Pill Head: The Secret Life of a Painkiller Addict (6 page)

Amy and I were also too concerned with finding a steady pot source to realize we had access to thousands of pills that would have made us feel a hundred times better. And looking back, I doubt Amy would have gone that far, had we known. Her parents were terrifyingly strict, and would have had us arrested.

“My entire senior year
of high school was devoted to snorting Percocet,” says Jared. His friend Tim, who was working at the drugstore, kept them in constant supply. “We were always telling ourselves, this is the best time we’re ever going to have in our lives,” he says. “We all had freshmen girlfriends. At that time we were really into Ecstasy, too. Me and three other guys all took our girlfriends to the prom, and on the way back we all took E. We had the limo drop us off at a park, and we were all just fucking in the grass.”

Most of the other kids in Jared’s high school were into drinking, dropping acid, and smoking pot. But he thinks there were probably
other small pockets of kids doing pills too. There were always various people who would drop in and out of his crowd and snort Percocets with them.

One of the girls from prom night wrote about their Ecstasy experience in a journal. Her dad ended up reading her diary and called the parents of all the kids who had been involved. “My parents grilled me about all the drugs I’d been taking,” Jared says. “I told them everything I’d been doing, except the pills. I wanted to keep that to myself. I didn’t care about admitting to taking acid or anything else, but I didn’t want them to know I was doing pills because I couldn’t imagine ever
not
doing them. All the other stuff I could give up if I had to.”

After graduation, Jared took a summer job as a counselor at a kids’ camp. “I didn’t have any pills up there,” he says. “This was after we’d been snorting pills literally every day for the past year. Now I know I was going through withdrawal, but at the time I was miserable and didn’t understand why. The symptoms were flulike, but the worst part was the mental stuff. I was in a constant state of horrible panic, and I was working with kids. I just wanted to get out of my body. By the end of the summer I finally felt all right, but I definitely wanted to get back to taking pills. I had no intention of stopping.”

That fall, Jared started college at a school about an hour and a half from his hometown, studying English and literature. Tim ended up going to college several states away, but Jared’s other main pill-snorting friend, Eric, got Tim’s old job at the pharmacy. Eric picked up right where Tim had left off, stealing as many pills as he could get away with. He would drive to visit Jared at school and leave him with a bunch of pills. Jared would keep some for himself, sell the rest to other students, and give the money back to Eric.

“The haul always varied, depending on what he could get,” Jared says. “Sometimes it would be hundreds and hundreds of pills. The students at my school were really into Valium and Xanax, so I could always sell those really easily. I’d keep the opiates for myself.”

This went on for months, until Eric’s bosses finally busted him. But since Eric was working in the pharmacy illegally to begin with, they couldn’t exactly press charges. He never got arrested and the
whole thing was settled out of court. But by the time that happened, Jared had been dealing on campus for so long that he had already developed other pill connections.

The first one was completely random. “I was walking down the street when some guy pulled up next to me in a car, rolled down his window, and said, ‘Anyone want some Percocets?’ It was the start of a long and fruitful relationship,” Jared remembers. “He was an army vet who had his own prescriptions, which he sold to me. I’d also discovered a whole ring of people who were selling pills in town, and that’s where I started getting OxyContin. I developed a very strict regimen. I’d snort Percocets throughout the day, just to give me a base high, and then spike that with a sixty-or eighty-milligram Oxy about three times a day.”

Despite his heavy addiction, Jared ended up graduating college with a 3.7 GPA. “No one had any idea,” he says. “I did well in school, but I looked bad. I had long hair, weighed about thirty or forty pounds less than I do now, and I had that sort of green, opiate look. The pills had stopped being fun since the middle of college. It just turned on me. There’s a distinct point where it just flips around completely, and I was taking them just to function. I wasn’t eating. I couldn’t take a shit, and when I did, it was the radius of a baseball bat (constipation is a common opiate side effect). The drugs weren’t fun anymore. They were horrible. But it was much worse without them.”

