An Israeli study finds that the cannabinoids in cannabis provide relief from anxiety due to stress. This study suggests that a treatment to heal a hyper-alert “fear memory” in post-traumatic stress disorder (PTSD) patients may exist.
Medical cannabis may also enhance PTSD behavior therapy treatments as an anti-anxiety agent that resets a damaged amygdala and may act as a superior psychiatric medicine to present-day antidepressants and anti-anxiety drugs.
The study: Cannabinoid activation in the basolateral amygdala blocks the effects of stress on the conditioning and extinction of inhibitory avoidance. Published in The Journal of Neuroscience, September 2009 [PDF]
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The endocannabinoid system has recently emerged as an important regulator of stress and anxiety in post-traumatic stress disorder, with supporting biological evidence in animal models starting to accumulate showing cause and effect.
All mammals are born with the same hardwired stress/fear pathway in their brains from birth. Its purpose is to help ensure survival by automatically triggering fight, flight or freeze behavior when faced with a threat to survival. This pathway is the common link upon which all anxiety disorders are based — overwhelming fear and anxiety.
The emotions present in anxiety disorders range from simple nervousness to bouts of terror. This automatic stress/fear body response is controlled by the four-part brain pathway called the “amygdala-hypothalamic-pituitary-adrenal axis.”
The amygdala holds a special “fear memory” which is separate from all other memories. It is located in as part of the brain called the limbic system. The amygdala scans the environment through the senses for threats to your existence.
Importantly, it vividly remembers all fearful events from your past, starting from infancy, by remembering all the details of the environment when threatened. The amygdala also controls coping and adapting to the stress of all challenges in your environment.
The hypothalamus/pituitary gland is the next controlling link from your brain to all the body’s glands, but in terms of fear and threats, the adrenal gland, sitting on top of your kidneys, is the next link. It releases two stress hormones that activate your muscles and immune system to respond to challenges and danger. Adrenaline (also called epinephrine) is a very short-acting hormone to get you out of danger fast.
The second stress hormone is called cortisol, also produced by the adrenal gland. If epinephrine is used for short-term stress, cortisol is used for long-term stress — the kind that takes place over days and weeks. Constant, unrelieved release of these two substances damages and rapidly ages the body.
Epinephrine makes your red blood cells sticky so wounds from combat clot quickly; long term, this leads to clogged blood vessels. Constant release of cortisol damages your immune system by breaking down white blood cells to be used as muscle fuel.
This whole system can be overwhelmed and damaged by terrifying life events, or by being in a very high-stress environment for extended periods of time. This could involve the threat of death to oneself or to someone else, or threats to one’s own or someone else’s physical, sexual, or psychological integrity overwhelming the individual’s ability to cope, or by constant high levels of unrelieved stress over a prolonged period. About 30 percent of people develop PTSD after such events.
When this system is activated over and over with very strong electrical nerve signals, the amygdala doesn’t come back to baseline, because it becomes damaged by getting stuck in the hyper-alert state of fear, pumping out adrenaline and cortisol in large amounts when it is reminded of the original event.
Symptoms for PTSD include re-experiencing the original trauma(s) through flashbacks or nightmares, avoidance of stimuli associated with the trauma, and increased constant arousal — such as difficulty falling or staying asleep-, anger, and hyper-vigilance. Formal diagnostic criteria require that the symptoms last more than a month and cause “significant impairment” in social, occupational, or other important areas of functioning.
Presently, cognitive-behavioral therapy is used as treatment for PTSD. This treatment takes a long time, requiring many cue exposure sessions where sights, sounds, images and memories that triggered the original fear are presented to the person with increasing realism. Avoidance behavior of anything that reminds the person of the event is addressed with breathing and muscle relaxation techniques that are learned and practiced while being exposed to reenacted memories.
What these sessions aim for is a cognitive override of the fight or flight response. Psychologists use the term “extinction” to describe the state when the sights and sounds no longer produce the reaction. However, these sessions are very vulnerable to reversal when high levels of stress are experienced in life.
Even if you have medical insurance, companies are reluctant to pay for such long-term treatment and would rather treat individuals with psychiatric drugs, many of which give only minor relief with many side effects.
