabolic syndrome, including weight gain, increased cholesterol, and increased risk of diabetes. This may be related to activity at histamine and 5HT2c serotonin receptors. The big three are clozapine, olanzapine, and (to a lesser extent) quetiapine. Aripiprazole and ziprasidone do not tend to be associated with weight gain.
This can be related to effects on histamine, muscarinic, and alpha adrenergic receptors. Individual medications vary in terms of which of these receptors they do or don’t effect, so there is a lot of variability in sedating effect.
The cholinergic signalling system is responsible for resting and digesting activities. When antipsychotics disrupt this, the result can be things like dry mouth and constipation. On a more positive note, this can decrease the likelihood of experiencing EPS. Again, there is a lot of variation from medication to medication as to anticholinergic activity.
Quetipine affects serotonin and norepinephrine signalling in addition to its action on dopamine, and this likely contributes to its beneficial effects on mood. The dose range varies widely, and for good antipsychotic effect the dose needs to be at the higher end of the range, approaching 1000mg/day.
Olanzapine is beneficial for mood. It has a low risk of EPS.
Of the atypicals, risperidone is the most likely to cause EPS and prolactin-related side effects. Risperidone is metabolized by the body into paliperidone, which carries a somewhat lower risk of side effects.
Aripiprazole has a unique mechanism of action. It’s a partial agonist at D2 receptors, meaning it tries to create something along the lines of the Goldilocks just-right bowl of porridge. It’s not sedating, and can actually help boost people’s energy. It’s not associated with weight gain. For all that it sounds like a pretty good drug, when I tried it several years ago I found my mood actually got worse.
Clozapine can be a wonder drug for people whose psychotic symptoms are resistant to other medications. It is the only antipsychotic that has been shown to decrease the risk of suicide in schizophrenia. However, it can be problematic in terms of side effects. It can increase the risk of seizures. It can cause drooling, which can be quite bothersome for some people. It can cause a dangerous drop in white blood cells, so bloodwork is required every 1-4 weeks. When starting clozapine, there is a small risk of an inflammatory reaction in the heart called myocarditis. It’s definitely not a first line medication, but sometimes you really do need to bring out the big guns.
Examples include loxapine, haloperidol, zuclopenthixol, and flupenthixol. The latter three are often given as long-acting injections, although there are more alternatives now as a number of atypicals have become available for injection.
There are a a number of typical and antitypical medications available as long-acting (“depot”) injections. These are generally given every 2-4 weeks. They are given intramuscularly into the shoulder (deltoid), hip (ventrogluteal) or upper buttocks (dorsogluteal) sites.
There are a number of benefits to long-acting injections. For some people it’s just easier to get an injection every few weeks than to take pills every day. Long-acting injections produce very steady levels of medication in the blood, and it can be hard to replicate this even if someone is fairly consistent with taking oral medications. Injections may be the treatment of choice for someone who is on some sort of community treatment order (the terminology and details around this vary depending on jurisdiction), particularly if they’re not keen on taking meds because they don’t have insight into their psychosis.
The downside to long-acting injections is that if people have side effects, they have to wait a while for the medication to clear out of their system. This can be avoided by trialling someone on the oral version and then switching to the injectable.
I hope that I haven’t confused you or totally turned you off of antipsychotics. Personally I’ve taken quetiapine for years and will continue to take it for many more. Antipsychotics can do a world of good, and I would say the most important thing is to work with your treatment provider to find what works best for you.
I’ll close with a brief anecdote. I once had a client who had been extremely psychotic when I first started working with him. We stabilized him on risperidone, and he responded beautifully except he was having sexual side effects. We lowered his risperidone and added some olanzapine, and now several years later he is an amazing peer leader and advocate. Meds gave this client his life back, and that’s priceless.
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I can be a bit (okay more than just a bit) of a geek, and one of my big interests is how medications work. Throw in the fact that I’m a mental health nurse, former pharmacist, and person who has tried piles of different psychiatric medication, and you get someone who will quite happily watch hours of continuing education webinars on the topic.
It can be really useful to understand how medications work, because it can make both the therapeutic effects and side effects make more sense. This is the first of a series of psych meds 101 posts I’m going to write that will break down different classes of medications. I’ll also address antipsychotics, mood stabilizers, anti-anxiety meds, and sleep meds.
