CONSEQUENCES OF ILLICIT DRUG USE ON HEALTH, FAMILY AND SOCIAL PROBLEMS

Kari Poikolainen

Finnish Foundation for Alcohol Studies, P.O. Box 220, FIN‑00531 Helsinki, Finland

Last updated June 25, 2002

Source: http://www.kolumbus.fi/kari.poikolainen/

Also published partly in: Poikolainen K. Quién pierde en esa apuesta: consecuencias del consumo de las drogas, In: La Drogadicción en México - indiferencia o prevención, ING Seguros, 2001, pp. 175-194.

Introduction

It is difficult to estimate the health and social risks related to any specific illicit drug. First, the users are not eager to tell about their clandestine activities. Secondly, the active drug dose in the street merchandise varies greatly. Thirdly, users of illicit drugs seldom stick to only one substance. Multiple use of illicit drugs, alcohol and tobacco is common. For example, at the end of a 33‑year follow‑up of narcotic addicts in California, 20.7% tested positive for heroin and 9.5% refused urine testing, 66.9% reported tobacco use, 22.1% were daily alcohol drinkers, 40.5% reported past‑year heroin use, 35.5% marijuana, 19.4% cocaine, 10.3% crack, 10.3% and 11.6% amphetamine use. The group also reported high rates of health problems, mental health problems, and criminal justice system involvement (Hser et al., 2001).

The risks are not only related to the drugs used, but also to the route of administration (oral, nasal, parenteral), technique of injecting (sterile, non‑sterile), sexual behaviour (protected, non‑protected), coexisting diseases (psychiatric, other) and subculture of drug users (criminal, marginalised, affluent). There are several types of drug users. For example, a Swedish study divided drug addicts into four categories. The largest one was characterized by an early onset of crime and deviance in adolescence, higher alcohol intake and more difficult childhood and adolescence conditions than in the other groups. Another group had fewer recorded acts of juvenile delinquency, and drug abuse was started later in life. Both these two groups had strong subcultural affiliation. The third group had weak subcultural affiliation and low crime rates. The fourth group was on the average emotionally unstable, had the best education, job situation and social relations and little or no criminality but reported mental and emotional problems (Byqvist and Olsson, 1998).

Risk of dependence

It is clear that use of a drug is a necessary cause for the onset of drug dependence. It is not sufficient, however. Genes, education, peer influences, availability of drugs and societal environment also play a role. Little is known about the risk of becoming dependent on a drug once one has tried it. Approximate estimates on risk are available from the U.S. National Comorbidity Survey, a probability sample of U.S. civilian population aged from 15 to 54 years (Anthony et al., 1994). According to the CIDI interview system, which may overestimate rates, the lifetime risk is as follows:

‑ cannabis 10%

‑ alcohol 15%

‑ opioids 23%

‑ nicotine 32%

During the Vietnam war, 47% of a random sample of U.S. soldiers who tried narcotics, mainly heroin or opium, became addicted. However, only 3.5% of those who felt to be addicted in Vietnam continued to feel addicted after returning home, and of those who ever injected drugs in Vietnam, 8.8% were interested in treatment after returning home (Robins et al., 1974). An analysis of the ECA Study in the U.S. found out that the earlier illicit drug use begins and the longer it lasts, the higher the likelihood of problems (Anthony and Petronis, 1995).

Mortality

Mortality is high among narcotic addicts who come to treatment because of their dependence. A large Swedish study found that after hospital treatment the death rate was 2.4% annually. Men had slightly higher mortality than women. This cohort consisted of the most severe cases 30‑40% of all illicit drug misusers. Compared with general population, indirectly standardized mortality ratio was 22‑fold among opioid users, 10‑fold among amphetamine users, 7‑fold among both cannabis users and multiple drug users (Adamsson Wahren et al., 1997). It should be noted that the drug refers here to the main cause of dependence during the index treatment episode. Other drugs may also have been used. Mortality among (mostly injecting) patients treated for opioid dependence has varied from 0.2 to 4.4 % annually between studies in various countries (Sanchez‑Carbonell and Seus, 2000). Mortality among untreated street addicts is likely to be higher than among those in treatment. In Sweden, the annual death rate among narcotic addicts either in no treatment or short‑term drug treatment was found to be 7.2% in the years 1979‑1984; during a longer follow‑up period between the 1967‑1988 annual death rate among addicts in methadone maintenance treatment was 1.4% (Grönbladh et al., 1990). The difference in death rates between these two series was entirely due to heroin‑related overdoses. Mode of administration and the level of know‑how in heroin use may influence the mortality rates in addict populations. There is no adequately controlled randomized study on the effectiveness of methadone maintenance treatment. However, the variation in death rates among addicts in or without methadone maintenance treatment reported in the literature suggests that this treatment reduces mortality among addicts (Barnett, 1999). The major causes of death among narcotic addicts are accidental overdoses, other accidents, suicide, homicide and infectious diseases.

