Best cbd oil for huntington’s

CBD for Huntington’s Disease

Huntington’s disease is a rare, genetic neurodegenerative disorder caused by an expansion of a repeating CAG triplet series in the huntingtin gene on chromosome 4. This causes the progressive degeneration of nerve cells in the brain, having a broad impact on the patient’s functional abilities, including motor, cognitive and psychiatric dysfunction.

Huntington’s disease is often called the quintessential family disease as it is inherited in an autosomal dominant fashion, meaning that each child of an affected parent has a 50% chance of inheriting the faulty gene and developing the disease.

As mentioned, Huntington’s disease manifests as a triad of motor, cognitive, and psychiatric symptoms that progresses insidiously over many years. The average length of survival after clinical diagnosis is typically 10 – 20 years. However, some people have lived thirty or forty years with late-stage Huntington’s disease lasting up to a decade or more.

As the disease progresses, a person with Huntington’s disease will eventually require help with all activities of daily living and care, eventually becoming bedridden and unable to speak. Huntington’s disease patients are however able to understand language and have an awareness of family and friends, although some won’t recognize family members.

Death is usually a result of pneumonia or other infections, injuries related to falls, complications related to the inability to swallow and often also suicide.

Symptoms of Huntington’s Disease

Huntington’s disease is often described as having ALS, Parkinson’s and Alzheimer’s simultaneously, with symptoms, usually appearing between the ages of 30 to 50, and worsening over a 10 to 25-year period.

The type of symptoms which appear first as well as symptom severity vary greatly from patient to patient. Some symptoms may also appear more dominant or have a greater effect on functional ability, although this can change during the course of the disease.

  • Involuntary jerking or writhing movements (chorea)
  • Muscle problems, including rigidity and muscle contracture (dystonia)
  • Slow or abnormal eye movements
  • Impaired gait, posture and balance
  • Issues with speech or speech changes
  • Difficulty swallowing
  • Ataxia and spasticity
  • Muscle weakness, a loss of muscle tissue and weight loss
  • Difficulty organizing, prioritizing or focusing on tasks
  • Lack of cognitive flexibility or dealing with changes in the environment and/or day-to-day schedule
  • The tendency to get stuck on a thought, behaviour or action (perseveration)
  • A lack of impulse control resulting in outbursts, acting without thinking and sexual promiscuity
  • Lacking awareness of one’s own behaviours and abilities
  • Slowness in processing thoughts or ”finding” words
  • Difficulty in learning and/or assimilating new information
  • Depression occurring due to injury to the brain and subsequent changes in brain function.
  • An obsessive-compulsive disorder marked by recurrent, intrusive thoughts and repetitive behaviours
  • Mania categorized by an exaggerated elevation in mood, overactivity, impulsive behaviour and inflated self-esteem
  • Bipolar disorder with alternating episodes of depression and mania
  • Feelings of irritability, sadness or apathy
  • Social withdrawal
  • Insomnia
  • Fatigue and loss of energy
  • Frequent thoughts of death, dying or suicide
  • Behavioural changes
  • Difficulty paying attention
  • A rapid, significant drop in overall school performance
  • Behavioural problems
  • Physical changes
  • Contracted and rigid muscles that affect gait (especially in young children)
  • Tremors or slight involuntary movements
  • Frequent falls or clumsiness
  • Seizures

Huntington’s Disease Medications & Treatments

There is no cure for Huntington’s disease and most interventions are aimed at lessening some symptoms of movement and psychiatric disorders. Multiple interventions can help a patient adapt more easily to changes in abilities. However, drugs that treat some symptoms may result in side effects that worsen other symptoms meaning that treatment goals must be regularly reviewed and updated.

Pharmaceutical Interventions

  • Tetrabenazine and deutetrabenazine are often prescribed to suppress involuntary jerking and writhing movements (chorea) although they do not have any effect on the progression of the disease. Possible side effects include drowsiness, restlessness, and the risk of worsening or triggering depression or other psychiatric conditions.
  • Antipsychotics like haloperidol and fluphenazine can suppress movements that can be beneficial in treating chorea. However, these drugs may worsen involuntary contractions (dystonia), restlessness and drowsiness. Other types of anti-depressant drugs such as risperidone, olanzapine and quetiapine may have fewer side effects but still should be used with caution, as they may also worsen symptoms.
  • Other medications that may help suppress chorea include amantadine, levetiracetam and clonazepam although poor side effect profiles limit their use.
  • Antidepressants such drugs as citalopram, escitalopram, fluoxetine and sertraline can help relieve depression but may also have some effect on treating obsessive-compulsive disorder. Side effects may include nausea, diarrhea, drowsiness and low blood pressure.
  • Antipsychotic drugs such as quetiapine, risperidone and olanzapine are prescribed to suppress violent outbursts, agitation, and other symptoms of mood disorders or psychosis. However, these drugs may themselves cause a variety of other types of movement disorders.
  • Mood-stabilizing drugs and anticonvulsants, such as Divalproex, carbamazepine and lamotrigine can help prevent the highs and lows associated with bipolar disorder.

Non-Pharmaceutical Interventions
Additional interventions that can help patients with Huntington’s disease can help them deal with behavioural, cognitive and day-to-day living difficulties. For instance, psychotherapy can help the patient and their families develop coping strategies, manage expectations during the progression of the disease and facilitate effective communication.

