ARTHRITIS BY MATT JACKSON, PHD
There are over 100 different types of arthritis that target bone joints. Osteoarthritis is the most common, affecting 27 million people in the U.S. who experience limited range of motion, swelling, stiffness, and chronic pain.1 It’s easy to take our joints for granted, but when the protective, slippery cartilage wears down, bone-on-bone contact can be intensely painful. It can affect all aspects of everyday life—simply moving in the night can wake you with pain.
Osteoarthritis can damage nerves, inflame the joint, and cause physical damage and bone spurs, which are bony projections on the edges of bones. The spurs can break off from the bone and float into the synovial fluid that lubricates the joint, acting like shrapnel. The chronic pain caused by osteoarthritis is difficult to treat. The first medication recommended by most professional medical organizations is acetaminophen, but some 50% of osteoarthritis patients don’t respond to it. Nonsteroidal antiinflammatory drugs (NSAIDs) and the selective serotonin norepinephrine reuptake inhibitor (SSNRI) duloxetine are often tried next—but again, not all patients respond.2 And let’s just not talk about opioids, which are addictive and have their own set of serious problems.
Considering 63% of osteoarthritis patients are unsatisfied with their current pain medication regimen,3 some are turning to medical cannabis for baseline pain management or to relieve the acute pains that “break through” their current medications. Cannabis might seem like a new alternative treatment, but cannabinoids are not. We have been treating chronic pain with cannabinoids for over 130 years. We just didn’t know it.
The story goes like this. Acetaminophen was first prescribed in 1887. Its widespread usage initially was put on hold by a competitor, which ended up causing kidney failure and cancer. Acetaminophen was mass produced in the 1950s and, despite safety concerns, became widely accepted as an over-the-counter medication by the 1970s.4 It may surprise you, but until recently, no one knew how acetaminophen worked. Then in 1991, a scientist in Israel, Dr. Raphael Mechoulam, discovered the first two endocannabinoids, AEA and 2-AG. It took almost two decades until we connected the dots and realized how acetaminophen truly works, and it’s an indirect action. When our bodies metabolize acetaminophen, it ends up amplifying our levels of the AEA and 2-AG. Those elevated endocannabinoids cause an ECS response, which is what is truly responsible for relieving pain and reducing inflammation.4
In fact, the synovial membrane that surrounds our joints have plenty of endocannabinoid receptors that are involved with both inflammation and the nervous system’s “pain pathway.” In osteoarthritis patients, the synovial fluid filling the joint contains both 48
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