David's Inferno (17 page)

As a one-man clinical trial, I'm often asked about specific meds. After trying to answer those questions for a while, I realized that while I could toss around acronyms like SSRI, NDRI, TCA, MAO, AED, and CNS with the best of them, there was something about the way that antidepressants are classified that didn't make sense.

All those years I thought I'd been trying to understand the difference between apples and apples, it turns out I was actually dealing with apples and oranges—with a few fish and fowl thrown in for good measure. As best I can tell, this is how it breaks down:
Drugs classified based on what they do in the brain
. Anything with an RI (that doesn't refer to the state where I was born) acts on the brain by
I
nhibiting the
R
euptake of neurotransmitters. Those are the various
S
elective
R
euptake
I
nhibitors (SRIs).

MAOIs (
M
ono
a
mine
O
xidase
I
nhibitors) are also named based on what they do in the brain. They inhibit the enzymes that are waiting to chow down some nice juicy used-up neurotransmitters.

In both cases, the goal is to have more synaptic connections.

Drugs classified based on the condition they treat
. Or, in many cases, the condition they were originally designed to treat. An AED, for example, is an
A
nti
-E
pileptic
D
rug. However, I, and many other people who have never had an epileptic fit, take them as mood stabilizers. They're also prescribed for bipolar. Still they're called AEDs.

Drugs classified based on their chemical structure
. For example, the “tricyclics.” This is the classification that's the most annoying. The researchers should be ashamed of themselves. Tricyclics are Reuptake Inhibitors too. They're just not as selective. They're named for what they
are
, not what they
do
. Their molecules have three (tri) rings of atoms—whatever that means. The cyclic part comes from the citric-acid
cycle
which is made up of seven chemical reactions, or maybe it's nine. I can't remember. Regardless, what goes around comes around. It's also known as the tricarboxylic acid cycle (TCA) or the Krebs cycle—and I don't think they mean Maynard G! Bottom line: tricyclics should be called PRIs: Promiscuous Reuptake Inhibitors.

Neither fish nor fowl
. The notorious “Atypicals.” This is almost as much of a scientific cop-out as the diagnosis NOS (Not Otherwise Specified). Atypical antidepressants and antipsychotics are called atypical because, at one time, they were different from the typical ones prescribed for a certain purpose. Although now they are often now prescribed more typically for that and other purposes.

To make matters worse, doctors often use brand and generic names interchangeably. And prescribe them for both FDA-approved and off-label conditions. So, for example, you might be taking a drug named sertaline, which is the generic version of Zoloft. It boosts serotonin levels by blocking reuptake and makes certain serotonin receptors more or less receptive. While it's selective for serotonin (i.e., an SSRI), it also blocks more dopamine reuptake than the other SSRIs. So you
could
call it an SDRI. Maybe that's why it seems to cause fewer problems with sexuality and weight gain. And why it's sometimes prescribed “off-label” for eating disorders, fibromyalgia, hot flashes, and migraines.

See? It's hard enough to figure out what's what and why without having to figure out what the heck it's supposed to do. So, if you're curious why your doctor prescribed what he or she prescribed for what ails you … ask. And keep asking. I mean, it's
your
mind. Even though it occasionally feels like someone else's.

Drug companies put a lot of effort into coming up with names. They need something with an obtuseness only a doctor could love (and prescribe). At the same time, they want to give patients at least a subliminal message of encouragement. Typically, they spend more than a million dollars to achieve these goals.

In retrospect, the name Prozac doesn't seem to fit that bill. Allegedly, it's just a mishmash of positive sounds. (I get the “pro” part. But “zac”?) Doesn't matter. The word has become so much a part of the lexicon that we don't question it anymore. The names Zoloft and Paxil are more calming and uplifting. Effexor certainly sounds effective. Wellbutrin suggests it may actually tame the beast. And, for some reason, Cymbalta has a relaxing ring, even though the image of crashing cymbals isn't exactly soothing. The name BuSpar seems unpleasantly Germanic, but does imply it'll put up a good fight. Abilify sounds like a performance-enhancing drug trying to pass as a mild-mannered pick-me-up.

Like Prozac, the brand named Valium has become so ingrained in our vocabulary that it makes most folks feel faintly drowsy just
hearing the word. At least it's a whole lot less sexist than “mother's little helper.” (Which included Librium and Quaaludes as well as Valium.)

“What are you taking?” Once you've identified someone as a fellow traveler, that's how you usually break the ice. Before you ask what they do for a living, whether they're in a committed relationship, have children, or root for the Red Sox or Yankees (correct answer revealed later), you want to know what drugs they're on. It's a bonding thing.

Once they answer, the proper response is a thoughtful, “Huh.” followed by a few pleasant stories about anyone you know who has ever taken that drug
successfully
.

