The Western Diet: Creates the "Munchies" in the Same Way as Marijuana

Marijuana (more specifically cannabis) has been used for thousands of years to treat a variety of ailments including those of the digestive system. Marijuana is technically a preparation of the Cannabis plant intended for use as a medicine or as a psychoactive drug. Cannabis is a genus of flowering plants that includes three putative varieties, Cannabis sativa, Cannabis indica, and Cannabis ruderalis. The major psychoactive component of marijuana, delta-9-tetrahydrocannabinol (Δ9-THC, or just THC). Following the discovery of the bioactive compound in marijuana it was determined that THC worked by binding to specific plasma membrane proteins which were referred to as the cannabinoid receptors. The identification of endogenous receptors for THC suggested that there must be endogenous ligands. And this indeed was proven true with the isolation and characterization of endogenous cannabinoid receptor ligands. These naturally occurring ligands are termed the endocannabinoids. The two best studied endocannabinoids are anandamide (N-arachidonoylethanolamine; AEA) and 2-arachidonoylglycerol (2-AG)

For more detailed information on the endocannabinoids go my website:

https://themedicalbiochemistrypage.org/endocannabinoids.php

Most individuals who smoke marijuana experience an increase in the desire to consume food, often referred to as "the munchies". Regulation of feeding behavior has long been associated with the cannabinoid system. Cannabis, in its various forms, increases appetite, particularly for palatable foods, and can also result in significant weight gain. Indeed, one of the most common medicinal uses for cannabis in the modern era is to stimulate the appetite of individuals undergoing cancer chemotherapy, in patients with AIDS, and in patients with other diseases associated with severe loss of appetite.

A recent paper published in the journal Physiology and Behavior describes the research carried out by investigators at my alma mater, the University of California, Riverside which demonstrates that the Western-style diet (high fat and high carbohydrate) induces an enhancement in feeding behavior through the activation of the endocannabinoid system.

Peripheral endocannabinoid signaling controls hyperphagia is western diet-induced obesity 

This study used mice as the animal model and compared the effects of a western-style diet (high fat and high sucrose) to a standard rodent chow on the levels of both anandamide and 2-AG in the intestines and the circulation. The animals were fed one or the other diet foe 60 days and then a number of parameters were examined. The western diet mice exhibited significant increases in the rate of feeding, the size of the meal consumed, total daily caloric intake, and not at all surprising significant increases in body mass when compared to the mice fed the standard chow.

The significance of the role of the endocannabinoid system in the western diet was demonstrated with the use of pharmacological inhibitors of the cannabinoid receptor, specifically the CB1R isoform (there are two cannabinoid receptors, CB1R and CB2R) which is the most abundant cannabinoid receptor. Of significance to endocannabinoid functions, the CB1R is the most abundant receptor of all receptor types within the brain.

The levels of anandamide and 2-AG were higher in the the intestines and blood of the western diet-fed mice compared to the standard chow-fed mice. In addition, the consumption of the western diet resulted in dysregulation in the expression of the genes encoding the primary components of the endocannabinoid system, those encoding the cannabinoid receptors  and those encodeing enzymes in the biosynthesis and metabolism of the endocannabinoids. When the CB1R was blocked there was a significant reduction in food intake in the western diet-fed mice but there was no effect on food intake in the standard chow-fed mice. Indeed, blocking the CB1R resulted in a meal size and rate of feeding in the western diet-fed mice that was equivalent to that in the standard chow-fed mice.

These results clearly demonstrate a correlation between the consumption of a high fat high sugar diet with disturbances in the endocannabinoid system leading to hyperphagia (an increased desire to consume more food). Of particular significance is that the hyperphagic behavior triggered by the dysregulated endocannabinoid system drives a preference for increased consumption of fatty foods.

The TAKE HOME from this study is quite clear: Eating a high fat and high sugar diet (even one that may not be in caloric excess) has a significant potential to interfere with ones control over their feeding behavior and make it that much harder to control ones weight and most assuredly make it extremely difficult to lose any weight. 

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