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diabetes and marijuana

Diabetes and Cannabis

“Munchies” & Your Metabolism: The Paradoxical Implications of Cannabis for Diabetes

Perhaps one of the most prominent side effects (or therapeutic effects, depending on your perspective) of medical cannabis is its appetite stimulating properties (1). This phenomenon has been colloquially dubbed as the “munchies”: an increased craving for food and an intensification of the sensory and hedonic properties of consuming it (2). Many clinicians consider this specific property of C. Sativa a blessing for their patients who have trouble eating and lack a healthy appetite. In fact, medical cannabis is often considered a godsend to many cancer patients due to its anti-nausea and anti-anorexic effects, both of which have immense clinical value when it comes to treating the debilitating side effects patients experience when undergoing chemotherapy (3). Therefore, it is not surprising that many people associate cannabis use with weight gain, due to this phenomenon of “the munchies”. But does smoking cannabis actually make you gain weight? Both cannabis use and obesity rates are dramatically rising across the world, with America placing 6th in the most obese countries in the world (4). It has been established in the scientific and medical communities that obesity is a significant risk factor for type 2 diabetes (also known as diabetes mellitus) (5). The question then becomes, could the increase in cannabis consumption among the global population have any relationship to this public health crisis (obesity and its pathological consequences), as a result of its appetite stimulating properties? The answer is more complex than you might think and, in fact, may surprise you! But first, a deeper look at the “munchies” and how that really works on a biological level.

 

What Are The “Munchies”: A Deeper Look Into Cannabis Induced Appetite Stimulation

“The munchies”, as defined in Beulaygue & French’s study, is described as the “compulsive eating of sweet and salty snacks while under the influence [of cannabis] and is often thought to be linked to added pounds” (4). The official, scientific term for this appetite stimulation is “hyperphagia” and is actually caused by a variety of phytocannabinoids (active constituents of the cannabis plant) and not just delta-9-THC, the primary psychoactive component of C. Sativa (1). Cannabinoids can be internally produced by our own bodies or exogenously introduced into our bodies through the consumption of cannabis. While cannabis-derived cannabinoids do not contain the exact same types of endocannabinoids our bodies make (which are 2-AG and Anandamide), both have been shown to cause hyperphagia across the board from animal studies to anecdotal reports to clinical trials (1). The two major receptor sites cannabinoids act upon are CB1and CB2, which are found mostly in the brain and the rest of the body respectively (5). In experiments and drug trials where a CB1 antagonist (a molecule or drug that blocks endogenous and exogenous cannabinoids from binding to CB1) was introduced to subjects, a marked decrease in appetite was present. However, when applying this clinically in the form of a drug that antagonized CB1, patients experienced severe depression and suicidality, causing the drug to be pulled off the market after only 2 years (1). But what if you could have your cake (and cannabis) and eat it too, without gaining the extra pounds and putting yourself at a higher risk for devastating metabolic disorders such as diabetes? Such an idea may not be as far-fetched as you may think. In fact, this is what makes the findings in Beulaygue’s and French’s paper exploring the relationship between heavy cannabis use and BMI all the more intriguing.

 

Cannabis Sativa & BMI: An Unlikely Epidemiological Trend

Obesity can lead to a multitude of health problems, with type 2 diabetes (Diabetes Mellitus) being one of the most common and most deadly (6). The notion of weight gain among cannabis users, as a result of their increased appetite (especially for sweet and/or salty snack foods), is a commonly held belief (4). The research in this area, however, is far from unanimous when it comes to drawing that conclusion. In fact, a 2016 study by Beulaygue & French out of the University of Miami, demonstrate a “negative association between marijuana use and BMI” in a “fixed-effects model” analyzing the relationship between cannabis use and BMI over time in almost 14 thousand patients listed in the National Longitudinal Survey of Adolescent Health (4). In fact, their data showed that heavy cannabis smoking (defined as multiple times a day, every day) is linked with statistically significant lower BMI’s, with a 3.1% reduction in daily female cannabis users and a 2.7% reduction in daily male cannabis users (4). Even when controlling for outside variables (called “confounding factors” in scientific terms) such as age, cigarette smoking, alcohol intake, anxiety, depression and physical activity (all of which could influence BMI outside of cannabis consumption alone). Dr. Beulaygue, the author of the study “Got Munchies?” and a close friend of mine, talked to me about how important it was to take these confounding factors into account since “the demographic of people using cannabis [either medically or recreationally] may already have a higher prevalence of [comorbidities, such as] depression, anxiety and/or other health-related issues”. Since there is documented evidence linking overeating, physical inactivity and tobacco smoking to both type 2 diabetes as well as cannabis use, it’s necessary to parse through the different variables and control for those that influence both clinical outcomes to isolate the effects of cannabis alone (4,7,8) . Only then can we better understand the seemingly paradoxical effects of cannabis on physiological, behavioral and metabolic factors relating to heavy cannabis use and a reduction in BMI in humans. Oddly enough, these results are not reproducible in animal models, adding further mystery to an already hazy relationship between heavy cannabis use and reduced BMI.

