Heroin in Vietnam: The True Story of the Robins Study

Editor's note: The famous Robins study 
on heroin use among Vietnam veterans
 has been so often—and so recently—misinterpreted 
that I felt motivated to reprint an older post on the subject.

[Originally posted 7/24/10]

In 1971, under the direction of Dr. Jerome Jaffe of the Special Action Office on Drug Abuse Prevention, Dr. Lee Robins of Washington University in St. Louis undertook an investigation of heroin use among young American servicemen in Vietnam. Nothing about addiction research would ever be quite the same after the Robins study. The results of the Robins investigation turned the official story of heroin completely upside down.

The dirty secret that Robins laid bare was that a staggering number of Vietnam veterans were returning to the U.S. addicted to heroin and morphine. Sources were already reporting a huge trade in opium throughout the U.S. military in Southeast Asia, but it was all mostly rumor until Dr. Robins surveyed a representative sample of enlisted Army men who had left Vietnam in September of 1971—the date at which the U.S. Army began a policy of urine screening. The Robins team interviewed veterans within a year after their return, and again two years later.

After she had worked up the interviews, Dr. Robins, who died in 2009, found that almost half—45 per cent—had used either opium or heroin at least once during their tour of duty. 11 per cent had tested positive for opiates on the way out of Vietnam. Overall, about 20 per cent reported that they had been addicted to heroin at some point during their term of service overseas.

To put it in the kindest possible light, military brass had vastly underestimated the problem. One out of every five soldiers in Vietnam had logged some time as a junky. As it turned out, soldiers under the age of 21 found it easier to score heroin than to hassle through the military’s alcohol restrictions. The “gateway drug hypothesis” didn’t seem to function overseas. In the United States, the typical progression was assumed to be from “soft” drugs (alcohol, cigarettes, and marijuana) to the “hard” category of cocaine, amphetamine, and heroin. In Vietnam, soldiers who drank heavily almost never used heroin, and the people who used heroin only rarely drank. The mystery of the gateway drug was revealed to be mostly a matter of choice and availability. One way or another, addicts found their way to the gate, and pushed on through.

“Perhaps our most remarkable finding,” Robins later noted, “was that only 5% of the men who became addicted in Vietnam relapsed within 10 months after return, and only 12% relapsed even briefly within three years.” What accounted for this surprisingly high recovery rate from heroin, thought to be the most addictive drug of all? As is turned out, treatment and/or institutional rehabilitation didn’t make the difference: Heroin addiction treatment was close to nonexistent in the 1970s, anyway. “Most Vietnam addicts were not even detoxified while in service, and only a tiny percentage were treated after return,” Robins reported. It wasn’t solely a matter of easier access, either, since roughly half of those addicted in Vietnam had tried smack at least once after returning home. But very few of them stayed permanently readdicted.

Any way you looked at it, too many soldiers had become addicted, many more than the military brass had predicted. But somehow, the bulk of addicted soldiers toughed their way through it, without formal intervention, after they got home. Most of them kicked the habit. Even the good news, then, took some getting used to. The Robins Study painted a picture of a majority of soldiers kicking it on their own, without formal intervention. For some of them, kicking wasn’t even an issue. They could “chip” the drug at will—they could take it or leave it. And when they came home, they decided to leave it.

However, there was that other cohort, that 5 to 12 per cent of the servicemen in the study, for whom it did not go that way at all. This group of former users could not seem to shake it, except with great difficulty. And when they did, they had a very strong tendency to relapse. Frequently, they could not shake it at all, and rarely could they shake it for good and forever. Readers old enough to remember Vietnam may have seen them at one time or another over the years, on the streets of American cities large and small. Until quite recently, only very seriously addicted people who happened to conflict with the law ended up in non-voluntary treatment programs.

The Robins Study sparked an aggressive public relations debate in the military. Almost half of America’s fighting men in Vietnam had evidently tried opium or heroin at least once, but if the Robins numbers were representative of the population at large, then relatively few people who tried opium or heroin faced any serious risk of long-term addiction. A relative small number of users were not so fortunate, as Robins noted. What was the difference? Was it a change in setting and circumstances that allowed most heroin users to quit? Or was it that the minority of soldiers who stubbornly became readdicted did so because, like Dr. Li’s rats, they were biochemically different from their friends who stayed clean?


