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Cannabinoids and Huntington’s disease

Manuel Guzmán is Professor of Biochemistry and Molecular Biology at Complutense University of Madrid, member of the Spanish Royal Academy of Pharmacy, and member of the Board of Directors of the International Association for Cannabinoid Medicines. His research focuses on the study of the mechanism of action and therapeutic properties of cannabinoids, especially in the nervous system. This work has given rise to more than one hundred publications in specialized international journals, as well as to several international patents on the possible therapeutic applications of cannabinoids as anticancer and neuroprotective drugs. He routinely collaborates with scientific reviewing and funding agencies.

Huntington’s disease (HD) is a devastating neurodegenerative disease that begins with choreic movements and goes on to include serious motor, behavioural and cognitive alterations (Walker, 2007).

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 (~95%) of the neurons in an area of the brain known as the “dorsal striatum” (or, more strictly, in humans the “caudate/putamen”), which monitors important neurobiological processes such as motor activity, cognitive functions and emotional control.

From a molecular point of view, it has been known for some time that HD results from the mutation of a single gene, which codes the protein known as “huntingtin” (The Huntington’s Disease Collaborative Research Group, 1993). However, the precise mechanisms by which the mutated huntingtin causes progressive degeneration of MSNs are extraordinarily complex and only partially known (Ross et al., 2014).

Cannabinoids and HD: preclinical data

The cannabinoid receptor CB1 (CB1R), the main molecular target of endocannabinoids and THC, is expressed in very high quantities in MSNs, which, as mentioned are the cells that primarily degenerate in HD. The receptor is also present in the terminals of “corticostriatal neurons”, which, as their name suggests, project from the cortex to the striatum and are responsible for fine controlling the activity of the MSNs (Fernández-Ruiz et al., 2011; Castillo et al., 2012). CB1R levels drop early and notably in MSNs in patients (e.g. Richfield y Herkenham, 1994; Glass et al., 2000; Allen et al., 2009) and animal models (e.g., Denovan-Wright y Robertson, 2000; McCaw et al., 2004; Casteels et al., 2011) of HD.

In contrast, CB1R expression is not affected in corticostriatal projections during HD (Chiodi et al., 2012; Chiarlone et al., 2014). The expression of other elements of the endocannabinoid system also changes during the development of HD (Fernández-Ruiz et al., 2011; Laprairie et al., 2015). Levels of the cannabinoid receiver CB2 (Palazuelos et al., 2009; Sagredo et al., 2009) and the FAAH enzyme (fatty acid amide hydrolase, the principal enzyme degrading anandamide; Blázquez et al., 2011) increase in the striatum of patients and animal models of HD, whereas levels of anandamide and other endocannabinoids are reduced (Bisogno et al., 2008).

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).

For many years it was hypothesized that an early and accentuated drop in the expression of CB1R in MSNs might play a pathogenic role in HD (Maccarrone et al., 2007; Fernández-Ruiz et al., 2011). However, selective genetic inactivation (Chiarlone et al., 2014) or selective genetic overexpression (Naydenov et al., 2014; Blázquez et al., 2015) of CB1R in the MSNs of mouse models of HD does not affect the motor impairments suffered by these animals. On the contrary, selective genetic inactivation of CB1R in their corticostriatal projections markedly worsens their motor behaviour (Chiarlone et al., 2014). From a biomedical perspective, therefore, it is very likely that the therapeutic target of the neuroprotective effects of cannabinoids in animal models of HD is the CB1R population located in the corticostriatal neurons and not that located in the MSNs.

Cannabinoids and HD: clinical data

Several clinical trials have been conducted to date with cannabinoids in HD. A first 6-week double-blind, crossover, placebo-controlled trial on 15 HD patients who were administered 10 mg/kg/day of CBD orally showed that this cannabinoid was safe but did not affect the severity of the chorea and other symptoms of the disease (Consroe et al., 1991).

Two additional uncontrolled single-patient studies using the synthetic cannabinoid Nabilone gave contradictory data on HD-associated chorea: one of the patients worsened (with 1.5 mg of Nabilone per day; Muller-Vahl et al., 1999), whereas the other improved (with 1 mg of Nabilone twice a day; Curtis y Rickards, 2006). Subsequently a double-blind, crossover, placebo-controlled trial was conducted in which Nabilone (1-2 mg per day) was administered to 37 HD patients during two 5-week periods, separated by a 5-week washout period (Curtis et al., 2009). The Nabilone was safe and well tolerated, but its effects were practically identical to those of the placebo in the different motor, cognitive, behavioural and neuropsychiatric scales analysed.

