AMERICAN ACADEMY OF PEDIATRICS
Committee on Substance Abuse
Marijuana: A Continuing Concern for Pediatricians
ABSTRACT. Marijuana, the common name for
prod-ucts derived from the plantCannabis sativa, is the most common illicit drug used by children and adolescents in the United States.1Despite growing concerns by the
med-ical profession about the physmed-ical and psychologmed-ical ef-fects of its active ingredient, D-9-tetrahydrocannabinol, survey data continue to show that increasing numbers of young people are using the drug as they become less concerned about its dangers.1
ABBREVIATION. THC, tetrahydrocannabinol.
B
ecause the decision of whether to usemari-juana is usually made by the time a young person reaches the age of 19 years,2,3
pediatri-cians must continue to be cognizant of the implica-tions of marijuana use. Widespread debate exists about marijuana and the possibility of legalizing its use or at least decriminalizing its possession.4 –7
Fur-thermore, marijuana is being promoted for medical purposes, such as the treatment of glaucoma and the management of nausea and anorexia related to can-cer chemotherapy.4,8,9Although these topics are
be-yond the scope of this statement, evidence suggests that pediatricians should continue their vigilant ef-forts to prevent the use of this drug by young people. The abuse of marijuana by adolescents is a major health problem with social, academic, developmen-tal, and legal ramifications.10 Marijuana is an
addic-tive, mind-altering drug capable of inducing depen-dency.11 Pediatricians are obligated to develop a
reasoned approach to dealing with its use by chil-dren and adolescents so they can provide appropri-ate care and counsel.12
EPIDEMIOLOGY
Between 1991 and 1997, the use of marijuana by young people increased dramatically.1In 1997, 23%
of eighth graders reported having used the drug at some time in their lives, an increase in use from 10% in 1991. Among 10th graders, the number nearly doubled from 23% in 1991 to 42% in 1997. In 1997, 50% of high school seniors reported having used marijuana compared with 37% 6 years earlier. The abuse of marijuana among teenagers has increased as the “perceived harmfulness” of regular use has de-creased and the perception of “peer acceptance” has increased.1,2
POTENCY
The potency of marijuana is defined as the percent-age of D-9-tetrahydrocannabinol (D-9-THC) in the dry weight of the sample. Increased sophistication in the selective breeding of marijuana plants has led to a substantial increase in the potency of street samples during the past 2 decades. In 1975, the average po-tency of THC in confiscated samples was 0.71%; by 1997, the average concentration was 3.71%—a five-fold increase. There is wide variation in the potency of smoked marijuana. Sensimilla (considered by many to be the finest product, produced from the flowering tops of the female hemp plant) had an average potency of 6.6% in 1997. Marijuana sold as loose plant material (leaves, stems, and seeds) had an average potency of 3.2%.13In addition, the method of
consumption (smoking as a rolled cigarette or in a pipe or packed into a hollowed-out cigar), as well as the presence of adulterating substances, affect the potency.
Because of the documented change in potency, pediatricians must be able to address with their pa-tients what seems to be “casual use” of marijuana. Trends suggest that the low-dose, self-experimenta-tion type of use typical of the 1960s may be giving way to the high-potency– high-reward pattern of compulsive marijuana use prevalent during the late 1990s.14
SOMATIC CONSEQUENCES
Marijuana should not be considered an innocuous drug. Regular use has been associated with cardio-vascular, pulmonary, reproductive, and immuno-logic consequences. The physioimmuno-logic effects of mari-juana use include an accelerated heart rate and a minimal rise in blood pressure.15,16 These effects,
which seem to be secondary toD-adrenergic vascular mechanisms, are transient and usually not deleteri-ous to the otherwise healthy adolescent. The imme-diate pulmonary effect of smoking marijuana is bronchodilation, although with long-term use the smoked particles act as an irritant, causing broncho-constriction and eventual airway obstruction.17–19The
chronic effects are similar to those of smoking to-bacco, and there seems to be a relationship between smoking marijuana and neoplastic changes in the lungs.20
Heavy marijuana use may be especially dangerous for adolescents during puberty. Such use has been associated with diminished sperm motility, de-creased sperm counts, dede-creased circulating testos-terone levels,21,22irregular ovulation, and decreased
pituitary gonadotropin levels.23,24The metabolites of
The recommendations in this statement do not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate.