Quotes from: Robins, Lee N. (1994). “Lessons from the Vietnam Heroin Experience.” Harvard Mental Health Letter. December.

Kratom: Mitragynine For Beginners

An organic alternative to methadone?

A disclaimer: Everything I know about kratom, I learned on the Internet and in science journals. I have no real world experience with this opiate-like plant drug, haven’t used it, don’t know very many people who have. Although it comes from a tree indigenous to Thailand and Southeast Asia, and has presumably been around forever, a recent journal article referred to kratom as “an emerging botanical agent with stimulant, analgesic and opioid-like effects.” Which makes it sound like a combination of heroin, amphetamine, and strong weed. In reality, however, it is evidently a fairly mild stimulant with additional sedative effects when the leaf is chewed. If that sounds contradictory, it is, but the overall effect is reported to be more in league with coca leaves than injected morphine. Addictive? Erowid notes that the leaves can vary widely in potency, but yes, potentially addictive. It’s not entirely surprising that kratom has been used in Asia, and increasingly in Europe and the U.S., as a self-managed treatment for pain and for opioid withdrawal. You can find kratom for sale all over the web. You will also find it in smoke shops and herbal outlets. But is any of it legal? And, as with methadone and buprenorphine: Is kratom part of the problem or part of the solution?

According to one web site maintained by kratom aficionados, the legality of kratom can be hard to determine. It is definitely illegal in Australia, Malaysia, Burma (Myanmar), and Thailand. However: “In the United States, access to county, state, and federal laws are often available online and it’s a simple matter of reading through the material (dense as it may be) to determine the actual legality of Mitragyna speciosa…. the only state where kratom is illegal in 2013 is Indiana. That’s not to say other state legislators haven’t tried to get kratom scheduled as an illicit substance. States to keep your eye on, especially if you’re a resident, are: Iowa, Hawaii, Vermont, Virginia, and Arizona. Louisiana hasn’t outright banned kratom, but they don’t allow it to be marketed as ‘for human consumption’ and thus we suggest, if you live in Louisiana, you exercise extra caution in your purchases.” In addition, you may rest assured that kratom is on the U.S. Drug Enforcement Administration (DEA) list of “Drugs and Chemicals of Concern.”

In other countries, kratom is controlled through licensing and prescription, similar in certain respects to the medical marijuana market in the United States. Nations in this category include Finland, Denmark, Romania, Germany, and New Zealand.

Kratom (Mitragyna speciosa) contains several psychoactive ingredients. The plant can be chewed, smoked, brewed into a tea—or made into an extract for sale as capsules or tablets (with accompanying arguments about “full-spectrum” extracts vs. “standardized” extracts).  According to Erowid, it is “unknown how long alkaloids retain their potency after being isolated from kratom leaves,” and furthermore, “many manufacturers are clearly exaggerating the potencies and quantities of whole leaf kratom used in their extracts.”

The leaves contain a plethora of psychoactive alkaloids, but the two primary stimulators of opioid receptors appear to be mitragynine and 7-hydroxymitragynine. These two compounds are considered to be stronger analgesics than euphorics, although users do sometimes report visual effects. Kratom is not considered toxic, but overdoses can be quite unpleasant, Erowid relates. Chronic heavy use reportedly leads to insomnia, dry mouth, constipation, and darkening of the skin.  Importantly, Erowid says they are “not aware of any cases of severe poisoning or death resulting from its use. Animal studies have found even very large doses of mitragynine (920 mg/kg) to be non-lethal.”

Last year, writer David DiSalvo, who blogs at Forbes, turned guinea pig, experimented with kratom, and blogged about the results. DiSalvo purchased an entirely legal supply of kratom—Lucky, Mayan, Nutmeg, and OnlineKratom by brand—and ran the self-experiment for a few weeks.

Here are excerpts from DiSalvo’s report: “My overall takeaway is that kratom has a two-tiered effect. Initially it provides a burst of energy very similar to a strong cup of coffee. Unlike coffee, however, the energy I derived from kratom was longer-lasting and level…. The second-tier effect was relaxing, but fell short of being sedating. I never felt sleepy while taking kratom, but I did experience a level relaxation that was pleasant, and balanced out the initial energy-boosting effects nicely.” Not surprisingly, DiSalvo’s major concern was that “it’s not easy to nail down the specific amount to take.” As for withdrawal, DiSalvo ranked it beneath caffeine withdrawal for severity.