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.

Conclusions

Numerous preclinical studies have demonstrated the neuroprotective power of cannabinoids in different animal models of neurodegeneration. This has raised hopes on possible clinical utility, especially in very serious diseases such as HD, for which no effective treatment is known.

However despite being globally safe and well tolerated, cannabinoids have not as yet shown any neuroprotective activity in humans. This discrepancy between the basic and clinical research may be due to factors such as the substantial biological differences between the animal models and human pathology or to inadequate design of the clinical trials, which have to date been geared towards assessing safety more than effectiveness. It therefore seems logical to suggest that future clinical trials should be conducted in earlier stages of HD with longer periods of treatment with cannabinoids. It might also be useful to know the pattern of cannabis use by HD patients and to have some biomarkers related to CB1R activity during the development of HD.

In all, the safety and tolerability shown thus far by different cannabinoids in clinical trials on HD should encourage more exhaustive future trials to assess whether these compounds might be used as therapeutic agents for treating this highly aggressive disease.

Bibliography

Allen KL et al. (2009) Cannabinoid (CB1), GABAA and GABAB receptor subunit changes in the globus pallidus in Huntington’s disease. J Chem Neuroanat 37:266-281.

Bisogno T et al. (2008) Symptom-related changes of endocannabinoid and palmitoylethanolamide levels in brain areas of R6/2 mice, a transgenic model of Huntington’s disease. Neurochem Int 52:307-313.

Blázquez C et al. (2015) The CB1 cannabinoid receptor signals striatal neuroprotection via a PI3K/Akt/mTORC1/BDNF pathway. Cell Death Differ 22:1618-1629.

Blázquez C et al. (2011) Loss of striatal type 1 cannabinoid receptors is a key pathogenic factor in Huntington’s disease. Brain 134:119-136.

Casteels C et al. (2011) Metabolic and type 1 cannabinoid receptor imaging of a transgenic rat model in the early phase of Huntington disease. Exp Neurol 229:440-449.

Castillo PE et al. (2012) Endocannabinoid signaling and synaptic function. Neuron 76:70-81.

Consroe P et al. (1991) Controlled clinical trial of cannabidiol in Huntington’s disease. Pharmacol Biochem Behav 40:701-708.

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Curtis A & Rickards H (2006) Nabilone could treat chorea and irritability in Huntington’s disease. J Neuropsychiatry Clin Neurosci 18:553-554.

Curtis A et al. (2009) A pilot study using nabilone for symptomatic treatment in Huntington’s disease. Mov Disord 24:2254-2259.

Chiarlone A et al. (2014) A restricted population of CB1 cannabinoid receptors with neuroprotective activity. Proc Natl Acad Sci USA 111:8257-8262.

Chiodi V et al. (2012) Unbalance of CB1 receptors expressed in GABAergic and glutamatergic neurons in a transgenic mouse model of Huntington’s disease. Neurobiol Dis 45:983-991.

Denovan-Wright EM & Robertson HA (2000) Cannabinoid receptor messenger RNA levels decrease in a subset of neurons of the lateral striatum, cortex and hippocampus of transgenic Huntington’s disease mice. Neuroscience 98:705-713.

Dowie MJ et al. (2010) Behavioural and molecular consequences of chronic cannabinoid treatment in Huntington’s disease transgenic mice. Neuroscience 170:324-336.

Fernández-Ruiz J et al. (2011) Prospects for cannabinoid therapies in basal ganglia disorders. Br J Pharmacol 163:1365-1378.

Glass M et al. (2000) The pattern of neurodegeneration in Huntington’s disease: a comparative study of cannabinoid, dopamine, adenosine and GABAA receptor alterations in the human basal ganglia in Huntington’s disease. Neuroscience 97:505-519.

Laprairie RB et al. (2015) Components of the endocannabinoid and dopamine systems are dysregulated in Huntington’s disease: analysis of publicly available microarray datasets. Pharmacol Res Perspect 3:e00104.

López-Sendón Moreno JL et al. (2016) A double-blind, randomized, cross-over, placebo-controlled, pilot trial with Sativex in Huntington’s disease. J Neurol 263:1390-1400.

Maccarrone M et al. (2007) The endocannabinoid pathway in Huntington’s disease: A comparison with other neurodegenerative diseases. Prog Neurobiol 81:349-379.

