Death Grip (15 page)

Like the other consummate downers—barbs, alcohol, and Miltown, with which they are cross-tolerant—benzos act on the receptors for gamma amino butyric acid (GABA). GABA, according to Tone, is the brain's “chief and most prolific inhibitory neurotransmitter”
22
and one to which, writes Dr. Heather Ashton, an emeritus professor of psychopharmacology at Newcastle University in the United Kingdom and the world's leading benzodiazepine expert, about 40 percent of the brain's neurons respond.
23
Indeed GABA, found throughout countless systems in the body, is what our brain and nervous system use to calm themselves—it's “inhibitory” in the sense that it decreases nerve-membrane excitability, reducing the rate of neuronal firing, or the “activating” messages that speed across the synapses like a crown fire through a parched aspen grove. (Restak writes that seizure and anxiety disorders alike are thought to result from too much of such overexcitation in the brain.
24
)

On a baseline chemical level, GABA inhibition begins when a nerve impulse releases the neurotransmitter from the presynaptic neuron; this GABA then crosses the synaptic cleft to bind with special GABA-receptor sites on the postsynaptic neuron.
25
(GABA sites, writes Tone, “modulate the emotional states associated with anxiety”; the brain's highest concentration of GABA receptors is in the amygdala, a limbic-system component key to emotional regulation.
26
) This transmission causes the receiving neuron to open and let a negatively charged chloride ion enter, while a positively charged potassium ion escapes. As Jack Hobson-Dupont puts it in
The Benzo Book
, “… the electrical potential of the membrane is [thus] increased, which then counteracts any electrical stimulation of the neural receptor.”
27
Or as Dr. Ashton frames it, the negative chloride ions “supercharge” the postsynaptic neuron, “making it less responsive to other neurotransmitters—like noradrenalin and epinephrine—which would usually excite it.”
28
In other words the activating neurotransmitters that trigger fight-or-flight, and hence panic attacks, are inhibited from spreading their message.

Benzodiazepines, however, are not synthetic GABA: They don't work by binding directly to GABA receptors but instead ligate to benzo-specific subreceptors along the GABA sites, with each subreceptor doing a slightly different duty (e.g., alpha 1 subreceptors are responsible for sedation, alpha 2 for antianxiety effects, and alphas 1, 2, and 5 for anticonvulsant effects, etc.)—though all benzos synch up to varying degrees with the various subreceptors, and all, writes Ashton, “enhance GABA activity in the brain.”
29
Taking a benzo can thus be said to
potentiate
GABA, increasing the strength with which the neurotransmitter binds to the GABA receptors. Benzos are therefore “GABA boosters,” allowing a greater number of chloride ions to enter the postsynaptic neuron and ultimately make it more excitation-proof. The pills aren't putting anything in your brain that's not already there, but are simply working with what you already have. (As Ashton phrased it in a phone interview, “All benzos do is enhance the action of GABA—they don't work on their own.”) Do you recall the locus coeruleus, the little blue spot in the brain that initiates the fight-or-flight response? Well, as Restak writes, “Drugs that decrease the firing rate of the locus stop the panic.”
30
And benzos, it turns out, are one of those drugs—by boosting GABA, they have a synergistic dampening effect on norepinephrine, which helps halt the panic response. That's why taking a fast-acting benzo like Xanax or Ativan or Klonopin mid-attack will knock it out—in that sense, the drugs are effective.

At least, that is, until they stop working. The problem is that if you consistently take benzos for too long—more than two to four weeks is a commonly cited time frame—something called down-regulation of the GABA receptors can occur. In this process, because the benzos have come to do so much of the receptors' work, the latter's ability to attract GABA, or GABA affinity, diminishes. The GABA receptors become less responsive, “so that the inhibitory actions of GABA and benzodiazepines are decreased,” writes Ashton in a scholarly paper.
31
In a conversation with me, Ashton framed it as GABA receptors essentially getting absorbed into the inside of the neuron so that they are no longer on the surface and accessible to the neurotransmitter. In essence, having been phased out by a robot down at the plant, they no longer show up for work and instead stay home to watch TV and eat Doritos. Meanwhile, the robot itself—benzos—needs more and more fuel to do its job.

