Can we please stop assuming that marijuana is harmful to young people?
This is a controversial topic, and it’s important that we look at the evidence, and not simply rest on our assumptions or politics. We do not want young people to use anything which is likely to harm them or interfere in their development; we also do not want to prevent young people from accessing anything which could protect them from harm or improve their quality of life. But which is marijuana? Is it good for the health, bad for the health, or both? Does the answer to that question depend on the age of the user?
Is there any proof that marijuana is bad for the health of its users?
Short answer: No.
Many types of pathology have been suspected of being caused by marijuana use or overuse, but so far none of them have stood up to empirical investigation. This is not for lack of trying. Three examples:
It’s intuitively obvious that habitual smoke inhalation would damage the throat and lungs, and habitual tobacco smoking certainly does. But after decades of research, it has become obvious that any damage from marijuana itself is clinically insignificant. Long term heavy users have actually been found on average to have greater lung capacities than non-users. They also exhale marginally more slowly, and since bronchitis is diagnosed by measuring the ratio between lung capacity and rate of exhalation, they are slightly more likely to meet the technical criteria for bronchitis, but this effect is driven primarily by *increased lung capacity* and it is dishonest to claim as proof of harm. Throat irritation and a cough however are real side effects, though rarely severe enough to be clinically significant. Avoiding this irritation is the main advantage of switching to vaporisers instead of smoking, but, for many smokers, the irritation remains an acceptable side effect, and evidence of long term harm is lacking. (1,2)
The munchies are not a myth (although not everyone gets them, and marijuana actually reduces appetite in a minority of users); on average, marijuana users eat ~50% more calories than non-users, sometimes gorging on “junk” foods. This would increase risk for Type II diabetes, were it not for marijuana’s anti-inflammatory and regulatory effects, which appear to protect the pancreas from damage. Several large epidemiological studies have now reported that there is no association, or a negative association, between marijuana use and diabetes. Marijuana users are evidently able to eat more food than non-users with less harm to the pancreas. (3,4,5)
Heavy use of marijuana often makes people feel foggy in the head, can slow reaction time, and moderately impairs some memory functions, so it seems reasonable to infer that this is related to damage. What people often do not realise, however, is that brain damage — whether triggered by a head injury, a virus, a seizure or emotional abuse — is mediated by excitotoxicity, which is when neurons are excited to the point that they fry themselves out. Marijuana reduces brain activity through multiple convergent mechanisms, and dramatically increases the activity of the system the brain uses to protect against excito-toxicity (the endocannabinoid system). This protects against brain damage, and there are many studies to prove it, and no studies which demonstrate brain damage from any level of marijuana use at any age: the brains of even very heavy long term users are no worse off than those of non-users. Marijuana users are even more likely to survive head injuries sustained in car accidents. The reason people are concerned about marijuana’s brain effects is precisely because it reduces activity, but it’s too MUCH activity which causes brain damage, not too little. In other words, not only is there no empirical evidence that marijuana causes brain damage in humans, it is also not biologically plausible that it would. (6,7,8,9,10,11,12,13)
It’s important to stress that the burden of proof is on the positive position, which is the claim that marijuana is causing harm. Absence of evidence should mean absence of concern — public policy should not be founded on the assumption that marijuana is causing harms which are both empirically and theoretically unsupported, despite decades of extensive research funded by organisations such as the National Institute on Drug Abuse. If it was harmful, wouldn’t they have proven it by now?
Is there a critical window of vulnerability in which young people are at risk if they use marijuana?
Short answer: No.
Despite the well documented absence of harm from marijuana use, the possibility has been suggested — and frequently repeated, not only by prohibitionists but also as a concession by marijuana advocates wishing to appear moderate — that teenagers might be experiencing harm from using even if adults are not. Increased concern about effects (of anything) on children makes sense, because anything which could interfere in ongoing neurodevelopment will have a ripple effect, and earlier exposure could have more negative effects than later exposure. This is certainly true of trauma: traumatic experiences in early childhood lead to more diverse symptoms and worse outcomes than traumas later in life. Unlike trauma, however, use of marijuana at an early age is not associated with cognitive impairment or poor health outcomes at a later age once other factors are controlled for. Trauma is, however, strongly associated with early onset of marijuana use, and especially with marijuana dependence, and so studies which examine people who became dependent on marijuana at an early age sometimes find evidence of trauma-related pathology when these people are compared with healthy controls. That is presented as evidence that marijuana is causing harm, even though the harms in question are not found in the majority of early-onset users, or even in the majority of heavy users, but only the most dependent early-onset users, and only in studies which did not control for trauma. Once childhood trauma is taken into consideration (unfortunately, it is usually ignored), the association between early marijuana use and harm evaporates. (14,15,16,17,18,19,20,21,22)
Obviously, the health of young people is very important, and we should not be overly hasty to dismiss possible risks. But there is no proof of any kind of harm at any age from any level of marijuana use, and it is dishonest to insist that there is. Thus there is no empirically sound public health argument for restricting marijuana availability or preventing young people from using it. Anybody who wishes to disagree would do well to perform a review of the literature with the confound of trauma in mind. If you would like more detail, citations, and in depth discussion of each of the harms spuriously associated with early-onset marijuana dependence (brain damage, depression, schizophrenia and IQ decline), contact me and I will furnish you with all you need. There is much to say, but for this article I’m trying to keep things brief: the bottom line is that nobody has ever clearly shown that teenagers who use marijuana are any worse off on average than if they had not used it.