McCaw EA et al. (2004) Structure, expression and regulation of the cannabinoid receptor gene (CB1) in Huntington’s disease transgenic mice. Eur J Biochem 271:4909-4920.

Mievis S et al. (2011) Worsening of Huntington disease phenotype in CB1 receptor knockout mice. Neurobiol Dis 42:524-529.

Muller-Vahl KR et al. (1999) Nabilone increases choreatic movements in Huntington’s disease. Mov Disord 14:1038-1040.

Naydenov AV et al. (2014) Genetic rescue of CB1 receptors on medium spiny neurons prevents loss of excitatory striatal synapses but not motor impairment in EH mice. Neurobiol Dis 71C:140-150.

Palazuelos J et al. (2009) Microglial CB2 cannabinoid receptors are neuroprotective in Huntington’s disease excitotoxicity. Brain 132:3152-3164.

Pietropaolo S et al. (2015) Chronic cannabinoid receptor stimulation selectively prevents motor impairments in a mouse model of Huntington’s disease. Neuropharmacology 89:368-374.

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.

Ross CA et al. (2014) Huntington disease: natural history, biomarkers and prospects for therapeutics. Nat Rev Neurol 10:204-216.

Sagredo O et al. (2009) Cannabinoid CB2 receptor agonists protect the striatum against malonate toxicity: relevance for Huntington’s disease. Glia 57:1154-1167.

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.

Walker FO (2007) Huntington’s disease. Lancet 369:218-228.

Weeding out the truth: can cannabis improve Huntington’s?

What can individual experiences with cannabis tell us about Huntington’s disease?

By Dr Michael Flower February 24, 2017 Edited by Professor Ed Wild

Cannabis, or medical marijuana, has been touted as a treatment for lots of conditions, and Huntington’s disease is no exception. Whenever it hits the news there’s a lot of interest, and recently cannabis found the spotlight again with videos claiming it can reverse the nerve cell damage in Huntington’s disease. These are extraordinary assertions that deserve to be explored.

What is cannabis?

It’s a plant, originally from Asia and India, that’s been known for thousands of years to have effects on the human brain. Many cultures have used it medically and recreationally. It’s psychoactive, which means that when taken – for example, by smoking its leaves – it alters the way our mind perceives things, characteristically inducing relaxation and euphoria, but it can also cause anxiety and paranoia.

Whether in synthetic or natural form, there is no proper scientific evidence that cannabis helps Huntington’s disease patients

It wasn’t until the 1940s that we discovered the active ingredients, which are oily chemicals called cannabinoids. Other plants make cannabinoids too, including some herbal teas, truffles and even cocoa.

How it works

In the late 1980s, we discovered that humans have tiny sensors, called receptors, for these cannabinoids on the surface of our cells. There are two main types of receptor – CB1 and CB2. Most CB1 receptors are in the brain and spinal cord. It’s these ones that are thought to produce the psychoactive effects. The receptors affect how active our nerve cells are, for example controlling the amount of pain a person feels. In contrast, CB2 receptors are found on immune cells that circulate in our blood, and activating them can have an anti-inflammatory effect. Normally there are very few CB2 receptors in the brain, and those that are there, are found on immune cells.

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.

‘Cannabinoid’ is the name we call any chemical that activates cannabinoid receptors. The ones that plants make are called phytocannabinoids. Phyto- comes from the Greek for plant. The ones our own bodies make are called endocannabinoids, derived from the Greek for ‘within’. It’s also possible to manufacture chemicals that activate these receptors, and we call these synthetic cannabinoids.

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’.

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.

The cannabis plant contains over 100 different cannabinoids, but the most psychoactive is tetrahydrocannabinol, otherwise known as THC, which potently activates CB1 receptors. The other main cannabinoid, cannabidiol (CBD), isn’t psychoactive. In fact, it reduces the activation of both CB1 and 2 receptors.

Cannabinoids can be extracted from plants and purified. Different strains of the plant are bred for different purposes, and each contains a different proportion of the cannabinoids. Hemp, for example, is a sturdy fibre that’s been used in paper and clothes and is low in the psychoactive chemical THC. Cannabis plants used recreationally tend to have high THC. Cannabis is illegal in some places, while elsewhere it is legal for medicinal or recreational use. Scientific research is going on to see if it could benefit people with Huntington’s disease.

Do cannabinoids improve Huntington’s disease?

