Background and purpose
This study aimed to assess the prevalence of illicit drug use among epilepsy patients and its effects on the disease.
New research published in Epilepsia, a journal of the International League Against Epilepsy (ILAE), suggests that an investigational neurological treatment derived from cannabis may alter the blood levels of commonly used antiepileptic drugs. It is important for clinicians to consider such drug interactions during treatment of complex conditions.
Cannabidiol (CBD), a compound developed from the cannabis plant, is being studied as a potential anticonvulsant, and it has demonstrated effectiveness in animal models of epilepsy and in humans. An ongoing open label study (Expanded Access Program) conducted by investigators at the University of Alabama at Birmingham is testing the potential of CBD as a therapy for children and adults with difficult to control epilepsy. The study includes 39 adults and 42 children, all of whom receive CBD.
Because all of the participants are also taking other seizure drugs while they are receiving the investigational therapy, investigators checked the blood levels of their other seizure drugs to see if they changed. “With any new potential seizure medication, it is important to know if drug interactions exist and if there are labs that should be monitored while taking a specific medication,” said lead author Tyler Gaston, MD.
Dr. Gaston and her colleagues found that there were significant changes in levels of the drugs clobazam (and its active metabolite N-desmethylclobazam), topiramate, and rufinamide in both adults and children, and zonisamide and eslicarbazepine in adults only. Except for clobazam/desmethylclobazam, however, the drug levels did not change outside of the normally accepted range. In addition, adult participants in the study taking clobazam reported sedation more frequently.
Tests also showed that participants taking valproate and CBD had higher ALT and AST (liver function tests) compared with participants not taking valproate. Very high ALT and AST indicate abnormal liver function, but significant ALT and AST elevation occurred only in a mall number of participants (4 children and 1 adult), and the levels returned to normal after discontinuation of valproate and CBD.
“While the interaction between CBD and clobazam has been established in the literature, there are currently no published human data on CBD’s potential interactions with other seizure medications,” said Dr. Gaston. “However, given the open label and naturalistic follow-up design of this study, our findings will need to be confirmed under controlled conditions.”
The findings emphasize the importance of monitoring blood levels of antiepileptic drugs as well as liver function during treatment with CBD. “A perception exists that since CBD is plant based, that it is natural and safe; and while this may be mostly true, our study shows that CBD, just like other antiepileptic drugs, has interactions with other seizure drugs that patients and providers need to be aware of,” said Dr. Gaston.
Article: Interactions between cannabidiol and commonly used antiepileptic drugs, Tyler E. Gaston, E. Martina Bebin, Gary R. Cutter, Yuliang Liu, Jerzy P. Szaflarski, and for the UAB CBD Program, Epilepsia, doi: 10.1111/epi.13852, published online 6 August 2017.
This study aimed to assess the prevalence of illicit drug use among epilepsy patients and its effects on the disease.
We systematically interviewed epilepsy outpatients at a tertiary epilepsy clinic. Predictors for active cannabis use were analysed with a logistic regression model.
Overall, 310 subjects were enrolled; 63 (20.3%) reported consuming cannabis after epilepsy was diagnosed, and 16 (5.2%) used other illicit drugs. Active cannabis use was predicted by sex (male) [odds ratio (OR) 5.342, 95% confidence interval (95% CI) 1.416–20.153] and age (OR 0.956, 95% CI 0.919–0.994). Cannabis consumption mostly did not affect epilepsy (84.1%). Seizure worsening was observed with frequent illicit (non-cannabis) drug use in 80% of cases.
Cannabis use does not seem to affect epilepsy; however, frequent use of other drugs increases seizure risk.
The hottest issue right now in the canna-sphere has to be the new information released and verified by the Federal Government about how cannabis can cure certain forms of cancer. However, just because the US Gov’t didn’t recognize these effects, doesn’t mean that private science didn’t. Literally hundreds of private studios were conducted and found these results. Why has it taken the Federal Gov’t so long to admit this? and now that they have, why arent they doing anything about it?
Here are 20 studys that show cannabis cures certain forms of cancer.
Cannabis has been making a lot of noise lately. Multiple states across the United States, along with many countries around the world, have successfully legalized medical marijuana, and the Uruguay parliament recently voted to create the world’s first legal marijuana market.
This is good news, as the health benefits of cannabis are vast, with multiple medical and scientific studies to confirm them. But what about the harmful effects? All psychological evaluations from the intake of cannabis are largely based on assumptions, suggestions, and observations (1). When we look at the actual science behind cannabis, it seems negative effects are difficult to confirm.
Let’s take a look at the science behind cannabis and cancer. Although cannabis has been proven to be effective for a wide range of ailments, this article will focus mainly on its effectiveness in the treatment of cancer. Cannabinoids may very well be one of the best disease and cancer fighting treatments out there. Cannabinoids refer to any of a group of related compounds that include cannabinol and the active constituents of cannabis. They activate cannabinoid receptors in the body. The body itself produces compounds called endocannabinoids and they play a role in many processes within the body that help to create a healthy environment. Cannabinoids also play a role in immune system generation and re-generation. The body regenerates best when it’s saturated with Phyto-Cannabinoids.
