Since cannabis has been shown to be harmless and non-toxic in numerous studies, researchers and many neurologists are currently recommending that ALL patients who have been diagnosed with ALS should begin cannabis therapy immediately. Researchers have discovered that a concentration of cannabinoids as found in cannabis, especially a derivative such as cannabis oil, is extremely therapeutic in the slowing of the progression of ALS, thanks to these and other studies addressing similar neurodegenerative disease states.These patients have a life expectancy of less than five years.
Says one expert who requested to remain anonymous:
"People have been using cannabis as a medicine for thousands of years. If it were me or my family member, we would be utilizing every possible administration of these neuroprotective substances, even if we were forced to move or break the law." Our source continued. "I mean seriously, what does a patient with ALS have to lose? We have shown clinically that this is a treatment with actual real time benefits that actually slow the progression of this horrid disease. What possible side effect could cannabis and its derivatives have that would make death preferable to the side effects?"A review of the scientific literature reveals an absence of clinical trials investigating the use of cannabinoids for ALS treatment. However, recent preclinical findings indicate that cannabinoids can delay ALS progression, lending support to anecdotal reports by patients that cannabinoids may be efficacious in moderating the disease’s development and in alleviating certain ALS-related symptoms such as pain, appetite loss, depression and drooling.Legal access to medicinal cannabis in the UK - SATIVEX
In 2006 the Home Office licensed Sativex so that:
– Doctors, at their own risk, could privately prescribe,
– Pharmacists could possess and dispense, and named patients with a prescription could possess.
Some studies:-
http://www.ncbi.nlm.nih.gov/pubmed/15204022
Effective treatment for amyotrophic lateral sclerosis (ALS) remains elusive. Two of the primary hypotheses underlying motor neuron vulnerability are susceptibility to excitotoxicity and oxidative damage. There is rapidly emerging evidence that the cannabinoid receptor system has the potential to reduce both excitotoxic and oxidative cell damage. Here we report that treatment with Delta(9)-tetrahydrocannabinol (Delta(9)-THC) was effective if administered either before or after onset of signs in the ALS mouse model (hSOD(G93A) transgenic mice). Administration at the onset of tremors delayed motor impairment and prolonged survival in Delta(9)-THC treated mice when compared to vehicle controls. In addition, we present an improved method for the analysis of disease progression in the ALS mouse model. This logistic model provides an estimate of the age at which muscle endurance has declined by 50% with much greater accuracy than could be attained for any other measure of decline. In vitro, Delta(9)-THC was extremely effective at reducing oxidative damage in spinal cord cultures. Additionally, Delta(9)-THC is anti-excitotoxic in vitro. These cellular mechanisms may underlie the presumed neuroprotective effect in ALS. As Delta(9)-THC is well tolerated, it and other cannabinoids may prove to be novel therapeutic targets for the treatment of ALS.
http://www.ncbi.nlm.nih.gov/pubmed/11467101
Marijuana has been proposed as treatment for a widening spectrum of medical conditions. Marijuana is a substance with many properties that may be applicable to the management of amyotrophic lateral sclerosis (ALS). These include analgesia, muscle relaxation, bronchodilation, saliva reduction, appetite stimulation, and sleep induction. In addition, marijuana has now been shown to have strong antioxidative and neuroprotective effects, which may prolong neuronal cell survival. In areas where it is legal to do so, marijuana should be considered in the pharmacological management of ALS. Further investigation into the usefulness of marijuana in this setting is warranted.
