Just this month, an article appeared in the Journal of Neuropsychology entitled "Early Onset Marijuana Use is Associated with Learning Inefficiencies." Young adults reporting early onset marijuana use have learning weaknesses, which accounted for the association between early onset marijuana use and delayed recall.
Results replicated a long line of prior research demonstrating poor delayed recall with marijuana use (Becker et al, 2014; Crane, Schuster, Mermelsteine, & Gonzales, 2015; Dougherty, et al, 2013; Gonzales et al, 2012; Hansan, et al, 2010; Harvey, Sellman, Pater, and Framptom, 200; Schuster, Crane, Mermelstein, & Gonzales, 2015; Solow et al, 2011).
Poor learning among early onset marijuana users may reflect a primary weakness in executive functioning. Executive functioning weaknesses have been documented among adolescent marijuana users, particularly among those who initiate use early. Early marijuana use may impede learning via disruption in brain regions, viz, prefrontal and parietal cortices that are neurologically implicated in the memory network (Dickerson and Eichenbau, 2010; Uncepher and Wagner, 2009). This hypothesis is supported by dense localization of CB1 receptors and anandamide, the endogenous cannabinoid in the prefrontal cortex, as well as frontal gray matter (Bhattacharyya et al, 2009; Bossong et al, 2012) and white matter disruptions in marijuana using adolescents (Aslor et al, 2011; Chorchrell, Lopez, Carson, and Yurgelin-Todd, 2010; Medina, Nagel, and Tapert, 2000; Yocel et at, 2010).
Learning weaknesses only in early onset marijuana users support early adolescence as a time of vulnerability to exogenous cannabinoids due to continued development of brain networks that mediate higher order cognitive capacities (Goglay et al, 2004; Tamnes et al, 2010).
Neuroimaging studies have found earlier age of marijuana use onset associated with abnormalities in cerebral gray and white matter (Batatha, et al, 2013; Lorensetti, Sulowj, Feranto, Loranzo, & Yucel, 2014) e.g., atypicial morphometry and neuropsychological correlates in the hippocampus (media, Scheinsburg, Cohen-Zion, Magel, and Tapent, 2007), prefrontal cortex (Media et al, 2009), as well as disruption in white matter integrity on frontal-temporal and the frontal-parietal pathways (Bera, et al, 2009; Brea & Tapert, 2010; Jacobos et al, 2009; Jacobos, Squeaglia, Bara, & Tapert, 2013). This research does not suggest that marijuana use later in adolescence is "safe," due to its impact on other cognitive capacities, mental health, and psychosocial functioning which still need to be fully understood.
Non-users and late onset marijuana users scored in the normative range (average-high average) on the CLVT-II. Weaknesses (possibly fragility of memory as well as deficits in cognitive processing) fell on the low end of the normative average range and were approximately 1/3 standard deviation from controls in late onset marijuana users. This does not constitute clinical impairments. Although the early onset sample was comprised of high functioning individuals, a critical question is that, given the relative weaknesses demonstrated by the data in learning, is marijuana keeping these young adults from achieving at a higher potential (MIQ=112).
Research findings of these investigations along with other studies shows a reduction in capabilities and intelligence across time (cognitive decline) (Mecer et al, 2012).
Adolescents using marijuana were found to have more difficulty learning new information and thus may not perform optimally (Lynskey and Hall, 2000), have lower grades (Medina, Hanson, et. al. 2007) and may need to work harder to achieve at grade level (Topert, et. al. 2007). These results suggest marijuana is detrimental to cognitive reserve.
The aforementioned study demonstrated that early onset marijuana use is associated with the acquisition of information into memory directly.
DSM-V defines cannabis-use disorder and the other cannabis-related disorders which includes problems associated with substances derived from the cannabis plant and chemically synthetic compounds.
The cannabinoids have diverse effects on the brain. Most significant is actions in CB1 and CB2 cannabinoid receptors found throughout the central nervous system. Individuals who regularly use cannabis can develop all of the symptoms of a substance abuse disorder. Cannabis use disorder (CUD) is not reflective of an isolated, benign item. CUD is commonly observed concurrently with other types of substance use disorders (i.e., alcohol, cocaine, opioids). Tolerance develops in individuals who use cannabis on a regular basis.
Abrupt cessation of daily or almost daily cannabis use results in development of cannabis withdrawal syndrome. Common symptoms of withdrawal include irritability, anger, anxiety, depressed mood, sleep difficulty and decreased appetite and weight loss. Periodic cannabis use and intoxication can negatively affect behavior and cognitive functioning and interfere with optimal performance at work or school or place the individual at increased physical risk when preforming activities that would be physically hazardous, such as driving a motor vehicle, playing certain sports, preforming manual work activities. Arguments with spouses or parents and the use of cannabis in the home, and using in the presence of children, can negatively impact family functioning and are common features of those with CUD.
