Your Brain on Weed: The Cannabis Effect on Mitochondria Function Explained
You might want to break out some sticky sativa and start grinding because I’ve got some pretty groundbreaking stuff coming your way. Today we start the series on how marijuana can paradoxically protect our brains and slow the process of aging.
Cannabinoid agonists (chemicals that bind cannabinoid receptors), once thought to impair the function of neurons in your brain, are now showing promise in addressing the cognitive deficits of neurodegenerative disorders, such as Alzheimer’s disease and Multiple Sclerosis.
Since the varied protective mechanisms employed by cannabis are a big bong hit of info, I decided to give it to you folks micro-dose style so you can get the most out of it.
Where the endocannabinoid system function intersects with the mitochondria function
The brain and central nervous system as a whole is extremely metabolically active; comprising only 2% of our body weight, yet consuming 20% of our metabolic caloric demands. The synaptic junction between nerves is a region of high energy demand and requires constant trafficking of mitochondria to this region.
Mitochondria are responsible for maintaining the delicate balance of energy production, while protecting against the free radical by-products formed in the process. Free radicals are generally highly reactive, and short live molecules.
Endocannabinoid System function:
Cannabinoid receptor signaling between the nucleus and the mitochondria is vital to ensuring that energy and housekeeping needs are met.
How aging affects the mitochondria’s function:
As we age this signaling path is not as robust, and energetic imbalance and toxic buildup ensues. The loss and dysregulation of synaptic mitochondria may be an important pathogenic factor in progression of cognitive decline. In plain terms, the aging of the mitochondrial function may be an important factor leading to mental deterioration.
The cognitive effects that we observe in a pathologically ageing brain result from alterations in nerve connectivity. Neighboring neurons in the brain are meant to transmit messages across the synapse between one another, but in an aging brain they cannot faithfully be relied upon to successfully transmit these messages.
This pattern of oxidative damage forming the basis of accelerated disconnection between the nerve synapses is demonstrated perfectly by Neurodegenerative disorders, like Alzheimer’s disease and Huntungton’s.
In fact, the fundamental core of senescence (process of deterioration) or aging of all cells in general, is based on accumulation of oxidative damage to lipid (fatty) membranes and genetic material. Free radical destruction of nerve fibers and their insulating myelin envelope leading to shrinkage of white matter brain volume and expansion of cerebrospinal fluid volume.
So how does Cannabis keep the function of Mitochondria young?[/caption]
Fortunately for us, phytocannabinoid molecules, such as THC and CBD, have anti-oxidant activity both while bound to the receptor and while free in solution. While unbound to its receptor, THC has direct buffering capacity to neutralize these ballistic free radical electrons before they can shred lipid membranes and genetic material.
Once cannabinoids do bind their intracellular cannabinoid receptor targets, they start a cascade of homeostatic mechanisms to turn on genes involved in mitochondrial defense against free radicals. Cannabinoid receptor signaling turns on a key regulatory gene that upregulates 3 key mitochondrial anti-oxidant systems. This brings me to a very important and little-known facet of our endocannabinoid systems.
Most of our cannabinoid receptors exist inside the cell, not on the cell’s exterior cell membrane. The CB1 receptors that live on the mitochondrial membrane respond to insult by protecting the mitochondrial components called cytochromes from leaking out of the cell when confronted with oxidative insult.
CB1 receptors live right on the surface of the mitochondrial membrane. Interestingly, when the cell receives a signal from the binding of cell membrane CB receptors, the signal is transmitted to the mitochondria FIRST and then to the nucleus after. This relationship is instinctive as it acts largely as the central command and mitochondria as the powerhouse behind it.
Further, the ECS (endocannabinoid system) protects from accelerated aging protecting the separation of charge to keep our energy currency of ATP pumping out. Mitigating calcium pore formation and leakage of toxic glutamate out of the cell prevents the dysregulated neuronal activity behind the progression of aging in our nerve cells.
In short, keeping our endocannabinoid system in balance supports our energy source that keeps us alive.
Thanks for stopping by and checking out my blog on cool topics surrounding cannabis medicine. Educating the cannabis community with high quality, peer-reviewed data brings me great joy. The pinnacle of fulfillment for me comes from helping a human live longer and healthier through useful wisdom. At the heart of the matter, destigmatizing cannabis use will be a slow process that will come through demystifying the public regarding cannabis data that is driven by scientific rigor rather than special interest folklore. Deliberate dissemination of credible info will, over time change the breakthrough knowledge of today into common knowledge of the future.
Royalsocietypublishing.org. 2020. The Endocannabinoid System In Normal And Pathological Brain Ageing | Philosophical Transactions Of The Royal Society B: Biological Sciences. [online] Available at: <https://royalsocietypublishing.org/doi/10.1098/rstb.2011.0388> [Accessed 17 November 2020].
Russo, Ethan B. “Cannabis Therapeutics and the Future of Neurology.” Frontiers, Frontiers, 1 Oct. 2018, www.frontiersin.org/articles/10.3389/fnint.2018.00051/full.
Marsicano, Giovanni, and Sharon Goodenough. “CB1 Cannabinoid Receptors and on-Demand Defense against Excitotoxicity.” MD Anderson Cancer Center, American Association for the Advancement of Science, 19 June 2015, mdanderson.elsevierpure.com/en/publications/cb1-cannabinoid-receptors-and-on-demand-defense-against-excitotox.