Huntington’s disease

Huntington’s disease (HD) is a genetically transmitted neurodegenerative disorder. The method of transmission is autosomal dominant of a gene on chromosome 4 that codes for a the protein huntingtin. This protein is mutated in this disease, due to a long “tail” of CAG (cytosine-adenine-guanine) repeats and deposits in mainly in the nucleus of the nerve cells where it does damage.


We know that HD runs in families and is of genetic origin. If your parent has this disease you have a 50% chance of getting it. The severity and transmission of this disease depends on the number of CAG repeats.

huntington's disease cag repeats

We still don’t  know why the huntingitn protein is toxic, why it is toxic in a selective way (it affects a very specific neuronal sub-population) and what is the pathogenic process of this disease.


Symptoms of these disease usually start showing between the ages of 35-45 although they can manifest in children (juvenile HD) as well as 80 year old patients. These symptoms are changes in physical skills, personality and cognition.
– “chorea” severe, involuntary writhing movements
– dystonia (involuntary tightening of muscles which results in “repetitive or twisting movements”)
– abnormal facial expression, and difficulties chewing, swallowing, and speaking
– progressing dementia characterised by deficits in maintaining cognitive flexibility
– sleep disturbances
– mood swings
– irritability
– apathy
– anxiety
– depression


From research, we know that during Huntington’s disease (HD) pathogenesis, the expression of genes in both the endocannabinoid system (ECS ) and dopaminergic system (DAS) is dysregulated.

huntington disease and ecs


An ideal treatment would be a constituent that could target these genes directly. Cannabigerol dose just that.

Cannabigerol (CBG) is a less known cannabinoid and derives from cannabigerolic acid (CBGA). CBGA is also the precursor of THCA, CBDA and CBCA so very little CBG is usuallly left in the plant. There are hoever some starins, especially hemp strains, which have a grater percentage of this compound. It can also be found in sprouting hemp seeds in the form of CBGA.

Researchers in a January 2015 study on mice, published in Neurotherapeutics pointed out:
“we were able to identify a series of genes linked to this disease…whose expression was altered in R6/2 mice but partially normalized by CBG treatment.”
“We also observed a modest improvement in the gene expression for brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and peroxisome proliferator-activated receptor-γ (PPARγ), which is altered in these mice, as well as a small, but significant, reduction in the aggregation of mutant huntingtin in the striatal parenchyma in CBG-treated animals.”
“In conclusion, our results open new research avenues for the use of CBG, alone or in combination with other phytocannabinoids or therapies, for the treatment of neurodegenerative diseases such as HD.” – Robert B et al., 2015

Patients should look for strains high in CBG and also cannabidiol (CBD), due to its anti-inflammatory, neuroprotective and neuroregenerative properties.
Tetrahydocannabinol (THC) should be present in small percentage, as it also has properties that alleviate some of the symptoms of HD.

The preferred method of consumption is via sublingual application of tinctures. Vaporising can also be used, but higher doses of constituents are usually needed than those achieved by vaporisation.