How to take cbd oil for als

CBD Oil for ALS (Lou Gehrig’s Disease)

ALS, also known as Lou Gehrig’s disease, is a degenerative disorder. Researchers named this disorder after the famous baseball legend Lou Gehrig, who was the first to be formally diagnosed with the condition. Characteristics of this disorder include gradually worsening muscle control and strength, which can eventually involve the inability to speak or swallow.

Most modern treatments for ALS focus on palliative care rather than curative solutions. Medical experts help patients to deal with chronic pain and discomfort, while also striving to extend life expectancy.

However, new research concerning ALS is underway. In recent years, there has been a focus on using cannabinoids, such as cannabidiol, to address ALS’s symptoms. This article addresses burgeoning research regarding possible uses of CBD in managing ALS symptoms. Various ways in which ALS can affect patients will also be discussed and examined.

What Is ALS?

ALS, or Amyotrophic Lateral Sclerosis, is a degenerative disease that causes the muscles in the body to weaken and atrophy. This makes it challenging to move the limbs, but it also adversely affects many functions within the body, including respiration and swallowing. With no known cure, ALS eventually leads to death by respiratory failure, as the body becomes incapable of even breathing properly without aid.

Common ALS Treatment Options

Unfortunately, despite the best efforts of scientists everywhere, there are currently no useful medical treatments that work to prevent or treat ALS. Instead, most medical professionals attempt to delay the onset of worsening symptoms.

Doctors often recommend ALS support group plans that work to improve the mental health of sufferers. It is also beneficial for patients as they can connect to others with the same diagnosis.

Since its approval in 1995, Riluzole, under the brand name Rilutek, has been the primary ALS treatment option. The drug works to slow the progression of ALS, all while prolonging the sufferer’s life expectancy after diagnosis.

The main problem is that these drugs are prohibitively expensive, at least in the USA, and they also tend to create extremely unpleasant side effects.

For example, patients commonly report excessive nausea, stomach pain, and general flu-like symptoms after regularly taking Riluzole, forcing them to choose between long-term health and short term pain.

However, CBD may address the side effects of drugs such as Riluzole, allowing patients to have less stress and discomfort. CBD may assist in making patients’ lives easier, allowing doctors and specialists to concentrate on long-range options and care.

What Is CBD & What Can It Do?

CBD is a chemical compound that works with the body to produce a variety of beneficial effects, many of which can mitigate symptoms.

It works because the body already has an endocannabinoid system (ECS), a health system designed to work with cannabinoids naturally. It is responsible for many different responses within the body, such as the release of helpful neurochemicals and even the body’s inflammatory response.

Most conditions that CBD may mitigate are related to these bodily responses – a reduction in anxiety as a result of interaction with the serotonin receptor, or controlling the pain of arthritis by helping diminish the inflammation. These are just two widespread uses of CBD.

What Do the Studies Say?

Over the years, more and more researchers have conducted studies to show CBD’s efficacy as a way to help those with ALS.

One example is a report by Sabrina Giacoppo and Emanuela Mazzon for the Journal of Neural Regenerative Research. It investigated the effects of various cannabinoid compounds on ALS progression and mortality.

The researchers found that delta-9-tetrahydrocannabinol (THC), cannabinol (CBN), Sativex (a 1:1 mixture of THC and CBD), and other compounds had positive effects. They included reducing oxidative stress, protecting the nervous system, and slowing disease progression.

Most of these findings were based on animal studies, meaning further research is warranted. However, the authors concluded: “…there is a valid rationale to propose the use of cannabinoid compounds in the pharmacological management of ALS patients. Cannabinoids indeed are able to delay ALS progression and prolong survival.”

Despite the lack of human clinical trials, a case report by Gerhard Nahler discussed the effects of co-medication with cannabidiol on ALS symptoms.

Co-medication works by pairing CBD with another conventionally used drug, as certain medications seem to work together and produce an increased efficacy rate. Experts observe this in those who have epilepsy, where they note a reduction in seizures when patients take a mixture of CBD and the conventional epilepsy drug, Clobazam.

The report demonstrated that CBD and Riluzole delayed the progression of the disease in a patient recently diagnosed with ALS. It improved symptoms such as muscle weakness and difficulties with speech and swallowing for approximately 12 months.

Finally, a 2019 study investigated the effects of CBD with THC on spasticity in 32 ALS patients. It found that there was a high level of satisfaction with the treatment, especially among those with moderate to severe symptoms. The researchers state that “THC:CBD may serve as a valuable addition in the spectrum of symptomatic therapy in ALS.” However, they also suggest that further research is necessary.

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So Is CBD Oil Only Useful as a Co-Medication?

