Last week, we covered what Selective Serotonin Reuptake Inhibitors (SSRIs) are marketed as and what it actually does (it’s different, but not far off), and this week, we’re going to cover what to expect.
It’s a little known fact that the second-leading cause of death amongst teenagers in Canada is suicide, followed by
stupidity accidents (Szatmari, 2014), while it is the eighth most prevalent for adults (Statistics Canada) and in an effort to alleviate this issue, more and more psychiatrists were prescribing psychotropic medications, namely SSRIs (Murray, Thompson, Santosh, & Wong, 2005). However, a different problem came up (as with many other things involving things where people rush to make more money) where more teenagers with this drug started reporting suicidal thoughts when they didn’t even have any prior to taking SSRIs (Ghaziuddin, Merchant, Dopp, & King, 2014), and this included adults (Nischal, Tripathi, Trivedi, 2012). This lead to the Food and Drug Association (FDA) in both Canada and the United States to issue a “black box” label on these medications. “Black box” meaning, “This shit can end you in very creative ways.”
(Imagine not being able to sue because the suicide method wasn’t creative enough though…)
So you may be wondering, “What is the point of taking these drugs if this is what it’s going to do to me?” Honestly, the law of averages…and the Swedes. In 2013, Björkenstam et al. of Uppsala University in Sweden discovered the Activation Syndrome.
Bit of background here, for any psychiatric medication, it takes about 3-6 weeks for the patient to start feeling the effects after continuous use (Parker et al., 2000), but it is during that time that is the most important because of this Activation Syndrome. Rest assured though that only 4% of those taking SSRIs feel these urges to self-terminate. So it’s not too bad if you play the numbers.
Now, with our SSRIs, it slowly starts to restructure and repair the hippocampus, returning it to normal after the damage done by excessive cortisol over time (as discussed in my previous post), and this is a crucial time that should be closely monitored by the patient’s medical practitioners and, most importantly, his or her support network. All parties involved must understand what is going on neurologically and scientifically in order to have a successful run against this particular type of mental illness. Knowledge (and individual mental strength) is power in this case because it relieves the fear of the unknown and that everything is going as it should be. Being ignorant about the problem is the worst thing anybody can do; I mean, just look at people against homosexuality.
(The word count before that paragraph ended was 420…ignorance also feeds the war on drugs…)
According to Björkenstam et al., the peak of the suicidal danger is (slightly) different between men and women. For dudes, it is between eight to eleven days at the start of therapy, while for dudettes, it is between ten to twelve.
Interestingly, I personally never felt the peak that late; it was closer to a 5-day maximum, with the peak being on Day 3. In my last go with SSRIs back in late April/early May, I felt pretty good after a week. I think it is because there are some variations with my hippocampus and how badly damaged it is after a decade or two of cortisol abuse, but now that I think about it, that’s not very likely considering the sample size Björkenstam et al. had; that variation should’ve been noticed in the stats crunching (or maybe they just didn’t report, who knows…).
So why only 4% of patients experiences this? No one really knows, as I’ll explain below, but my personal hunch on this is it is dependent on how damaged your hippocampus is from said cortisol exposure and duration in a person’s life and their own personal trains of thoughts. I know that this new format is to look at depression and the like in a scientific point of view, but much like everything else in psychology, both the environment and genetics plays a role in a person’s development.
At the end of the proverbial day, Björkenstam et al. couldn’t find anything that would trigger these symptoms, but could only confirm its existence. Surprisingly, there are also no known rates of suicide that are caused by the Activation Syndrome (Safer & Zito, 2007; Gibbons, Hur, Baumik, & Mann, 2005). My guess is because it is harder to forensically prove that a simple pill killed someone when it’s pretty obvious that the person hung/shot/poisoned/take your death pick themselves. Keep in mind that the Bjökenstam study was published only two years ago and I’m sure there is research going on as I write and you reading this, so (much) more time is needed.
I was having lunch with my defenseman with a neuroscience BsC degree the other day and we were talking about how far we’ve come in understanding the human brain on an actual scientific level. While neuroscience and psychology were considered as one discipline for a long time, it has only been the past hundred years or so that we have really begun to understand it, especially with the advent of fMRI machines. With that said, we are completely ignorant of what’s going on with the Activation Syndrome, and please don’t hold your breath until we find out or else that’ll be some other form of oxygen-starved brain damage.
So that’s it for this week, hope it was fun and riveting. Keeping with the tradition of this blog, I’ve been writing while my hippocampus was starved for serotonin and SSRIs, and I’m seeing that I’m a pretty sadistic asshole! Haha! This weening thing isn’t working out as well as I’d like it to. Whoops!
Next week, we’ll delve into the nitty-gritty (kitty) brain science of suicide.
By the way, I’ve never seen a single episode of this show…don’t even know what it’s about…
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