Who are the Victims? What is the Cause?

by Linda S. Wong and Bruce K. Alexander

Linda S. Wong is a student at Simon Fraser University, Burnaby, British Columbia V5A 156, Canada. Bruce K Alexander, Ph.D., is a professor of psychology at the same university. This article was adapted from a chapter in Drug Policy 1989-1990: A Reformer's Catalog.

Since the death of college basketball star Len Bias in 1986, people have commonly claimed that recreational use of cocaine causes death. In fact, Bias died of a combination of large quantities of very pure cocaine and alcohol used during an all-night celebration. Studies indi-cate that recreational uses of powdered cocaine is not normally lethal.

We do not want to deny that heavy doses of cocaine can cause death. Co-caine overdose has been known for decades and is easily diagnosed. The victims generally become excited and confused shortly after a large dose of cocaine, and subse-quently undergo convulsions, depression, coma and, in severe cases, death from respiratory depres-sion or heart failure. Over-dose death usually occurs within two hours, often sooner, and levels of cocaine in blood plasma are high. This syndrome has been well documented in human beings since the 19th century and can be replicated in experimental animals.

However, studies fail to provide substantial evidence to support claims that moderate doses in recreational use can cause death. Instead, many interpretations of medical literature have gratuitously assumed that people harmed by using cocaine are moderate users rather than heavy users.

In 1979, the Journal of the American Medical Association published "Death Caused by Recreational Cocaine Use," a well known article by C.V. Wetli and R.K. Wright that provides an ex-ample of carel ess logic used to attribute great danger to moderate cocaine use. The article has been widely cited, but it contains no evidence whatsoever that justifies the ominous assertion in its title.

By searching the records of the Dade County, Fla., (Miami) coroner's office between 1969 and 1978, Wetli and Wright located 68 people who had cocaine in their body at the time of death. But to say that this relatively small number of deaths was "caused by recreational cocaine use" is a some-what loose interpretation of the events. Virtually all of the bodies had other drugs besides cocaine in their systems, particularly the synthetic lidocaine, which is mixed with street cocaine in Miami. Heroin, barbiturates, alcohol, valium and numerous other drugs were also found in the blood of these bodies, so there was no possibility of determin-ing the effect of cocaine by itself. In fact, 29 of the 68 deaths were officially at-tributed to "multiple-drug intoxication." Fifteen of the remaining 39 death s were officially attributed to "trauma," in-cluding automobile accidents, drown-ing and gunshot wounds.

Of the 24 remaining cases, five were shown to be traffickers who died when cocaine-laden condoms burst inside their bodies or when they swallowed massive doses to conceal it from the police. The sixth victim apparently overdosed to commit suicide.

In the end, Wetli and Wright suc-ceeded in documenting 18 people over a 10-year period (less than two per year) who could have died from recreational use of cocaine. However, not one of these was actually shown to be a rec-reational user, rather than a depend-ent or addicted person. It is entirely possible that none of them were recreational users!

The greatest problem with the argument that cocaine causes heart attacks is that the number of reported cases is so few compared with the mil-lions of North Americans who have used cocaine at least experimentally. Most of the dozens of published studies report only a case or two. Moreover, in the majority of cases, the patients had other risk factors for coronary disease. A majority were smokers, used other illicit drugs, and many had obstructive coronary artery disease. In a thorough review published in the Western Jour-nal of Medicine in 1988, C.K Bates wrote, "It is not possible to unequivo-cally state that cocaine abuse causes myocardial infarction."

The significance of these isolated reports remains to be seen. It seems judicious to conclude at this point that use of cocaine might produce a variety of severe adverse reactions on rare occasions, especially in conjunc-tion vvith other drugs and in persons with pre-existing pathology. However, this would simply put cocaine in the same category as most other drugs that are in daily, legal use.

The infrequent adverse reactions produced by cocaine appear to be com-parable in frequency and severity to those produced by many other common legal drugs. In fact, 650 ofevery 100,000 tobacco users die from their drug use, 74 of 100,000 alcohol users and 25 of every 100,000 cocaine users. Whereas the evidence that recreational use of cocaine is life threatening is inferential and dubious, there is direct evidence that moderate doses of pure cocaine, administered intranasally, are reasonably safe.

References

C.K. Bates, "Medical Risks of Cocaine Use," Western Journal of Medicine, No.148,1988. P. Devenvi and M.A. McDonough, "Cocaine Abuse and Endocarditis," Annals of Inter-nal Medicine, No. 109, 1988.

J.D. Haines and S. Sexter, "Acute Myocar-dial Infarction Associated vvith Cocaine Abuse," Southern Medical Journal, No. 80, 1987.