Using Cannabinoids to Treat Symptoms of Post-Traumatic Stress Disorder
A study published in late 2015 in the journal “Neuroendocrinology” reported the discovery of a biological mechanism linking the modulation of the human body’s endocannabinoid receptors to the treatment of post-traumatic stress disorder (PTSD) symptoms. PTSD manifests as intrusive and frightening memories in people who have experienced severe trauma, such as violence or death, leading to chronic stress, increased anxiety and irritability, panic attacks, and other forms of social dysfunction.
Key Research Findings
During the study, a group of scientists from Canadian and U.S. universities observed 46 volunteers who had experienced the 9/11 terrorist attack in New York City. The participants were divided into two groups: 24 people with PTSD symptoms and 22 who did not develop the disorder despite the trauma.
An in-depth analysis of the PTSD group showed that their levels of anandamide—an endogenous cannabinoid similar in structure and function to THC—were significantly lower than those in the control group. Anandamide activates the same cannabinoid receptors as THC, CBD, and other related compounds.
Researchers note that anandamide is the main activator of the CB1 endocannabinoid receptor, which is found throughout the body, especially in the central and peripheral nervous systems and in brain regions responsible for emotions. Anandamide acts as a neuromodulator of fear, helping suppress panic, confusion, and sadness—emotions typical of traumatic experiences. A deficiency of anandamide in the brain, due to impaired production, disrupts the modulation of negative emotions, making it difficult for people with PTSD to overcome their traumatic memories. This deficiency can also lead to increased fearfulness, chronic stress, and short-term memory problems due to impaired memory consolidation in the brain.
Supporting Studies and Broader Implications
Other studies have also found a link between PTSD and dysfunction of the body’s endocannabinoid system. In 2009, researchers from Virginia Commonwealth University described a connection between low anandamide levels and conditions like PTSD and various forms of epilepsy. A year later, scientists from the University of Rome found a similar link between low anandamide in spinal fluid and temporal lobe epilepsy.
Dr. Ethan Russo, a leading U.S. medical cannabis expert, summarizes that anandamide deficiency may contribute to many chronic conditions, including migraines, fibromyalgia, irritable bowel syndrome, epilepsy, and even neurodegenerative diseases like Alzheimer’s and Parkinson’s. He notes that this deficiency can often be quickly corrected by consuming phytocannabinoids, which have a rapid and strong therapeutic effect on many symptoms of these conditions.
According to Dr. Russo, endocannabinoid levels vary from person to person. Healthy eating and physical activity boost anandamide production, while stress, chronic fatigue, poor diet, and negative emotions suppress it. He also highlights that frequent alcohol consumption and diets high in sugar or artificial sweeteners threaten anandamide balance.
Other research teams have linked anandamide deficiency to the progression of various forms of depression, especially chronic depression. Dr. Matt Hill of Rockefeller University notes that blood serum analysis shows people with depression have significantly lower levels of endocannabinoid metabolites than healthy individuals.
Stress, Anandamide, and the Brain
Animal studies have shown that chronic stress and fear reduce anandamide levels in rats, leading to increased anxiety and slower nerve signal transmission via CB1 receptors. When exposed to stress or threats, a healthy endocannabinoid system stimulates anandamide release in specific brain regions to modulate emotional responses. Chronic stress, however, overstimulates the glands that produce endocannabinoids, eventually reducing their output and causing dysfunction in other biological systems. This can result in symptoms ranging from migraines and physical discomfort to accelerated progression of cancer and neurodegenerative diseases. Anandamide deficiency also disrupts fat metabolism, explaining why PTSD and depression can be accompanied by sudden changes in body shape.
In 2012, Brazilian scientists found that chronic stress not only affects anandamide production in the hippocampus but also suppresses CB1 receptor sensitivity and expression. Since the hippocampus is responsible for memory consolidation, this suppression slows the process of overcoming fear, sadness, and aggression.
Dr. Alexander Neumeister of New York University explains that chronic stress increases the production of the enzyme fatty acid amide hydrolase (FAAH), which breaks down anandamide and other complex fat-containing compounds. Excessive FAAH activity quickly depletes anandamide, and this phenomenon may negatively affect future generations by influencing genes that regulate these compounds, potentially leading to inherited tendencies toward substance use or certain behaviors.
In short, chronic stress leads to excessive FAAH production, causing anandamide to be broken down too quickly. In contrast, calm states help restore normal anandamide levels throughout the body.
CBD and Its Therapeutic Potential
The phytocannabinoid CBD can suppress FAAH synthesis, slowing the breakdown of anandamide and making it effective in treating PTSD and depression symptoms. Brazilian researchers found that CBD extracts reduced stress in animals, even in the presence of previous stressors. CBD binds to the 5HT1A receptor, which is responsible for serotonin production and has a calming effect, as well as reducing nausea and vomiting. Human studies confirm that CBD also binds to this receptor, explaining some of its therapeutic effects.
Based on these findings, scientists are now seeking ways to enhance CBD’s effects on 5HT1A and CB1 receptors and to find alternative methods for sustained activation. Nevertheless, significant therapeutic benefits can be achieved through regular, moderate use of cannabis or its extracts with high CBD content. Experience from Israeli and U.S. doctors shows that even a single joint of high-CBD cannabis can quickly and effectively relieve most physiological and psychological symptoms in even the most severe PTSD cases for an entire day.
Legal and Pharmaceutical Perspectives
Although U.S. and European authorities were slow to act, ongoing cannabis reform has led to partial legalization for therapeutic, industrial, and sometimes recreational use. This “thaw” has greatly increased opportunities for independent research into cannabis and its extracts, and has empowered organizations like MAPS (Multidisciplinary Association for Psychedelic Studies) to study the plant’s benefits.
While most U.S. doctors support federally sponsored trials of cannabis therapy for PTSD, some experts, like Dr. Neumeister, remain skeptical about using cannabis flowers or natural extracts in medicine. He points out that while CBD shows potential for suppressing PTSD symptoms, its effect is relatively weak without the synergistic action of THC, which is more psychoactive and can cause unpleasant side effects and a high risk of psychological dependence if overdosed. He stresses the need for safer, more controlled alternatives to phytocannabinoids.
Currently, the main alternative to natural cannabinoids is synthetic substances that completely suppress FAAH production. However, Dr. Neumeister warns that while these substances eliminate FAAH, they may have serious health consequences, as the accumulation of endocannabinoids and suppression of CB1 activity can cause dysfunction in various biological systems.
Despite the fact that many people in the U.S., Europe, and elsewhere openly or secretly use cannabis flowers and oils to manage PTSD and related psychological conditions, pharmaceutical companies largely support the development of synthetic cannabinoid substitutes, undermining reforms that have already given patients access to safe and effective medicine. At the same time, all attempts to create safe synthetic FAAH inhibitors have failed, sometimes fatally, further confirming the lack of need for such alternatives to an already relatively safe therapy.