IN MY OWN CASE,
and I think this is true for the majority of pill heads I’ve met, I was self-medicating for some form of depression. I say this because, well, not only did I know I was depressed, but there’s a whole emerging field of study about depression manifesting itself as physical pain. Cymbalta, a popular antidepressant, has even incorporated this idea into its advertising campaigns. Depression
hurts
, the ads declare.

Dr. Carol Boyd’s initial questions about painkiller use were developed back in 2003, and she is now developing new questions to address this theory linking depression and pain.

“All I was asking is, ‘Why are you using it?’ and they said, ‘Because I have pain.’ We didn’t explore it enough,” she says. “If I get funded again this time around, I’ll be following kids around from the time they are eleven and specifically asking them why they are using and what kind of pain they have. I’ll also be asking about any other health problems they have and what other pills they are on. Because one important thing we found is that if we controlled for antidepressant use in this group, that is, if they were already on antidepressants, they were not bigger nonmedical users of prescription opiates. In other words, it’s possible that the kids who are using opiates are self-treating
a mood disorder. We can’t prove it yet, but my data is looking like that.”

She isn’t alone in this theory. As far back as 1995, an article was published in the
Journal of Clinical Psychopharmacology
by lead author J. Alexander Bodkin, now the director of the Clinical Psychopharmacology Research Program at Harvard University’s McLean Hospital. The article was entitled, “Buprenorphine Treatment of Refractory Depression.” First released in the United States in 1985, buprenorphine was a Schedule V narcotic analgesic in an injectable formulation marketed under the trade name Buprenex. Since 2002 it has been sold in the United States under the trade name Subutex, which is a sublingual (under the tongue) formulation, but federal regulations prohibit dispensing the drug for pain and have raised it to Schedule III. It may be used only to treat opiate withdrawal, much as methadone is used to treat heroin withdrawal. A special formulation of buprenorphine called Suboxone includes naloxone, a compound that immediately kicks narcotics off pain receptors. Naloxone is added specifically to prevent abuse, since it takes effect only if the tablets are crushed and injected, rather than taken orally. (Naloxone is commonly used for overdoses, and there’s a growing movement to make it widely available to heroin and other opiate abusers through needle-exchange programs.)

The Bodkin study followed ten depressed patients who hadn’t responded to other depression treatments and were given a small opiate dosage. Three dropped out because of side effects, but most of the other seven “showed striking improvement in both subjective and objective measures of depression.” It should also be noted that two of the positive responders had had former opiate addictions or experiences in the past. (One of the former drug abusers actually deteriorated.)

Dr. Bodkin first became interested in buprenorphine while working on an entirely different class of drugs, monoamine oxidase inhibitors (MAOIs), a strong form of antidepressant, like Parnate (tranylcypromine) and Nardil (phenelzine). “The classic case with MAO inhibitors is that a person suffering from depression will go from being sluggish, unmotivated, and downhearted to being highly energized and ever so slightly euphoric. It’s really striking when you
see it the first few times. Prozac had just hit the market, and Prozac sure doesn’t do that.”

Prozac is in the family of SSRIs, or selective serotonin reuptake inhibitors. In the simplest of explanations, messages are passed between nerve cells in the brain via a
synapse,
a small gap between the cells. The cell that is releasing information does so by sending neurotransmitters into the gap. Neurotransmitters called monoamines (serotonin, norepinephrine, and dopamine) are recognized by receptors on the surface of the receiving cell, which then relays the signal. Around 10 percent of the neurotransmitters are lost in this process and the other 90 percent are released from the surface of the receiving cell to be taken up again by the sending cell, a process called reuptake. Some theories believe that depression is linked to the lack of stimulation by the receiving cell. SSRIs work by keeping the neurotransmitter serotonin in the gap between the cells longer, so that the receiving cell can be stimulated longer. Besides Prozac, other common brands of SSRIs include Zoloft, Paxil, Lexapro, and Celexa.

