Medical marijuana

The history of medical marijuana

The use of marijuana for medicinal purposes has a long history. It began around 2737 B.C.E. The 1868 US Dispensatory purported that the tincture made by soaking marijuana in alcohol improved appetite, sex drive, mental disorders, gout, cholera, hydrophobia, and insomnia. The Squibb Company in the early 1900s had a product called chlorodyne which was a combination of morphine and cannabis intended to treat stomach problems. There were a variety of other cannabis-based products popular in the 1930s, but the Marijuana Tax Act of 1937, which imposed a transport fee of $100 per ounce (a lot of money in 1937), killed the market. Marijuana remains a Schedule I substance under the controlled substances act and illegal under federal law. Conversely, 62% of Americans favor legalization of marijuana (up from 31% in 2000). Marijuana is legal by state law for medicinal use in 33 states and for recreational use in 10. It is also legal in the District of Columbia, Guam and Puerto Rico. A recent poll showed that 13% of American adults use marijuana up from 7% in 2013. As the use of cannabis products becomes a larger part of our culture, it is apparent that pro-active policies are needed. Any policy should be developed with local legal counsel. The purpose of this article is not to create policy. It is intended to provide food for thought.


Marijuana and impairment

In 1964, scientists identified the psychoactive substance in marijuana, delta-9-tetrahydrocannabinol (THC). Since THC is psychoactive, there must be receptors for it in the brain. Devane and Howlett found evidence of cannabinoid receptors in the brain in 1988. There are two types of cannabinoid receptors CB1, responsible for brain effects, and CB2, which has a role in the immune system. The receptors are not specifically designed for marijuana. There must be some naturally occurring substances that use the same receptors. The first such substance, anandamide, was identified in 1992. There are a few others. These naturally occurring neurotransmitters are called endocannabinoids and are different from other neurotransmitters. Most neurotransmitters are stored in neurons and released when the neuron fires. Endocannabinoids are made when needed, rather than stored. As you recall from physiology class, neurotransmitters are released by the presynaptic neuron, cross the synapse and bind to receptors on the postsynaptic neuron. Endocannabinoids are retrograde. They are released by the postsynaptic neuron and bind to CB1 receptors on the presynaptic neuron. By functioning as regulators, they prevent too much excitation or inhibition. CB1 receptors are found all over the brain in areas responsible for motor control, fear, anxiety and in the midbrain dopamine reward circuit.

Given the widespread distribution of cannabinoid receptors, it is no surprise that there are many ways in which marijuana use can cause impairment. Note that the word is impairment-not intoxication. You don’t need to be stoned out of your mind to have your brain not function properly. Impairment varies from individual to individual and for an individual. One can’t anticipate the same response with each use. Also, an individual’s perception of the level of function may be inaccurate. Impairment can be affected by route of administration (smoking, eating, vaping, skin patch), individual metabolism, history (first time, acute, chronic), other substances ingestion and dosage. Dosage is tough to measure. Potency varies. Marijuana can be as much as 30 times stronger than it was a couple of decades ago.

Impairment may be expressed as problems concentrating, attending to details, focusing on goals, performing two actions simultaneously and learning new, complex information. Time perception is altered. Brief intervals are perceived as longer than they are. Driving simulator studies have shown that the perceived distance between objects increased. Impaired people don’t distinguish colors well. They process three dimensional visual cues differently, have impaired mathematical performance, and have increased reaction time. It’s not surprising that studies have shown an association between marijuana use and risk of motor vehicle crashes. A meta-analysis quantified the increased risk as 20%-30%. Unfortunately, blood levels are not predictive of the level of impairment associated with marijuana use.


Conclusion

I have recently discussed this issue of medical marijuana with several medical transportation providers. None had addressed it. One opined that he could legitimately argue that all of his employees were in safety sensitive positions, but he was unable to articulate how the laws in his state defined them.  Another stated that since marijuana remains illegal under federal law as a Schedule I, no action is required. The development of a well-reasoned, legally sound policy is crucial. The policy will not be effective unless it is adequately communicated and enforced.


References

  • Polk, TA, “The Addictive Brain”,Virginia: The Great Courses, 2015
  • Iverson, LI, “Understanding Marijuana: A New Look at the Scientific Evidence”, New York: Oxford University Press, 2002.
  • Vargas, S, “Clearing the Air on Marijuana”, Safety and Health, April 2019
  • Erickson, CK, “The Science of Addiction from Neurobiology to Treatment”, New York: W.W. Norton and Company, 2007
The information provided in this article is intended for general informational purposes only and should not be considered as all encompassing, or suitable for all situations, conditions, and environments. Please contact us at losscontrol@markel.com or your attorney if you have any questions. The article may not be linked to, copied, reproduced, republished, posted, or distributed in any way by non-policyholders of Markel®, without permission.