How is the Endocannabinoid System (ECS) Disrupted in Endometriosis?
Many components of the ECS are found in endometrial tissue and their levels are regulated by the menstrual cycle in rodent models of the disease. These include cannabinoid receptors type 1 and type 2 (CB1 and CB2), N-acyl phosphatidylethanolamine phospholipase D (NAPE-PLD), an enzyme that synthesizes endocannabinoids, and fatty acid amide hydrolase (FAAH), and enzyme that breaks down endocannabinoids. The highest concentration of the endocannabinioid anandamide (AEA) in the reproductive system is found in the uterus.
Endometriosis is linked to endocannabinoid deficiency (ECD). Women with endometriosis have lower levels of CB1 receptor in endometrial tissue. Reduced ECS function leads to growth of endometriosis throughout the body and more pain, and endometriosis pain is mediated through the CB1 receptor.
Human endometriosis cells proliferated (divided and grew) less when stimulated with a synthetic cannabinoid called WIN 55212-2. Rodent studies of endometriosis found animals had more pain when treated with AM251, a drug that inhibits the cannabinoid receptors, and less pain when treated with WIN 55212-2.
Why is the ECS disrupted in women with Endometriosis?
Environmental toxins such as dioxin have been linked to endocannabinoid deficiency. Dioxin decreases levels of CB1 in endometrial tissue. As we are subjected to pollution in our air, water, grass, and food as well as BPA in water bottles and receipts, it’s no wonder why so many women in developed countries now have severe endometriosis. In the future we are certain more toxins will be linked to endometriosis risk as well as endocannabinoid deficiency.