MAOIs work differently. Remember the 10 percent of neurotransmitters lost in the process of relaying a signal? They’re not technically lost, they get burned up by an enzyme called monoamine oxidase, which is also found in the lining of the gut and other body tissues. Most of the relevant antidepressant-related MAO in the brain is in the pre-synaptic neuron (the sending cell), and inhibiting it with MAOIs allows a build-up of monoamine stores to be released as needed, thus easing depression symptoms. MAO is also responsible for the breakdown of monoamines such as serotonin. MAOIs block this breakdown process in the brain, making more neurotransmitters available.

“There were a lot of cokeheads at the time in the business class,” Dr. Bodkin says. “I thought that maybe at least some of these people might be unknowingly self-treating an otherwise MAO-responsive condition with cocaine. I did a little more research and discovered that some cocaine addicts were responding well to a new opioid, buprenorphine.”

Dr. Bodkin knew that opioids had been used to treat mood
disorders at the turn of the century before becoming widely stigmatized because of their abuse potential. But researchers were now presenting buprenorphine as a safe opiate because not only did the high feeling disappear after a day or two, it also didn’t have the same withdrawal symptoms associated with other opioids. Laboratory testing showed a long delay before the drug disassociated from the neuron: it bound tenaciously to the receptor, reducing withdrawal problems. Another positive feature: as the dosage rises, respiratory depression only reaches a certain point, levels out, and then actually reverses itself a bit, so there was little danger of overdose. It had been used by urologists for postsurgery treatment since the 1980s because it was thought to have less effect on urinary retention than other commonly used opiates. (I can attest to the fact that opiates cause urinary retention—all in all, I’ve probably spent about two entire weeks of my life staring at the porcelain tiles above a urinal, trying to pee while high out of my mind.)

“Back in those days,” Dr. Bodkin explains, “it wasn’t a tremendously complicated thing to get permission to carry out an open trial. I was finishing up my residency and doing a fellowship here at McLean, and it was really quite exciting to see that some previously treatment-unresponsive depressed people had a fabulously good response to buprenorphine.”

In the trial, all patients were taken off their previously prescribed psychotropic medications, except for benzodiazepines. They were given 0.15 milligram of buprenorphine every morning, and the dosage was titrated (meaning that more is added as one’s body becomes used to a certain dose and it stops being effective) throughout the trial depending on each patient’s tolerance and the clinical benefit they were receiving from the drug. The maximum daily dosage ended up being 1.8 milligrams.

At the end of the trial, Dr. Bodkin tried to raise money for more studies. “I’m not terribly enthusiastic about the application process,” he admits, “so I didn’t go absolutely to the mat with it, but I sent out several proposals and got nowhere with them. I ran into another group who were trying to raise money for a similar study. They had gotten stuck at the level of the institutional review board at one of the
major medical centers. I realized, ‘Jesus, opiates are so stigmatized that they aren’t going to give this a shot,’ although it remains in my armamentarium, as it did then, for treating people who really need it. You’ve really got to get informed consent, and you’ve got to be careful. When I first published that article, I had an awful lot of people showing up for treatment, and I was a little too young and naïve to realize that a fair number of them were drug abusers who thought they’d found a doctor who was cool enough to prescribe to them. That’s one of the things that made me less of a passionate advocate than I otherwise would have been.”

After Dr. Bodkin realized he had been prescribing to drug abusers, he took them off the medication and they sued him for injury. “It was really ugly,” he sighs. “It took years to get it over with, and it was the nightmare of my life at the time. I was a fool. I should have been able to see at the door that there were personality problems. I started out with the position that people were just trying to make themselves feel normal and well, but I quickly discovered that there are several other groups of people with motivations to specifically seek out opiates who are very self-destructive, and destructive to others.”

Like me.

Dr. Bodkin knows of one doctor who prescribes oxycodone to treat depression. “He thinks it’s sensible to go with the most euphoriant of the pills. For a period of time he needed other doctors to cover his patients for him for various personal reasons, and I was one of them. In those situations I made every effort to switch people over to standard antidepressants or buprenorphine because I didn’t want to be involved with prescribing oxycodone.”

