Adolescence and Drug Abuse: Biomedical Consequences


Many facets of the biomedical aspects of substance abuse in adolescents have not yet been adequately researched. Little is known about the biological elements, if any, that contribute to the genesis of substance abuse. In the instance of alcoholism a genetic vulnerability appears to be established from the studies of identical twins, one raised by the natural parent and the other placed at an early age in the home of nonalcoholic foster parents. In the studies conducted both in this country () and in Denmark () the incidence of problem drinking of both groups of twins was similar. It is well established that among people of Mongolian descent, a widespread sensitivity to alcohol, based upon the rapid accumulation of acetaldehyde, is observed (). Facial flushing and more upsetting symptoms, including asthma and hypotension, can be present. In those with marked discomfort after drinking small amounts of ethanol, a certain preventive role is probably played by this inborn racial change in the ability to metabolize alcohol.

Such genetic factors have not yet been uncovered for other psychoactive drugs. With the recent identification of opiate () and benzodiazepine () receptor sites, and the hint that other drug-specific receptors will be found, it becomes conceivable that receptor site or endogenous ligand deficiency or excess may come to constitute one of the variables in the pathogenesis of the dependency disorders.

A fair amount of clinical and investigational information of varying “hardness” is available about the biomedical consequences of adolescent drug abuse. What remains essentially unknown is whether juveniles and adults respond to the mind-altering chemicals in a manner that is qualitatively or quantitatively different. Do young organism manifest a relative psychophysiologic vulnerability to any of the drugs of abuse, as compared to the mature organism? Is it possible that differences in the rates of absorption, distribution, metabolism, and excretion my exist? Alternatively, adaptive mechanism on a cellular or on the human level are likely to be differentially developed.

Since adolescence is a period of high drug abuse, and since subsequent careers of drug-taking are established and fixed at this time, the medical sequelae are of considerable interest. These effects will vary according to the drug group involved. In polydrug-using individuals the consequences tend to be greater than in monodrug abusers because of drug synergism, intensified psychic state, or drug-drug interactions.


As the most widely used illicit drug, the impact of cannabis is of particular interest, especially since a more potent product is being smoked by younger age groups, with more daily smokers being counted. A controversy exists regarding the exact amount of harm that consistent smoking of marijuana can do. Dosage levels are obviously one of the interacting variables that determine whether adverse effects will occur.

The immediate side effects of cannabis use consist of acute anxiety, panic, and confusional and paranoid states. These side effects are infrequent, however. A small number of case reports of schizophreniform reactions has been reported in the American literature (). These are probably psychotic reactions precipitated by marijuana in predisposed individuals. Impaired psychmotor performance for complex tasks has been well demonstrated (). The impairment of immediate recall also seems well documented ().

Intermediate side effects include flashbacks (an uncommon event) (), tracheobronchitis that is similar to tobacco smoker’s cough (), and psychologic dependence (). Immunologic (), chromosomal (), cellular protein synthesis (), and hormonal changes () have been described, but these are difficult to evaluate, not only because they have not been invariably confirmed, but also because much of the work has been done on in vitro and animal preparations and their relevance to the human condition remains to be established. Now, nevertheless, sufficient evidence is accumulating, and these findings cannot be ignored.

Perhaps the most frequently asked question about cannabis is whether the amotivational syndrome () that appears to occur most often in adolescents and young adults is a drug-related event, or whether the loss of drive and goal-directedness is primarily a psychosocial process that marijuana reinforces. It is most likely that both possibilities occur. For some, consistent usage will promote passivity and loss of motivation, for others who drop out because of situational and personality difficulties, marijuana will act as a satisfactory reinforcer.

The reduction in drive states seen in certain young users may have a biologic substrate. It may be a reflection of lowered drive hormones like testosterone or leutinizing hormone (). It could represent the limbic system changes described by Heath et al. (1979). It is also quite likely that a good part of the picture can be accounted for by the sedative quality of marijuana. It is employed by some people for its tranquilizing and sleep-inducing effects. When large amounts of a sedative are used during the waking hours, it must be expected that a loss of ability to perform and a drop in motivation will result. Alcohol, opiates, and hypnosedatives will induce similar effects.

The long-term changes of concern include the possibilities of chronic obstructive lung disease and pulmonary carcinogenicity (). The comparison with tobacco is justified, since similar coal tars are present in both plants. The combined use of both products may be particularly undesirable (). Whether cannabis produces physical dependence is contingent on dosage. In amounts not commonly used on the street at present, tolerance and a withdrawal syndrome are discernible on sudden discontinuance ().


