Marijuana Damages Brain Cells: Anti-Drug Propaganda or Legitimate Health Concern?

Jordan Levy

10/4/09

Introduction

As the most commonly abused illicit drug in the United States (http://www.medicinenet.com/marijuana/page3.htm), marijuana has received its fair share of negative publicity. According to the National Survey on Drug Use and Health, in 2007, 14.4 million Americans aged 12 or older used marijuana at least once in the month prior to being surveyed, and about 6,000 people a day in 2007 used marijuana for the first time—2.1 million Americans, 62.2 percent of which were younger than 18 years of age (http://www.nida.nih.gov/infofacts/marijuana.html).

Since its use is so widespread, especially among American youth, it’s no wonder there are a lot of claims circulating about the drug, many of them negative. For instance, one website dedicated to keeping teens from using marijuana claims that “the drug can make you mess up in school, in sports or clubs, or with your friends. If you’re high on marijuana, you are more likely to make mistakes that could embarrass or even hurt you. If you use marijuana a lot, you could start to lose interest in how you look and how you’re getting along at school or work” (http://www.drugabuse.gov/MarijBroch/Marijteenstxt.html). Information presented in this way can be misleading, as it provides no scientific evidence for these lofty claims. As a result of websites such as this, many individuals have distorted information regarding marijuana and both its short-term and long-term effects on the human body.

One of the most common claims about marijuana is that it can kill brain cells, damage brain function, and causes learning and memory impairment. This may seem like a bold claim, but in a society dedicated to keeping teens off drugs, it often seems appropriate to use intimidating statistics in order to yield results. For many years, these ideas have been simply accepted as correct, but recently scientists have developed interest in the severity of such a lasting claim, and many studies have been done which attempt to answer this very question: does marijuana really damage brain function and impair memory?

Immediate Effects of Marijuana on the Body

The active ingredient in marijuana is delta-9-tetrohydrocannabinol, commonly referred to as THC. THC binds to and activates specific receptors in the brain, known as cannabinoid receptors (http://www.ctprevention.org/saac/Saac_Files/fs_marijuana_brain.pdf). When these receptors are activated, THC interferes with the normal functioning of various areas of the brain, including the cerebellum, part of the brain responsible for balance, posture, and coordination of movement, and the hippocampus, which is involved with memory formation. As a result, individuals under the influence of marijuana may experience impairment in motor control and compromised short-term memory. In the intoxicated state, memory is often selectively impaired in a dose-dependent fashion similar to alcohol (Deahl 1991). Marijuana also affects receptors in the cerebral cortex that are responsible for sensory perception, which can cause users to experience altered sensory experiences in areas such as touch, sight, hearing, taste, and smell. It can cause distorted perception, impaired coordination, difficulty in thinking and problem solving, and problems with learning and short-term memory (http://www.nida.nih.gov/infofacts/marijuana.html).

The immediate effects of marijuana intoxication on an individual are commonly accepted and are generally undisputed. However, the long-term effects have received a great deal of debate, as scientific research has yielded contradictory results.

Physical Effects of Marijuana on the Brain

In response to many negative claims against marijuana use, Morgan and Zimmer (1991) compiled existing literature and data into a single document in order to discredit what they felt were widespread myths about the drug.

One of these myths was that marijuana damages brain cells, and that this damage causes memory loss, cognitive impairment, and learning difficulties. They report that this claim is based on a study by Heath et. al (1980), in which structural changes in several regions of the brain were found in two rhesus monkeys exposed to THC, the active chemical in marijuana. These changes occurred primarily in the hippocampus, the area of the brain known to play an important role in learning and memory, which suggested that exposure to THC in humans would yield similar negative results.

However, according to Morgan and Zimmer, in order to achieve these damaging results, doses of up to 200 times the psychoactive dose in humans would have to be given. Even studies in which subjects were given 100 times the human dose failed to cause any structural impairment of the brain. Additionally, in a more recent study of rhesus monkeys by Slikker et. al (1992), in which the monkeys were exposed to the equivalent of 4-5 joints per day through face-mask inhalation for an entire year, seven months later there was no observed change in hippocampal structure, cell size, cell number, or synaptic configuration. As a result of these studies, Morgan and Zimmer concluded that the claim that marijuana causes physiological damage to brain cells is incorrect.