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Excerpts From The Study
“The main finding of the present study is that cannabinoids receptor activation in the basolateral reverses the enhancing effects of the environmental stress on inhibitory avoidance and its impairing effects on extinction”
“Acute stress elevates corticosteroid levels, and CB1 receptor activation in the basolateral amygdala significantly reduces this stress-induced elevation“
“Indeed, pharmacological augmentation of cannabinoids reduces anxiety-related behavioral response”
“Manipulation of the endogenous cannabinoid system has become a major focus of current search for novel therapeutics to treat many common mental illnesses, including anxiety disorders, depression, and drug addiction”
The Experiment In Brief
(from Science Daily/Science News)
Using a synthetic form of marijuana which has similar properties to THC in natural plant form, this synthetic cannabinoid called WIN55,212-2 was delivered directly into the basolateral amygdala, which is the location of the fear memory for past traumatic life-threatening events. Drug delivery was conducted by surgically implanting a micro cannula into this area for exact cause and effect.
“The potential therapeutic value of cannabinoid is underscored by the dense expression of the cannabinoid CB1 receptor in regions known to be significant for anxiety and emotional learning, particularly the basolateral amygdala.”
The CB1 receptor into which THC fits is the fix, by resetting the damaged amygdala. The exact process is called “depolarization-induced suppression of inhibition.”
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”The first stage of the research examined how long it took for the rats to overcome a traumatic experience, without any intervention. A cell colored white on one side and black on the other was prepared. The rats were placed in the white area, and as soon as they moved over to the black area, which they prefer, they received a light electric shock. Each day they were brought to the cell and placed back in the white area. Immediately following exposure to the traumatic experience, the rats would not move to the black area voluntarily, but a few days later after not receiving further electric shocks in the black area, they learned that it is safe again and moved there without hesitation.”
Next, the researchers introduced an element of stress. A second group of rats were placed on a small, elevated platform after receiving the electric shock, which added stress to the traumatic experience. These rats abstained from returning to the black area in the cell for much longer, which shows that the exposure to additional stress does indeed hinder the process of overcoming trauma.
The third stage of the research examined yet another group of rats. These were exposed to the traumatic and additional stress events, but just before being elevated on the platform received an injection of synthetic marijuana in the amygdala area of the brain — a specific area known to be connected to emotive memory.
These rats agreed to enter the black area after the same amount of time as the first group — showing that the synthetic marijuana cancelled out the symptoms of stress. Refining the results of this study, the researchers then administered marijuana injections at different points in time on additional groups of rats, and found that regardless of when exactly the injection was administered, it prevented the surfacing of stress symptoms.
This is where cannabinoids make all the difference in the world, because they activate CB1 receptors found in great numbers in the amygdala!
Bottom line #1: The results of this study show that cannabinoids can play an important role in stress-related disorders. “The results of our research should encourage psychiatric investigation into the use of cannabinoids in post-traumatic stress patients.”
Bottom line #2: “It is generally appreciated that the recreational use of cannabinoids is related to their positive modulatory effects on the brain-rewarding processes along with their ability to positively influence emotional states and remove stress responses to environmental stimuli.”
Watching the sad news from the Japanese earthquake and tsunami, how many survivors will develop PTSD in the weeks and months to come?
How many more soldiers are going to come home from war with PTSD?
How many people suffer in silence from tragic events beyond their control in childhood?
So can medical cannabis repair the damaged fear memory in PTSD-affected brains? How about some human studies with volunteers, using real marijuana?
Imagine that! Here is a non-toxic plant that helps people survive the emotionally painful memories inflicted on them by child abuse, crime, rape, violence, war, and natural disasters.
Cannabis is the healing of the nations… Indeed.
More Supporting Evidence
6. Adaptations in endocannabinoid signaling in response to repeated homotypic stress: a novel mechanism for stress habituation
7. Regulation of endocannabinoid signaling by stress: implications for stress-related affective disorders
8. Involvement of the endocannabinoid system in the neurobehavioral effects of stress and glucocorticoids
9. Suppression of amygdalar endocannabinoid signaling by stress contributes to activation of the hypothalamic-pituitary-adrenal axis