Speech can help improve patients’ ability to swallow, eat and speak clearly, or teach them how to use communication devices. Similarly, physical therapy can enhance strength, flexibility, balance and coordination that can help maintain mobility as long as possible and may reduce the risk of injury. In addition, occupational therapy can help with strategies that can assist the patient, family members and caregivers on environmental changes and the use of assistive devices that improve functional abilities, including the installation of handrails at home, assistive devices for activities such as bathing and dressing and eating and drinking utensils adapted for people with limited fine motor skills.

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CBD for Huntington’s Disease

Research & Scientific Evidence of using CBD for Huntington’s Disease

Research into the use of cannabidiol (CBD) for Huntington’s disease goes as far back as the 1980s with a few, although sometimes contradicting studies on both animal and human subjects being available. However, most recent studies and clinical trials show that CBD has several properties that can help relieve many symptoms of Huntington’s disease including neurodegeneration, oxidative stress and inflammation as well as motor impairments such as tardive dyskinesia and cognitive decline.

In a 2016 review paper published in Pharmacological Research, the authors evaluated the available evidence showing the CBD’s neuroprotective properties for application in neuropsychiatric disorders. They concluded that CBD has potential therapeutic effects over a broad range of neuropsychiatric disorders including Huntington’s disease.

Although the exact mechanisms are still unclear, from the data available it seems clear that CBD attenuates brain damage associated with neurodegenerative and/or ischemic conditions. This seems to be due to CBD’s ability to affect synaptic plasticity and facilitates neurogenesis through interactions with the endocannabinoid system (ECS), 5HT1A receptors, Oxidative stress and peroxisome proliferator-activated receptors (PPAR), the inhibition of adenosine uptake, immune mediators, brain-derived neurotrophic factor (BDNF), and other related mechanisms.

They also found that CBD also has positive effects on attenuating psychotic-, anxiety- and depressive-like behaviours, which taken together with its neuroprotective and neurogenesis properties, makes CBD a potential therapeutic agent for neuropsychiatric disorders.

In another 2016 study published in Frontiers in Pharmacology, however this time on animals, scientists investigated the efficacy of CBD in preventing motor and cognitive impairments induced in rats.

The induced tardive dyskinesia (motor impairment) that is accompanied by cognitive deficits in rats through the repeated administration of reserpine. Male Wistar rats received four injections of CBD (0.5 or 5 mg/kg) or a placebo from day two to five after symptoms onset. On days 3 and 5, the animals also received one injection of 1 mg/kg reserpine or vehicle. Locomotor activity, vacuous chewing movements, and catalepsy were assessed from days one to seven. On days eight and nine, they evaluated animals’ performance on the plus-maze discriminative avoidance task, for learning/memory assessment.

They found that both CBD dosages of 0.5 and 5 mg/kg was able to reduce motor and cognitive impairments that is suggestive of it being an effective and safe pharmacological intervention for reducing tardive dyskinesia and cognitive impairments in neurodegenerative diseases.

From the data they found that CBD how 51–84% protection against the huntingtin-induced cell death caused by the huntingtin gene that causes Huntington’s disease, possibly by exert a protective effect through antioxidant mechanisms. In addition, they found that CBD reverses or attenuates 3-NP-induced alterations in the mRNA for antioxidant enzymes that reduces striatal (a cluster of neurons in the subcortical basal ganglia of the forebrain) damage and oxidative injury.

They concluded that from the data reviewed CBD plays a protective role in the treatment and/or prevention of some movement disorders and seems to be especially effective in treating both primary and secondary dystonic movements. They do however mention that in the case of Huntington’s disease, combining CBD with Δ9-THC in a 1:1 ratio (as in Sativex) is preferred for optimal benefits.

Anecdotal Evidence

As with the review study above, most Huntingdon’s patients that use cannabinoids for symptom relief use medical cannabis or a combination of CBD and THC. However, the internet is full of stories like this one, of people claiming that they have had life-changing improvements in their condition. Nonetheless, for patients that do not have access to medical cannabis, CBD can still be effective for symptom relief at the right dosages.

CBD as a Complementary Treatment in Huntingdon’s disease

In addition, CBD can be helpful as a complementary therapy for patients with Huntington’s disease in other ways. As mentioned, many patients have co-existing conditions like depression, anxiety and in the case of juvenile Huntington’s, seizures with which CBD can help. CBD’s powerful anticonvulsant properties can help prevent, control and reduce seizures. Similarly, as an anti-depressant, CBD can help alleviate the clinical depression that is commonly experienced with Huntington’s while its anxiolytic properties can help control anxiety and hyperactivity.

Bottom Line

To date, research on CBD for Huntington’s disease is still rare, with more focus being on investigating Sativex – a drug with a 1:1 ration of CBD to THC. However, CBD does have several properties that can directly help manage and reduce many Huntington’s disease symptoms such as oxidative stress, inflammation, tardive dyskinesia and cognitive decline. For instance, it has repeatedly been shown that CBD has neuroprotective, antispasmodic, anxiolytic, anti-depressant, anti-oxidant and anti-inflammatory properties. This also makes CBD a powerful ally when used as a complementary therapy for depression and anxiety. If you are considering using CBD for Huntington’s disease, always speak to your treating physician first. CBD is contraindicated with use with certain medications. They can also monitor dosage, symptom severity and other clinical parameters, to ensure that your CBD treatment is both safe and effective.

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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.

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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.

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