A study by Block et. al (1999) yielded similar results, finding that “frequent marijuana use does not produce clinically apparent MRI abnormalities or detectable global or regional changes in brain tissue volumes of gray or white matter, or both combined”. However, the study notes that anatomical abnormalities could occur at a microscopic level that cannot be measured by an MRI, so the true results of the study remain somewhat unclear.

Despite this, Morgan and Zimmer acknowledge that there is evidence that marijuana, especially in high doses, can interfere with users’ ability to transfer new information into long-term memory. Thus, although while under the influence of marijuana, learning is less efficient, there is no evidence that marijuana users suffer permanent structural impairment.

Heavy Marijuana Use and Psychiatric Illness

In addition to the hypothesis that heavy marijuana use can cause impairment to memory and brain function, it has also been suggested that extremely heavy marijuana use can lead to a mental condition that is often referred to as “cannabis psychosis.” (Iverson 2003) This condition generally results from taking very large doses of the drug, and can often be serious enough to lead to the subject being admitted to the hospital, as the symptoms are often confused with those of schizophrenia. These symptoms include delusions of control, grandiose identity, persecution, thought insertion, auditory hallucinations, changed perception, and blunting of emotions. However, this condition is a result of the acute toxicity of marijuana, and is generally unrelated to long-term use of the drug.

Despite this, additional studies have also found a correlation between heavy marijuana use and a display of schizophrenic symptoms. As reported by Hall and Solowji (1998), one study in Sweden of 50,000 individuals found a dose-response relation between the frequency of marijuana use by age 18 and the risk of a diagnosis of schizophrenia over the subsequent 15 years. In the study, it was determined that the relative risk of schizophrenia in those who had used cannabis before was 2.4 times greater than in non-users, and for individuals who had used marijuana more than 50 times in their lifetime the risk was 6 times greater than non-users. The results of this study suggest that cannabis use can exacerbate the symptoms of schizophrenia, and can bring out the symptoms in individuals who are predisposed to a future diagnosis of schizophrenia.

Additional studies have yielded similar results. Hambrecht and Hafner (2000) studied 232 patients in Germany with first-episode schizophrenia and found that 13% had a history of cannabis use, a rate twice that of matched normal controls. While these results seem convincing, however, they don’t necessarily prove a cause-and-effect relationship between marijuana and schizophrenia. Rather, it could be that both marijuana use and schizophrenia are related to a common predisposing factor. For instance, many marijuana users come from deprived social backgrounds, which is a known risk factor for schizophrenia-like psychosis (Iverson 2003). Other reports from New Zealand, Australia, and France have also concluded that the development of cannabis dependence in young adults is associated with increased rates of psychiatric symptoms (Patton et al., 2002). While schizophrenic patients often use marijuana and other psychoactive drugs as a form of “self-medication,” they can often make the symptoms of delusions and hallucinations worse, and can also counteract the anti-psychotic effects of drugs used to treat schizophrenia (Negrete et al., 1986; Linzen et al., 1994).

However, though there exists a clear correlation between heavy marijuana users and psychiatric illness, it is still unclear whether or not this is a causative relationship. If marijuana use were truly a causative factor for schizophrenia, the United States likely would have seen a large increase in cases of schizophrenia in the last 30 years as a result of increased use in the 1960s and 1970s. However, a review of epidemiological evidence up to 1990 failed to show these results, suggesting the relationship between marijuana use and psychiatric illness is not completely direct (Thornicroft 1990).

Frequency of marijuana use and effect on brain function

Procedure

A study by Block and Ghoneim (1992) compared the performance of 144 adult marijuana users and 72 non-marijuana users in order to study the impairments of human cognition and learning that resulted from frequent marijuana use. These individuals were recruited through advertisements, and classified their own average weekly marijuana use as “not at all,” “less than once,” “light” (1-4 times), “intermediate” (5-6 times), or “heavy” (7 or more times), as well as the duration of their use at this frequency. They also filled out a questionnaire that documented the number of occasions in which they had used various other drugs in their lifetime, during the last 12 months, and the previous month. Additionally, and perhaps most importantly (as this is a crucial part that is often left out of similar experiments), the individuals were matched on intellectual functioning before the onset of drug use based on their scores received during the Iowa Tests of Basic Skills standardized test. Finally, in order to ensure that the test results would not be influenced by the effects of other drugs, subjects had to abstain from alcohol from 6 PM the night before each session up through the entire day of the session. Additionally, subjects had to abstain from marijuana and other drugs 24 hours before each subsequent session.

