Lou Gehrig’s Disease, aka Amyotrophic Lateral Sclerosis (ALS) and Medical Cannabis
Definition
ALS is a progressive disease that causes the death of neurons controlling voluntary muscles. ALS is also known as Lou Gehrig’s disease or motor neuron disease (MND).
Potential Efficacy / Quality of Evidence (Low, Average, High) of Medical Marijuana for ALS
Low
Cannabinoids, Terpenes/Terpenoids, Strains and Ratios that May Help
As with many other neurological and neurodegenerative conditions, THC and CBD may help reduce nervous system inflammation.
Delta-3 carene may help dry the mouth and prevent drooling.
Medical MMJ Pros
Cannabinoids – in particular CBD – may help slow the progression of ALS in some instances.
May help treat many of the symptoms associated with ALS, in particular cachexia, dementia, drooling, muscle spasticity.
Medical MMJ Cons
Few human trials.
May make some problems associated with ALS worse, e.g. memory problems, muscle weakness.
More About the Condition
ALS is characterized by muscle weakness and wasting – which gets progressively worse – until death ensues typically due to respiratory muscle failure. Generally, ALS patients present a number of clinical symptoms, including weakness, spasticity, cachexia, dysarthria and drooling, and pain secondary to immobility, among others. Cannabinoids may possibly slow the progression of ALS, and there is certainly evidence that cannabis can help treat some of the symptoms of ALS, especially spasticity, cachexia, drooling and chronic pain.
Amyotrophic lateral sclerosis (ALS) affects around 1 – 3 people per 100,000 population in a given year. Around 90% of cases of ALS are sporadic, meaning that the patient need not have relatives with ALS. Around 10% of cases of ALS are familial, meaning they have inherited ALS. For those who have inherited ALS, there is an issue with the superoxide dismutase-1 gene (SOD-1), which encodes for a key antioxidant enzyme.
There are also mutations in TAR-DNA binding protein-43 (TDP-43) and FUS (fused in sarcoma) which encode proteins involved in pre-mRNA splicing, transport and stability. mutation in non-coding hexanucleotide repeat sequence (GGGGCC) in the C9orf72 gene was considered as the most common genetic cause of ALS. Mutations in the C9orf72 gene have also been seen in patients with dementia.
Like most studies, the use of cannabis to treat ALS has mostly only been examined in preclinical experiments, usually on mice. Some of these studies suggest that cannabinoids may be used to slow the onset of ALS, and therefore increase life expectancy and generally reduce the burden of the disease.
There is little evidence from human trials on whether or not cannabis is effective for ALS, although there are some anecdotal reports, the most famous of which are the stories of Cathy Young and Bob Strider, who believe that cannabis has helped them. Scientific observations with humans demonstrated cannabinoids relieving hyperalgesia and adjusting muscular spasticity, but once again, this is just one overview, and far more human trials are needed in order to say anything for definite.
Cannabinoids’ neuroprotective effects may also play a role in helping treat ALS. Just like with many medications, cannabinoids may work for some types of ALS, but not others. This may be due to different genetic mutations.
Quotes from Experts
“There is a growing body of evidence that cannabinoids (the active ingredient in cannabis) may hold a significant therapeutic benefit for patients with amyotrophic lateral sclerosis (ALS). Moreover, through manipulation of the endocannabinoid system, cannabis may hold disease-modifying potential in ALS (92–105). There are a number of animal studies suggest that the endocannabinoid system is implicated in the pathophysiology of ALS (93–99). This may be through a direct action or disease mechanism. Conversely this may be as part of a failure of homeostatic functioning of the neuromuscular system that may be governed by this system. There is now good animal based evidence that cannabinoids are capable of slowing disease progression of ALS in mice (93–96).” Source: ‘Complementary and Alternative Therapies in ALS‘, Bedlack, Richard S et al. Neurologic clinics vol. 33,4 (2015): 909-36. doi:10.1016/j.ncl.2015.07.008
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