http://www.ncbi.nlm.nih.gov/pubmed/18781981
Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative condition characterised by the selective loss of motor neurons from the spinal cord, brainstem and motor cortex. Although the pathogenic mechanisms that underlie ALS are not yet fully understood, there is significant evidence that several neurotoxic mechanisms including excitotoxicity, inflammation and oxidative stress, all contribute to disease pathogenesis. Furthermore, recent results have established that although primarily a motor neuron specific disorder, ALS is not cell-autonomous and non-neuronal cells including astroglia and microglia play a critical role in mechanism of disease. Currently the only licensed therapy available for the treatment of ALS is the anti-glutamatergic agent Riluzole, which has limited therapeutic effects. However, there is increasing evidence that cannabinoids and manipulation of the endocannabinoid system may have therapeutic value in ALS, in addition to other neurodegenerative conditions. Cannabinoids exert anti-glutamatergic and anti-inflammatory actions through activation of the CB(1) and CB(2) receptors, respectively. Activation of CB(1) receptors may therefore inhibit glutamate release from presynaptic nerve terminals and reduce the postsynaptic calcium influx in response to glutamate receptor stimulation. Meanwhile, CB(2) receptors may influence inflammation, whereby receptor activation reduces microglial activation, resulting in a decrease in microglial secretion of neurotoxic mediators. Finally, cannabinoid agents may also exert anti-oxidant actions by a receptor-independent mechanism. Therefore the ability of cannabinoids to target multiple neurotoxic pathways in different cell populations may increase their therapeutic potential in the treatment of ALS. Recent studies investigating this potential in models of ALS, in particular those that focus on strategies that activate CB(2) receptors, are discussed in this review.
Therapeutic options for amyotrophic lateral sclerosis (ALS), the most common adult-onset motor neuron disorder, remain limited. Emerging evidence from clinical studies and transgenic mouse models of ALS suggests that cannabinoids, the bioactive ingredients of marijuana (Cannabis sativa) might have some therapeutic benefit in this disease. However, Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the predominant cannabinoid in marijuana, induces mind-altering effects and is partially addictive, compromising its clinical usefulness. We therefore tested whether cannabinol (CBN), a non-psychotropic cannabinoid, influences disease progression and survival in the SOD1 (G93A) mouse model of ALS. CBN was delivered via subcutaneously implanted osmotic mini-pumps (5 mg/kg/day) over a period of up to 12 weeks. We found that this treatment significantly delays disease onset by more than two weeks while survival was not affected. Further research is necessary to determine whether non-psychotropic cannabinoids might be useful in ameliorating symptoms in ALS.
http://www.ncbi.nlm.nih.gov/pubmed/17241118
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss, paralysis and death within 2-5 years of diagnosis. Currently, no effective pharmacological agents exist for the treatment of this devastating disease. Neuroinflammation may accelerate the progression of ALS. Cannabinoids produce anti-inflammatory actions via cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2), and delay the progression of neuroinflammatory diseases. Additionally, CB2 receptors, which normally exist primarily in the periphery, are dramatically up-regulated in inflamed neural tissues associated with CNS disorders. In G93A-SOD1 mutant mice, the most well-characterized animal model of ALS, endogenous cannabinoids are elevated in spinal cords of symptomatic mice. Furthermore, treatment with non-selective cannabinoid partial agonists prior to, or upon, symptom appearance minimally delays disease onset and prolongs survival through undefined mechanisms. We demonstrate that mRNA, receptor binding and function of CB2, but not CB1, receptors are dramatically and selectively up-regulated in spinal cords of G93A-SOD1 mice in a temporal pattern paralleling disease progression. More importantly, daily injections of the selective CB2 agonist AM-1241, initiated at symptom onset, increase the survival interval after disease onset by 56%. Therefore, CB2 agonists may slow motor neuron degeneration and preserve motor function, and represent a novel therapeutic modality for treatment of ALS.