There were two sessions of the experimental testing. The first, lasting about 3 hours, consisted of four tests from the Iowa Tests of Educational Development, as well as the Short Test of Educational Ability. All of these tests were multiple choice pencil-and-paper tests. The second session, which lasted 2.5 hours, involved cognitive and psychomotor tests, which were taken on a computer.

The first session assessed 5 functions: the ability to do quantitative thinking (solving mathematical problems), the correctness and appropriateness of expression (recognizing misspelled words and correcting grammar errors), vocabulary (recognizing synonyms for a given word), the ability to interpret literary materials (answering questions about a given text), and a short test of educational ability (answering questions about vocabulary, arithmetic, letter series, and symbol manipulation).

The second session consisted of 6 different tests. In the first, Buschke’s test, a list of 16 nouns, half of which were “high imagery words,” which are easily visualized, and half were “low imagery words,” which are more difficult to visualize, was presented on the screen at a rate of 3 seconds/word. The subject tried to recall as many words as possible on seven consecutive learning and test trials. The subject tried to recall the whole list on each test trial, but after the first learning trial, the subject was reminded only of the words missed on the immediately preceding test trial. This procedure made it possible to test several aspects of memory, as well as total recall.

The second test measured concept formation by having the subjects study a picture of 2 different hypothetical families for one minute, then showing them 20 new faces, half from each family, and had the subject indicate to which family the individual belonged. One of the families portrayed a “clear concept,” while the other portrayed a “fuzzy concept,” which the subjects had to recognize in order to correctly match the families.

The next test measure text learning, in which the subject read a paragraph from a magazine article and then recalled as much as possible during three minutes. Then, the subject reread the paragraph and recalled it again. The subject then repeated this entire procedure with a different paragraph. The subject’s recall was tape-recorded in order to be scored for text learning.

The fourth test measured free and constrained associations, in which a subject was presented with 100 words and was asked to give a single word as an association. For the first 50 words, the subject could give a free association, but for 10 words each, the subject had to provide one of five different types of “constrained associations,” in which the response had to be related to the stimulus in a specified way.

The fifth test measured paired associate learning, in which the subject was shown a list of 30 pairs of words. The initial word from each pair was then presented to the subject, who had to try and respond to the second word from each pair. This was repeated once with the same set of words, and then the entire procedure was repeated with a different list.

Finally, the sixth test was a series of psychomotor tests. In the first, the subject viewed two light-emitting diodes: one which was flickering and the other which was not. The subject had to indicate which of the diodes was flickering, and the computer determined the flicker fusion threshold. The second half of the test measured discriminate reaction time, in which the subject viewed a series of digits that flashed for 100 milliseconds each and pressed a button following each “4” that appeared. The computer altered the interstimulus interval depending on the subject’s accuracy. This procedure was repeated four times.

Results

The results of the first session were conclusive: heavy marijuana users showed impairments in mathematic ability and verbal expression on the twelfth grade Iowa Tests compared to non-users. However, heavy users were unimpaired on the other three tests: vocabulary, ability to interpret literary materials, and short tests of educational ability.

On the second session, the results were somewhat mixed. In Buschke’s Test, heavy marijuana users showed impairment relative to non-users in long-term retrieval for high imagery words, although not for low-imagery words. However, interestingly enough, intermediate marijuana users achieved a higher percentage of correct answers than non-users for “fuzzy” concepts on the concept formation test. On the other computerized tests, including text learning, paired associate learning, free and constrained associations, and critical flicker fusion and discriminate reaction time, there was no evidence of the effects of marijuana use.

