Brain Injury Causes Cannabis Search, But A Study Previously Discussed in Veterans Missed One Possible Cause – Endocannabinoid Deficiency. Inflammation is a major aftershock after primary injury. Excessive degradation of endocannabinoids then follows the neuroinflammatory attack. Consequently, 2-AG deficiency was specifically identified as a symptom of trauma in a study by researchers from the University of Texas Health Science Center. However, secondary injuries, such as inflammation, can, unfortunately, last anywhere from days to years after a TBI.
Immunity of injured mind
Injuries to the brain shift a person’s behavior and sense of character. Less noticeably, however, neurological damage from trauma can alter the immune system and cause chronic neuroinflammation. Cells within the brain respond to blunt impact and release inflammatory cytokines. From here, the enzymes that degrade 2-AG are affected by a constellation of inflammatory events. In particular, traumatic brain injury can lead to the stimulation of an inflammatory factor known as COX-2. Although a less common metabolic process, COX-2 breaks down the endocannabinoid, 2-AG into further metabolites during an injury. Trauma leads to degradation of the endocannabinoid, 2-AG, causing a vicious cycle. The breakdown cycle is promoted by enzymes such as COX-2, for example, but more so than MAG-lipase. Optimistically, MAG-l and COX-2 are both blocked by CBG, which will prevent the degradation of 2-AG.
Stop endocannabinoid degradation after TBI, CBG versus THC
2-AG is an endocannabinoid found throughout the body and facilitates incredible neuroprotection. And THC, the intoxicating cannabinoid of cannabis, helps release 2-AG. Therefore, doses of THC will offer some relief, but they work effectively as a bandage. Treating TBI with THC is like continuing to draw water from a vessel without patching the hole. While both the active leak and the current flood must act to successfully save the boat. Instead of continuing to promote 2-AG production with THC doses. A better solution for traumatic brain injury is to stop rapid degradation of 2-AG. To do this, one can use specific phytocannabinoids to block the enzymes that degrade 2-AG, especially CBG and THCa.
Reduces the tone of endocannabinoids
Different enzymes break down 2-AG, but the degradation usually depends on the location of the endocannabinoids. 85% of the endocannabinoid is degraded in neurons by the enzyme MAG-lipase. Substances that block the breakdown of endocannabinoids should eventually stop damaging neuroinflammation after TBI. 2-AG is an endocannabinoid that, like THC, disrupts the two cannabinoid receptors, CB1 and CB2. However, it activates cannabinoid receptors without causing intoxication. To better regulate neuroinflammatory cytokines, however, 2-AG targets an additional receptor – PPARy. Regulating inflammation is vital, as traumatic brain injury also leads to cognitive impairment and dementia in severe cases. Neurological symptoms occur due to the accumulation or breakdown of certain proteins, such as beta-amyloid and tao. Fortunately, CBG prevents the rapid breakdown of endocannabinoid, 2-AG, which can heal secondary injury after TBI. Keep in mind that further research is needed to ensure the benefits of CBG in the clinical setting. Leave a comment if you have been successful in treating any condition with CBG. And don’t forget to read this story to read about a root cause behind a genetic endocannabinoid deficiency.
Show your work
MAG-lipase operates within the presynaptic region of the CB1 receptor and 2-AG transmits in advance. Elevated presynaptic 2-AG is known to desensitize CB1 receptors. Thus, MAG-1 inhibitors cause some addiction and tolerance concerns.
