Medical Marijuana Helps Cure Chronic Disease

Medical Marijuana Helps Cure Chronic Disease

“The medicinal power of Marijuana is well documented throughtout history

Back in 2700 BC, According to Chinese lore, the Emperor Shen Nung, considered the Father of Chinese medicine, in 2700 BC ,discovered the healing properties of Marijuana as well as Ginseng and Ephedra.

Throughout recorded history, the use of Medical Marijuana  has been linked to the ancient Egyptians, Persians, Greek civilizations, George Washington, Queen Victoria and even mainstream medicine by the 1840s.

From the 1850s to Y 1942, Marijuana was listed in the United States Pharmacopeia, an official public standards-setting authority for all prescription and over-the counter medicines, as a treatment for tetanus, cholera, rabies, dysentery, alcoholism, opiate addiction, convulsive disorders, insanity, excessive menstrual bleeding and many other health problems. My father was a Dental doctor and had a license to dispense the drug, pharmacies carried it back then.

During that same time frame prohibition gained popularity, that along with a growing “faith” in federal government.

By Y 1937, the United States passed its 1st federal law against Marijuana despite objections by the American Medical Association (AMA).

In fact, Dr. William C. Woodward, testifying on behalf of the AMA, told the US Congress:

“The American Medical Association knows of no evidence that Marijuana is a dangerous drug.”

He warned that a prohibition “loses sight of the fact that future investigation may show that there are substantial medical uses for Cannabis.”

Today, we see a growing trend of acceptance of Marijuana for its medicinal purposes.

Dr. Sanjay Gupta, CNN’s chief medical correspondent, reversed his Y 2009 opinion against Marijuana when he said, “We have been terribly and systematically misled for nearly 70 yrs in the United States, and I apologize for my own role in that.”

Now people including lawmakers are seeing the legalization of Marijuana in states like Colorado and Washington for “recreational” purposes. Most Americans are in favor of Medical Marijuana,  and the legalization of this drug.

The Big Q: why does the federal government want to ban its usage?

The Big A: it is all about control and money, and there is a major market for it, plus it poses a major threat to the pharmaceutical industry.

Below are just a few of the many health benefits associated with Medical Marijuana:

1. It can stop HIV from spreading throughout the body.
2. It slows the progression of Alzheimer’s.
3. It slows the spread of cancer cells.
4. It is an active pain reliever.
5. It can prevent or help with opiate addiction.
6. It combats depression, anxiety and ADHD.
7. It can treat epilepsy and Tourette’s.
8. It can help with other neurological damage, such as concussions and strokes.
9. It can prevent blindness from glaucoma.
10. Its connected to lower insulin levels in diabetics.

Contrary to popular notions, many patients  experience health benefits from Medical Marijuana without “getting stoned.””

http://www.livetradingnews.com/medical-marijuana-helps-cure-chronic-disease-55569.htm#.U6VjgZRX-uY

CB2 cannabinoid receptors as an emerging target for demyelinating diseases: from neuroimmune interactions to cell replacement strategies

Figure 2

“Amongst the various demyelinating diseases that affect the central nervous system, those induced by an inflammatory response stand out because of their epidemiological relevance. The best known inflammatory-induced demyelinating disease is multiple sclerosis, but the immune response is a common pathogenic mechanism in many other less common pathologies (e.g., acute disseminated encephalomyelitis and acute necrotizing haemorrhagic encephalomyelitis).

In all such cases, modulation of the immune response seems to be a logical therapeutic approach.

Cannabinoids are well known immunomodulatory molecules that act through CB1 and CB2 receptors. While activation of CB1 receptors has a psychotropic effect, activation of CB2 receptors alone does not. Therefore, to bypass the ethical problems that could result from the treatment of inflammation with psychotropic molecules, considerable effort is being made to study the potential therapeutic value of activating CB2 receptors.

In this review we examine the current knowledge and understanding of the utility of cannabinoids as therapeutic molecules for inflammatory-mediated demyelinating pathologies. Moreover, we discuss how CB2 receptor activation is related to the modulation of immunopathogenic states.

The activation of CB2receptors results in the modulation of the inflammatory response, restraining one of the agents responsible for the progress of demyelination and neuronal death, the ultimate causes of the symptoms in pathologies such as MS and EAE.

The modulation of inflammatory molecules through CB2 receptors could also enhance remyelination, stimulating the survival of oligodendrocyte precursors and neural stem/precursor cells, and their development into mature oligodendrocytes.

…this raises the possibility that CB2 agonists could have the potential to promote brain repair.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219542/#!po=48.0769

A restricted population of CB1 cannabinoid receptors with neuroprotective activity.

“The CB1 cannabinoid receptor, the main molecular target of endocannabinoids and cannabis active components, is the most abundant G protein-coupled receptor in the mammalian brain…

The data unequivocally identify the restricted population of CB1 receptors located on glutamatergic terminals as an indispensable player in the neuroprotective activity of (endo)cannabinoids, therefore suggesting that this precise receptor pool constitutes a promising target for neuroprotective therapeutic strategies.”

http://www.ncbi.nlm.nih.gov/pubmed/24843137

Targeting the Endocannabinoid System for Neuroprotection: A 19F-NMR Study of a Selective FAAH Inhibitor Binding with an Anandamide Carrier Protein, HSA.

“Fatty acid amide hydrolase (FAAH), the enzyme involved in the inactivation of the endocannabinoid anandamide (AEA), is being considered as a therapeutic target for analgesia and neuroprotection…
The endocannabinoid system has been implicated as a therapeutic target for analgesia, anti-emesis, and neuroprotection… These findings provide a potential new therapeutic modality for neuroprotection through dual inhibition of FAAH and anandamide carrier proteins…”

Figure 1

Protective Effects of Cannabidiol Against Hippocampal Cell Death and Cognitive Impairment Induced by Bilateral Common Carotid Artery Occlusion in Mice.