There is growing interest in the therapeutic potential of marijuana (cannabis) and cannabinoid-based chemicals within the medical community and, particularly, for neurological conditions. This interest is driven both by changes in the legal status of cannabis in many areas and increasing research into the roles of endocannabinoids within the central nervous system and their potential as symptomatic and/or neuroprotective therapies. We review basic science as well as preclinical and clinical studies on the therapeutic potential of cannabinoids specifically as it relates to movement disorders. The pharmacology of cannabis is complex, with over 60 neuroactive chemicals identified to date. The endocannabinoid system modulates neurotransmission involved in motor function, particularly within the basal ganglia. Preclinical research in animal models of several movement disorders have shown variable evidence for symptomatic benefits, but more consistently suggest potential neuroprotective effects in several animal models of Parkinson’s (PD) and Huntington’s disease (HD). Clinical observations and clinical trials of cannabinoid-based therapies suggests a possible benefit of cannabinoids for tics and probably no benefit for tremor in multiple sclerosis or dyskinesias or motor symptoms in PD. Data are insufficient to draw conclusions regarding HD, dystonia, or ataxia and nonexistent for myoclonus or RLS. Despite the widespread publicity about the medical benefits of cannabinoids, further preclinical and clinical research is needed to better characterize the pharmacological, physiological, and therapeutic effects of this class of drugs in movement disorders.
The American Academy of Neurology published an evidence-based systematic review of randomized controlled trials using marijuana (Cannabis sativa) or cannabinoids in neurologic disorders. Several cannabinoids showed effectiveness or probable effectiveness for spasticity, central pain, and painful spasms in multiple sclerosis.
The review justifies insurance coverage for dronabinol and nabilone for these indications. Many insurance companies already cover these medications for other indications. It is unlikely that the review will alter coverage for herbal marijuana. Currently, no payers cover the costs of herbal medical marijuana because it is illegal under federal law and in most states. Cannabinoid preparations currently available by prescription may have a role in other neurologic conditions, but quality scientific evidence is lacking at this time.
Endocannabinoids: Windows to the Brain
Katherine H. Taber, Ph.D. and Robin A. Hurley, M.D.
Cannabis sativa (hemp) is a flowering annual that has been in use as a structural material (cordage, cloth, paper) and in medicine for thousands of years.5–7 Reference to the psychoactive effects of its phytochemical products have been found in writing throughout the ancient world. Cannabis herb (marijuana) is made by drying the leaves and flowering tops. Cannabis resin (hashish) is made by collecting the fluid secreted by the plant during the flowering phase.
A recent review indicates that studies of this plant have identified more than 500 compounds within the plant.6 The principle psychoactive cannabinoids in Cannabis sativa are 8 and 9 tetrahydrocannabinol (THC)6,7 9 THC is considered the major psychoactive constituent as it is considerably more abundant in the plant and more potent in effect. The amount of 9 THC varies greatly across plant strains and is also affected by farming and preparation techniques.8Studies suggest an increasing content of 9 THC in street cannabis over the past few decades (e.g., 1.5% in 1980, 4.47% in 1997, 5.11% in 2002).8 9 THC is converted to 11-hydroxy-9 THC in the lungs and liver.7 Onset of action depends on both dose and method of administration. Following ingestion by smoking, initial effects may appear within the first minute, whereas following oral ingestion first effects may appear in 15–30 minutes.8,9 Onset, duration and nature of action (pleasant versus unpleasant) are affected by other factors, as well, such as individual differences in absorption, method of smoking, previous history, anxiety level, and environmental context.8,10Early acute effects commonly include light-headedness and euphoria, with some individuals experiencing tachycardia and hypotension. Later acute effects may include time dilation, relaxation, increased body awareness, increased appetite, sleepiness, impaired memory, and impaired concentration.7–9,11 Adverse reactions do occur (e.g., anxiety, panic, paranoia, psychotic symptoms), but are much less common.8,9,11,12 Functional imaging studies indicate that intoxication is associated with increased regional cerebral blood flow and metabolism, particularly in frontal and limbic regions as well as the cerebellum.8
Both tolerance and dependence can develop with chronic use.9,11–13 Withdrawal is characterized by nervousness, tension, anxiety, and sleep disturbances. While long-term cognitive impairment has been reported in some studies, the evidence for this is not strong.7–9,11,12 Some studies support an influence of cannabis use on the development of psychiatric disorders, particularly schizophrenia and mood disorders.11,12,14
A surge in research into the mechanism of action for 9 THC in the brain followed its isolation and identification in the 1960s.6 This led to the identification of endogenous cannabinoid (endocannabinoid) receptors in brain tissue. Research intensified following the cloning of these receptors (CB1 and CB2) in the early 1990s.6,7,15,16 Identification of the first endocannabinoid, N-arachidonoylethanolamine (anandamide, from the Sanskrit for “eternal bliss”) was achieved soon after.6 A decade later the modulatory action of endocannabinoids at synapses was discovered.17 Both the CB1 and CB2 receptors are cell surface proteins that span the membrane and are coupled intracellularly to one of the G-proteins.7,16–18 The distributions and actions of the CB1 and CB2 receptors are quite different.6,7,9,15–19 CB1 receptors are located predominately on axon terminals in both the central and peripheral nervous system and on some peripheral tissues (e.g., liver, gut, adrenal, muscle, fat). CB2 receptors are found principally peripherally on immune cells (e.g., spleen, macrophages, tonsils, monocytes, neutrophils), and were originally not thought to occur in the brain. More recently they have been identified on both neurons and glial cells, where they may participate in immune functions.6,7,9,17,20–22 This article will focus on the CB1 receptor and compounds that interact with it, as this system mediates most or all of the psychotropic actions of cannabinoids.
…If an epilepsy patient and their doctor feel that marijuana is their best treatment option then they need to have safe, legal access to medical marijuana and they need that access now…