Scientists around the world have been studying their effects in Huntington’s disease. Most work has been done in cells grown in the lab, or in animals bred to have the disease-causing gene. Some research suggests that CB1-targeting chemicals may protect cells against toxins. In the brains of Huntington’s mice, CB1 receptor levels have been found to be reduced and CB2 levels are increased. Loss of CB1 receptors may be involved in some symptoms of the disease, because Huntington’s mice that lack the CB1 receptor tend to have worse movement control. The increase in CB2 receptors may be one of the body’s ways of dealing with HD. This theory is strengthened by research showing that mice treated with CB2-targeting chemicals have less nerve cell death – possibly because this calms down the immune system in the brain.

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.

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But this video on the internet shows cannabis works for HD!

Proper clinical trials, with ‘blinded’ and ‘placebo-controlled’ designs, are how to find out whether a drug really works.

Searching the internet, you’ll find several videos and news stories suggesting people’s Huntington’s disease has been reversed by cannabis. We’re very pleased that these individual patients have found something that works for them.

But unfortunately, these anecdotes aren’t scientific evidence. Based on these brief snapshots, it’s impossible to tell whether they have actually improved overall. Huntington’s symptoms naturally vary, and are influenced by many factors, like sleep and infections. We don’t know about these patients’ genetic mutations, the stage of their disease or what other medications they’re taking. We also have to bear in mind the powerful placebo effect of therapies like this, where a significant proportion of people are known to improve because they believe strongly in a treatment, rather than because of any properties of the drug itself. There’s also a strong bias in mainstream and social media towards the publication of success stories like these, but nobody writes about all the people who tried cannabis and didn’t improve, or felt worse afterwards.

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.

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.

But where’s the harm in it?

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.

Right now there is no evidence to show that cannabinoids work in Huntington’s disease, for symptoms or slowing down progression.

The natural world is chock-full of potential treatments for all manner of diseases. Aspirin, penicillin and even some cancer drugs were purified from natural sources. But even drugs from natural sources can be harmful. Recreational cannabis use is known to carry a risk of psychosis, and medical cannabinoids can also cause sedation, anxiety, depression, dizziness, and nausea. They can interact with other medicines like antihistamines and antidepressants. Trials in multiple sclerosis have also raised a possible risk of epilepsy. These aren’t reasons to stop studying cannabinoids as a potential therapy for Huntington’s, but they do mean we should be very careful and ideally study them in properly monitored clinical trials.

Letting the smoke clear

Right now there is no evidence to show that cannabinoids work in Huntington’s disease, for symptoms or slowing down progression. That doesn’t negate anyone’s personal experience, but it does mean that individual anecdotes or videos need to be interpreted with healthy caution – especially when the people making the claims are the people who stand to make profit from the ‘cure’.

The research community hopes that cannabinoids will be shown to be effective and safe enough to be able to prescribe, but we don’t have the evidence to make that decision yet. Whilst cannabinoid research is telling us a lot about the biology of Huntington’s disease, it’s certainly not the only avenue under investigation, and exciting trials in other treatments may change the playing field in the not-too-distant future. The best way to fight Huntington’s disease is through rigorous scientific research to develop treatments that are effective, reliable and safe.

The authors have no conflicts of interest to declare. For more information about our disclosure policy see our FAQ.

CBD Oil and Huntington’s Disease: Benefits, Dosage, & Side-Effects

CBD will not cure Huntington’s disease — nothing will.

However, CBD oil may ease symptoms and improve your quality of life.

Learn how it works, how to use it safely, and what dose to take.

Article By

Huntington’s disease is a genetic disorder affecting the brain.

Unfortunately, there’s no cure for this slowly progressing, but deadly disease.

Recent evidence, however, suggests that CBD oil may offer support to this condition, slowing its progression and improving quality of life for those affected.

Here, we investigate these claims and discuss how CBD can be used to support Huntington’s disease. We also go over how you can start using the neuroprotective effects of CBD to your advantage.

MEDICALLY REVIEWED BY

Carlos G. Aguirre, M.D., Pediatric Neurologist

Updated on January 12, 2022

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What Are The Benefits of CBD Oil For Huntington’s Disease?

The problem with Huntington’s disease is that dysfunctional proteins (huntingtin) build up around the nerve cells which begin to impede their ability to function.

Over long periods of time (10-20 years) this results in widespread inflammation and death of the neurons.

This causes severe neurological symptoms and a gradual reduction in the quality of life.

The primary benefits of CBD oil for Huntington’s disease include:

  • Reduces inflammation in the brain
  • Alleviates common side effects of Huntington’s disease
  • Offers powerful neuroprotective benefits

Although there are no conclusive clinical trials yet involving CBD on Huntington’s disease patients, there are a lot of compelling animal trials and case studies published.