Most of the serious adverse consequences of opiate use are secondary to the contamination of the injected bolus. The exceptions include overdose and anaphylactic reactions (). Of the infections resulting from inattention to sterile techniques, hepatitis is the most frequent, almost invariable complication. Endocarditis, thrombophlebitis, and a variety of pulmonary insults are not infrequent. Metastatic infections originating from the heart valves and lungs can lodge in any organ and cause inflammatory reactions or abcess formation.

The dangers in the life of a heroin user must be noted: they include the “hot shot” (an intentionally lethal dose provided by the dealer) and other homicidal events, accidents due to oversedation, and diseases caused by malnutrition and poor hygiene. The rigors of withdrawal are not great at present, since only small mounts of the drug are to be found in the “bag,” and detoxification facilities are generally available.


The intoxicated state, with its hazards from poor judgment, impaired motor skills, and irritability, contributes to accident proneness. Violent behavior is seen just as in the closely related alcohol-intoxicated states. Sedatives are the most frequently used chemicals for suicidal purposes, with the barbiturates being the preferential drugs for this use ().

Physical dependence occurs with continued use of sedatives. The withdrawal syndrome is more impressive than opiate withdrawal, and it can be life-endangering. Another ominous feature is that, although tolerance to large amounts of barbiturates takes place, the lethal dose may be only a few capsules more than the well-tolerated amount.

The combined use of sedatives with a related drug such as alcohol has resulted in fatalities even when the blood levels of both substances were at less than lethal concentrations. Barbiturates also interfere with the metabolism of a number of classes of therapeutic drugs, and may nullify the efficacy of these agents.

Adolescents appear to react much like adults to acute or chronic sedative abuse.

Volatile Solvents

Volatile solvents have particular relevance for youths: they may be the initial drug abused by grammar and junior high school students ().

Bass (1970) described a sudden sniffing death, that is, a cardiac arrest from a combination of the solvent, the relative unavailability of oxygen, and sensitization of the pacemakers of the heart to the overproduction of adrenalin in response to stress.

Depending upon the solvent, occasional peripheral nerve cell, liver, kidney, or bone marrow damage might occur. Heavy usage in children has resulted in neuropsychological deficits that have not cleared over a few months of abstinence ().


The acute toxicity of drugs such as LSD consists of anxiety, panic, and psychotic reactions. Prolonged psychotic reactions are likely to be underlying schizophrenic disorders unleashed by the hallucinogenic experience. Flashbacks are not uncommon and are more apt to occur in those who have had multiple LSD exposures ().

Certain features of the phencyclidine (PCP) state permit its inclusion with the hallucinogens (). In addition, hypertension, ataxia, analgesia, amnesia, confusion, agitation, and depersonalization combine to induce behavioral toxicity greater than that seen with the LSD-type hallucinogens. A toxic and a schizophreniform psychosis have often been seen, the latter being difficult to differentiate from acute paranoid schizophrenia without blood or urine tests for phencyclidine. Therefore, acute psychotic breaks in youngsters should be checked with urinary PCP and amphetamine tests. A severe depression may occur during the waning phase of the experience.

PCP-related death can be caused by suicide, homicide, accident, respiratory depression, convulsions, or cerebral hemorrhage. The schizophrenic-like state may persist for weeks or months. Recurrences of the psychosis after recovery are possible without further drug ingestion. Multiple psychoses are observed in individuals who return to the use of PCP, in sane instances because of amnesia regarding the psychotic experience. Violence is a real problem. During the sober interval after many PCP exposures, mood and thought disturbance may continue to be measurable.


The amphetamines are prototypical compounds of the stimulant class. Hypertension, arterial wall changes, heart rhythm disturbances, and convulsions are some of the occasional complications of high dose or prolonged use. The actual hypertension my cause cerebral hemorrhage and, as with PCP, this group is to be considered in instances of teenage stroke. Overdose is infrequent. A paranoid thought disorder or paranoid psychosis will emerge when the amphetamines are used in increasing quantities over time ().