You're now strung out; you're officially dependent. You “need more and more benzos to get this calming effect,” says Ashton. “Or, if you stay on the same dose you go into withdrawal while you still take the benzos”—a bleak phenomenon called
tolerance withdrawal.
In this closed feedback loop, doses climb and receptors invert until your baseline anxiety level is higher than ever, perhaps with thickening storms of panic attacks. You might see temporary relief at each dosage increase, but it's short-lived as down-regulation continues apace. Neither can you keep upping your dose indefinitely, milligram by milligram, for the rest of your life—at a certain point you'll become toxic. Meanwhile you might start to feel “interdose anxiety,” common to the fast-acting benzos like Ativan, Klonopin, Xanax, and Halcion. These pills bind more tightly to receptors and have a shorter half-life than, say, Librium and Valium—they're metabolized much more rapidly, increasing anxiety symptoms between doses and inciting a “craving” for the next pill. (I say “craving” in quotes because, unlike pleasure-center drugs like cocaine and heroin, which flood the brain with serotonin and dopamine, benzos are what Ashton calls “depunishing drugs.” Through their GABA-ergic action they “protect against punishing stimuli”
32
—namely anxiety—but won't necessarily get you high except if abused in large doses. They're not really much fun to take.)

The first benzo I took was in February 1992, that spring semester back in Boulder. I'd gone over to some friends' house to watch
Blade Runner
, buying a gallon jug of Carlo Rossi white for us all. Still edgy with free-floating anxiety and also a little bit curious about the pills, I popped one as we cued up the movie. It hit ten minutes later as we watched Harrison Ford track his Replicants, a warm, billowing fog that swelled to fill the room. The Ativan imparted a feeling of
everything is fine.
Not,
everything is GREAT!
, as you might feel after a rail of coke or a few Vicodin. Just,
everything is fine
, as in nothing is wrong, and everything always has been and always will be okay. For the first time in months, my connection to the bodily scrutiny and catastrophic thoughts had been severed. I could not have had a panic attack had someone held a gun to my head.

The Ativan was very seductive. In a way—and perhaps because of the alcohol—I did feel “high.” It reminded me of the first time I'd been stoned on marijuana, one July night down in Albuquerque, the summer after I'd graduated from the Challenge Program. Leaving The Big Apple, a few of us punks had snuck into a dirt lot across the way and hidden behind a berm. I'd been around weed before but never inhaled, though this night someone explained how I needed to take the smoke down into my lungs and hold it. I did so, coughed, and then did it again. A few minutes later as we walked back toward the club, the world began coming in frames, like overlaid snapshots of itself stitched back together. I felt happy and giddy—almost reassured by the hallucinations. This was a better, more interesting version of reality: the siren song of any psychoactive substance. As my feet crunched tangibly over the dirt, I could pick out every pebble and grain of sand, elucidated in crystalline whiteness by the security lights across the way.

Benzos and weed, they didn't feel so different. With both, that initial message that the world was a warm, secure, glowy place and that I was safe in my body was impossible to ignore. I could see why the psychiatrist had urged caution: Notwithstanding the chemical component of addiction, on a purely psychic level if you pick up that smooth, laidback, easy-listening station over the airwaves once you'll want to tune in again, even if in trying to banish anxiety forever you end up worsening it beyond your darkest imaginings.

 

CHAPTER 7

With the benefit of hindsight, my first experience with benzodiazepine withdrawal came in Italy and Greece, in the summer of 1995. I'd been taking too many pills, and then ran out. I'd been living in Torino (Turin) in northern Italy that spring semester, junior year, for a study-abroad program, but had come mainly to be with my girlfriend, Luisa, an Italian five years my junior. I'd met this lovely girl with bright brown eyes, a rich laugh, nose ring, and dark, lustrous hair at a Christmas dinner at my father's over winter break 1993–94. Luisa lived with close family friends in Albuquerque as an exchange student. As dinner ended, I'd asked Luisa—bored to death, she said, in Albuquerque—if she wanted to ski in Taos, and we'd hit it off on the slopes: my first “date” in five years. Smitten not only with her but certainly also with the notion of female company, once she returned to Italy I'd begun sending Luisa frankly embarrassing missives that professed my infatuation. We started talking weekly by phone. She must have felt something, too, because she agreed to a one-month Eurail trip in the summer of 1994 despite having spent only one day with me. Never mind that she had a boyfriend, who came stumbling into her house drunk and peevish the day I arrived in Torino. By the time Luisa and I hit central Europe, midway through our trip, I'd convinced her of the superiority of the American male. It was either that backrub in Berlin's Tiergarten or the white wine straight from the bottle one night in Prague's Centre Plaza, but I'd convinced her in my own awkward, fumbling way.