Whenever using CBD for medical conditions like this, it’s important to speak with your doctor first and to use only the highest grade CBD Oils available.

What’s The Dose of CBD Oil For Huntington’s Disease?

Dosing CBD is difficult because everyone reacts differently to it.

To get started, use our CBD oil dosage calculator to find your estimated dose based on your weight and desired strength.

In the context of something like Huntington’s disease, it’s likely that a stronger dose is going to provide more results than a weaker dose.

Some of the studies being done involving this disease have used very high dosages, in the realm of around 700 mg of pure CBD per day.

This compares to the usual dosage range of about 10-120 mg per day.

Of course, the full-spectrum hemp oils tend to require lower doses because of something called the entourage effect. This is the idea that the other compounds in the cannabis plant improve the effects of CBD by enhancing its absorption, helping it pass the blood-brain barrier, and slowing its breakdown.

For this reason, we prefer a premium full-spectrum hemp oil when using CBD for neurological conditions like Huntington’s disease.

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What is Huntington’s Disease?

Huntington’s disease is a progressive brain disorder characterized by uncontrollable muscle movements, inability to control emotions, and a gradual reduction in cognitive function.

It’s a serious and life-long condition caused by a genetic mutation.

Living with Huntington’s disease comes with unique challenges. There’s no cure, but there are a few options that can help slow the progression of the disease and improve quality of life.

One such option growing a lot in interest is cannabidiol (CBD), the main non-psychoactive cannabinoid in the marijuana plant.

Symptoms of Huntington’s Disease

Most of the symptoms involved with Huntington’s disease are the direct result of neuronal death. Proteins build up in the brain, interfering with the nerve cells.

Over time, problems with normal nerve function start to appear, and will gradually get worse over the course of 10-15 years.

Early-Stage Symptoms:
  • Chorea (Involuntary movements)
  • Irritability
  • Depression
  • Small involuntary movements
  • Poor coordination
  • Trouble learning new information or making decisions
Late-Stage Symptoms:

What Causes Huntington’s Disease?

Huntington’s is a genetic disorder.

The disease affects an estimated 3-7 people every 100,000, primarily of European descent. The disease is very rare in African and Asian populations.

The disorder comes from a mutation in a gene referred to as HTT.

This gene encodes a protein called huntingtin. Scientists still aren’t sure what it does, but it appears to play a critical role in the ability of the nerve cells function.

People who have Huntington’s disease produce abnormally long huntingtin proteins.

These long proteins are unstable and will break down into smaller chunks, which can tangle together and accumulate around the neurons. Over time these tangles interfere with the neuron’s ability to function and will eventually cause the neurons to die.

This is what causes the gradual onset of symptoms associated with the condition such as involuntary movements, speech difficulty, and confusion.

This is a similar process to the one that happens with Alzheimer’s disease, but Alzheimer’s involves another protein known as TAU. Protein tangles in the neurons cause them to break down over time.

HTT Gene Mutation

In the healthy HTT gene, proteins are repeated 10 to 35 times, however, in people with Huntington’s disease, these proteins are repeated anywhere from 36 to 120 times (specifically the CAG proteins).

In general, anything less than 39 repeats won’t cause any symptoms; however, over 40 repeats will almost always result in symptoms of Huntington’s disease.

The child inherits this mutation from the parents. It’s very rare for someone to develop Huntington’s disease without a parent who also has the condition.

If you did not receive the gene from your parents, you cannot pass it on to your children. You need to have the genetic mutation in order to pass it on.

As the gene is passed down the generations, the number of repeats tend to increase in size.

People with adult-onset Huntington’s disease tend to have about 40-50 repeats, while people with juvenile-onset usually have at least 60 repeats.

These repeats are important because this is how doctors test for the disease.

When Does Huntington’s Disease Start Showing Symptoms?

There are two main types of Huntington’s disease; each indicates when the disease will first start showing signs and symptoms:

1. Adult-Onset Huntington’s disease

Adult-onset describes the age in which symptoms begin to appear. In all people with Huntington’s disease, they have had the disorder from birth; however, it sometimes won’t produce problematic symptoms until adulthood.

Usually, symptoms for adult-onset Huntington’s disease will begin to appear around age 30 or 40.

2. Juvenile-Onset Huntington’s Disease

Juvenile onset Huntington’s disease starts much earlier, either in early childhood or during puberty.