Is cannabis an effective means to cope with mood, sleep, pain and other physiological and psychological problems? Comprehensive assessment typically reveals reports of cannabis use contributing to exacerbation of these very same symptoms as well as other reasons for frequent use, e.g., to experience euphoria, forget problems, in response to anger, and as an enjoyable social activity. Some individuals who use cannabis multiple times daily do not perceive themselves as spending an excessive amount of time under the influence and recovering from the effects of cannabis, despite being intoxicated on cannabis or coming down from its effects. Symptoms of acute and chronic use includes red eyes (conjunctival injection), cannabis odor on clothing, yellowing of finger tips (from smoking joints), chronic cough, burning of incense (to hide the odor) and marked craving and impulse for specific foods.
In terms of development and course, the DSM-V notes that recent acceptance of by some of the use and availability of "medical marijuana" may increase the rate of onset of CUD among older adults. In terms of functional consequences of CUD, many areas of psychosocial cognitive or health functioning may be compromised in relation to CUD. Contrary to what individuals state such as "it helps me think clearly," cognitive function, in particular, higher executive functions, appears to be compromised in cannabis users. The relationship appears to be dose dependent acutely and clinically.
This in turn is conducive to problems at school and work. Cannabis use has been related to reduction in pro-social goal-directed ability, which some have labeled amotivational syndrome manifested in poor social performance and employment problems. Moreover, cannabis-related problems with social relationships are reported in these with CUD. Accidents due to involvement in potentially dangerous behaviors while under the influence (driving, recreational, sport activities) are also of concern. Cannabis smoke contains high levels of carcinogenic compounds and place chronic users at risk for respiratory illnesses similar to tobacco smokers. Thus, the trend of control of tobacco products and legalization of cannabis products places the public at risk for health and cognitive and psychological disorders.
Chronic cannabis use may contribute to onset of exacerbation of many other mental disorders. In particular, concern has been raised about cannabis use as a causal factor in schizophrenia and other psychotic disorders. Cannabis use can contribute to onset of an acute psychotic episode, can exacerbate some symptoms and can inherently affect treatment of a major psychotic illness. This author has observed many cases of "marijuana psychosis." It is a very real phenomenon. There is a subset of the population in which there are psychiatric disorders in relation to marijuana use.
Cannabis has been commonly thought as a "gateway" drug. This is due to the thought that individuals who frequently use cannabis have a significantly greater lifetime probability than non-users of using more dangerous substances, e.g., opioids and cocaine. It is difficult to understand why marijuana is used for pain management when Cognitive Behavioral Therapy is the Gold Standard and non-pharmacologic pain management as well as pain management groups and biofeedback. As someone said on NFL Today, "Why are people talking about use of marijuana for pain when there is an opioid epidemic in this country." The goal should be for the patient to be in control of their care and not to become dependent on substances that are carcinogenic.
Co-occurring mental conditions are common in CUD. Cannabis use has been associated with poorer quality of life, increases in mental health treatment and hospitalization as well as higher rates of depression, anxiety disorder, suicide attempts, and conduct disorder. Individuals with past year or lifetime CUD have high rates of alcohol use disorder (>50%) and tobacco use disorder (53%). Among those seeking treatment for a CUD, 74% report problematic use of a secondary or ternary substance: alcohol (40%), cocaine (12%) methamphetamine (6%) and heroin and other opiates (2%). In those younger than 18, the rates are significantly higher.
Individuals with past year or lifetime diagnosis of CUD also exhibit higher rates of concurrent mental disorder: Major Depressive Disorder (11%), anxiety disorder (24%), bipolar disorder (13%) are quite common among individuals with a past year diagnosis of CUD as are antisocial (30%) obsessive-compulsive (19%), paranoid (18%) personality disorders.
The most significant health effects of cannabis involve the respiratory system. Chronic cannabis users exhibit high rates of respiratory systems of bronchitis, sputum production, shortness of breath and wheezing.
The evidence for the severe adverse health and psychological effects of marijuana is supplied by a large body of research and replicated studies. Legalization of marijuana may be explicable in light of deleterious effects when one considers the profit motive of cities and individuals.
As with any other product, let the buyer beware! Stay strong! Fight On!
Dr. Perrotti received his PhD in Clinical Psychology from Alliant University in San Diego, CA. He is a licensed psychologist in California and Pennsylvania. Dr. Perrotti is a member of the National Register of Health Service Provider in psychology and the National Academy of Neuropsychology. He was an Assistant Professor of Psychiatry and Behavioral Sciences at the Keck School of Medicine, USC from 2005-2006. Dr. Perrotti is the author of numerous publications in forensic psychology and assessment, traumatic brain injury in college, professional sports and military populations, and child trauma and complex PTSD.
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