 

“If You Give a Mouse a Cookie”: The Effects of Cannabis Induced “Munchies” in Animals

Humans and animals have different metabolic, behavioral and physiological pathways. Thus, it’s important to note that this unintuitive and paradoxical effect that seemingly links heavier cannabis smoking to lower BMI is surprisingly observed in clinical trials and not in in-vivo (“in-living”) animal trials, as per a 2001 Nature article by Di Marzo and colleagues (9). Instead, they observed the expected correlation: cannabis-induced appetite stimulation leads to weight gain in mice when stimulated by both exogenous cannabinoids (from the cannabis plant) and their own endocannabinoids (naturally produced, lipid-based neurotransmitters with the strikingly similar resemblance in structure and function to exogenous cannabis-derived cannabinoids) (9). Clearly, there are some unique factors in play when assessing cannabis-induced appetite stimulation in humans and subsequent weight gain (or the lack thereof). While these factors have not yet been extensively identified or comprehensively understood, it does hold promise for diabetic patients seeking new, more efficacious treatments for their disease. In fact, the research shows just that; cannabis ironically has therapeutic properties when it comes to treating Type II diabetes.

 

Medical Cannabis as a Novel Treatment for Diabetes Mellitus

As discussed earlier, preclinical animal studies have shown cannabis to both stimulate appetite and cause weight gain by stimulating CB1 receptors in the brain, causing hyperphagia, as well as CB1 receptors in the liver, causing insulin-resistance (10,11). Excessive weight gain and resistance to insulin have both been identified as major risk factors for diabetes (2). Luckily, however, humans seem to show the opposite effects of cannabis on weight gain and insulin-resistance. In fact, studies to date have shown either lower odds or a negligible difference when it comes to cannabis use and a diagnosis of diabetes (12,13). In fact, some studies have gone so far to show a “protective” effect of smoking cannabis on insulin sensitivity, reducing the likelihood for insulin resistance, as seen in earlier animal models (13). Exactly how this works is still a mystery to scientists, but ample research is being done to find out. As noted in Beaulaygue’s and French’s paper, bureaucratic barriers to cannabis research, especially on humans in a clinical setting, can be difficult due to various hurdles enforced by the DEA, NIH, and NIDA because of the schedule I status of the drug (4). Nonetheless, the available data make clear that cannabis and, more generally, all cannabinoids, play an integral role in energy intake, lipid and glucose metabolism in peripheral organs, and direct actions in skeletal and pancreatic systems (10). More longitudinal studies, involving greater numbers of patients, are being performed to assess correlation and causation between cannabis use and diabetes. A study observing 18,000 Swedish people over time found no association between cannabis use and the subsequent development of type 2 diabetes (14). While the data is beginning to become clear that the “munchies” in daily smokers either reduces the risk or does not affect the risk of diabetes mellitus, scientists and researchers are still left in the dark as to why this happens. Beulaygue & French hypothesize on their results by citing literature that points to increased energy expenditure leading to more calories burned, increased metabolic rate, faster glucose metabolism in the brain and lower levels of fasting insulin (4). Indeed, these are all factors that may be at play when considering the effects of cannabis on human metabolism and how they may relate to diabetes. Further research is necessary to uncover these physiological mechanisms so novel cannabinoid-based treatments may potentially be utilized in the prevention and treatment of diabetes and other metabolic syndromes.