marijuana cross the human placenta and are also found in human milk. Although the consequences of the presence of such metabolites in human milk have yet to be identified,25–27infants born to mothers who
smoke marijuana during pregnancy are shorter, weigh less, and have smaller head circumferences at birth.27,28Marijuana and some of its components
in-fluence the immune system and affect the body’s antitumor activities. Marijuana receptors have been identified on macrophages and T and B lympho-cytes, suggesting a molecular basis for immunosup-pression by THC.29 –31
NEUROPHARMACOLOGY
The psychoactive effects ofD-9-THC are receptor-mediated. The cannabinoid receptor sites in the brain are particularly dense in the outflow nuclei of the basal ganglia, the hippocampus, and the molecular layers of the cerebellum, implicating roles for canna-binoids in the disruption of cognition and coordina-tion. Sparse densities in the lower brainstem areas controlling cardiovascular and respiratory functions
may explain why high doses of D-9-THC are not
lethal.32
Anandamide, a derivative of arachidonic acid, is an endogenous chemical in the brain that binds with cannabinoid receptors.33 Like D-9-THC, it has been
shown to affect muscle coordination, produce anal-gesic and tranquilizing effects, and inhibit secretion of follicle-stimulating hormone, prolactin, and growth hormone.34The use of anandamide as a
mar-ijuana antagonist has substantial effects on rats con-ditioned to self-treatment with THC33,34 and has
helped elucidate the mechanism by which cannabi-noids exert their biological and psychologic effects.
The most pervasive common pathway among drugs of abuse, including cocaine, heroin, opiates, and marijuana, is the stimulation of release of the neurotransmitter, dopamine.35–38 This endogenous
catecholamine stimulates certain dopaminergic pro-jections of the medial forebrain bundle—the brain’s so-called reward circuitry.39 Psychoactive drugs,
in-cluding marijuana, derive substantial abuse liability from enhancing these circuits; and it is the psycho-active ingredient of marijuana,D-9-THC, that stimu-lates the release of dopamine, mediated through the cannabinoid receptors.40,41
In both animal and human experiments, subjects self-administer marijuana. They predictably select high-potency marijuana over low-potency marijua-na,42 supporting the hypothesis that the reinforcing
effect and abuse liability of marijuana are positively related to theD-9-THC content.
Marijuana is lipophilic and is stored in the brain and other fat-rich areas of the body, forming what has been described as a “depot.”43The slow release
of marijuana and its metabolites from lipid stores may explain the carry-over effects of marijuana on driving and other cognitive and behavioral chang-es,44 as well as the absence of acute signs of
with-drawal after abrupt discontinuation of use.45
BEHAVIORAL AND COGNITIVE CONSEQUENCES Marijuana affects the brain, resulting in behavioral and cognitive effects. Acutely, marijuana produces euphoria, relaxation, and disinhibition. Persons un-der the influence of the drug show impaired prob-lem-solving skills and difficulty in organizing thoughts and conversing. Other adverse conse-quences of marijuana use include interference with coordination; the ability to judge elapsed time, speed, and distance; the ability to track a moving object; and reaction time.46 – 49 There is little doubt
that marijuana intoxication contributes substantially to accidental deaths and injuries among adolescents, especially those associated with motor vehicle crashes, and is frequently involved in incidents re-lated to driving while intoxicated.50,51
Regular use of marijuana also exerts a negative effect on short-term memory, learning, and attention span. Three methodologically strong studies pre-sented compelling evidence that these functions were impaired in frequent users of marijuana (de-fined as using 20 to 30 days per month), even up to 6 weeks after discontinuation of use,52and noticeable
impairment in attention and memory was evident even after 24 hours of abstinence.53,54Clearly, young
people who are frequent users of marijuana experi-ence residual neuropsychologic effects with an im-paired ability to learn.53
An “amotivational syndrome” has been described in chronic heavy marijuana users. This syndrome is characterized by the inability to sustain attention on environmental stimuli and to maintain goal-directed thinking and behavior.55An additional source of
con-cern is the occasional occurrence of dysphoric reac-tions that may range from mild fear to depersonal-ization to frank paranoia.56,57
Finally, marijuana use often precedes the use of other more dangerous drugs. Although marijuana use does not necessarily predict progression to the use of “harder” drugs, adolescents who use mari-juana are 104 times as likely to use cocaine compared with peers who never smoked marijuana.4,58
There-fore, the use of marijuana as a risk behavior and its role as a “gateway drug” for some teenagers must be considered.