It starts with emotional changes, clumsiness, frequent falling, rigidity, slurred speech, drooling, and a decline in school performance.

Some children with the disease will also experience seizures. This happens in about 3-50% of those affected.

Compared to adult-onset Huntington’s, juvenile-onset tends to progress quickly.

As we’ll discuss in more detail below, people with juvenile-onset tend to have a more severe genetic mutation than those with adult-onset.

How is Huntington’s Disease Diagnosed?

Doctors start by considering the symptoms.

“Does the patient show any signs of Huntington’s disease?”

Next, they consider the patient’s ethnic background and family history.

“Are they of European descent? Do they have other family members who have had the condition?”

Huntington’s is an inherited disease, so if there are other family members with the condition, the patient will be a lot more likely to also carry that particular gene mutation.

Doctors will look at the gene through a number of specialized genetic tests and count the number of repeats.

Huntington’s Diagnosis Criteria:
  1. Less than 26 repeats: Negative for Huntington’s disease.
  2. Between 27 and 35 repeats: Negative for Huntington’s disease, but risk of having children within the Huntington’s disease range.
  3. Between 36 and 39 repeats: Low risk for developing Huntington’s disease. At higher risk of having children with the disease.
  4. 40 or more repeats: High likelihood of developing symptoms of Huntington’s disease and having children with the disease.

How is Huntington’s Disease Treated?

Unfortunately, Huntington’s Disease cannot be slowed or stopped; however, there are a few drugs that can help ease some symptoms. Antidepressants and anxiolytics can help treat mood disorders brought on by the disease. Antipsychotics can be prescribed to help control hallucinations and outbursts. Tetrabenazine and deuterabenazine can treat chorea, the uncontrollable movements often associated with Huntington’s.

Some drugs can interact with CBD and cause adverse reactions, so always speak to your doctor before taking CBD. Never stop or adjust the dose without a doctor’s supervision.

What The Research Says: CBD For Huntington’s Disease

The research involving CBD for this condition is still in its infancy.

There have only been a small handful of clinical trials investigating this relationship. The trials we do have are significantly lacking in key areas of focus.

They’re too short, too small, and involve patients with the wrong focus of symptoms.

We are getting much closer, however.

In order to conduct these large and expensive clinical trials, we first need to confirm that there are benefits from CBD oil towards the pathophysiology involved in Huntington’s disease, through cell cultures and animal testing. The next step is to conduct small human-based trials, before moving on to larger and more widespread clinical trials.

We’ve done plenty of animal studies, many of which have shown that CBD and THC are able to slow the progression of Huntington’s disease in rats [3].

On top of this, there are some case reports of people with Huntington’s disease using CBD and synthetic THC. Some of these reports involve significant improvement in symptoms like chorea (involuntary movement), and speech difficulties [2].

There have so far only been a handful of clinical trials involving CBD and Huntington’s disease. One such trial only investigated the use of CBD in patients not experiencing the main symptom of involuntary movements. This is interesting because the primary theories behind how CBD can be used to improve the symptom is by treating these involuntary movements.

This particular study was also only done over the course of about 6 weeks, which is of little value when you consider the fact that Huntington’s progresses over 20 years. No changes should be expected in as little as 6 weeks, especially in people who have already developed symptoms of Huntington’s disease.

To no surprise, members of the study taking CBD showed little or no improvement over the course of the study. This has little value to the role CBD may play in the treatment of this disease, however, it’s a good starting point because it proved that CBD doesn’t make the condition any worse (after 6 weeks, at least), which some people originally theorized could happen.

A Note on Mitochondria Dysfunction & Huntington’s Disease

The mitochondria, the powerhouse of the cell, has also been implicated as playing a role in the process behind Huntington’s disease, which CBD has been shown to offer potent modulatory benefits towards [5].

More research is needed to see how mitochondrial dysfunction is linked to Huntington’s and whether or not CBD can be used to correct these dysfunctions.

Moving Forward: Future Applications of CBD For HD

CBD is a valuable medicinal constituent of the cannabis family of plants.

Its ability to regulate both neurological and immune function— both of which are heavily involved in the progression of Huntington’s disease make it a prime candidate for future treatment options for this condition.

There has been a growing collection of evidence to support CBD’s ability to slow the progression of Huntington’s disease and improve the quality of life in people suffering from this debilitating condition.

More research needs to be done to understand the extent this compound can help those diagnosed with the condition.

We look forward to seeing this space develop further in the coming years as high-quality clinical trials are published on the topic.

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