The human brain is the most complex structure in the known universe. 

Scientific exploration of the human mind has mostly focused on the brain and its chemistry. However we cannot expect to quantify what we barely understand. Treating the brain as a predictable stimulus-response system has turned out to be a dubious approach. 

Our bodies are not machines. Every cell is a conscious being.

The complexity of the mind is mirrored in the complexity of nature.

Therefore we should be able to inform psychiatry with plant medicine to treat mental disorders like Post-Traumatic Stress Disorder (PTSD).

This article will explore how we’re beginning to do exactly that. 

PTSD Rewires the Brain

Mental health disorders like PTSD continue to be a major challenge in our overly stressed, terrorized, and traumatized world. Trauma binds us all regardless of the circumstances of our birth.

Right now it binds us, but it should unite us.

Grief, war, abuse, natural disasters, and crippling illness, these traumatic experiences alter the fluidity of the brain (neuroplasticity). The traumatized brains becomes hyperactive and hypersensitive, resulting in symptomatic Post-Traumatic Stress Disorders (PTSD). 

Our brains are equipped with an alarm system (amygdala) that ensures our survival. It is responsible for signaling flight or fight responses. Certain stimuli trigger the amygdala for PTSD patients, causing the frontal cortex to malfunction. Thus the brain loses the ability to discern between safety and danger. 

Neurophysiology of PTSD

PTSD causes a change in the physical structures of the brain.

Namely, PTSD patients tend to have decreased volume in the prefrontal cortex (executive function of the brain), and in the hippocampus (memory center of the brain), thus creating an increased fear response, nightmares, arousal, impulsivity, flashbacks, and intrusive thoughts. During these PTSD episodes, a cortisol (stress hormone) surge is most likely to happen and leads to adrenal exhaustion, which results in a dysfunctional hypothalamic-pituitary axis. This creates a decrease in cortisol level and an increase in the negative feedback system, thus creating hyperarousal and hypervigilance.

Research evidence shows how PTSD can lead to an increase in norepinephrine, glutamate, and a decrease in serotonin, which contributes to physical, mental, and emotional symptoms of PTSD. 

Veterans & PTSD 

While several traumatic events can trigger PTSD, as stated above, it is most prevalent in war veterans. A 2017 study shows that about 12.9% of veterans who participated in the study were diagnosed with PTSD. 

War veterans are more likely to experience mental disorders like PTSD and depression, no thanks to several exposures to traumatic events during their active service. Research shows that about 14% to 16% of US service members deployed to Afghanistan and Iraq had PTSD or depression. Some other common mental disorders that may arise from these traumatic experiences include suicide, traumatic brain injury (TBI), substance abuse, and interpersonal violence. 

Each of these comorbidities, and potential treatments, involves the endocannabinoid system. 

Why ECS Signaling Can Treat PTSD

PTSD may have a direct link to the endocannabinoid system. 

Several researchers have reported that PTSD patients have increased brain scan activity with decreased effective activation of CB-1 receptors.

It was observed in PTSD patients. There are also cases where an alteration in the receptors was observed in depressed individuals. Note that the stimulation of receptors in the prefrontal cortex, amygdala, and hippocampus may relieve anxiety and cause CB-1 receptor-mediated G-protein signaling sensitization. By activating the CB-1 receptors in the amygdala, scientists have reported a decrease in aversive memories, anxiety, and fear. When CB-1 receptors in the hippocampus are stimulated, they can increase the average concentration of serotonin and thus, provide antidepressant properties

The ECS is an electric field of with trillions of charge exchanges per second.

Think of cannabinoid receptors as recipients while CBGA and  other cannabinoid are donors. The cannabinoids donate charges and molecules that signal the ECS to switch activities on and off wherever the cannabinoids receptors are found. 

This is why cannabis and other plant medicines are critical to a new age in mental healthcare.

While the brain is rewired to continually exist in a flight mode during PTSD, active interaction between cannabinoids and their receptors can reverse that. CBGA is therefore an excellent donor, thanks to its phenolic and carboxyl groups.

CBGa’s resemblance to natural cellular structures allows for a charge exchange that triggers the brain to restore normal activities.

The body treats CBGa as its own while supplying life-giving nourishment to the ECS unlike any molecule we’ve seen so far. 

This is how CBGa can treat virtually any chronic disorder of oxidative stress.

Recall that cannabinoids offer modulatory roles. This means they are capable of cushioning the effect of unbalanced mental alertness. They can trigger the formation of new brain cells via neurogenesis, reduce the adverse effects of free radicals, and ultimately affect a chemical harmony in cannabinoid receptors directly linked to stress and mental alertness. 

Increased neurogenesis triggered by CBG and CBGA can decrease hypervigilance, hyperarousal, and intrusive memories, and normalization of cortisol can be related to CB-1 receptors being agonized in the hippocampus. 

Much energy goes into the interaction between cannabinoids and binding sites on their receptors. Although these binding energies are yet to be fully measured, the strong interaction between proteins in the binding sites of the receptors and cannabinoids makes a good team. 

Clinical Trials

Cannabinoids are often regarded as biomarkers of psychiatric disorders. 

Research into the role of marijuana and psychiatry disorders shows a direct link between CB1 receptors in stress regulation, development of mood disorders, PTSD, schizophrenia, ADHD, and eating disorders. The manipulation of this receptor via cannabinoid therapy was found to inhibit the action of degrading enzymes through modulation of CB2 receptors. This resulted in anxiolytic, antidepressive, and antipsychotic effects. 

Cannabinoid administration in human models showed an improvement in insomnia and reduced the frequency of nightmares. Cannabinoid administration can also reduce the frequency of fear and anxiety associated with hyperactivity in the amygdala. CBGa improves mood levels while neutralizing the harmful effect of free radicals.

The use of Cannabinoid-derived isolates like CBGA-Q and CBGA-Q-Na Salt was found to have neuroprotective effects in Parkinson’s disease. While this was tested in Parkinson’s disease, the neuroprotective role of CBGA and other rare cannabinoid molecules cannot be neglected.