All this might lead some to believe that the only use CBD oil has is in conjunction with conventional drugs used to treat ALS.

However, while CBD oil can be useful when combined with other drugs, the fact remains that those taking CBD oil still enjoy the various potential benefits that this unique oil would provide. For example, CBD users have stated that this substance reduces stress, increases relaxation, and eases pain, and it is known to have pain-relieving and anti-anxiety properties.

Another potential benefit of CBD for ALS patients is its ability to regulate the immune system and quell inflammation. Experts have suggested that immune dysfunction may contribute to the development of ALS and research has shown that people with the condition often have excessive levels of inflammation.

Although there is currently no evidence that CBD can reduce inflammation in ALS, specifically, it may well have positive effects. While CBD seems to be a worthwhile option, some might be wondering why patients use CBD oil rather than whole-plant, medical marijuana. , In fact, there are a few reasons why some experts don’t recommend regular cannabis for treating ALS.

Why Not Just Smoke Regular Marijuana?

While there are many people who smoke cannabis regularly to manage many of the underlying symptoms of ALS, there are a few significant drawbacks that make taking CBD oil a preferable option.

For starters, THC’s psychogenic effects can potentially be a problem for those with ALS. While some people may find the high pleasant, others may not enjoy the sensation. Furthermore, THC can cause various side effects, including dizziness, confusion, or increased anxiety levels.

Furthermore, marijuana sales are not currently allowed in a variety of jurisdictions in the USA, making it all the more difficult for doctors to recommend it as a useful option to assist with ALS symptoms.

There is also a more practical issue with smoking cannabis – the ability to smoke it at all. As ALS develops, the ability to breathe independently can be impaired, making it challenging to attempt to smoke marijuana. This is often one of the main reasons why CBD oil is preferable, as it is far easier to take for someone with reduced motility.

Final Verdict About CBD Oil for ALS

ALS patients may now use CBD oil to mitigate or reduce their symptoms as it is readily available in many places. Studies show that there is great promise in how people can benefit from CBD.

Although there is still plenty of research to be done, CBD oil seems to be a compelling choice for those looking to lessen the effects of many ALS symptoms.

Can cannabinoids be a potential therapeutic tool in amyotrophic lateral sclerosis?

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.


Amyotrophic lateral sclerosis (ALS) is the most common degenerative disease of the motor neuron system. Over the last years, a growing interest was aimed to discovery new innovative and safer therapeutic approaches in the ALS treatment. In this context, the bioactive compounds of Cannabis sativa have shown antioxidant, anti-inflammatory and neuroprotective effects in preclinical models of central nervous system disease. However, most of the studies proving the ability of cannabinoids in delay disease progression and prolong survival in ALS were performed in animal model, whereas the few clinical trials that investigated cannabinoids-based medicines were focused only on the alleviation of ALS-related symptoms, not on the control of disease progression. The aim of this report was to provide a short but important overview of evidences that are useful to better characterize the efficacy as well as the molecular pathways modulated by cannabinoids.

Keywords: amyotrophic lateral sclerosis, cannabinoids, symptomatic ALS treatment, experimental ALS model, clinical trials, mechanisms of neuroprotection

Amyotrophic Lateral Sclerosis (ALS)

Amyotrophic lateral sclerosis (ALS) is the most common degenerative disease of the motor neuron system. The incidence is about 1–3 cases per 100,000 population per year. In Italy it is estimated that at least 3,500 patients and 1,000 new cases per year ( ALS is characterized by relentless progression of muscle wasting and weakness 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 (Zarei et al., 2015).

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The most abundant forms of ALS are sporadic (90%), but the disease may be also familiar (10%), associated with mutations in the superoxide dismutase-1 gene (SOD-1), that encodes for a key antioxidant enzyme, and also in TAR-DNA binding protein-43 (TDP-43) and FUS (fused in sarcoma) which encode proteins involved in pre-mRNA splicing, transport and stability (Hardiman et al., 2011). Recently, mutation in non-coding hexanucleotide repeat sequence (GGGGCC) in the C9orf72 gene was considered as the most common genetic cause of ALS (Matamala et al., 2016). The exact function of this protein remains undefined; however, it seems to play a major role in cellular trafficking, mainly in neurons (Williams et al., 2013). The C9orf72 mutation was found also in frontotemporal dementia (FTD) patients (Farg et al., 2014). Since 20% of ALS patients develops dementia with a frontotemporal phenotype, this mutation may explain the link between familial FTD and ALS (Farg et al., 2014).