There are
some
people who respond by telling stories of people they know who took that drug and broke out in hives, had brain-crushing headaches, and/or ended up in an Inpatient Psychiatric Unit.

I consider this to be in extremely bad form.

Despite my uncertainty, if not total ignorance, about these things, when I used to hear what drug someone was taking, I thought I had something useful to contribute to the discussion. After all, I did much better with Lamictal than Depakote. Celexa made me crazy (literally) this time around after working for years. Wellbutrin helped even out my moods in the late 1990s; this time, it did little more than blunt the occasional edge—just enough so that when I told folks I felt a little better, I didn't feel I was perjuring myself. Seroquel left me uncomfortably numb. When combined with Depakote I felt drugged (a delineation that might seem meaningless in my case). Lorazepam made me feel just weird. Buspirone has a short half life and allegedly doesn't cause cognitive or memory impairment. I took it two or three times a day and it made me feel stupid. Valium was addictive for me. But, for whatever reason, I can take Klonopin on and off with no problem.

The point is that my experience is irrelevant
. All my opinions and attitudes
are based on the assumption (delusion) that how something affected me might affect you.

I'm not trying to show off here. (Well I am, kind of.) It's just that understanding the dysfunctional categorizing and fairly irrelevant nomenclature of drugs helps me understand what the ones I take are supposed to do, how they relate to each other, and how they relate to other ones I've taken in the past. Call it idle curiosity. Call it an obsessive thirst for knowledge. Call it empowering. When I learn this stuff, it makes me feel better.

For example, I've always wondered why there are so many different SSRIs. Seemed to me that a drug inhibits serotonin reuptake or it doesn't. It turns out that there are a whole lot of different molecules that can inhibit serotonin uptake. And they all do it a little differently. In particular, they all influence different combinations of receptors and metabolize at different speeds.

The speed of metabolism is particularly important for anyone who wants to understand what's happening in their brain when they take a psychotropic medication. Because it explains a drug's average “half-life.” (Average because of everyone's different size, shape, metabolism, etc.) A half-life defines how long it takes for half of the drug to get out of your system. Which helps explain:

You can have a basic understanding of
all
these things just from knowing the half-life of the drug you're taking. Because, unlike the Strontium 90 they just found in the soil near my friendly neighborhood nuclear plant—which has a half-life of about 30 years—the half-life of most medications can be measured in minutes, hours, or days. Obviously, the longer the half-life, the less problematic it is to miss one dose. Again, we're talking
average
half-lives. And none of us is average.

Here's a case in point. One morning, well after I'd stabilized, I realized I was running out of Lamictal. I called for a refill, but, having no other excuse to go downtown, I decided to split my two doses that day (i.e., 50 mg twice a day instead of 100 mg twice day).

The next morning, I took a whole 100 mg pill because I was
sure
I'd get downtown sometime that day. But I didn't. Maybe it was snowing or something. So, I took 50 mg that night and 50 mg the next morning. I can't remember why I didn't go to the pharmacy
that
day. In any event, I took my last 50 mg that night. I knew had had to go downtown the next morning. No matter what.

The writers of those tiny-type prescription inserts whip themselves into a frenzy about how you can break into weird rashes, send your blood pressure soaring, and/or die if you lose at medication roulette. But, at least with the antidepressants I've taken, they're rather la-di-da about missing
one
dose: don't double up, just take your next regular dose and get on with your life.

They do
not
, unfortunately, include the warning, “Hey, Dave … yeah you, the guy in Vermont … we're assuming you're not an idiot.
In other words, that you'll go downtown and get a refill ASAP after you realize you're out.”

The half-life of Lamictal is particularly variable, ±25 hours seems to be the accepted average for someone taking it on a regular basis. So, on the day after a given dose, you have about 50% of
that
dose left in your system; 25% the next; 12.5% the next, and so on. Since, in this case, over the previous three days I'd taken about half as much as usual … well, you do the math. (I get really confused when I try.) Bottom line, I was reducing my blood levels way faster than I would have if going off intentionally.

As I said, half-lives depend on a lot of subjective factors, e.g., how much you weigh, other drugs you're taking, and whether your kidneys and/or liver are operating at full power. For example, if you're also taking valproate acid (Depakote), the half life of Lamictal is considerably longer; i.e., you need significantly less. That's why, when I segued from Depakote to Lamictal, my psychiatrist gave me a special pack that dispensed exactly the correct amount to take of each, every day over a five-week period.

Statistics aside, when I woke up around 6 a.m. the fourth morning, I was seriously agitated. But the pharmacy wouldn't open for a few hours. I took a Klonopin, which calmed my mind a little but didn't do much for the shakes. By the time I was in the car, my heart was racing, I was beginning to cold-sweat, and it took all my powers of persuasion to convince myself I wasn't having a heart attack. At one point, I almost pulled over and called 911.