Overall, the experimental results suggest that heavy marijuana users do show overall impairments relative to non-users in the areas of mathematics and verbal expression, but not in any other abilities. These impairments may indicate that the regular use of marijuana 7 or more times in a week can damage the central nervous system beyond the acute effects of the drug. However, there are a few confounding variables that may affect the validity of the above claim.

Block and Ghoneim acknowledge that the association between impairments in brain function and marijuana use may be more indirect than the results suggest. For instance, if marijuana users go to school high, they might learn less or remember less of what they learn as a result of acute marijuana intoxication and not the long-term brain effects of extended use. Thus, the lower test scores of heavy marijuana users may be attributed to the short-term effects of marijuana use and not the potential impairment caused by excessive long-term use. As a result, although this experiment was one of the better-designed studies of the effects of marijuana use on the brain because it matched subjects on intelligence before the onset of marijuana use, it is still someone inconclusive. Though the results suggest that heavy marijuana use may affect the mathematical and verbal expression abilities of an individual, the link was not direct enough to completely attribute these impairments to the effects of extensive marijuana smoking over time and not acute marijuana intoxication.

Conclusion

Despite significant amounts of research in existence regarding the potential damaging effects marijuana can have on brain cells, memory, and brain function, experimental results present conflicting information regarding the validity of the claim.

The results of the studies discussed above demonstrate that many heavy users of marijuana experience some form of memory or brain impairment, whether it be difficulty transferring new information into the long-term memory, lower mathematical and verbal abilities, or an increased likelihood of displaying symptoms of psychiatric illness. However, in each of these studies, there was not enough evidence to prove that marijuana is a direct cause for these problems – rather, it could possible that individuals who are predisposed to heavy marijuana use are also predisposed to these impairments.

Additionally, analyses of the physiological structure of the brain of heavy marijuana users did not display any difference from non-users, although the studies also suggest that brain abnormalities could exist in an undetectable form.

One aspect the research seems to have concluded is that the risk for brain damage exists solely for heavy marijuana users, and those who use it less than 7 times a week generally do not show any more risk for brain damage than do non-users.

Thus, although significant amounts of research have been conducted regarding marijuana’s long-term effect on the brain, it is still impossible to reach a definite conclusion about the potential damaging effects the drug may have. Although the current research suggests a link between heavy marijuana use and damage in brain function, more research needs to be conducted in order to determine whether or not this link is causative. While the occasional joint is unlikely to cause much damage to an individual’s brain, until more research has been conducted, heavy users should evaluate their habits, as they may potentially be causing significant damage to their health.





References

Block, R. I. & Ghoneim, M.M. (1993). Effects of chronic marijuana use

on human cognition. Psychopharmacology, 110, 219-228.

Block, R.I., O’Leary, D. S., Ehrhardt, J. C., Augustinack, J.C., Ghoneim, ] M.M., Arndt, S., & Hall, J.A. (1999). Effects of frequent marijuana

use on brain tissue volume and composition. NeuroReport, 11(3),

491-496.

Deahl, M. (1999). Cannabis and memory loss. British Journal of

Addiction, 86, 249-252.

Hall, W. & Solowij, N. (1998). Adverse effects of cannabis. The Lancet,

352, 1611-1616.

Iversen, L. (2003). Cannabis and the brain. Oxford Journals, 126(6),

1252-1270.

Marijuana drug information. (2008). Retrieved October 4, 2009,

from MedicineNet Web site:

http://www.medicinenet.com/marijuana/article.htm

Marijuana: facts for teens. (2008). Retrieved October 4, 2009, from the

National Institute of Drug Abuse Web site:

http://www.drugabuse.gov/MarijBroch/Marijteenstxt.html

Marijuana: the brain’s response to drugs. (1997). Retrieved October 4,

2009, from the Connecticut Clearinghouse Web site:

http://www.ctprevention.org/saac/Saac_Files/fs_marijuana_brai

n.pdf

Morgan, J. P. & Zimmer, L. (1995). Exposing marijuana myths: a review

of the scientific evidence. Open Society Institute.

NIDA InfoFacts: marijuana. (2009). Retrieved October 4, 2009, from

the National Institute of Drug Abuse Web site: http://www.nida.nih.gov/infofacts/marijuana.html