“Having now experienced the product myself for a number of weeks,” he wrote “I can see no reason why it should be banned, or on what basis such a product would be banned if people can walk into a typical coffee shop and buy an enormous cup of an addictive substance that’s arguably more potent than any kratom available anywhere.”

In September, Larry Greenemeier examined the case for kratom legalization in an article for Scientific American that tracks the herb’s “strange journey from home-brewed stimulant to illegal painkiller to, possibly, a withdrawal-free treatment for opioid abuse.” Greenemeier interviewed Edward Boyer, director of medical toxicology at the University of Massachusetts Medical School, who first became familiar with kratom after a software engineer who had been using kratom tea for pain ended up at Massachusetts General Hospital after combining kratom with modafinil and suffering a seizure. (The case was reported in the June 2008 issue of Addiction).

According to Boyer, mitragynine “binds to the same mu-opioid receptor as morphine, which explains why it treats pain. It’s got kappa-opioid receptor activity as well, and it’s also got adrenergic activity so you stay alert throughout the day.” As if that weren’t enough, kratom also binds with serotonin receptors. “Some opioid medicinal chemists would suggest that kratom pharmacology might reduce cravings for opioids while at the same time providing pain relief. I don’t know how realistic that is in humans who take the drug, but that’s what some medicinal chemists would seem to suggest…. So if you want to treat depression, if you want to treat opioid pain, if you want to treat sleepiness, this compound really puts it all together.”

And again, unlike heroin and prescription painkillers, which can lead to respiratory difficulties and death, “in animal studies where rats were given mitragynine, those rats had no respiratory depression,” according to Boyer.

However, Boyer cautions that, like any other opioid, kratom has abuse liability. “Heroin was once marked as a therapeutic product and later was criminalized,” he reminds us. 

Photo Credit: https://hampedia.org/wiki/File:Kratom.jpg

Heroin in Vietnam: The Robins Study Reexamined

How everything we knew about heroin was wrong.

Editor's note: The famous Robins study on heroin use among Vietnam veterans has been so often—and so recently—misinterpreted that I felt motivated to reprint an older post on the subject.

[Originally posted 7/24/10]

In 1971, under the direction of Dr. Jerome Jaffe of the Special Action Office on Drug Abuse Prevention, Dr. Lee Robins of Washington University in St. Louis undertook an investigation of heroin use among young American servicemen in Vietnam. Nothing about addiction research would ever be quite the same after the Robins study. The results of the Robins investigation turned the official story of heroin completely upside down.

The dirty secret that Robins laid bare was that a staggering number of Vietnam veterans were returning to the U.S. addicted to heroin and morphine. Sources were already reporting a huge trade in opium throughout the U.S. military in Southeast Asia, but it was all mostly rumor until Dr. Robins surveyed a representative sample of enlisted Army men who had left Vietnam in September of 1971—the date at which the U.S. Army began a policy of urine screening. The Robins team interviewed veterans within a year after their return, and again two years later. 

After she had worked up the interviews, Dr. Robins, who died in 2009, found that almost half—45 per cent—had used either opium or heroin at least once during their tour of duty. 11 per cent had tested positive for opiates on the way out of Vietnam. Overall, about 20 per cent reported that they had been addicted to heroin at some point during their term of service overseas.

To put it in the kindest possible light, military brass had vastly underestimated the problem. One out of every five soldiers in Vietnam had logged some time as a junky. As it turned out, soldiers under the age of 21 found it easier to score heroin than to hassle through the military’s alcohol restrictions. The “gateway drug hypothesis” didn’t seem to function overseas. In the United States, the typical progression was assumed to be from “soft” drugs (alcohol, cigarettes, and marijuana) to the “hard” category of cocaine, amphetamine, and heroin. In Vietnam, soldiers who drank heavily almost never used heroin, and the people who used heroin only rarely drank. The mystery of the gateway drug was revealed to be mostly a matter of choice and availability. One way or another, addicts found their way to the gate, and pushed on through. 