SUMMARY
The seriousness of the behavioral consequences of marijuana use is sufficient to cause great concern and should prompt the pediatrician to counsel young people against any use of the drug. Such counsel should be based on health concerns, including the relationship of marijuana use to trauma associated with intoxication and the effect on memory and learning during this important period of develop-ment. Additional reasons for concern and counsel include anxieties and uncertainties about the poten-tial harm that marijuana use may cause to adoles-cents during a period of rapid change in hormonal secretion, possible teratogenicity, and the known consequences of long-term use.
A discussion of drug use, including the use of marijuana, should be a routine part of primary health
AMERICAN ACADEMY OF PEDIATRICS 983
at Viet Nam:AAP Sponsored on August 30, 2020
www.aappublications.org/news
care clinical preventive services for every child and adolescent. An assessment of potential drug use gives the pediatrician the opportunity to offer antic-ipatory guidance before the onset of drug use, to intervene and minimize consequences if drug use has begun, and to detect and address issues of long-term or heavy use.
Although all users should be counseled about the dangers of the drug and the illicit nature of its use, marijuana is an addictive drug and is capable of producing dependency. Marijuana-dependent teen-agers should be offered treatment options, rather than simply punishment, for their illness.
Committee on Substance Abuse, 1998 –1999
Richard B. Heyman, MD, Chairperson Trina M. Anglin, MD
Stuart M. Copperman, MD Alain Joffe, MD
Catherine A. McDonald, MD Peter D. Rogers, MD, MPH Rizwan Z. Shah, MD
Liaison Representatives
Marie Armentano, MD
American Academy of Child and Adolescent Psychiatry
Gayle M. Boyd, PhD
National Institute of Alcohol Abuse and Alcoholism Dorynne Czechowicz, MD
National Institute on Drug Abuse
REFERENCES
1. University of Michigan News and Information Services.Monitoring the Future Study[news release]. Ann Arbor, MI: University of Michigan News and Information Services; 1997
2. Johnson LD. Changing trends, patterns and nature of marijuana use. In:
Conference Highlights, National Conference on Marijuana Use: Prevention, Treatment and Research. Bethesda, MD: National Institute on Drug Abuse, National Institutes of Health; 1996. NIH publication 96-4106: 17–19
3. Kandel D. Relationship between marijuana use and the use of other drugs and other antisocial problem behaviors. In:Conference Highlights, National Conference on Marijuana Use: Prevention, Treatment and Research. Bethesda, MD: National Institutes of Health; 1996. NIH publication 96-4106:48 –51
4. Grinspoon L, Bakalar JB. Marihuana as medicine: a plea for reconsid-eration.JAMA. 1995;273:1875–1876
5. Kleber HD. Deglamorising cannabis.Lancet. 1995;346:1241
6. Kassirer JP. Federal foolishness and marijuana.N Engl J Med. 1997; 336 –366-367
7. Geddes D. Decriminalisation of cannabis.Lancet. 1995;346:1709 –1710 8. Smith D. From the president. Am Soc Addict Med News.
January-February 1997:4
9. Workshop on the Medical Utility of Marijuana.Report to the Director. Rockville, MD: National Institutes of Health, National Institute on Drug Abuse; 1997
10. Jaffe SL, Compton MT. Marijuana update for child and adolescent psychiatrists.AACAP News. 1997;28:7–9
11. American Psychiatric Association.Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994:216 –221
12. American Academy of Pediatrics, Committee on Adolescence and Com-mittee on Substance Abuse. Marijuana: a continuing concern for pedi-atricians.Pediatrics. 1991;88:1070 –1072
13. National Institute on Drug Abuse.Quarterly Report: Potency Monitoring Project. Rockville, MD: National Institute on Drug Abuse; 1997. Report No. 62, April 1 to June 30
14. Gold M. The pharmacology of marijuana. In: Graham AW, Schultz TK, eds.Principles of Addiction Medicine. Chevy Chase, MD: American Soci-ety of Addiction Medicine; 1998:163–171
15. Beaconsfield P, Ginsburg J, Rainsbury R. Marijuana smoking: cardio-vascular effects in man and possible mechanisms.N Engl J Med. 1972; 287:209 –212
16. Weiss JL, Watanabe AM, Lemberger L, Tamarkin NR, Cardon PV. Cardiovascular effects of delta-9-tetrahydrocannabinol in man. Clin Pharmacol Therapy. 1972;13:671– 684
17. Vachon L, FitzGerald MX, Solliday NH, Gould IA, Gaensler EA. Single-dose effects of marijuana smoke: bronchial dynamics and respiratory-center sensitivity in normal subjects.N Engl J Med. 1973;288:985–989 18. Tashkin DP, Shapiro BJ, Frank IM. Acute pulmonary physiologic effects
of smoked marijuana and oral 9-tetrahydrocannabinol in healthy young men.N Engl J Med. 1973;289:336 –341
19. Wu TC, Tashkin DP, Djahed B, Rose JE. Pulmonary hazards of smoking marijuana as compared with tobacco.N Engl J Med. 1988;318:347–351 20. Cottrell JC, Sohn SS, Vogel WH. Toxic effects of marihuana tar on
mouse skin.Arch Environ Health. 1973;26:277–278
21. Hembree WC, Nahas GG, Zeidenberg P, et al. Changes in human spermatozoa associated with high dose marihuana smoking. In: Nahas GG, Paton WDM, eds.Marijuana Biological Effects: Analyses, Metabolism, Cellular Responses, Reproduction and Brain. New York, NY: Pergamon Press; 1979:429 – 439
22. Kolodny RC, Masters WH, Kolodner RM, Toro G. Depression of plasma testosterone levels after chronic intensive marijuana use.N Engl J Med. 1974;290:872– 874
23. Asch RH, Smith CG, Siler-Khodr TM, Pauerstern CJ. Effects of delta-9-tetrahydrocannabinol during the follicular phase of the rhesus monkey.
