Marijuana Smoking and Genetic Damage
Marijuana Smoking and Genetic Damage
According to the data reported by the National Institute of Drug Abuse (1), marijuana is the most popular drug of abuse within United States. Despite the claims and reported list of adverse effects, marijuana use is increasing in young adults. It is usually smoked as bongs or joints (hand rolled cigarettes) in addition to marijuana cookies and brownies.
The primary active compound that is responsible for the euphoric effects of marijuana is delta-9-tetrahydrocannabinol (or THC). Once smoked, the active compound is rapidly absorbed into the blood stream from the lungs and can almost instantaneously stimulate the specialized receptors in the brain to produce the sense of pleasure or ‘high’.
Can Marijuana Cause Genetic Damage?
Nicotine cigarettes have long been associated with a wide variety of malignancies due to DNA alterations. Although almost all the recreational drugs are known to cause debilitating damage to the vital organs, most of these were considered non-carcinogenic. However, according to the latest research, marijuana smoking can lead to genetic damage in addition to many other adverse effects. Based on the results of an experimental study published in the journal Chemical Research in Toxicology (2), investigators reported that the carcinogenic potential of the marijuana is attributed to compounds like Acetaldehyde. Lead investigator Singh suggested that Acetaldehyde has the capacity to alter the stable structure of DNA to cause mutations; leading to cancers and other ailments.
Another study reported in the Journal of Toxicological Sciences (3) suggested that marijuana smoke induces oxidative stress in the biological cells. As a result of stress, reactive oxygen species are produced that are known to cause gene mutations and resulting DNA damage.
Human DNA is the basis of life. It carries all the necessary information to protect and prevent the cellular existence from significant harm. However, if the molecular insult is severe, the DNA damage is almost inevitable. It is imperative to keep in mind that DNA damage is the primary etiological factor that promotes carcinogenesis (or tumor formation).
John Charles A. Lacson and associates (4) conducted an experimental study to compare if the cancer producing potential of marijuana is similar to other recreational drugs of abuse like cocaine. After extensive analysis, it was concluded that in comparison to cocaine, marijuana increases the risk of developing testicular tumor almost 2-folds in the consumers.
Other adverse effects that are usually reported in the setting of chronic marijuana consumption are:
Changes in Memory and Cognition:
Most characteristic symptoms are:
- Learning disabilities
- Deficits in coordination
- Deficits in brain development
- Low level of intelligence and intellectual capacity
This is mainly because marijuana receptors are highly concentrated in the higher brain centers (parts of brain that are associated with intellectual thinking and memory consolidation). Clinical data suggests that chronic consumption of marijuana can interfere with problem solving capacity, intellectual thinking, time perception, sensory perception and emotional intelligence.
Chronic marijuana smokers develop respiratory infections (marked by chronic cough and production of sputum). Study conducted by Kim and associates also suggested that marijuana smoking cam lead to lung cancer (5).
Marijuana consumption is followed by changes in heart. According to clinical investigations, marijuana can increase the heart rate up to 20 to 100% soon after the absorption of active compound in the blood. It is also suggested that the risk of myocardial infarction increases up to 4.8-folds in some susceptible subjects.
Individuals who have a personal or positive family history of psychiatric illnesses (such as paranoia, schizophrenia, depression etc.) are more prone to develop psychiatric issues or even psychosis in the setting of marijuana intake.
It is highly recommended to seek help if you are psychologically dependent on marijuana to minimize the risk of developing malignant lesions and end-organ damage.
- Singh, R., Sandhu, J., Kaur, B., Juren, T., Steward, W. P., Segerback, D., & Farmer, P. B. (2009). Evaluation of the DNA damaging potential of cannabis cigarette smoke by the determination of acetaldehyde derived N2-ethyl-2′-deoxyguanosine adducts. Chemical research in toxicology, 22(6), 1181-1188.
- Kim, H. R., Jung, M. H., Lee, S. Y., Oh, S. M., & Chung, K. H. (2012). Marijuana smoke condensate induces p53-mediated apoptosis in human lung epithelial cells. The Journal of toxicological sciences, 38(3), 337-347.
- Lacson, J. C. A., Carroll, J. D., Tuazon, E., Castelao, E. J., Bernstein, L., & Cortessis, V. K. (2012). Population‐based case‐control study of recreational drug use and testis cancer risk confirms an association between marijuana use and nonseminoma risk. Cancer, 118(21), 5374-5383.
- Falek, A. (2012). Genetic studies of marijuana: Current findings and future directions. Marijuana and Health Hazards: Methodological Issues in Issues in Current Research, 1.