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

Δ9-tetrahydrocannabinol prevents methamphetamine-induced neurotoxicity.

“Methamphetamine (METH) is a potent psychostimulant with neurotoxic properties…

Preclinical studies have shown that natural (Δ9-tetrahydrocannabinol, Δ9-THC) and synthetic cannabinoid CB1 and CB2 receptor agonists exert neuroprotective effects on different models of cerebral damage. Here, we investigated the neuroprotective effect of Δ9-THC on METH-induced neurotoxicity…

Our results indicate that Δ9-THC reduces METH-induced brain damage via inhibition of nNOS expression and astrocyte activation through CB1-dependent and independent mechanisms, respectively.”

http://www.ncbi.nlm.nih.gov/pubmed/24844285

Full-text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028295/

Relationship between working-memory network function and substance use: a 3-year longitudinal fMRI study in heavy cannabis users and controls.

“The aim of this 3-year longitudinal neuro-imaging study was to investigate the relationship between substance use (e.g. alcohol, cannabis, nicotine, illegal psychotropic drugs) and working-memory network function over time in heavy cannabis users and controls.

Within the group of cannabis users, cannabis-related problems remained stable, whereas alcohol-related problems, nicotine dependence and illegal psychotropic substance use increased over time. At both measurements, behavioral performance and network functionality during the n-back task did not differ between heavy cannabis users and controls. Although n-back accuracy improved, working-memory network function remained stable over time.

Within the group of cannabis users, working-memory network functionality was not associated with substance use.

These results suggest that sustained moderate to heavy levels of cannabis, nicotine, alcohol and illegal psychotropic substance use do not change working-memory network functionality.

Moreover, baseline network functionality did not predict cannabis use and related problems three years later, warranting longitudinal studies in more chronic or dependent cannabis users.”

http://www.ncbi.nlm.nih.gov/pubmed/24589297

Changes in Cerebral CB1 Receptor Availability after Acute and Chronic Alcohol Abuse and Monitored Abstinence.

“Involvement of the type 1 cannabinoid receptor (CB1R) in the effects of alcohol on the brain is supported by animal experiments…

In conclusion, whereas the acute alcohol effect is an increase in CB1R availability, chronic heavy drinking leads to reduced CB1R availability that is not reversible after 1 month of abstinence. Longer follow-up is required to differentiate whether this is a compensatory effect of repeated endocannabinoid overstimulation or an enduring trait-like feature.

An enhanced CB1R signaling may offer a new therapeutic direction for treatment of the negative affective state produced by alcohol withdrawal and abstinence, which is critical for the maintenance of alcohol addiction.”

http://www.ncbi.nlm.nih.gov/pubmed/24553924

Basolateral amygdala CB1 cannabinoid receptors mediate nicotine-induced place preference.

“In the present study, the effects of bilateral microinjections of cannabinoid CB1 receptor agonist and antagonist into the basolateral amygdala (intra-BLA) on nicotine-induced place preference were examined in rats.

Taken together, these findings support the possible role of endogenous cannabinoid system of the BLA in the acquisition and the expression of nicotine-induced place preference. Furthermore, it seems that there is a functional interaction between the BLA cannabinoid receptors and nicotine in producing the rewarding effects.”

http://www.ncbi.nlm.nih.gov/pubmed/24468643

Use of Dronabinol for Cannabis Dependence: Two Case Reports and Review

“Based on recent laboratory studies, dronabinol (delta-9-tetrahydrocannabinol) has been shown to reduce cannabis withdrawal symptoms and the subjective effects of marijuana.

Given that agonist agents have been found to be effective for opiate and nicotine dependence, the clinical utility of dronabinol for cannabis dependence is a reasonable approach…

It is clear from the two cases that both patients found the induction onto dronabinol helpful.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2733248/

Dronabinol for the Treatment of Cannabis Dependence: A Randomized, Double-Blind, Placebo-Controlled Trial

“… there are no effective medications for cannabis dependence. The purpose of this study was to evaluate the safety and efficacy of dronabinol, a synthetic form of delta-9-tetrahydrocannabinol, a naturally occurring pharmacologically active component of marijuana, in treating cannabis dependence.

This is the first trial using an agonist substitution strategy for treatment of cannabis dependence. Dronabinol showed promise, it was well-tolerated, and improved treatment retention and withdrawal symptoms…

In conclusion, agonist substitution pharmacotherapy with dronabinol, a synthetic form of THC, showed promise for treatment of cannabis dependence, reducing withdrawal symptoms and improving retention in treatment…

The trial showed that among adult cannabis-dependent patients, dronabinol was well accepted, with good adherence and few adverse events.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154755/

 

Cannabinoid type-1 receptor ligands, alone or in combination with cocaine, affect vigilance-related behaviors of marmoset monkeys.

“Endocannabinoids (eCB) have been functionally linked to cocaine’s rewarding effects.

…changes in CB1r function – alone and in combination with cocaine – affected stereotyped vigilance-related behaviors… further implicating the eCB system in the neurobiological mechanisms of cocaine addiction.”

http://www.ncbi.nlm.nih.gov/pubmed/24445195

Nabiximols as an Agonist Replacement Therapy During Cannabis Withdrawal: A Randomized Clinical Trial.

“The cannabis extract nabiximols (Sativex), developed as a multiple sclerosis treatment, offers a potential agonist medication for cannabis withdrawal…

Nabiximols treatment significantly reduced the overall severity of cannabis withdrawal…

The data support further evaluation of nabiximols for management of cannabis dependence and withdrawal in treatment-seeking populations.”

http://www.ncbi.nlm.nih.gov/pubmed/24430917

Pharmacological blockade of either cannabinoid CB1 or CB2 receptors prevents both cocaine-induced conditioned locomotion and cocaine-induced reduction of cell proliferation in the hippocampus of adult male rat.

“Addiction to major drugs of abuse, such as cocaine, has recently been linked to alterations in adult neurogenesis in the hippocampus. The endogenous cannabinoid system modulates this proliferative response as demonstrated by the finding that pharmacological activation/blockade of cannabinoid CB1 and CB2 receptors not only modulates neurogenesis but also modulates cell death in the brain.

In the present study, we evaluated whether the endogenous cannabinoid system affects cocaine-induced alterations in cell proliferation…

These results indicate that the changes in neurogenic, apoptotic and gliotic processes that were produced by repeated cocaine administration were normalized by pharmacological blockade of CB1 and CB2. The restorative effects of cannabinoid receptor blockade on hippocampal cell proliferation were associated with the prevention of the induction of conditioned locomotion but not with the prevention of cocaine-induced sensitization.”

http://www.ncbi.nlm.nih.gov/pubmed/24409127