Updated: Aug 29
Among Facebook friends familiar with my work, dozens of conversations have started by their linking me to relevant pieces on, for example, the racial disparities of marijuana legalization, the therapeutic application of psychedelics, and, perhaps less pressing but no less appreciated, the varieties of ways our ancestors got high.
As much as I try to stay up on my drug news, sometimes people scoop me. This most recently happened last month when I received an article with a fantastically understated title: “Groundbreaking Treatment could be the End of Cocaine Addiction.” It was certainly enough to make a skeptical drug historian smile (and chuckle at the layered humor of Yahoo Finance covering anything related to the stockbroker’s culturally purported substance-of-choice).
Leonardo DiCaprio’s Jordan Belfort fulfilling every stereotype
Cocaine addiction is probably here to stay for the foreseeable future, but the new treatment, called a cocaine “vaccine,” offers some promise. It’s certainly groundbreaking at least. Dr. Ronald Crystal, principal investigator for currently-enrolling clinical trials at New York-Presbyterian/Weill Cornel Medical Center, correctly notes that, “While there are drugs like methadone designed to treat heroin, there aren’t any therapeutics available to treat cocaine addiction.” Addiction research scientists understand fairly well how our opioid receptors operate but most are perpetually vexed by cocaine’s complex neurotransmitter influence.
The vaccine, named dAd5GNE, combines parts of a common cold virus with a particle molecularly similar to cocaine, triggering an immune response against both. “Once immune cells are educated to regard cocaine as the enemy,” Crystal explains, “it produces antibodies, from that moment on, against cocaine the moment the drug enters the body.” The idea is to neutralize cocaine particles before they pass the blood-brain barrier, blunting their effects. This is a key distinction among addiction medications like methadone, which partially block opioid receptors once drugs like heroin cross over.
Crystal concedes that the process may not reliably pan out for humans. Years ago, his team observed vaccinated rats appearing less hyperactive after cocaine use than non-vaccinated rats, and the isolated antibody absorbing cocaine particles in a test tube, but scaling up is not necessarily linear. “We need to find out if the vaccine will cause enough anti-cocaine antibodies to be produced so that it works in humans, too.”
Crystal’s cautious optimism is not reflected in articles like the one my friend shared (though author Melody Hahm is considerably more measured in the main text). Once Crystal began experimenting on primates after mice, an article from The Fix invited readers to “[i]magine that cocaine addiction could be eradicated, poof, with a simple vaccine. [Crystal] now thinks his team has actually figured out a very clever trick to make that dream a reality.” A recent article in the New York Post calls the treatment a potential “saving grace” for addicts.
Methadone did little to alleviate the structural inequalities that contributed to drug addiction, as elaborated in this 1966 pamphlet
Poof! The drug historian continues smiling. In the early 1960s, scientists Vincent Dole and Marie Nyswander began using the synthetic opioid methadone to treat heroin addiction. Soon, journalists began proclaiming the drug as the “magic bullet” solution to the nation’s growing heroin problem. (But not without reason; the uniquely favorable conditions of early methadone trials, which featured rigorous screening processes for applicants and included staggered patient cohorts in cumulative retention data, produced impressive results: anywhere from 71 to 94 percent of users ceased criminal activity, found steady employment, and/or enrolled in college.) But heroin addiction was most prevalent in poor, high-stress urban neighborhoods characterized by racial discrimination in housing and employment. Methadone didn’t alter the scene much in places short on opportunity and long on reasons to use and sell dope. For decades, critics have credited the drug with simply perpetuating social conditions that give rise to drug use in the first place.
dAd5GNE may face similar charges. It doesn’t eliminate craving for cocaine, it just reduces the drug’s effect. Research suggests cocaine must occupy at least 47 percent of a dopamine transporter to produce a characteristic high and Crystal’s vaccinated primates never reached levels above 20 percent. But committed human addicts may accidentally overdose trying to bridge the gap, assuming they stick with the vaccination booster regiment at all, while polydrug users have an easier workaround. In any case, neither the setting or consequences of cocaine use on a social or individual level will probably change much. And, like its opioid-blocking counterparts, the cocaine vaccine gets us no closer to answering questions about addiction’s natured and (or?) nurtured etiology.
However, the vaccine has one major advantage over most opioid maintenance therapies: it has virtually no addictive potential. Twelve-step adherents and other abstemious interests liken methadone maintenance to substituting one drug – read: addiction – for another. Opioid replacement drugs can induce a mild euphoria, create physical tolerance, and even be fatal at certain dosage thresholds, which, at least theoretically, are non-issues for vaccine boosters administered weeks apart.
However, this treatment is not for everyone who does cocaine. The vast majority of users enjoy it as a fun or utilitarian stimulant without adverse outcomes. Many have no desire to stop. But even for problem users hoping to quit, the cocaine vaccine may go the way of methadone, Antabuse, and nicotine patches: magic bullets for some, stopgaps for others, nothing for most. (Assuming, of course, that trials confirm dAd5GNE is viable for human use.) But for anyone who earnestly desires to break patterns of destructive behavior, here’s hoping for more poofs in the future than the past.