What to know about your Endocannabinoid System (ECS)

Many of us have heard of some of the transmitter systems within our bodies, such as the sympathetic nervous system, which gives us our fight-or-flight response. Fewer have heard of the more recently discovered endocannabinoid system (ECS), which is amazing when you consider that the ECS is critical for almost every aspect of our moment-to-moment functioning. The ECS regulates and controls many of our most critical bodily functions such as learning and memory, emotional processing, sleep, temperature control, pain control, inflammatory and immune responses, and eating. The ECS is currently at the center of renewed international research and drug development.

What is the ECS?

The ECS comprises a vast network of chemical signals and cellular receptors that are densely packed throughout our brains and bodies. The "cannabinoid" receptors in the brain — the CB1 receptors — outnumber many of the other receptor types on the brain. They act like traffic cops to control the levels and activity of most of the other neurotransmitters. This is how they regulate things: by immediate feedback, turning up or down the activity of whichever system needs to be adjusted, whether that is hunger, temperature, or alertness.

To stimulate these receptors, our bodies produce molecules called endocannabinoids, which have a structural similarity to molecules in the cannabis plant. The first endocannabinoid that was discovered was named Anandamide after the Sanskrit word Ananda for bliss. All of us have tiny cannabis-like molecules floating around in our brains. The cannabis plant, which humans have been using for about 5,000 years, essentially works its effect by hijacking this ancient cellular machinery.

A second type of cannabinoid receptor, the CB2 receptor, exists mostly in our immune tissues and is critical to helping control our immune functioning, and it plays a role in modulating intestinal inflammation, contraction, and pain in inflammatory bowel conditions. CB2 receptors are particularly exciting targets of drug development because they don't cause the high associated with cannabis that stimulating the CB1 receptors does (which is often an unwanted side effect).

How CBD interacts with your ECS

When you take CBD, it’s as if it elbows its way to the front of the cannabinoid line, pushes aside 2AG and anandamide, and takes priority seating on the canoe. That means that your natural cannabinoids hang around on the surface of your cells longer, which gives them more time to activate your CB1 and CB2 receptors, until the next ride comes along to transport your endocannabinoids inside the cell, where they are ultimately deactivated by metabolic enzymes.

In essence, CBD acts a “reuptake inhibitor” that prolongs the natural life cycle of our own natural endocannabinoids so they can confer more therapeutic benefits. Much like you tone weak biceps by lifting weights and exposing your muscle fibers to extra muscle-making stimulus, CBD boosts the “tone” of your endocannabinoid system by exposing it to an extended dose of cannabinoid activity. This may be a key mechanism whereby CBD helps to protect the brain, buffer stress, and fight disease.

THC binds directly to both CB1 and CB2 cannabinoid receptors like a key fitting into a lock and activates these receptors, causing them to send a signal that culminates in a physiological response (less pain, less inflammation, lower blood pressure, mild euphoria, relaxation, etc.). But CBD doesn’t work this way. Instead of binding with cannabinoid receptors to initiate a signal itself, CBD fine-tunes the signaling that’s been triggered by THC or an endogenous cannabinoid.

To recap: CBD can elevate the levels of your endogenous cannabinoid compounds, anandamide and 2AG, which activate your cannabinoid receptors and cause them to signal. CBD can also finetune the way your cannabinoid receptors function, turning down the volume at CB1 while augmenting CB2 in a manner that balances the body and promotes good health.

These statements have not been evaluated by the Food and Drug Administration.