Does marijuana help with stress and trauma-related pathology?
Short answer: Yes.
That marijuana has anti-inflammatory properties and can assist in stress relief is widely known. However, the relevance of these facts to the question of pathology has not been properly considered by most writers on the subject. Childhood trauma is strongly associated with all of the harms spuriously associated with marijuana use, and these harms are driven by neuro-inflammation, which marijuana use reduces. It’s helpful to understand the system marijuana works upon, the endocannabinoid system, which is a system the brain uses to protect itself from inflammation and excitotoxicity. Chronic stress however can cause this system to fail, producing an endocannabinoid deficiency which allows damage to proliferate. Marijuana’s main effect is boosting the activity of this system, which can compensate for or reverse the loss of feedback inhibition associated with chronic stress and trauma. This is why so many people with traumatic childhoods are dependent on marijuana: it helps. The critical question, then, is whether excessive marijuana use can cause the endocannabinoid system to downregulate, leading to a loss of this protection, but, even though this is often claimed by organisations such as NIDA, their own data shows it not to be the case. Marijuana use does not suppress the endocannabinoid system, it enhances it, and this make it extremely useful in inflammatory conditions, such as those related to trauma and chronic stress. (23,24,25,26,27,28,29,30)
Childhood trauma explains the modestly elevated pathology observed in cannabis-dependent adolescents. It explains why they begin using it, why they sometimes become dependent on it, why they have brain damage which sometimes turns up in badly designed studies trying to look for marijuana effects without controlling for trauma, and an examination of the mechanisms involved reveals no biologically plausibility that marijuana is worsening any of these conditions.
So can we please stop saying that it harms children when there’s no evidence of that, and when there’s much clearer evidence that it’s helping?
And can we please not design legislation which makes preventing young people from accessing it a goal in and of itself?
It’s high time we actually focused on improving outcomes for people at risk, and stopped blaming their problems on the things they find helpful.
(1) Tashkin DP. 2013. “Effects of Marijuana Smoking on the Lung” Annals of the American Thoracic Society 10(3):239-247
(2) Kempker J, Honig E, Martin G. 2014. “Effects of marijuana exposure on expiratory airflow: a study of adults who participated in the US National Health and Nutrition Examination Study” Ann Am Thorac Soc [epub ahead of print]
(3) Rajavashisth TB, Shaheen M, Norris KC, Pan D, Sinha SK, Ortega J, Friedman TC. 2012. “Decreased prevalance of diabetes in marijuana users: cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) III” BMJ Open 2:e000494
(4) Le Strat Y, Le Foll B. 2011. “Obesity and Cannabis Use: Results from 2 Representative National Surveys” American Journal of Epidemiology doi: 10.1093/aje/kwr200
(5) Rodondi N, Pletcher MJ, Liu K, Hulley SB, Sidney S. 2006. “Marijuana use, diet, body mass index and cardiovascular risk factors (from the CARDIA study)” American Journal of Cardiology 15;98(4): 478-84
(6) Weiland B, Thayer R, Depue B, Sabbineni A, Bryan A, Hutchison K. 2015. “Daily marijuana use is not associated with brain morphometric results in adolescents or adults” Neurobiology of Disease 35(4): 1505-1512
(7) Fagan S, Campbell V. 2013. “The influence of cannabinoids on generic traits of neurodegeneration.” British Journal of Pharmacology 2014: 171; 1347-1360
(8) Sánchez-Blázquez P, Rodríguez-Muñoz M, Vicente-Sánchez A, Garzón J. 2013. “Cannabinoid receptors couple to NMDA receptors to reduce the production of NO and the mobilization of zinc induced by glutamate” Antioxid Redux Signal 19(15): 1766-1782
(9) Nguyen B, Kim D, Bricker S, Bongard F, Neville A, Putnam B, Smith J, Plurad D. 2014. “Effect of marijuana use on outcomes in traumatic brain injury” Am Surg 80(10): 979-83
(10) Katona I, Freund T. 2008. “Endocannabinoid signaling as a synaptic circuit breaker in neurological disease” Nat Med 14(9): 923-30
(11) Tzilos G, Cintron C, Wood J, Simpson N, Young A, Pope H Jr, Yurgelun-Todd D. 2005. “Lack of hippocampal volume change in long-term heavy cannabis users” Am J Addict 14(1):64-72