“Perhaps our most remarkable finding,” Robins later noted, “was that only 5% of the men who became addicted in Vietnam relapsed within 10 months after return, and only 12% relapsed even briefly within three years.” What accounted for this surprisingly high recovery rate from heroin, thought to be the most addictive drug of all? As is turned out, treatment and/or institutional rehabilitation didn’t make the difference: Heroin addiction treatment was close to nonexistent in the 1970s, anyway. “Most Vietnam addicts were not even detoxified while in service, and only a tiny percentage were treated after return,” Robins reported. It wasn’t solely a matter of easier access, either, since roughly half of those addicted in Vietnam had tried smack at least once after returning home. But very few of them stayed permanently readdicted.

Any way you looked at it, too many soldiers had become addicted, many more than the military brass had predicted. But somehow, the bulk of addicted soldiers toughed their way through it, without formal intervention, after they got home. Most of them kicked the habit. Even the good news, then, took some getting used to. The Robins Study painted a picture of a majority of soldiers kicking it on their own, without formal intervention. For some of them, kicking wasn’t even an issue. They could “chip” the drug at will—they could take it or leave it. And when they came home, they decided to leave it.

However, there was that other cohort, that 5 to 12 per cent of the servicemen in the study, for whom it did not go that way at all. This group of former users could not seem to shake it, except with great difficulty. And when they did, they had a very strong tendency to relapse. Frequently, they could not shake it at all, and rarely could they shake it for good and forever. Readers old enough to remember Vietnam may have seen them at one time or another over the years, on the streets of American cities large and small. Until quite recently, only very seriously addicted people who happened to conflict with the law ended up in non-voluntary treatment programs.

The Robins Study sparked an aggressive public relations debate in the military. Almost half of America’s fighting men in Vietnam had evidently tried opium or heroin at least once, but if the Robins numbers were representative of the population at large, then relatively few people who tried opium or heroin faced any serious risk of long-term addiction. A relative small number of users were not so fortunate, as Robins noted. What was the difference?

Quotes from: Robins, Lee N. (1994). “Lessons from the Vietnam Heroin Experience.” Harvard Mental Health Letter. December.

See also:

Robins, Lee. N. (1993) “Vietnam veterans' rapid recovery from heroin addiction: a fluke or normal expectation?” Addiction. 88(8), 1037 – 1167.

Origins of the Disease Model of Addiction (Part 1) can be found HERE.

Photo Credit:  soldiersupportproject.org

A New/Old Treatment for Opiate Addiction

 

Gov makes naltrexone legit for heroin.

Last week, the government officially sanctioned the use of naltrexone, trade name Vivitrol, for use in the treatment of heroin addiction. Approved years ago by the FDA for use in the treatment of alcoholism, naltrexone is a long-acting opiate receptor antagonist that has been widely used for heroin detoxification, withdrawal, and maintenance for some time. In that light, the official approval was a bit of an anticlimax, and of less scientific interest than naltrexone’s earlier approval for alcohol dependence. 

While naltrexone has yet to become the huge treatment breakthrough for alcoholism that addiction researchers hoped for it, naltrexone did, in the end, prove to be the first anti-craving medication widely available for alcoholics. Using an opiate antagonist as an aid to the prevention of alcoholic relapse would have been unthinkable without the underpinnings of a neurophysiological model of addiction. Various investigators have also speculated that naltrexone, the drug used as an adjunct of heroin withdrawal therapy, may find use against symptoms of marijuana withdrawal in people prone to marijuana dependence

Naltrexone has something of a mixed reputation, however, in part due to its use in the highly controversial practice of “rapid detox.” Naltrexone, like methadone and buprenorphine, blocks the heroin high in a relatively neutral manner. It does so by knocking the opiate molecule off its receptors and replacing it with “dead weight,” so to speak. Naltrexone would seem to be the perfect drug for heroin addicts—but it is not. It does little to reduce cravings. Like acamprosate for alcohol, another blocking approach, its record of accomplishment is mixed, and the dropout rate is high. There is not even a mild drug-like effect to provide cross-tolerance and dampen the effects of withdrawal, as with methadone. Recently, naltrexone for heroin addiction has been offered as a form of rapid detoxification. The addict is anesthetized and placed on a respirator, then injected with naltrexone. The result: complete detoxification in a matter of hours, as the naltrexone molecules knock the opium molecules off their receptors. It can be lethal if not carefully controlled and supervised. The problem, as always, is that the detoxified addict is just as vulnerable to heroin addiction as before. Rapid detox does nothing to combat subsequent cravings, and relapse is frequent.