Most antidepressants affect the three major neurotransmitters implicated in depression: serotonin, norepinephrine, and dopamine. Nerve cells (neurons) communicate with other neurons via connections known as synapses. The neuron sending the signal is referred to as presynaptic, and the neuron receiving the signal is referred to as postsynaptic. The presynaptic neuron releases neurotransmitter molecules in the synaptic cleft (the space between the two neurons), and the neurotransmitters act at specific receptors on the postsynaptic neuron.
Why does that matter? Many antidepressants are reuptake inhibitors, meaning they block recycling pumps on the presynaptic side that would normally take up and recycle some of the neurotransmitter that had been released. This means there is more neurotransmitter floating around the synaptic cleft, available to act at receptors on the postsynaptic neuron. Over time, this actually changes the number of receptors that the postsynaptic neuron produces, which may explain the delayed onset of action for antidepressants.
Other antidepressants may block certain types of receptors on either pre- or post-synaptic neurons, and this may influence the release of one or more types of neurotransmitters.
A lot of medications are messy, in the sense that they don’t only do want them to. Some antidepressants affect histamine receptors, and this can cause side effects such as sedation and weight gain. Activity at muscarinic receptors can cause sedation, dry mouth, and constipation.
There are multiple different kinds of serotonin and norepinephrine receptors, and they impact various processes in the body. When serotonin gets busy at certain types of receptors it can do things that we don’t want it to, causing things like insomnia, weight gain, or sexual dysfunction. Norepinephrine can act at certain receptors to affect things like blood pressure, causing lightheadedness.
These inhibit the activity of the presynaptic serotonin recycling pumps. Escitalopram is the most “clean” in that it does what it’s supposed to and not much else. Other medications in this class include citalopram, sertraline, fluoxetine, and paroxetine.
These inhibit the presynaptic recycling pumps for both serotonin and norepinephrine. Some people are not as responsive to meds that act on serotonin alone, and respond better when there is action on norepinephrine. Drugs in this class include venlafaxine, desvenlafaxine, and duloxetine.
Bupropion inhibits the presynaptic recycling pumps for norepinephrine and dopamine. Because of the different mechanism of action, it can be used in combination with SSRI for a triple-whammy sort of effect.
These inhibit the recycling pumps for serotonin and norepinephrine. However, they are quite “messy” and affect a number of different receptors, meaning they tend to cause more side effects. They are dangerous in overdose because they can potentially disrupt the heart rhythm. Several years ago a psychiatrist wanted to put me on nortriptyline, and while I reluctantly agreed, I soon stopped it because I didn’t think it was a safe medication to have at home given that I do get suicidal thoughts in the context of depression. Other examples of TCAs include amitriptyline and imipramine. This class of medications is also used to manage nerve pain.
These inhibit the monoamine oxidase (MAO) enzyme, which acts inside neuronal cells and is involved in breaking down serotonin, norepinephrine, and dopamine. They are an older class of medications and despite being very effective antidepressants they are seldom used because of the need to restrict dietary intake of tyramine. Tyramine is normally broken down in the gut by MAO, but if MAO is blocked by medication, tyramine is absorbed into the bloodstream and sends blood pressure through the roof. This condition is referred to as hypertensive crisis. Tyramine is found in a number of different foods, including aged cheeses and fermented foods.
Tranylcypromine is the most commonly used MAOI. Moclobemide is a variation of an MAOI called a RIMA (reversible inhibitor of monoamine oxidase) that acts reversibly on the MAO enzyme, so that tyramine is still able to get broken down safely by MAO in the gut.
There are a variety of other medications such as mirtazapine and vortioxetine that work in novel ways, which I won’t get into here. The combination of mirtazapine and venlafaxine is sometimes referred to as “California rocket fuel”; this is part of my current treatment plan, and while I’m not getting a rocket fuel effect it has helped. There are also other medications that can be used to augment antidepressant therapy, including lithium, atypical antipsychotic medications, and liothyronine (a form of thyroid hormone).