Dr. Bodkin believes it’s usually unwise to prescribe oxycodone or other strong opiates for depression. “People who do it tend to get in trouble,” he says. “Even if it were a lifesaver for a patient—and who knows? it might be in some patients—prison isn’t a nice place to spend your adulthood. And although oxycodone is an extremely useful pain medication, even very respected physicians can get investigated by the DEA and occasionally go to jail, and the sentences can be blood-curdlingly long. It’s almost a religious matter in some circles, in the same way that there is a kind of religious opposition to the use of
marijuana for people getting chemotherapy. People are dying and there are organizations out there saying, ‘Don’t spoil their souls—they won’t get into heaven!’”

These days Dr. Bodkin is focusing more research on MAO inhibitors. I’m biased against these antidepressants, because I had a bad experience with one when I was a teenager.

The main problem with MAOIs is that monoamines don’t just burn up neurotransmitters; they also burn up a molecule called tyramine, which affects blood pressure. So when monamine oxidase is blocked, tyramine levels rise too.

I was prescribed Parnate when I was eighteen. It was for depression, which at the time was manifesting itself in me as hatred for my parents—pretty much like any other teenager. According to the newly revised twelfth edition of
The Pill Book: The Illustrated Guide to the Most Prescribed Drugs in the United States
(now includes self-injectables!), Parnate is prescribed for major depression that doesn’t respond to other drugs. It is also prescribed for a variety of conditions, including “bulimia, cocaine addiction, night terrors, post-traumatic stress disorder, and symptoms of multiple sclerosis.”

I’d never been on any other antidepressants before. All I knew is that Parnate got me high. It was a speedy, sleepless high that I quickly grew addicted to. During the few months I was on Parnate my diet consisted solely of Coca-Cola and Ritz crackers. There were bizarre side effects, like brown semen and tremors.

The sleeplessness was the worst. I felt an unexplainable need for pressure on top of me, so I’d sleep between the box spring and the mattress, like a bed sandwich. And all I could think about was waiting until morning so I could take another one of my pills. No one was monitoring my use of this drug. I was simply handed a prescription from our family therapist/psychiatrist (who the family only saw five times since that was all that was covered by our insurance), with a list of strict instructions, which included a long list of foods I couldn’t eat, like cheese and soy sauce, because they contained an excess of tyramine. But I barely had an appetite, so it hardly mattered.

I began taking Parnate during the summer after my senior year of high school and continued into my first year of community col
lege. During that time, my older sister got married. The wedding was to take place at my grandmother’s house in Tennessee, and I took a bus down to Philadelphia, where my father was living with his new wife. The plan was for all of us to drive down to Tennessee together from there. I arrived giddy and restless from having to sit still for so long on the bus. And I was hungry. They didn’t have any Ritz crackers at my dad’s house, but my stepmother offered me ramen noodles.

I didn’t know that she liked to spice them up with soy sauce.

Halfway through the bowl, I put my spoon down and said, “Something’s wrong.”

My stepmother glanced up at me from across the room where she was packing for the trip and asked, “You okay?” before looking back down at her suitcase.

A terrifying feeling was starting at the base of my spine, a sharp stabbing pain right above my butt, and my body filled with adrenaline. I couldn’t breathe.

“Something’s wrong,” I repeated, pushing back the chair and trying to stand up. I leaned forward over the table, knocking aside the bowl of ramen. The pain that had started at the bottom of my spine was traveling upward. The stabbing sensation had reached the middle of my back, and I realized it was crawling straight up toward my head.

The taste in my mouth suddenly became vividly familiar. “Is there soy sauce in this?” I yelled.

My stepmother nodded, a scared look on her face.

“Oh god, get Dad,” I said. She ran to the door and shouted his name out toward the parking lot, where he had been loading up the car for our trip.

“Please god please god please god,” I whispered. The pain had reached my neck. I ran to my bag and grabbed the bottle of Parnate. My dad came running into the room, and I shoved the bottle of pills into his hand just as the pain exploded into my head, like a fountain of churning acid that had been traveling through a narrow tube, finding its pool of release.