 Naltrexone combined with buprenorphine is marketed as Subutex, and represents another treatment modality for opiate addiction.  In addition, a University of Minnesota study of kleptomania—the compulsion to steal—showed that naltrexone drastically reduced stealing among a group of 25 shoplifters.

Naltrexone will be offered as a monthly injection, an approach that has not been widely tested on opiate addicts, but is potentially an advantage over frequent visits to methadone clinics or daily ingestion of other treatment drugs. Unfortunately, naltrexone is a potential problem for people with liver disease or hepatitis.  At high doses, naltrexone has been implicated in liver damage. More common adverse effects include dizziness, lethargy, and headache.

 Graphics Credit: http://www.cancercenter.ph/

The Perils of Polydrug Abuse

Methadone and benzodiazepines.

For patients in opiate treatment programs, benzodiazepine use represents both a barrier to recovery and a potentially life threatening situation. The combination of benzodiazepines and methadone can lead to fatal overdose.

The five most commonly prescribed benzodiazepines fall into two major categories. High potency medications include Xanax (Alprazolam), with a short half-life of six to 12 hours, and Ativan (Lorazepam), with a slightly longer half-life. The low-potency benzodiazepines are represented by the short-lived Restoril (Temazepam), and the longer-lasting Valium (Diazepam), with a half-life of 20 to 100 hours. The fifth popular benzodiazepine, Klonopin (Clonazepam) is a high-potency drug with a half-life of 18 to 50, the highest in its class. Their primary clinical uses include the treatment of anxiety disorders, insomnia, convulsions, and muscle spasms. They also find use in the treatment of acute mania, catatonia, and detoxification from alcohol.

While some patients are able to use benzodiazepines safely at low dosage for years, patients with a history of opiate addiction are a high-risk category for these medications. Tolerance develops quickly in patients who use benzodiazepines to “boost” the effect of methadone, or as a sedative during opioid withdrawal. Since high doses of benzodiazepines cause respiratory depression, even among opioid users who have developed a high tolerance to such effects, the combination increases the risk of severe intoxication, injuries, or fatal overdose.

In addition, benzodiazepines and methadone interact pharmacologically through the actions of the CYP450 liver enzyme, which detoxifies both substances. If the work load for CYP450 becomes too great, the result can be an accumulation of high levels of methadone in the body.

It has been estimated that “80 percent of benzodiazepine abuse is part of polydrug abuse, most commonly with opioids.” In a two-year study by the National Institute of Drug Abuse (NIDA), 73 per cent of heroin users also used benzodiazepines more often than weekly.

According to a recent Canadian study of 172 subjects, the reported lifetime prevalence of benzodiazepine abuse in methadone maintenance patients ranged from 67 to 94 percent, with two-thirds of the patients reporting benzodiazepine use during the past 6 months. Patients who took benzodiazepines also reported more previous opioid overdoses, according to the study. And women are more likely than men to abuse benzodiazepines. In a study by Australia’s National Drug and Alcohol Research Centre (NDARC), researchers conducting a five-year study of heroin overdoses in New South Wales found that attempted suicide by benzodiazepine overdose was more common than attempted suicide by heroin overdose.

Methadone maintenance patients need to be questioned carefully about benzodiazepine use. By doing so, physicians and other caregivers can work toward actively decreasing the likelihood of treatment failure or fatal methadone overdose.

Photo Credit: www.drug.uz

OxyContin Back in Court

Kentucky goes after makers of “hillbilly heroin”

The attorney general for the state of Kentucky filed a lawsuit last week against Purdue Pharma L.P., makers of OxyContin, seeking to recover damages related to widespread addiction to the painkiller commonly known as “hillbilly heroin.”

Brought to widespread attention by Rush Limbaugh’s well-publicized addiction, OxyContin is a prescription narcotic for which a thriving black market has been established. It did not take drug users long to discover that OxyContin could also be ground up and either snorted or injected for a heroin-style high. Hundreds of deaths have been attributed to the street use of this Schedule II narcotic. Kentucky state officials say the social costs associated with fighting addiction have increased dramatically since the drug’s introduction. Others states are prepared to make the same argument.