Before I left for Italy, I'd visited the psychiatrist in Boulder to stock up on Paxil and Ativan. He wrote a prescription for sixty Ativan, but the two-milligram size this time, with the idea that it would be easier to travel with fewer pills that I could break in half. I must confess that, with the Ativan, I'd begun to blur the distinction between use and abuse: I'd horde pills the first few weeks of each month, and then wash down one or two a night with wine over the final week. (I dozed through more than a few survey classes the day after my one-man “parties.”) It was just like it had been with food: Deprive myself five days out of seven, then indulge to excess the other two. By then I had so few panic attacks that I felt comfortable monkeying around with the pills—I'd even gone off Paxil once or twice, when I didn't feel like I needed it. An improved diet helped as well: I now tried to eat three square meals a day.

That spring in Italy, however, I had had a panic flare-up—heart palpitations, sleeplessness, and night terrors. It would be easy to blame living in a foreign city, or to blame struggling with a new language and culture shock, but that just wasn't the case. I lived only two blocks from Luisa and her family in central Torino, renting an attic room from a mother-and-daughter pair who happened to be friends of Luisa's family. The Italians took great pains to include me in their lives and to help me learn the language. Luisa's parents also had ties to the climbing world—Luisa's father, Luigi, was the director of an Italian publishing house—and he and Luisa's mother, Sandrina, had introduced me to the Torinese climbing community. I had regular partners whom I'd meet weekly at a giant artificial wall at the Palazzo a Vela velodrome or with whom I'd load into tiny Euro-sedans and zip up to cliffs in the nearby Alps. Sandrina loaned her two-door Renault to Luisa and me, and we took weekend trips to Finale Ligure, a spectacular place with pocketed bellies of white limestone dotting lush canyons above the Riviera.

The real problem was that I was starving myself again. The Italians are small, thin hobbit-people, the climbers even more so, and with my thick musculature I'd garner the occasional blunt but well-meaning, “
Sei un po' più grosso di noi Italiani, pero scali come un animale!
” (“You're a little bigger than us Italians, but you climb like a beast!”) This only fueled my Climborexia. My main partner was a sometime motorcycle racer, Freddino, a thin man with a moustache who drove like a maniac on the
autostrade
and loved a cliff called Campambiardo, a gneissic plug levering out over a chestnut-covered hillside in Val di Susa. Freddino lived in an apartment building with his extended family and seventeen adopted stray cats, and peppered his speech with colorful, made-up slang like “tanardi” (little cliff critters, like chipmunks). Freddino, at age fifty, could climb 5.13 and had legs twiggy as an ostrich's. “Ciao, big!” he'd say when he greeted me. “Ciao, strong American boy!” It was the only English he knew. With Freddino, I onsighted my first European 8a (5.13b) at a crag called Donnaz in Val d'Aosta, an overhanging face tilted out over an ancient Roman viaduct.

On the hungriest nights I lay awake in bed, the attic ceiling close above as predawn trolleys clacked and echoed along the cobblestone canyon of Via Carlo Alberto outside. Heart palpitations came in waves, quieting only after half an Ativan and a ball of mozzarella scavenged from the kitchen. I was in Europe, the birthplace of hard sport climbing, and I needed to
perform
, which meant staying skinny. And I was climbing harder than ever: I'd redpointed a 5.13d, a few 5.13c's, and was routinely onsighting routes up to 5.13b, which among Torino's rock jocks conferred an intoxicating semistardom as
L'Americano forte
(“the strong American”). The study-abroad program demanded little more than reading art-history books and visiting local castles, so I had plenty of time to frequent the cliffs. One day amidst this manic climbing fest, I became so malnourished that, as I lowered off a 5.13, I could feel my heart squirting dull, barely-there beats, then pounding fiercely to catch up.
Thudda-thud … retreat … pause … pause … pause … THUD-THUD-THUD-THUD-THUD.
Frightening stuff—a group of us were up at the shadowy black shale plug of Gravere high in Val di Susa, springtime cherry blossoms on the breeze, larch and chestnuts budding along an aqueduct below. My Italian friends talked
frichettone,
climber slang, at the base of the wall, oblivious to my plight. Postcard-perfect Alps shimmered snow-covered across the way, mammoth waterfalls spilling from their flanks.
Was I finally having that heart attack? Were these mountains the last thing I'd see?
But never:
What, exactly, was I doing to myself?
I snuck off to pop an Ativan, as I'd learn to do all too covertly and well, returned, and tied back in, setting off up another climb, now feeling a druggie's indifference toward my shaky hands and erratic heartbeat.