It should be noted that narcotic addicts who come to treatment are likely to be the most severely addicted group of all. Drug users in the general population are likely to had lower risk of death. Addicts registered by law to the Home Office in England and Wales contain a good deal of addicts who are not in treatment. In this population, mortality in the age‑group 15‑19 years was 0.13% for men and 0.09% for women. Of all deaths, 24% were due to methadone and 21% due to heroin overdose. During a 20‑year follow‑up, the mortality rates in this cohort were 0.52% for men and 0.35% for women (Oyefeso et al., 1999). The U.S. Epidemiologic Catchment Area study compared never drug users with drug users and adjusted for age, sex, race, and smoking. The relative risk of death for persons who met the Diagnostic Interview Schedule criteria for drug dependence and reported using drugs less than five times a week was 1.7 (95% confidence interval 1.0, 2.9) and for daily users 2.0 (1.0, 4.0) (Neumark et al., 2000). These relative risks are considerably less than the age‑and‑sex‑adjusted 7‑22‑fold risks for treated narcotic addicts. Further adjustment for social factors and alcohol intake might additionally decrease the risk estimates. A U.S. study found that mortality among addicts after treatment was increased by alcohol use, age and religious activity (Joe et al., 1982).

Morbidity and social problems

All major illicit drugs may cause poisonous overdose, dependence and withdrawal syndrome. There is clear evidence that non‑sterile injection of any drug may cause AIDS, hepatitis B, hepatitis C, infective endocarditis and other infectious diseases (English et al., 1995). Drug addicts with hepatitis C infection commonly drink alcohol although this increases the risk of liver cirrhosis and liver cancer. A British study found out the methadone maintenance patients aware of being hepatitis virus C (HVC) positive drank only slightly less alcohol than those who were HVC negative (McCusker, 2001).

Drugs can be a part of the glamorous life of the rich and famous and they can be a part of a criminal subculture. The rich are likely to suffer from dependence and withdrawal symptoms, the poor are likely to have additional problems related to violence, mental health and crime. The latter problems are seldom directly due to drug effects. Rather, the risk of violence is increased by aggressive personality, interpersonal conflict, and expectations of drug effects. Mental disorders may predispose to drug use. Criminal behaviour often starts earlier in life than drug use, and increases because of the need to finance drug use (Physicians, 2000).

Opioids. There is some limited evidence that opioid use causes antepartum hemorrhage, low birthweight, perinatal deaths and suicide (English et al., 1995) . A study on patients in methadone maintenance treatment in the U.S.A. showed that crime patterns established before opioid addiction tended to persist throughout the addiction career and were intensified by addiction (Nurco et al., 1989).

Stimulants. There is clear evidence that both cocaine and all major amphetamine derivatives can cause a withdrawal syndrome and psychosis. There is some evidence that the long‑term, heavy use of "ecstasy" (MDMA or 3,4‑methylenedioxymethamphetamine) may cause sleep disorders, depressed mood, persistent anxiety, impulsiveness and hostility, and selective impairment of episodic memory, working memory and attention. The cognitive deficits may persist for at least 6 months after abstinence (Morgan, 2000) . There is some limited evidence that cocaine use causes antepartum hemorrhage and low birthweight (English et al., 1995) . Among U.S. men, chronic cocaine use has been found to increase physical health problems, controlling for prior health status, current cocaine use, use of other drugs and sociodemographic characteristics. In turn, poor health contributed to continued cocaine use (Chen et al., 1996) . Cocaine use has also been found to increase the risk of syphilis even when adjusted for other risk factors, such as the number of sexual partners and frequency of sex with prostitutes (Rolfs et al., 1990) . Cocaine exposure during pregnancy has been found to be unrelated to the school‑age intelligence of the child (Wasserman et al., 1998).

Cannabis. Cannabis products have become more potent during the last three decades, which undermines the value of early research in the assessment of the effects of cannabis. The most potent psychoactive substance in cannabis products is delta‑9‑tetrahydrocannabinol (THC). In the 1970's, a reefer contained on the average 10 mg of THC, at present the content may be 15‑30‑fold (Ashton, 2001).

A follow‑up study of adolescents in the U.S.A. found, after adjusting for sex, race, degree of risk taking, disciplinary problems in school, working 1‑10 hours per week, drinking on 1‑2 days during the past month, and involvement in sports, that lifetime use of marijuana equal to 1‑5 occasions was related to increased incidence of injuries (Alexander et al., 1992). Flight simulation has showed that aircraft piloting performance is decreased (Leirer et al., 1991). Driving simulator studies have shown that cannabis worsens driving ability. This is often consciously compensated by slowing down the speed. The latter might explain why culpability studies have found no evidence that cannabis alone increases the risk of road traffic fatalities or injuries needing hospital treatment (Bates and Blakely, 1999). There is inadequate evidence that cannabis causes schizophrenia or low birthweight (English et al., 1995) . Long‑term use may increase the risk of chronic bronchitis and constructive obstructive pulmonary disease. Cannabinoids are carcinogenic but the risk of laryngeal, pharyngeal or lung cancer remains unknown (Van Hoozen and Cross, 1997) . A large follow‑up study of African American and Puerto Rican adolescents found that early adolescent marijuana use increased the risk in late adolescence of not graduating from high school, delinquency, having multiple sexual partners, not always using condoms, perceiving drugs as not harmful, smoking tobacco and marijuana, drinking alcoholic beverages, and having more friends who exhibit deviant behaviour. These risks were controlled for age, sex, ethnicity, and, when available, earlier psychosocial measures (Brook et al., 1999) . Cannabis use has been found to weaken educational achievement in school and learning of new things (Tanner et al., 1999) . This is in agreement with neuropsychological findings suggesting that some executive functions, mainly attentional behaviour, visual analysis and hypothesis testing seem to be impaired because of prenatal cannabis exposure (Fried and Smith, 2001).

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