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Amyotrophic lateral sclerosis (ALS) is a degenerative, usually terminal neurological disease generally showing up between the ages of 40 and 70. It is also known as Motor Neuron Disease (MND). Initial symptoms present subtly as muscle stiffness or weakness but continue to progress until patients are unable to speak, walk or even breathe by themselves. There is no specific known cause or cure; several mechanisms are thought to cause motor neuron degeneration. Approximately 1900 Australians suffer from ALS and the number seems to be growing with the aging population.

The endocannabinoid system has been implicated in both relieving symptoms and possibly slowing disease progression of ALS patients. Cannabidiol (CBD) is a potent antioxidant and has been shown to mediate the body’s inflammatory response. Both of these properties are desirable in the treatment of ALS.


This image is a simplification for website aesthetics only. For more information please refer to the clinical studies referenced below.

Postulated causes of motor neuron damage
Abnormal glutamate metabolism
Glutamate is chemical found in the brain and an excitatory neurotransmitter responsible for signalling between neurons. While this chemical is important it is also toxic to cells in excess. Glutamate concentration can spike by either an increased release from neurons or by defective transport and metabolism.

Free radicals and oxidative stress
Free radicals are molecules with an unpaired electron, a property that makes these compounds highly reactive within the body. Free radicals damage the proteins and lipids within nerve cells if they are allowed to build up. In ALS, free radicals accumulate and create an oxidative environment or oxidative stress that, in turn, damages motor neurons.

Inflammatory damage

Evidence suggests that an inappropriate immune response may be implicated in the progression of ALS. The body’s immune response initiates synthesis of specific proteins, increases intracellular calcium levels and releases inflammatory mediators, all of which are thought to damage motor neurons.
Specific benefits of Endocannabinoid Activation with Cannabidiol
One characteristic seen in ALS is an increase in glial cells in the CNS, causing neuroinflammation and eventually damage to the motor neurons. CBD is a potent anti-inflammatory, clinically shown to cause apoptosis (death) of the glial cells, reducing inflammation and offering symptomatic relief as well a preventative measure against ALS.


Neurons are sensitive to changes in their environment, particularly oxidative stress, which can cause irreparable damage. Through many different mechanisms including its antioxidant properties, CBD both protects neurons from possible damage and helps to heal damaged neurons.

An anxiolytic is a medication or other intervention that is used to control anxiety and depression, a common secondary symptom of ALS. The endocannabinoid system is a proven regulator of mood and cognition. Additionally, CBD mimics natural serotonin in its ability to bind to some of the same receptors, most importantly the 5HT1A receptor. Activation of this receptor has been shown to improve mood and reduce anxiety and depression.

Pertinent Studies:

Carter, G. T., & Rosen, B. S. (2001). Marijuana in the management of amyotrophic lateral sclerosis. American Journal of Hospice and Palliative Medicine, 18(4), 264-270.
Fowler, C. J., Rojo, M. L., & Rodriguez-Gaztelumendi, A. (2010). Modulation of the endocannabinoid system: neuroprotection or neurotoxicity?. Experimental neurology, 224(1), 37-47.
Hampson, A. J., Grimaldi, M., Axelrod, J., & Wink, D. (1998). Cannabidiol and (−) Δ9-tetrahydrocannabinol are neuroprotective antioxidants. Proceedings of the National Academy of Sciences, 95(14), 8268-8273.
Kaufman, J., Almasy, K., Boller, A., Dahodwala, N., Elman, L., Kelley, M., & McCluskey, L. (2014). Medical Marijuana Utilization and Perceived Therapeutic Value in Patients with ALS (P3. 014). Neurology, 82(10 Supplement), P3-014.
Moreno‐Martet, M., Espejo‐Porras, F., Fernández‐Ruiz, J., & Lago, E. (2014). Changes in Endocannabinoid Receptors and Enzymes in the Spinal Cord of SOD1G93A Transgenic Mice and Evaluation of a Sativex®‐like Combination of Phytocannabinoids: Interest for Future Therapies in Amyotrophic Lateral Sclerosis. CNS neuroscience & therapeutics, 20(9), 809-815.