There is ongoing controversy as to whether cannabis use increases or decreases the risk of type 2 diabetes.

Cannabis contains within it hundreds of chemicals known as cannabinoids.  The chemical Δ9-THC produces almost all of the psychoactive effects associated with the plant. The cannabinoids that are produces by this plant bind to the CB1 receptor in the human brain and the CB2 receptor in the immune system.

Of all the risk factors that result in diabetes, obesity is by far the largest contributor.  The fat in the obese person that places them at increased risk is visceral fat.  This contrasts with subcutaneous fat, which is more affectionately known as “baby fat”.

What is already known and accepted in the medical arena are the following risk factors for diabetes: increased body weight, physical inactivity, unhealthy food intake, and increased age.  The only risk factor that cannot be controlled is age.  As people get older, the body deteriorates, including the ability of the pancreas to meet the metabolic needs of the body.  When the pancreas can no longer meet the metabolic needs of the body, serum glucose levels rise and the patient becomes predisposed to diabetes.  However, all the other risk factors are within the control of the patient.  One can control their weight, activity status, and the types of foods they consumes.  Some of these very same risk factors within our control are also affected by cannabis.  The question remains as to whether cannabis increases, decreases, or has no effect on these risk factors.

Cannabis stimulates the CB1 receptor in the brain which promotes food craving.  Intuitively, this becomes a concern, because if one takes a substance that causes hunger, then eating increases, the weight increases, the insulin requirements of the body increases, and thus the incidence of diabetes will also increase.But this was not what was found in the studies reviewed.

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A large study, whereby 17,967 men and women were followed from 2002 until 2010 to find out if there was any relationship between cannabis use and the development of diabetes. As there are many factors that might increase or decrease the incidence of diabetes, the study attempted to control these variables. These variables were age, sex, BMI, physical inactivity, smoking, alcohol use, and occupational position.  This study found that there was no association between cannabis use and subsequent development of type 2 diabetes.  What the study also found was that cannabis users had lower rates of being overweight or obese than nonusers.

In a study of 10,623 adults, followed from 1988-1994, called the Third National Health and Nutrition Examination survey (NHANES III), it was found was that the mean BMI was lower in current cannabis users that non-current users.

In a study of 7,233 women followed for 21 years called the Mater-University of Queensland Study of Pregnancy (MUSP) the prevalence of overweight or obesity was inversely associated with cannabis use.

In a study for 4,657 people between 2005 and 2010, the association of cannabis use and glucose, insulin, and insulin resistance was assessed. The study found that fasting insulin was lower, insulin resistance was lower, waist circumference was lower, and the HDL subcomponent of cholesterol was higher.  In other words, cannabis not only “protected” the patient from developing diabetes, but the use of marijuana also resulted in an improvement in the metabolic syndrome.  This translated into a cardiovascular benefit as well as a reduced risk for diabetes.  The mechanism proposed in this study for the reduced risk of diabetes was the CB2 receptor in adiponectin, which is found in subcutaneous “baby” fat.  When adiponectin is stimulated, it results in improved insulin sensitivity.  Improved insulin sensitivity is the most important contributor for improving the metabolic syndrome.

I propose another reason for the seemingly paradoxical relationship between cannabis use and diabetes.

Every person who has ever used cannabis knows full well how it gives you the “munchies”.  The physiological reason for this is that Δ9-THC centrally stimulates the craving for sugar.  The increased appetite caused by cannabis, one would logically reason, would result in weight gain and increased risk of full-blown diabetes.  Diabetes occurs when the insulin produced by the pancreas is not enough to support the metabolic needs of the body.  In other words, the pancreas is too small to support the overweight body.  As the body gets fatter, the pancreas cannot produce enough insulin to store glucose.  The result is persistently elevated serum glucose which often translates to diabetes.

The paradox is this:  If cannabis makes you hungry, and specifically hungry for concentrated sweets (high-caloric foods) then why is it that one usually does not gain weight and one usually does not develop diabetes?

The answer is simple.  It lies in the question of why one uses cannabis in the first place.   One uses marijuana because of pain – physical pain, emotional “pain”, or psychiatric “pain”.   It can be the pain of multiple sclerosis, the pain of spinal stenosis, the “pain” of insecurity and loneliness, or the “pain” of a myriad of psychiatric disorders such as depression and schizoaffective disorder. These reasons result in one’s gravitating towards the calming and (yes) pain-relieving effects of cannabis.

Then there is also another question relating to the risk factors seen in the future diabetic.  Why does one overeat in the first place, which leads to weight gain, and then may unfortunately lead to diabetes?  Why do many people eat more than the requirement of their body’s caloric needs?  Why do people continue to eat even after the stomach is full and they are endocrinologically satiated?  Because a full stomach gives one a sense of comfort and calmness. – the very same effects of cannabis.

When one feels comfort and when one feels calm, then one is psychologically satiated.  And when one is psychologically satiated, one loses their inclination to overeat because the reasons for doing so are no longer present.

[Image credit- Wikimedia.Commons]

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Dr. Leah has been a physician of Internal Medicine for 30+ years. Her career began with acceptance to a select six-year medical school program immediately after graduating high school. Dr. Leah spent the vast portion of her career as an Attending Physician and Professor in major metropolitan hospitals, with direct responsibility for administering, supervising and training physicians during their residency. Dr. Leah is traditionally trained but very receptive to new conceptual ways of patient treatment. The well-being of every patient is her primary focus. Her firm belief is that our understanding of medicine can never be static as there is always more to learn. Physicians should always re-evaluate their knowledge and continually seek better and more effective ways to help their patients.

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