There are also new outside of the box treatments being studied such as ketamine, which affects the action of the neurotransmitter glutamate. I am really excited about this, and will write more about it in future posts.
If you’ve made it this far, good for you! I hope you’ve found some of this useful, and maybe it’s even given you some added insight into medications you have taken or are taking. In the upcoming post Psych Meds 101: Mood Stabilizers, I’ll talk about the treatment of bipolar depression, and why antidepressants have a limited role to play.
I guess I should start by explaining what Uzbek is. It’s the language of Uzbekistan, a former Soviet republic in central Asia that was part of the Silk Road that once wound through Asia. It’s an area of the world where there are still people living the traditional nomadic lifestyle involving yurts, riding horseback, and drinking fermented mares’ milk (a delicacy I just couldn’t bring myself to try).
So how does this relate to antidepressants? That’s where I have a story to tell. In 2015, I spent 5 weeks backpacking in Uzbekistan, Kazakhstan, and Kyrgyzstan. During that time, I was hauling around a veritable pharmacy: a sufficient supply of my 5 different psych meds, plus my standard round-up of just-in-case backpacking meds to cover motion sickness, travel’s diarrhea, and other such fun adventures.
I landed in Tashkent, the capital city of Uzbekistan, around 10pm. I was exhausted from the long flight, and just wanted to fall into bed somewhere. I thought it seemed a bit odd that the customs declaration form asked for a list of any medications I was carrying, but I dutifully listed them all. The rather ghetto-seeming airport wasn’t inspiring much confidence, but I hoped that as is often the case my Canadian passport would get me waved right through.
When my turn in line came, I handed my declaration form to the customs officer. He stared confusedly at my mammoth list of medications. Then he wanted to see them, although I’m not sure why, as that didn’t seem to make things any easier. He appeared to have no idea what to do, so he consulted some of his colleagues. I told them that they were for depression, but they didn’t seem to have any idea what I was talking about. There was much talking, looking confused, and phone calls until finally they waved me along.
I thought that would be the end of it; if only I could be so lucky. I hadn’t booked a hostel room because it hadn’t struck me as necessary; I was an experienced traveller and had never had problems before. Tashkent is no great tourist mecca, so that might have worked out okay, except there was some sort of international sporting competition going on in town and everything was booked up solid.
By midnight, I had given up on Tashkent and instead turned up at the Uzbekistan-Kazakhstan border, thinking I might have better luck across the border. Except that meant another customs declaration form, and much more confusion over my bag of meds. The customs officers tried to be nice, but spoke very minimal English. They wanted to know what the meds were for, and I didn’t think antidepressant would be in their lexicon, so I kept pointing at my head. Maybe that made them more confused, or maybe it made me look more like a psych patient – who knows. When they saw I’d just arrived in Uzbekistan that night, they decided they needed to call customs staff at the airport. Talk about the blind leading the blinder. Eventually I think they just took pity on me and let me go.
Travelling with psychiatric medications in non-Western countries can be a bit dicey, even aside from the issue of border crossings. Replacement meds can be hard to come by if meds get stolen, and that’s something I always try to remain cognizant of. That saved my butt on one occasion in India when I was sleeping in an upper bunk on an overnight train. My backpack was shoved underneath the lower bunk, and during the night someone stole everything in the backpack other than clothing. If my bag of meds hadn’t been tucked in beside me on the bunk, they would’ve been gone.
I haven’t really been well enough to travel in the last couple of years, but hopefully I’ll get back into it even with the depression. I still may be able to pull off my 40 by 40 goal: 40 countries visited by age 40. And next time I go somewhere off the English-language track, I might look up the local word for antidepressant ahead of time… just in case.
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What do mental illness and sex have to do with each other? Quite a bit, actually, both in terms of the illness itself and the medications to treat it.
Let’s start with meds. Antidepressants that affect serotonin (such as the SSRI class) can do a real number on sex drive/function. This tends to be mediated by a particular type of serotonin receptor known as 5HT2a, which means that some antidepressants that affect serotonin are less likely to cause this problem, such as mirtazapine and vilazodone. Another option is something like bupropion, which doesn’t act on serotonin receptors. I talk more about antidepressants in my psych meds 101 post.