 

The Last Bite: A Final Note on Cannabis & Diabetes

The common depiction of a cannabis user among society at large is sluggish, lethargic and, by way of the “munchies”, overweight. The National Institute of Drug Abuse (NIDA), claims deleterious changes in the “function and structure of brain regions related to reward, decision making, and motivation” (4). However, Beulaygue & French’s findings demonstrate the exact opposite. Indeed, with the spread of decriminalization and legalization of cannabis around the United States, it is clear that as a society, we have come a long way from the times of “Reefer Madness” and intense anti-cannabis propaganda. Nonetheless, there is much left to uncover about this versatile plant species that contains a plethora of active compounds with potential therapeutic benefits across various spectrums of disease and physiology. It is crucial that, as a society of people looking out for humankind’s best interests, we remove the often insurmountable hurdles of clinical trials involving cannabis due to its schedule I status. For now, Beulaygue & French want to make it very clear that they do not advocate for cannabis use as a dieting strategy, despite the fact their study shows a strong correlation between heavy cannabis use and lower BMI among women and men. It is important to note that these results are specific to the smoking of cannabis and not cannabis use in its other forms (e.g. edibles, vaping, transdermal patches, etc). Also, this author would like to point out that it is difficult to generalize all strains and types of cannabis by just categorizing all it’s seemingly infinite genotypes and phenotypes as simply “cannabis”. Unlike pharmaceutical medications, cannabis is living medicine, with each strain and even each plant within the same strains, having a diverse array of cannabinoid and terpenoid proportions and ratios, all of which plausibly affect each individual person differently. Taking an average among large sample sizes and studying them over time, like in Beulaygue & French’s study, is an intuitive and necessary method for approaching this complex area of research. In the end, the high safety profile and low probability for adverse drug interactions seen in cannabis medicine, make it a favorable option for both clinicians and patients. Hopefully, in the years to come, a solid understanding of the metabolic and pathophysiologic pathways that exist between cannabis and metabolic disorders, such as diabetes, are uncovered for the benefit of patients everywhere. Until then, don’t feel terribly guilty about that chocolate chip cookie or slice of deep-dish pizza you decide to enjoy if you get the “munchies” yourself.

 

About the Author: Gaurav Dubey is a clinical researcher in the Department of Pediatric Cardiovascular Thoracic Surgery at Rush Medical Center downtown Chicago. He is also an active scientific blogger and content creator with a curious passion for all things medical cannabis. He is the Staff Writer for The Medical Cannabis Community & a new freelance contributor for Green Flower Media.

 

Huge thanks to one of my dearest and brightest friends’, Dr. Isabelle C. Beulaygue, Post-Doctoral Research Fellow at the Boston University Center for Promise and author of the study “Got Munchies? Estimating the Relationship Between Marijuana Use and Body Mass Index”. Your collaboration on this paper and insight into your study was fascinating and invaluable to its success. Thank you, Isabelle!  To learn more about Isabelle and see her official Boston University profile, click her photo!

 

 

References

  1. Brierley, D. I., Samuels, J., Duncan, M., Whalley, B. J., & Williams, C. M. (2016). Cannabigerol is a novel, well-tolerated appetite stimulant in pre-satiated rats. Psychopharmacology, 233(19-20), 3603-3613. 10.1007/s00213-016-4397-4 Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/27503475
  2. Kirkham, T. C. (2009). Cannabinoids and appetite: Food craving and food pleasure. International Review of Psychiatry (Abingdon, England), 21(2), 163-171. 10.1080/09540260902782810
  3. Abrams, D. I. (2016). Integrating cannabis into clinical cancer care. Current Oncology (Toronto, Ont.), 23(2), S8. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/27022315
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  9. Di Marzo, V., Goparaju, S. K., Wang, L., Liu, J., Bátkai, S., Járai, Z., . . . Kunos, G. (2001). Leptin-regulated endocannabinoids are involved in maintaining food intake. Nature, 410(6830), 822-825. doi:10.1038/35071088
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