
As I thought about the NFL using CBD to minimize brain trauma, I thought next about the fact that one of my sons played Pac-10 and high school football. As he was my son, he was a kicker and not a line backer, but even he got hit a time or two.
I often discuss with friends and patients what I would think if one of my grandkids got big enough to play real contact football or other sports requiring a helmet. In fact, any sport that requires a helmet is a sport where brain trauma is possible.
We have been seeing a lot of benefit using CBD for childhood seizures and we are beginning to see brain trauma being treated with CBD. It is just starting, but why not consider giving some CBD to kids or young adults for brain damage “early intervention” or prevention. It is likely that very low doses would be effective. Virtually all THC can be avoided and the child would not be altered in any manner.
One could also easily argue to use the CBD at night, as a number of animal studies show neuro protection.
Here is one of MANY PubMed articles:
We examined the cerebroprotective mechanism of cannabidiol, the non-psychoactive component of marijuana, against infarction in a 4-h mouse middle cerebral artery (MCA) occlusion model. Cannabidiol was intraperitoneally administrated immediately before and 3h after cerebral ischemia. Infarct size and myeloperoxidase (MPO) activity, a marker of neutrophil, monocyte/macropharge, were measured at 24h after cerebral ischemia. Activated microglia and astrocytes were evaluated by immunostaining. Moreover, high-mobility group box1 (HMGB1) was also evaluated at 1 and 3 days after MCA occlusion. In addition, neurological score and motor coordination on the rota-rod test were assessed at 1 and 3 days after cerebral ischemia. Cannabidiol significantly prevented infarction and MPO activity at 20h after reperfusion. These effects of cannabidiol were not inhibited by either SR141716 or AM630. Cannabidiol inhibited the MPO-positive cells expressing HMGB1 and also decreased the expression level of HMGB1 in plasma. In addition, cannabidiol decreased the number of Iba1- and GFAP-positive cells at 3 days after cerebral ischemia. Moreover, cannabidiolimproved neurological score and motor coordination on the rota-rod test. Our results suggest that cannabidiol inhibits monocyte/macropharge expressing HMGB1 followed by preventing glial activation and neurological impairment induced by cerebral ischemia. Cannabidiol will open new therapeutic possibilities for post-ischemic injury via HMGB1-inhibiting mechanism.