Tuesday, December 13, 2016

Are there hidden consequences to cannabis use?

In 1988, DEA Chief Administrative Law Judge, Francis Young, said that “In strict medical terms marijuana is far safer than many foods we commonly consume.... Marijuana in its natural form is one of the safest therapeutically active substances known to man. By any measure of rational analysis marijuana can be safely used within the supervised routine of medical care.”

28 years later, researchers still continue to study the potential risks of marijuana use. The Substance Abuse and Mental Health Services Administration, in a 2007 National Survey on Drug Use and Health, revealed that 1 in 10 users developed cannabis dependence, with over 4 million Americans meeting DSM-IV diagnostic criteria for cannabis dependence. As this figure is likely to grow with increasing legalization across all 50 states, an understanding of the effects of cannabis on executive functions is more critical than ever in anticipation for its upcoming widespread clinical relevance.

THC, the primary psychoactive constituent of cannabis, is primary responsible for the cognitive effects and addictive potential of cannabis. THC intoxication has been shown to impair cognitive function on a number of levels—from basic motor coordination to more complex tasks, such as the ability to plan, organize, solve problems, make decisions, remember, and control emotions and behavior.

Unfortunately, it is less clear how long cognitive and motor deficits endure. Back in 2002, traditional research methods showed deficits cleared away after a month of abstinence of cannabis use (1). However, with advancements in neuroimaging technology, more recent reports reveal more subtle, long-term effects of cannabis use on brain morphology and physiology. A recent study explored cannabis-related episodic memory deficits and hippocampal morphological differences between healthy individuals and schizophrenics (2).

It found that both healthy and schizophrenic individuals with cannabis use disorder (CUD) were characterized by distinct cannabis-related hippocampal morphological differences and deficits in episodic memory (EM). Shape differences observed in healthy individuals with CUD  were associated with poorer EM, while shape differences observed in schizophrenics with CUD were associated with a longer duration of CUD and shorter duration of CUD abstinence. In conclusion to the study, a past history of CUD was possibly associated with notable differences in hippocampal morphology and EM impairments among adults with and without schizophrenia (2).

However, it is important to highlight some qualifications to these results. Despite similar degrees of sensitivity to cannabis use, between healthy and schizophrenic individuals, the morphological effects seem qualitatively different as CUD could just be exaggerating left-hemisphere hippocampal distortions that were already present due to schizophrenia. Additionally, the schizophrenic hippocampal morphological distortions weren't consistent with all prior research, possibly reflecting simple neurological susceptibility to cannabis abuse.

Most notably from the study, there is an inability to infer a causal relationship between past history of cannabis use and chronically impaired EM or differences in hippocampal morphology given the nature of the data obtained, but EM impairment was observed even after a lengthy period of abstinence. Future studies could build on this one by collecting biological markers of cannabis use to support dose-response observations of cannabis use on episodic memory.

References
  1. Pope H.G., Gruber A.J., Hudson J.I., Huestis M.A., Yurgelun-Todd D. (2002). Cognitive Measures in Long-Term Cannabis Users. The Journal of Clinical Pharmacology, 42: 41S–47S. doi:10.1002/j.1552-4604.2002.tb06002.x
  2. Smith M.J., Cobia D.J., Reilly J.L., Gilman J., Roberts A.G., Alpert K.I., Wang L., Breiter H.C., Csernansky J.G. (2015). Cannabis-related episodic memory deficits and hippocampal morphological differences in healthy individuals and schizophrenia subjects. Hippocampus, 25(9), 1042–1051. http://doi.org/10.1002/hipo.22427

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