(12) Block R, O’Leary D, Ehrhardt J, Augustinack J, Ghoneim M, Arndt S, Hall J. 2000. “Effects of frequent marijuana use on brain tissue and composition” Neuroreport 11(3): 491-6
(13) DeLisi L, Bertisch H, Szulc K, Majcher M, Brown K, Bappal A, Ardekani B. 2006. “A preliminary DTI study showing no brain structural change associated with adolescent cannabis use.” Harm Reduct J 3: 17
(14) Cornelius J, Kirisci L, Reynolds M, Clark D, Hayes J, Tarter R. 2009. “PTSD contributes to teen and young adult cannabis use disorders” Addictive Behaviors 35(2):91-94
(15) Butters J. 2002. “Family stressors and adolescent cannabis use: a pathway to problem use” J Adolesc 25(6): 645-54
(16) Hyman S, Sinha R. 2009. “Stress-Related Factors in Cannabis Use and Misuse: Implications for Prevention and Treatment” J Subst Abuse Treat 36(4): 400-413
(17) Barnes G, Barnes M, Patton D. 2005. “Prevalence and predictors of “heavy” marijuana use in a Canadian youth sample” Subst Use Misuse 40(12): 1849-63
(18) Murphy J, Houston J, Shevlin M, Adamson G. 2013. “Childhood sexual trauma, cannabis use and psychosis: statistically controlling for pre-trauma psychosis and psychopathology” Soc Psychiatry Psychiatr Epidemiol 48:853-861
(19) Dube SR, Felitti VJ, Dong M, Chapman DP, Giles WH, Anda RF. 2003. “Childhood abuse, neglect, and household dysfunction and the risk of illicit drug use: the adverse childhood experiences study.” Pediatrics 111(3):564-72
(20) Gupta M. 2013. “Review of somatic symptoms in post-traumatic stress disorder” Int Rev Psychiatry 25(1): 86-99
(21) D’Andrea W, Ford J, Stolbach B, Spinazzola J, van der Kolk B. 2012. “Understanding Interpersonal Trauma in Children: Why We Need a Developmentally Appropriate Trauma Diagnosis” American Journal of Orthopsychiatry 82(2): 187-200
(22) Kaffman A. 2009. “The Silent Epidemic of Neurodevelopmental Injuries” Biol Psychiatry 66(7): 624-626
(23) Alshaarawy O, Anthony J. 2015. “Cannabis smoking and serum C-reactive protein: a quantile regressions approach based on NHANES 2005-2010” Drug Alcohol Depend 147: 203-207
(24) Gaffal E, Cron M, Glodde N, Tuting T. 2013. “Anti-inflammatory activity of topical THC in DNFB-mediated mouse allergic contact dermatitis independent of CB1 and CB2 receptors” Allergy68(8): 994-1000
(25) Cabral G, Raborn E, Griffin L, Dennis J, Marciano-Cabral F. 2008. “CB2 receptors in the brain: role in central immune function” Br J Pharmacol 153(2): 240-251
(26) Greer G, Grob C, Halberstadt A. 2014 “PTSD symptom reports of patients evaluated for the New Mexico medical cannabis program” Journal of Psychoactive Drugs 46(1): 73-77
(27) Neumeister A, Normandin M. 2013. “Elevated Brain Cannabinoid CB1 Receptor Availability in Posttraumatic Stress Disorder: A Positron Emission Tomography Study” Molecular Psychiatry 18(9): 1034-1040
(28) Passie T, Emrich H, Karst M, Brandt S, Halpern J. 2012. “Mitigation of post-traumatic stress symptoms by Cannabis resin: a review of the clinical and neurobiological evidence” Drug Test Anal 4(7-8):649-59
(29) Rossi S, de Chiara V, Musella A, Kusayanagi H, Mataluni G, Bernardi G, Usiello A, Centonze D. 2008. “Chronic psychoemotional stress impairs cannabinoid-receptor-mediated control of GABA transmission in the striatum” J Neurosci 28(29): 7284-92
(30) McPartland J, Guy G, Di Marzo V. 2014. “Care and feeding of the endocannabinoid system: a systematic review of potential clinical interventions that upregulate the endocannabinoid system” PLOS ONE 9(3) e89566
I acknowledge that marijuana is not useful in every situation, that some people react badly to it and should not use it, and that young people should be educated about appropriate and inappropriate dosage strategies, and not simply encouraged to use all day every day. However, I insist that our focus should be on preventing trauma and alleviating its effects, not on denying access to a plant which many trauma survivors, of any age, find to be incredibly helpful. If future study reveals conclusive evidence of harm, I will gladly revise my position accordingly, but the more evidence emerges, the less plausible that seems. If it was harmful, there would be proof by now. Don’t pretend that this is totally uncharted territory — thousands of studies have been performed, and yet the claims of harm remain unsupported. It’s time we stopped assuming and insisting that marijuana has health effects which it demonstrably does not have.