“The present study investigated whether cannabidiol (CBD), a major non-psychoactive constituent of marijuana, protects against hippocampal neurodegeneration and cognitive deficits induced by brain ischemia in adult mice…

These findings suggest a protective effect of CBD on neuronal death induced by ischemia and indicate that CBD might exert beneficial therapeutic effects in brain ischemia. The mechanisms that underlie the neuroprotective effects of CBD in BCCAO mice might involve the inhibition of reactive astrogliosis.”

http://www.ncbi.nlm.nih.gov/pubmed/24532152

Therapeutic potential of cannabinoid medicines.

Drug Testing and Analysis

“Cannabis was extensively used as a medicine throughout the developed world in the nineteenth century but went into decline early in the twentieth century ahead of its emergence as the most widely used illicit recreational drug later that century. Recent advances in cannabinoid pharmacology alongside the discovery of the endocannabinoid system (ECS) have re-ignited interest in cannabis-based medicines.

The ECS has emerged as an important physiological system and plausible target for new medicines. Its receptors and endogenous ligands play a vital modulatory role in diverse functions including immune response, food intake, cognition, emotion, perception, behavioural reinforcement, motor co-ordination, body temperature, wake/sleep cycle, bone formation and resorption, and various aspects of hormonal control. In disease it may act as part of the physiological response or as a component of the underlying pathology.

In the forefront of clinical research are the cannabinoids delta-9-tetrahydrocannabinol and cannabidiol, and their contrasting pharmacology will be briefly outlined. The therapeutic potential and possible risks of drugs that inhibit the ECS will also be considered. This paper will then go on to review clinical research exploring the potential of cannabinoid medicines in the following indications: symptomatic relief in multiple sclerosis, chronic neuropathic pain, intractable nausea and vomiting, loss of appetite and weight in the context of cancer or AIDS, psychosis, epilepsy, addiction, and metabolic disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/24006213

http://onlinelibrary.wiley.com/doi/10.1002/dta.1529/abstract

Neuroprotection and reduction of glial reaction by cannabidiol treatment after sciatic nerve transection in neonatal rats.

“The clinical use of neurotrophic factors is difficult due to side effects and elevated costs, but other molecules might be effective and more easily obtained. Among them, some are derived from Cannabis sativa.

Cannabidiol (CBD) is the major non-psychotropic component found on the surface of such plant leaves.

The present study aimed to investigate the neuroprotective potential of CBD…

The present results show that CBD possesses neuroprotective characteristics that may, in turn, be promising for future clinical use.”

http://www.ncbi.nlm.nih.gov/pubmed/23981015

CB1 and CB2 Cannabinoid Receptor Antagonists Prevent Minocycline-Induced Neuroprotection Following Traumatic Brain Injury in Mice.

“Traumatic brain injury (TBI) and its consequences represent one of the leading causes of death in young adults. This lesion mediates glial activation and the release of harmful molecules and causes brain edema, axonal injury, and functional impairment. Since glial activation plays a key role in the development of this damage, it seems that controlling it could be beneficial and could lead to neuroprotective effects. Recent studies show that minocycline suppresses microglial activation, reduces the lesion volume, and decreases TBI-induced locomotor hyperactivity up to 3 months. The endocannabinoid system (ECS) plays an important role in reparative mechanisms and inflammation under pathological situations by controlling some mechanisms that are shared with minocycline pathways. We hypothesized that the ECS could be involved in the neuroprotective effects of minocycline. To address this hypothesis, we used a murine TBI model in combination with selective CB1 and CB2 receptor antagonists (AM251 and AM630, respectively). The results provided the first evidence for the involvement of ECS in the neuroprotective action of minocycline on brain edema, neurological impairment, diffuse axonal injury, and microglial activation, since all these effects were prevented by the CB1 and CB2 receptor antagonists.”

http://www.ncbi.nlm.nih.gov/pubmed/23960212

Regulation of neuroinflammation by herbal medicine and its implications for neurodegenerative diseases. A focus on traditional medicines and flavonoids.

“Herbal medicine has long been used to treat neural symptoms. Although the precise mechanisms of action of herbal drugs have yet to be determined, some of them have been shown to exert anti-inflammatory and/or anti-oxidant effects in a variety of peripheral systems.

 Now, as increasing evidence indicates that neuroglia-derived chronic inflammatory responses play a pathological role in the central nervous system, anti-inflammatory herbal medicine and its constituents are being proved to be a potent neuroprotector against various brain pathologies.

 Structural diversity of medicinal herbs makes them valuable source of novel lead compounds against therapeutic targets that are newly discovered by genomics, proteomics, and high-throughput screening.”

http://www.ncbi.nlm.nih.gov/pubmed/15956812

Emerging role of the cannabinoid receptor CB2 in immune regulation: therapeutic prospects for neuroinflammation.

“There is now a large body of data indicating that the cannabinoid receptor type 2 (CB2) is linked to a variety of immune events. This functional relevance appears to be most salient in the course of inflammation, a process during which there is an increased number of receptors that are available for activation. Studies aimed at elucidating signal transduction events resulting from CB2 interaction with its native ligands, and of the role of exogenous cannabinoids in modulating this process, are providing novel insights into the role of CB2 in maintaining a homeostatic immune balance within the host. Furthermore, these studies suggest that the CB2 may serve as a selective molecular target for therapeutic manipulation of untoward immune responses, including those associated with a variety of neuropathies that exhibit a hyperinflammatory component.”

Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768535/