http://www.ncbi.nlm.nih.gov/pubmed/20439484
Significant advances have increased our understanding of the molecular mechanisms of amyotrophic lateral sclerosis (ALS), yet this has not translated into any greatly effective therapies. It appears that a number of abnormal physiological processes occur simultaneously in this devastating disease. Ideally, a multidrug regimen, including glutamate antagonists, antioxidants, a centrally acting anti-inflammatory agent, microglial cell modulators (including tumor necrosis factor alpha [TNF-alpha] inhibitors), an antiapoptotic agent, 1 or more neurotrophic growth factors, and a mitochondrial function-enhancing agent would be required to comprehensively address the known pathophysiology of ALS. Remarkably, cannabis appears to have activity in all of those areas. Preclinical data indicate that cannabis has powerful antioxidative, anti-inflammatory, and neuroprotective effects. In the G93A-SOD1 ALS mouse, this has translated to prolonged neuronal cell survival, delayed onset, and slower progression of the disease. Cannabis also has properties applicable to symptom management of ALS, including analgesia, muscle relaxation, bronchodilation, saliva reduction, appetite stimulation, and sleep induction. With respect to the treatment of ALS, from both a disease modifying and symptom management viewpoint, clinical trials with cannabis are the next logical step. Based on the currently available scientific data, it is reasonable to think that cannabis might significantly slow the progression of ALS, potentially extending life expectancy and substantially reducing the overall burden of the disease.
Legal access to medicinal cannabis in the UK
Legal access to medicinal cannabis within the UK is limited to the pharmaceutical cannabis based medicine Sativex. This can only be prescribed to MS sufferers and is at your doctors discretion, so differing postcodes can effect access. It should also be noted that although the NHS in Wales will subsidise Sativex, the NHS in England will not, so typical treatments can cost up to £500 a month. All other cannabis use or production in the UK is Illegal.
EIGHT things you need to know about Sativex:-
1. With the connivance of the UK Home Office and government, GW Pharmaceuticals has been allowed to develop a monopoly cannabis business against all the provisions of the Misuse of Drugs Act 1971 and the UN Single Convention on Narcotic Drugs 1961. Cannabis is a very effective and safe medicine for a wide variety of conditions but in order to facilitate GW’s monopoly, the British public has been systematically misled and misinformed by government propaganda. Most seriously, people in pain, suffering and disability, seeking to provide their own cannabis medicine, have been ruthlessly and cruelly pursued by a corrupt law enforcement policy.2. Sativex IS cannabis. It is pharmacologically identical to the plants from which it is made. It is NOT just an extract of THC and CBD, it contains all the cannabinoids, terpenes, flavonoids and other compounds included in cannabis. As GW founder and chairman, Geoffrey Guy, says “Most people in our industry said it was impossible to turn cannabis into a prescription medicine. We had to rewrite the rule book. We have the first approval of a plant extract drug in modern history. It has 420 molecules, whereas every other drug has just one.”3. Sativex DOES get you high, just as every form of cannabis (except industrial hemp). See the Sativex Summary of Product Characteristics (SPC) which describes “euphoric mood” as a “common” side effect.4. GW’s licence to cultivate cannabis issued in 1998 was for research purposes only. Since at least 2003, GW has been involved in commercial exploitation of cannabis and has therefore been acting unlawfully. The Home Secretary RETROSPECTIVELY LEGALISED GW’s licence by statutory instrument dated 13th March 2013. For the 10 years prior to that, GW, its directors and employees should have been subject to the same criminal penalties as anyone else producing a class B drug.5. GW is engaged with the Home Secretary in an unlawful conspiracy falsely to distinguish Sativex from cannabis.Note that when re-scheduling Sativex in schedule 4 it has used a 75 word definition whereas every other drug in all five other schedules is defined by one word. The definition of Sativex even includes its method of delivery by an oral-mucosal spray. No other drug is scheduled by its method of delivery.6. GW is engaged with the Home Secretary in an unlawful conspiracy to protect its unlawful monopoly of medicinal cannabis with the support of the British police which acts as armed enforcers of a private commercial interest.7. The Home Office overrides doctors prescriptions for medicinal cannabis produced by Bedrocan, the Dutch government’s official producer. Home Office officials intimidate and threaten GPs who write such prescriptions.8. Sativex is fantastically expensive. The NHS is charged at least 10 times the price for Sativex that organised crime sells cannabis for on the streets and between six and 17 times what Bedrocan is available for.
