There currently aren’t any treatments capable of curing Huntington’s disease, so some might think sufferers have nothing to lose from trying alternative therapies. However, there are risks.
Through proper clinical trials, researchers can prove whether a potential treatment is both effective and safe. This is the standard that all other medicines are held to, and it shouldn’t be any different for cannabinoids.
Having found sensors for cannabinoids in the human body, the logical conclusion was that we might also naturally make cannabinoids. And indeed, the first of these was found in the early 1990s, followed shortly after by several more. Nerve cells use them as a way of regulating their own activity level. Normally one nerve cell passes information to another by sending a neurotransmitter chemical. Cannabinoids are a way for the second nerve cell to pass a message back to first, telling it to calm down.
What can individual experiences with cannabis tell us about Huntington's disease?
These results in cells and animals are encouraging, but humans are a lot more complex. Bitter experience has taught us that very often results can be inconsistent, or even completely different, when therapies are scaled up for use in humans. Unfortunately, no cannabinoids have translated into effective treatments in people with Huntington’s disease yet. Several clinical trials with cannabis extracts or synthetic cannabinoids didn’t reduce the abnormal movements, like chorea, or affect the course of the disease.
Whether in synthetic or natural form, there is no proper scientific evidence that cannabis helps Huntington’s disease patients
Different cannabinoids have stronger or weaker effects at each receptor, so they can have varied effects on our bodies. Once in the body, they are eventually broken down by the liver. Some are also stored in fatty tissues, along with their breakdown products from the liver, and these can be detected for several weeks afterwards in blood ‘drug tests’.
Claims that there’s a solid body of evidence supporting the use of cannabinoids in Huntington’s disease are highly misleading, and there’s certainly no evidence that they can cure or reverse the disease. However, it’s also worth remembering that there are several exciting potential drugs being trialled around the world right now that hold great promise. Cannabinoids are just a small part of the big picture, and real progress is being made in understanding and treating Huntington’s disease.
“We are pleased with the DEA’s cooperation and support to facilitate our company mission to service the unmet needs of patients suffering from these chronic diseases,” he added.
The cannabis plant produces a variety of compounds known as cannabinoids, including THC and CBD, two of the most abundant found in the plant. CBD, the non-psychoactive component of cannabis, is believed to have neuroprotective properties, while THC is the main psychoactive constituent of cannabis.
A specialty pharmaceutical solutions company will help MMJ with specialized liquid encapsulation solutions, and make sure MMJ follows FDA protocol and DEA manufacturing guidelines.
Currently, several academic institutions are in touch with MMJ to prepare studies of cannabis as a treatment for Huntington’s disease and MS.
“MMJ clinical trials will provide the necessary data to prove that cannabis can treat essential tremors, a neurological disorder that causes involuntary shaking. Ultimately, there’s so much interest in THC and CBD as a treatment modality, so MMJ will be providing the clinical research data necessary to prove patient dosing, safety, and efficacy,” Moynahan stated.
MMJ-001 and MMJ-002 are two of MMJ’s lead therapeutic candidates, and are liquid formulations of highly purified THC and CBD.
The company is developing MMJ-001 to treat spasticity (abnormal muscle tightness) in MS, and MMJ-002 to treat Huntington’s-associated chorea — a neurological condition marked by involuntary spasms or writhing movements.
There is currently no known cure for HD. It leads to the death of the patient between 10 and 20 years from the onset of the symptoms. The disease has an approximate prevalence of 1 case per 10,000 and is caused primarily by the degeneration of a specific population of neurons, called “medium spiny neurons” (MSNs). These cells make up practically all (
Richfield EK & Herkenham M (1994) Selective vulnerability in Huntington’s disease: preferential loss of cannabinoid receptors in lateral globus pallidus. Ann Neurol 36:577-584.
Cannabinoids and HD: preclinical data
The Huntington’s Disease Collaborative Research Group (1993) A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington’s disease chromosomes. Cell 72:971-983.
Finally, a double-blind, crossover, placebo-controlled trial was performed in which Sativex was administered (approximate average dose: 20 mg of THC and 20 mg of CBD per day) to 24 HD patients for two 12-week treatment periods, separated by a 4-week washout period (Lopez-Sendon Moreno et al., 2016). The Sativex was safe and well tolerated, but no significant effects were observed either in the motor, cognitive, behavioural and functional parameters or in the biomarkers assessed.
Studies carried out by two independent laboratories have shown that genetic inactivation of CB1R aggravates HD in mouse models of the disease (Blázquez et al., 2011; Mievis et al., 2011). Analogously, administration of THC (2 mg/kg/day; Blázquez et al., 2011) or the synthetic cannabinoid WIN-55.212-2 (0.3 mg/kg/day; Pietropaolo et al., 2015) in mice models of HD delays the onset and attenuates the pathology and motor symptoms of the disease. Nonetheless, an additional study found no beneficial effects of THC (albeit at a very high dose, 10 mg/kg/day), the synthetic cannabinoid HU-210 (0.01 mg/kg/day) or the inhibitor of FAAH URB597 (0.3 mg/kg/day) in a mouse model of HD (Dowie et al., 2010).