Although the pathogenic mechanisms that underlie ALS are yet unknown, it is believed that ALS could have a multifactorial etiology, where environmental factors can greatly contribute to pathology triggering. Moreover, several mechanisms including mitochondrial dysfunction, protein aggregation, oxidative stress, excessive glutamate activity, inflammation and apoptosis are involved in ALS pathogenesis leading to motor neuron cell death in the brain and spinal cord (Zarei et al., 2015).

To date, the only therapy available for ALS is the glutamate-antagonist riluzole that was able to inhibit the presynaptic release of glutamate, most likely by blockade of voltage-gated sodium channels. However, riluzole has limited therapeutic efficacy and also it is able to moderately prolong patient survival (Miller et al., 2007). Therefore, new innovative and safer therapeutic approaches are urgently needed, at least aimed at delaying the neurodegenerative processes of the ongoing disease.

Over the last years, a growing interest has been focused to cannabinoids, the bioactive compounds of Cannabis sativa, for their antioxidant, anti-inflammatory and anti-excitotoxic effects exhibited in preclinical models of central nervous system disease (Croxford, 2003). Here, we provided an overview of the potential usefulness of cannabinoid agents in the management of ALS.

Overview on Cannabinoids

The Cannabis plant, also known as marijuana, contains over 500 natural compounds and about 70 of these are classified as cannabinoids (Fischedick et al., 2009). The discovery of Δ9 -tetrahydrocannabinol (THC) as the major psychoactive principle in Cannabis, as well as the identification of numerous non-psychoactive cannabinoids such as cannabidiol (CBD), cannabigerol (CBG), cannabinol (CBN), cannabichromene (CBC), Δ9 -tetrahydrocannabivarin ( Δ9 -THCV) and cannabidivarin (CBDV), has led to a significant growth in research aimed at understanding the therapeutic effects of these compounds.

Cannabinoids exert many of their activities by binding cannabinoid (CB) receptors. To date, two types of receptors have been identified to have different tissue distribution and mechanisms of signaling. CB1 receptors are expressed mainly on neurons and glial cells in various parts of the brain, CB2 receptors are found predominantly in the cells of immune system. Both CB1 and CB2 receptors belong to the family of G-protein coupled receptors (GPCRs) that, after cannabinoid agonist binding and signaling, exert an inhibitory effect on adenylate cyclaseactivity, activation of mitogen-activated protein kinase, regulation of calcium and potassium channels, and other signal transduction pathways (Munro et al., 1993). Moreover, there is increasing evidence supporting the existence of additional cannabinoid receptors (no-CB1 and no-CB2) in both central and peripheral system, identified in CB1 and CB2-knockout mice, involving intracellular pathways that play a key role in neuronal physiology. This kind of receptors includes transient receptor potential vanilloid type 1 (TRPV1), G protein-coupled receptor 55 (GPR55), G protein-coupled receptor 18 (GPR18), G protein-coupled receptor 119 (GPR119) and 5-hydroxytryptamine receptor subtype 1A (5-HT1A) (Pertwee et al., 2010). Δ9 -THC, of which is well-known psychotropic effects, is believed to perform the majority of itsactions in the CNS binding CB1 and CB2 receptors. Non-psychotrophic phytocannabinoids exert multiple pharmacological effects via CB1/CB2 receptors as well as no-CB1 and no-CB2 receptors (Pertwee et al., 2010).

Overall, recent studies showed that cannabinoids inhibit the release of pro-inflammatory cytokines and chemokine in neurological preclinical models suppressing in this way the inflammatory response (Velayudhan et al., 2014). They show also a potent action in inhibiting oxidative and nitrosative stress, modulating the expression of inducibile nitric oxide synthase and reducing the production of reactive oxygen species (ROS) (Velayudhan et al., 2014). Moreover, cannabinoids were found to exert anti-glutamatergic action by inhibiting glutamate release and enhancing the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) (Croxford, 2003). Just about all these properties exhibited by these compounds, have prompted researchers to investigate their potential therapeutic effects in ALS, providing interesting results.

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Neuroprotective Effects of Cannabinoids in Experimental Model of ALS

Recent in vivo studies support that cannabinoids may be beneficial as neuroprotective agents in ALS. The most commonly used murine model for human ALS is the hSOD (G93A) transgenic mouse, which is genetically engineered to develop clinical symptoms similar to those observed in humans with ALS.