Oxycontin racked up sales of $2 billion for the year ended August 2005. At least two companies, Pain Therapeutics (PTIE) and Alpharma, (ALO) are aiming at the market for more abuse-proof versions of OxyContin. “The big issue,” writes The Motley Fool’s Brian Lawler, “is whether insurers and government health programs will be willing to pay the premium price for an abuse-resistant drug.”

Oxycodone, as the drug is known medically, is a semi-synthetic derivative of thebaine, an alkaloid found in opium. It was developed in Germany in the early years of the 20th Century as a morphine substitute. Today, oxycodone is used extensively and very effectively for pain relief in terminal cancer patients. The Food and Drug Administration (FDA) approved the used of OxyContin in a time-release version in 2004.

Purdue Pharma said it will contest the lawsuit, which charges fraud, conspiracy and negligence--but the company recently settled other litigation with West Virginia and the U.S. Department of Justice for $685 million in cases alleging illegal marketing and promotion of the drug. U.S Attorney John Brownlee of the Western District of Virginia said that company sales reps falsely implied that OxyContin had less potential for addiction and abuse than similar prescription narcotics. Several other states were parties to those complaints, in which Purdue Pharma officials pled guilty last year to charges of misleading the public. Several states have taken a similar approach toward Merck, the manufacturers of Vioxx.

The Kentucky attorney general’s office said OxyContin addiction was so widespread that officials in Pike County were forced to build a $5.6 addition to the county jail to cope with increased convictions for oxycodone addiction. “It’s ironic that those who manufacture a drug that is meant to ease the pain of those suffering from debilitating diseases… have in fact inflicted so much pain by being deceptive and greedy,” said Country Judge-Executive Wayne Rutherford.

With the plethora of state lawsuits brought on behalf of Medicaid programs and law-enforcement agencies against OxyContin, “I think we have the answer as to whether government health programs will cover the costs of these abuse-resistant drugs,” Lawler concludes. “Count this as one less hurdle for Pain Therapeutics, Alpharma, and the other developers of these abuse-resistant compounds."

Vaccinating Against Vices

Developing a pill or a vaccine for a specific drug addiction has long been one of the tantalizing potential rewards of addiction research. Now a company in Florida has garnered national attention, a spate of clinical trails, and a positive response from the National Institute on Drug Abuse (NIDA) with a compound called NicVAX, aimed at nicotine addiction. In addition, Celtic Pharma in Bermuda is working on a similar product for cocaine addiction.

The idea of vaccinating for addictions is not new. If you want the body to recognize a heroin molecule as a foe rather than a friend, one strategy is to attach heroin molecules to a foreign body--commonly a protein which the body ordinarily rejects--in order to switch on the body’s immune responses against the invader. The idea of a vaccine for cocaine, for example, is that the body’s immune system will crank out antibodies to the cocaine vaccination, preventing the user from getting high. A strong advantage to this approach, say NIDA researchers, is that the vaccinated compound does not enter the brain and therefore is free of neurological side effects.

Preliminary research at the University of Minnesota showed that a dose of vaccine plus booster shots markedly reduce the amount of nicotine that reaches the brain. Animal studies have shown the same effect. NicVAX, from Nabi Biopharmaceuticals, consists of nicotine molecules attached to a protein found in a species of infectious bacteria. When smokers light up, antibodies attack the protein-laden nicotine molecules, which, further encumbered by these antibodies, can no longer fit through the blood-brain barrier and allow the user to enjoy his smoke.

That, at least, is the idea. It is a difficult and expensive proposition, the closest thing to a miracle drug for addiction, but it does not specifically attack drug craving in addicted users. The idea of vaccination is that, once a drug user cannot get high on his or her drug of choice, the user will lose interest in the drug.

This assertion is somewhat speculative, in that users of the classic negative reinforcer, Antabuse, have found ways to circumvent its effects--primarily by not taking it. There remain a wealth of questions related to the effects of long-lasting antibodies. And it is sometimes possible to “swamp” the vaccine by ingesting four or five times as much cocaine or nicotine as usual.

Drugs that substantially reduce the addict’s craving may yet prove to be a more fruitful avenue of investigation. While several anti-craving medications have been approved for use by the Food and Drug Administraton (FDA), no vaccines have made it onto the approved least yet.

For more on pharmaceutical approaches to fighting drug addiction, see my website at http://www.dirkhanson.org