J Clin Endocrinol Metab. 1981;52:50 –55
24. Cohen S. Marijuana and reproductive functions.Drug Abuse Alcohol News. 1985;13:1
25. Fried P. Perinatal and developmental effects of marijuana. In:Conference Highlights: National Conference on Marijuana Use: Prevention, Treatment, and Research. Rockville, MD: National Institute on Drug Abuse, National Institutes of Health; 1995. NIH publication 96-4106. 1995:32–34 26. Fried PA. Prenatal exposure to marihuana and tobacco during infancy,
early and middle childhood: effects and an attempt on synthesis.Arch Toxicol Suppl. 1995;17:233–260
27. Zuckerman B, Frank DA, Hingson R, et al. Effects of maternal marijuana and cocaine use on fetal growth.N Engl J Med. 1989;320:762–768 28. Shrono PH, Klebanoff MA, Nugent RP, et al. The impact of cocaine and
marijuana use on low birth weight and pre-term birth: a multicenter study.Am J Obstet Gynecol. 1995;172:19 –27
29. Cabral G. Effects of marijuana on the brain, endocrine system and immune system. In:Conference Highlights: National Conference on Mari-juana Use: Prevention, Treatment and Research. Rockville, MD: National Institute on Drug Abuse, National Institutes of Health; 1996. NIH publication 96-4106; 1996:21–24
30. Bhargava HN, House RV, Thorat SN, Thomas PT. Cellular immune function in mice tolerant to or abstinent from 1-trans-delta 9-tetrahy-drocannabinol.Pharmacology. 1996;52:271–282
31. House RV, Thomas PT, Kozak JT, Bhargava HN. Suppression of im-mune function by non-peptide delta opioid receptor antagonists. Neu-rosci Lett. 1995;198:119 –122
32. Herkenham M, Lynn AB, Little MD, et al. Cannabinoid receptor local-ization in brain.Proc Natl Acad Sci U S A. 1990;87:1932–1936 33. Devane WA, Hanus L, Breuer A, et al. Isolation and structure of a brain
constituent that binds to the cannabinoid receptor.Science. 1992;258: 1946 –1949
34. Musty RE, Reggio P, Consroe P. A review of recent advances in canna-binoid research and the 1994 International Symposium on Cannabis and the Cannabinoids.Life Sci. 1995;56:1933–1940
35. Leshner AI. Drug abuse and addiction are biomedicinal problems.Hosp Pract (Off Ed).–A Special Report. 1997:2– 4
36. Self DW. Neurobiological adaptations to drug use.Hosp Pract–A Special Report. 1997:5– 8
37. Koob GF. Neurochemical explanations for addiction.Hosp Pract–A Spe-cial Report. 1997:12–14
38. Volkow ND, Fowler JS, Gatley SJ, et al. PET evaluation of the human brain dopamine system of the human brain.J Nucl Med. 1996;37: 1242–1256
39. Self DW, Nestler EJ. Molecular mechanisms of drug reinforcement and addiction.Annu Rev Neurosci. 1995;18:463– 495
40. Rodriguez de Fonseca F, Carrera MRA, Navarro M, Koob GF, Weiss F. Activation of corticotropin-releasing factor in the limbic system during cannabinoid withdrawal.Science. 1997;276:2050 –2054
41. Tanda G, Pontieri FE, Di Chiara G. Cannabinoid and heroin activation of mesolimbic dopamine transmission by a common mu1 opioid recep-tor mechanism.Science. 1997;276:2048 –2050
42. Chait LD, Burke KA. Preference for high- versus low-potency mari-juana.Pharmacol Biochem Behav. 1994;49:643– 647
9th ed. New York, NY: McGraw Hill; 1996:572–573
44. Leirer VO, Yesavage JA, Morrow DG. Marijuana carry-over effects on aircraft pilot performance.Aviat Space Environ Med. 1991;62:221–227 45. Wickelgren I. Marijuana: harder than thought? Science. 1997;176:
1967–1968
46. Lundqvist T. Chronic cannabis use and the sense of coherence.Life Sci. 1995;56:2145–2150