Behavioral toxicity causes much of the morbidity and mortality associated with stimulant abuse, and its biochemical basis consists of increased availability of dopamine and norepinephrine at the neuronal synapse. Hyperactivity, impulsiveness, aggressiveness, and paranoid thinking combine to cause accidents and homicides. Suicide is a possibility during the withdrawal phase when serious depression can occur. A decade ago the fad of injecting enormous quantities of amphetamines became rather popular. This was was the “speedfreak” phenomenon (). Apparently, because of the intensity of the state and the miserable withdrawal period, the fad eventually subsided and hardly exists at present.

As a rule, adolescents only use cocaine occasionally, since it is priced out of the market for regular use. The intravenous use, and particularly the smoking of cocaine base () is much more likely to provoke adverse effects than snorting. These effects consist of strong psychological dependence, paranoid modes of thinking, heart rhythm irregularities, and the behavioral toxicity of the other stimulants.


Alcohol is mentioned here because it is a substantial adolescent problem in its own right () and is often combined with the other drug classes already mentioned. In adolescents the excessive use of alcohol produces impaired behavioral controls. This can result in belligerence, accident proneness (especially while driving), impaired school performance, and problems involving the law. Young people drink less consistently than older people, but tend to consume more on a single drinking occasion (Third Special Report 1978). Therefore, the various chronic organ impairments are less likely to occur in youths than in adults. However, the age of first diagnosis of cirrhosis of the liver is decreasing, and 25- to 30-year-olds with cirrhosis, which takes 10 years or more of heavy drinking to develop, are being seen. The acute effects of heavy drinking, such as gastritis or bleeding peptic ulceration are more likely in the adolescent.

If heavy drinking patterns are established during the early years of life, they tend to persist. Then the biomedical consequences are considerable. Damage to the pancreas, liver, nerves, muscles, endocrine glands, heart, and brain become likely. In large quantities alcohol is a protoplamic poison affecting all cells. Its first metabolic product, acetaldehyde, is believed to be responsible for some of the tissue damage () in heavy drinkers. In addition, the acidic shift associated with alcohol metabolism affects carbohydrate, fat, and protein metabolism, producing a large array of disease states.


The consequences of excessive drug use may be substantial. This is true for every abused drug, the only requirement being that sufficiently large amounts be taken over a sufficiently long period of time. In some instances the untoward effects are imediate, during the period of acute intoxication; in others they may be delayed for decades.

The adolescent, at a stage of psychophysical development when adaptive responses are being learned, is probably more vulnerable to the loss of learning time than the adult. If intoxication with the depressant class of drugs occupies much or all of the waking hours, or if the overuse of drugs becomes the only learned technique for coping with life stresses, the developmental process stops.

Since youth is a period of exploratory, risk-taking, sensation-seeking behavior, it is this group that has traditionally become over-involved in experiences such as drug misuse. It would be a major undertaking to understand the nature of adolescence and to develop strategies to reduce its destructiveness.

Future Research Directions

1. It is important to cane to an understanding of the risk factors in cannabis use by adolescents, particularly the effect on the gonadal hormones and the question of amotivation. The matter of cannabis’ carcinogenetic potential should also be studied. Certain clinical questions, such as whether daily cannabis use leads to increased vulnerability to infections in pre-adolescents and adolescents, could be determined with well-designed investigations of large samples.

2. It may be necessary to await additional basic information before a search for biomedical causes of various types of drug abuse in juveniles can be designed.

3. A search for any differences between adolescent and adult drug abuse effects would be well worth undertaking. An appropriate animal could be used for such comparative work.

4. Animal work with abusable psychoactive drugs should sometimes include younger experimental groups when the drug involved is favored by the youthful population, e.g., when the pharmacology of the solvents is being examined.

5. When certain drugs, PCP for example, are particularly damaging and are widely used by teenagers, research into early intervention strategies seem worthwhile.

6. Something might be learned from a retrospective look at former “speedfreaks,” why they quit, and their subsequent history. Perhaps the information may be applicable to some of today’s drug abuse problems.

7. The causes and careers of amotivation require immediate research attention.

8. Cannabis use in the 8- to 11-year-old group must be studied to confirm or refute the impression that this age group is becoming more heavily involved.

Sidney Cohen, M.D.


Selections from the book: “Drug Abuse And The American Adolescent”. Dan J. Lettieri, Ph.D., and Jacqueline P. Ludford, M.S., eds. Review Report, emphasizing use of marijuana: epidemiology, socio-demographic and personality factors, family and peer influence, delinquency, and biomedical consequences. National Institute on Drug Abuse Research Monograph 38, 1981.