Vince Lombardi (former American football player, coach and executive in the NFL) once said “Football is not a contact sport, it’s a collision sport – dancing is a contact sport.” When it comes to TBI (Traumatic Brain Injuries) and CTE (Chronic Traumatic Encephalopathy), there is little doubt that American football is the sport that’s attracted the most publicity in terms of head injuries, thanks largely to NFL litigation and the 2015 Hollywood film “Concussion”, based on Dr. Bennett Omalu’s work in the fields of TBI and CTE.
Whilst the film certainly increased public recognition of the dangers of concussions, other sports such as Ice Hockey, Rugby, Soccer, Boxing and of course MMA have also given rise to lawsuits. The increasing body of evidence suggesting a link between TBI and CTE makes harsh reading for current and former sports professionals and amateur, young and old. So where does all this leave us?
Playing sports is certainly not the only cause however, the number of people with TBI or CTE is difficult to assess accurately as it’s much larger than most people would expect. According to the Centers for Disease Control and Prevention, “every year at least 1.7 million Traumatic Brain Injuries occur in the United States across all age groups, and they are a contributing factor in about a third (30.5%) of all injury-related deaths (Faul, Xu, Waldo, & Coronado, 2010).”
The report, “Endogenous cannabinoids mediate effect of BDNF at CA1 inhibitory synapses in the hippocampus”, published by the Department of Neuroscience, University of Connecticut School of Medicine, Farmington, CT in the journal Synapse last week, suggested that cannabinoids may help the brain heal after injury.
The article authors (Selvam, Yeh, and Levine) explain that the human brain is capable of producing cannabis-like substances in response to Traumatic Brain Injury. These are called “endo” cannabinoids (endogenous, or produced inside the human body). The system that produces these endocannabinoids is called the endocannabinoid system. Phytocannabinoids (the cannabinoids produced by plants, such as the cannabis plant and others) nourish the endocannabinoid system.
The authors further stated that “Brain derived neurotrophic factor (BDNF) in the hippocampus [triggers] sIPSCs,” or Induced Pluripotent Stem-Cells created by an injured brain in order to heal itself. More BDNF equals more IPSC’s and greater healing. “Further, postsynaptic eCB [endocannabinoid] re-uptake inhibition enhanced the effect of BDNF.” Simply, the higher the level of cannabinoids in the injured brain, the greater may be the potential for healing.”
According to a report from the Industry of Medicine, more than 100 million people in North America suffer from chronic pain and inflammation. That same report estimates the pain-price tag for medical treatments and lost productivity at more than $600 billion annually, making chronic pain and inflammation major drains on the economy.
Centers for Disease Control and Prevention, has also grown. Clearly, there is an urgent need for effective and safe solutions to address the growing problem of chronic pain and inflammation.
Dr. Brazos Minshew, MSc, ND and President of the Abattis Medical Advisory Board, explains, “chronic pain occurs when internal systems within our body break down and fail to produce important endogenous chemicals. One of our body’s key pain management systems works through the production of bioactive lipids known as endocannabinoids which bind to and activate the CB-1 and CB-2 cannabinoid receptors. When activated, CB-1 and CB-2 modulate neural activity, helping our bodies cope with pain without being overwhelmed. Our body’s other principal pain management system works through the production of endorphins that interact with opiate receptors to reduce our perception of pain.”
“When our bodies experience pain that is too severe or lasts too long, our ability to produce endocannabinoids and endorphins slows and eventually exhausts, and we join the millions of people disabled or impaired by chronic pain.” added Dr. Minshew.
Comfort, is Abattis Bioceuticals newest proprietary nutraceutical, which contains Alpinia Galangal and Capsicum Annuum was developed by Abattis scientists to activate the endocannabinoid system and nourish endorphin release in response to chronic pain. Comfort will be manufactured in accordance with Canadian Natural Health Products (NHP) monographs and under the US Food and Drug Administration’s (FDA) Current Good Manufacturing Practice (CGMP) regulations. Comfort is scheduled for public release on Cyber Monday, being November 26, 2018.
Brain derived neurotrophic factor (BDNF), traditionally known for promoting neuronal growth and development, is also a modulator of synaptic transmission. In addition to well-characterized effects at excitatory synapses, BDNF has been shown to acutely suppress inhibitory neurotransmission, however the underlying mechanisms are unclear. We have previously shown that at inhibitory synapses in layer 2/3 of somatosensory cortex, BDNF induces the mobilization of endogenous cannabinoids (eCBs) that act retrogradely to suppress GABA release. Here, we hypothesized that in the hippocampus, BDNF acts similarly via eCB signaling to suppress GABAergic transmission. We found that acute application of BDNF reduced spontaneous inhibitory postsynaptic currents (sIPSCs) via postsynaptic TrkB receptor activation. The suppressive effects of BDNF required eCB signaling, as this effect on sIPSCs was prevented by a CB1 receptor antagonist. Further, blocking postsynaptic eCB release prevented the effect of BDNF whereas eCB re-uptake inhibition enhanced the effect of BDNF. These results suggest that BDNF triggers postsynaptic release of eCBs. To identify the specific eCB release by BDNF, we tested the effects of disrupting the synthesis or degradation of 2-arachidonoylcglycerol (2-AG). Blocking 2-AG synthesis prevented the effect of BDNF and blocking 2-AG degradation enhanced the effect of BDNF. However, there was no change in the effect of BDNF when anandamide degradation was blocked. Collectively, these results suggest that in the hippocampus, BDNF-TrkB signaling induces the postsynaptic release of the endogenous cannabinoid 2-AG, which acts retrogradely at presynaptic CB1 receptors to suppress GABA release. This article is protected by copyright. All rights reserved.