47. Lundqvist T. Specific thought patterns in chronic cannabis smokers observed during treatment.Life Sci. 1995;56:2141–2144
48. Mendelson JH, Meyer RE. Behavioral and biological concomitants of chronic marihuana smoking by heavy and casual users. In:Marijuana: A Signal of Misunderstanding. 1972;1:68 –246
49. Naditch MP. Acute adverse reactions to psychoactive drugs, drug usage and psychopathology.J Abnorm Psychol. 1974;83:394 – 403
50. Logan BK, Schwilke EW. Drug and alcohol use in fatally injured drivers in Washington State.J Forensic Sci. 1996;41:505–510
51. Crouch DJ, Birky MM, Gust SW, et al. The prevalence of drugs and
alcohol in fatally injured truck drivers.J Forensic Sci. 1993;38:1342–1353 52. Schwartz RH, Gruenewald PJ, Klitzner M, Fedio P. Short-term memory impairment in cannabis dependent adolescents.Am J Dis Child. 1989; 143:1214 –1219
53. Block RI, Ghoneim MM. Effects of chronic marijuana use on human cognition.Psychopharmacology (Berl). 1993;110:219 –228
54. Pope HG, Yurgelun-Todd, D. The residual cognitive effects of heavy marijuana use in college students.JAMA. 1996;275:521–527
55. Weller RA. Marijuana: effects and motivation.Med Aspects Hum Sexu-ality. 1985;19:92–104
56. Keeler MH. Adverse reaction to marijuana: classification and suggested treatment. Am J Psychiatry. 1967;124:674 – 677
57. Weil AT. Adverse reactions to marihuana: classification and suggested treatment.N Engl J Med. 1970;282:997–1000
58. National Institute on Drug Abuse.Drug Use Among Racial/Ethnic Minor-ities. Rockville, MD: National Institute on Drug Abuse; 1995. NIH publication 95-3888
AMERICAN ACADEMY OF PEDIATRICS 985
at Viet Nam:AAP Sponsored on August 30, 2020
www.aappublications.org/news
DOI: 10.1542/peds.104.4.982
1999;104;982
Pediatrics
Committee on Substance Abuse
Marijuana: A Continuing Concern for Pediatricians
Services
Updated Information &
http://pediatrics.aappublications.org/content/104/4/982
including high resolution figures, can be found at:
References
http://pediatrics.aappublications.org/content/104/4/982#BIBL
This article cites 39 articles, 6 of which you can access for free at:
Subspecialty Collections
http://www.aappublications.org/cgi/collection/substance_abuse_sub
Substance Use
http://www.aappublications.org/cgi/collection/for_your_benefit
For Your Benefit
following collection(s):
This article, along with others on similar topics, appears in the
Permissions & Licensing
http://www.aappublications.org/site/misc/Permissions.xhtml
in its entirety can be found online at:
Information about reproducing this article in parts (figures, tables) or
Reprints
http://www.aappublications.org/site/misc/reprints.xhtml
DOI: 10.1542/peds.104.4.982
1999;104;982
Pediatrics
Committee on Substance Abuse
Marijuana: A Continuing Concern for Pediatricians
http://pediatrics.aappublications.org/content/104/4/982
located on the World Wide Web at:
The online version of this article, along with updated information and services, is
by the American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.
the American Academy of Pediatrics, 345 Park Avenue, Itasca, Illinois, 60143. Copyright © 1999 has been published continuously since 1948. Pediatrics is owned, published, and trademarked by Pediatrics is the official journal of the American Academy of Pediatrics. A monthly publication, it
at Viet Nam:AAP Sponsored on August 30, 2020
www.aappublications.org/news