Treatment with Δ9-THC in ALS hSOD(G93A) mice, either before or after signs onset, improves motor impairment and increases survival by 5% probably via its anti-glutamatergic and anti-oxidant activity (Raman et al., 2004). Moreover, it was demonstrated that Δ9 -THC attenuates oxidative stress in ALS hSOD(G93A) mouse spinal cord primary cultures, that were exposed to the oxidant tert-butyl hydroperoxide (TBH) in the presence of Δ9 -THC and SR141716A, the CB1 receptor antagonist, as assessed by lactate dehydrogenase (LDH) and SOD-1 release. Specifically, the antioxidant effect of Δ9 -THC was not CB1-receptor mediated; since the CB1 receptor antagonist SR141716A did not diminish the antioxidant effect (Raman et al., 2004). Δ9 -THC was found also to protect against excitotoxicity produced by kainic acid in primary neuronal cultures, obtained from ALS hSOD(G93A) mouse spinal cord, by activation of CB1 receptor. In this case, the neuroprotective effect was blocked with the CB1 receptor antagonist, SR141716A, indicating a receptor-mediated effect (Raman et al., 2004). Therefore, treatment with cannabinoids may reduce elevated glutamate levels observed during ALS by modulating excitotoxicity events.

Moreover, treatment with cannabinol (CBN), a non-psychotropic cannabinoid, through its residual affinity to CB1 receptors, is able to delay significantly disease onset in ALS hSOD(G93A) mice subcutaneously implanted with osmotic mini-pumps. However, the molecular mechanisms remain undefined. On the contrary, survival was not affected (Weydt et al., 2005).

Likewise, a significant delay in disease progression was found when CB1/CB2 receptor agonist WIN 55,212-2 was intraperitoneally administered to ALS hSOD(G93A) mice beginning after onset of motor impairment and tremor (at 90 days old), however, survival was not extended (Bilsland et al., 2006). Genetic ablation of the fatty acid amide hydrolase (FAAH) enzyme, which results in raised levels of the endocannabinoid anandamide, prevented the appearance of disease signs in 90-day-old to ALS hSOD(G93A) mice. However, elevation of cannabinoid levels with either WIN55, 212-2 or FAAH ablation had no effect on life span. On the contrary, CB1 deletion had no effects on disease onset in ALS hSOD(G93A) mice, but extend lifespan by 15 days, a 13% increase in survival. Therefore, the beneficial effects exhibited by cannabinoids may be mediated by non-CB1 receptors, but presumably by CB2 ones. Moreover, the neuroprotective effects of cannabinoids were ascribed to a decrease of microglial activation, presynaptic glutamate release and formation of ROS (Bilsland et al., 2006).

Also, it was demonstrated that mRNA, receptor binding and function of CB2, but not CB1, receptors are dramatically and selectively up-regulated in the spinal cords of ALS hSOD(G93A) mice in a temporal pattern paralleling disease progression (Shoemaker et al., 2007). It was found that daily intraperitoneal administration of the selective CB2 agonist, AM-1241, initiated after disease onset in ALS hSOD(G93A) mice, delayed motor impairment and increased survival by 56%. The beneficial effects of cannabinoids could potentially be mediated via CB2 receptor-mediated suppression of microglial/macrophage activation in the spinal cords of symptomatic G93A mice and that CB2 receptors are selectively up-regulated in spinal cords as a compensatory, protective measure (Shoemaker et al., 2007).

Few years ago, the neuroprotective effects of a mixture of two extracts in approximately a 1:1 ratio (2.7 mg of Δ9 -THC and 2.5 mg of CBD) commercially known as Sativex® were investigated by using ALS hSOD(G93A) transgenic mice (Moreno-Martet et al., 2014). Sativex® was found to be effective in delaying ALS progression in the early stages of disease and in animal survival, although the efficacy was decreased during progression of disease. Also, it has been demonstrated that changes occur in endocannabinoid signaling, particularly a marked up-regulation of CB2 receptors in SOD(G93A) transgenic mice together with an increase of N-acyl phosphatidylethanolamine phospholipase D (NAPE-PLD) enzyme, which is responsible for the generation of anandamide (N-arachidonoylethanolamine), the ligand of cannabinoid and vanilloid receptors (Moreno-Martet et al., 2014). Therefore, the efficacy of cannabinoids in slowing ALS progression, in extending life expectancy and in reducing the overall gravity of the disease is mainly due to activation of CB2 receptors. More specifically, it was widely demonstrated that drugs activating CB2 receptors, expressed predominantly in immune cells and non-neuronal tissues, successfully improve the symptoms of several inflammatory diseases (Walter and Stella, 2004). However, further studies are necessary to assess the neuroprotective effects of cannabinoids that target CB2 receptors. Molecular mechanisms underlying cannabinoids-driven neuroprotective effects in ALS hSOD(G93A) mice model are illustrated in Figure 1 .

Schematic illustration of the neuroprotective mechanisms of action of cannabinoids into ALS hSOD(G93A) mice.