Antipsychotics can also be problematic (more on this in psych meds 101). Antipsychotics work by blocking dopamine receptors, but if there is too much dopamine blockade along a certain pathway in the brain (the tuberoinfundibular pathway to get really geeky with it), you disrupt levels of the hormone prolactin, and boom, you get sexual dysfunction. Different antipsychotics vary in their potential to affect prolactin, so having sexual side effects with one doesn’t mean you will necessarily have the same effect with another medication.
Some mood stabilizers such as valproic acid are quite teratogenic, meaning they’re likely to cause fetal malformations. This means reliable birth control is something that has to be considered along with everything else that goes with a mood disorder. This is easier said than done for a woman in the midst of a manic episode.
Then there is the illness itself. As a nurse, I’ve spoken to clients who are deeply ashamed of reckless sexual behaviour they’ve engaged in while manic or psychotic, things that under normal circumstances they would never even consider doing. At the other end of the spectrum, depression can shut down sex drive and sexual function. These are issues that it’s not easy or comfortable to talk about, so they tend to hide in the shadows, but they can have a huge effect both on an individual level and on a relationship. I don’t have any great insights or answers to share with you, but I do think it’s important to talk about it. It’s also worth considering sex as a potential barometer of your mental health. I remember at one point when my depression was starting to improve I met a man who actually made me feel turned on, and I thought wow, this is the most normal thing that I’ve felt in a very long time.
I’ll close with a quick word on autoerotic activity, to borrow a term from Seinfeld. Orgasm releases happy hormones like oxytocin and dopamine, so it seems to me a little bit of self-love once in a while can’t hurt. And really, we all deserve some self-love, whether it’s in an erotic sense or not.
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Society is obsessed with how we look, and in particular what size we are. Even people who are generally quite polite feel entitled to comment on our weight and body shape, without having any idea what the backstory might be. In the case of mental illness, there is often a great deal of backstory.
Over the last 10 years, there’s been about an 80 pound span between my lowest weight and my highest, and I’ve ranged from a size 6 to a size 16. When I’m depressed, I tend to lose my appetite, and at times have lost significant amounts of weight because of this. When I’m really unwell, I could easily go days without eating, but I know that I should eat, so I try to force food down. When this is too hard I try to choke down something like Boost instead. The only time I have ever counted calories was when I was pushing myself to cram in 1000 Calories a day, about half of what I should actually be taking in. When people complimented me on my weight loss, I would have thrown those bottles of Boost at them if I had the energy. Why did these people see skinny sick me as somehow better than curvy well me? It was almost certainly done out of ignorance rather than malice, but that shouldn’t make it okay to essentially say “you look better when you’re sick”.
For the last several years I’ve been on a trifecta of weight gain-inducing meds (quetiapine, mirtazapine, and lithium) that tipped the scales to over 200 pounds. I had mixed feelings as the weight piled on. I wasn’t thrilled about the changes in my body, especially since it felt so out of my control. Still, that med combo kept me well for a few years, and that was really my priority. After a solid period of stability on this med combo, I decided to try going off the Seroquel, hoping that would bring my weight down a bit. What actually ended up happening was that I had a relapse of my depression. At that point I decided it was time to just fully accept my new body, because if I wanted to be well I needed these meds.
Earlier this year I began seeing a naturopath. I had gotten depressed again despite my med cocktail, and I was willing to try anything that might help. Based on my history and bloodwork, one of her recommendations was an anti-inflammatory diet. It’s not a weight loss diet; instead, it’s all about putting healthy foods into your body and keeping unhealthy things out. I have ended up losing some weight as a result, and I’m feeling more comfortable in my body, but I’ve faced the issue again of people commenting on my weight loss. Yes, the weight loss is a healthy thing this time around, but people don’t know anything about that when they make comments. My body should not be theirs to pass judgment on.
I don’t recall ever actually saying anything in response to the people have commented on the changes in my body. There’s just too much backstory to be able to fit into a one-line zinger. Our bodies may reflect to some extent what’s going on inside of us, but often not in a way that is consistent with societal expectations around body size and shape. From anorexia nervosa to depression to binge eating disorder, our bodies can be warped by our illnesses. I just hope that someday more people will understand that.
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