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Medical Marijuana: Legality and Efficacy


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It's seems that amongst the many many potions, pills and panacea talked about in relation to easing benzodiazapine withdrawal (BW) we inevitably come across the idea of cannabis being in some way useful.

 

Personally, just like the other super foods and what-have-you, I don't think it makes a bit of difference to the withdrawal process.  At best it masks the symptoms at worse it exacerbates them.  At present nothing but time with help with withdrawal.

 

 

With this in mind I thought I'd throw together a little bit of info about medical marijuana (MM),  all taken from simple google searches.

 


 

An example of the authorized uses of MM.

 

 

Washington State

 

(a) Cancer, human immunodeficiency virus (HIV), multiple sclerosis, epilepsy or other seizure disorder, or spasticity disorders;

 

(b) Intractable pain, limited for the purpose of this chapter to mean pain unrelieved by standard medical treatments and medications;

 

© Glaucoma, either acute or chronic, limited for the purpose of this chapter to mean increased intraocular pressure unrelieved by standard treatments and medications;

 

(d) Crohn’s disease with debilitating symptoms unrelieved by standard treatments or medications;

 

(e) Hepatitis C with debilitating nausea or intractable pain unrelieved by standard treatments or medications; and

 

(f) Diseases, including anorexia, which result in nausea, vomiting, wasting, appetite loss, cramping, seizures, muscle spasms, or spasticity, when these symptoms are unrelieved by standard treatments or medications.

 

 

 

New Jersey State

 

(1)  one of the following conditions, if resistant to conventional medical therapy: seizure disorder, including epilepsy; intractable skeletal muscular spasticity; or glaucoma;

 

(2)  one of the following conditions, if severe or chronic pain, severe nausea or vomiting, cachexia, or wasting syndrome results from the condition or treatment thereof: positive status for human immunodeficiency virus, acquired immune deficiency syndrome, or cancer;

 

(3)  amyotrophic lateral sclerosis, multiple sclerosis, terminal cancer, muscular dystrophy, or inflammatory bowel disease, including Crohn’s disease;

 

(4)  terminal illness, if the physician has determined a prognosis of less than 12 months of life; or

 

(5)  any other medical condition or its treatment that is approved by the department by regulation.

 

 

 

http://www.aclu-wa.org/sites/default/files/attachments/Medicalmarijuanabrochure_6_10.pdf

 

http://www.njleg.state.nj.us/2008/Bills/PL09/307_.HTM

 

 

 

From the above sample we can clearly see that whilst BW might mimic some of the above illnesses in some small aspects, there is nothing relating to the use of MM as palliative against withdrawal from any substance.

 


 

Whilst the pharmacology of benzodiazapines and tetrahydrocannabinol (THC the active compound in MM) are understood to some point, their interactions with other bodily systems are not.

 

Let's have a quick poke at benzodiazapines.

 

Very simply, when we use benzodiazapines, GABA receptors increase the function of chloride ions as a dampener on the nervous system, they inhibit neural activity.

 

Someone who is in BW has a damaged GABA system, they are constantly overstimulated, the GABA receptors have stopped binding with GABA so readily due to the external benzodiazapine taking the role of GABA.

 

If we look quickly at THC we see it initially raises levels of glutamate, a major excitatory neurotransmitter, giving rise to some of the following physiological effects.

 

    * Loss of coordination. Cannabinoid receptors located in parts of the brain associated with coordination and movement can drastically inhibit motor skills and coordination. This is why many users become quite clumsy and unable to efficiently conduct themselves when they are “high”. This type of result is usually moderately pronounced, though it tends to taper off as the individual begins to sober up.

 

 

    * Audio or visual distortion. This is a result of cannabinoid receptors that are located in the parts of the brain associated with hearing or vision. These receptors set off a chemical reaction within the brain that can cause many different effects, from slurred speech to the inability to piece together a coherent sentence. It can also result in “looping” audio, where one particular sound (that is usually one syllable in duration) will repeat over and over again, as perceived by the user, until it is either replaced by a different sound or the effects of THC begin to wear off.

 

 

    * Lack of time perception. Once again, this is the result of the cannabinoid receptors location in relation to the time perception areas of the brain. This can create feelings of longevity, or “time passing by slowly; this can also create the sense that time is passing quite quickly. Given the nature of the symptom, there is no way to quantitatively state when it begins to manifest.

 

    * Feelings of euphoria, insecurity, joy, or paranoia. As THC triggers various reactions within the brain, different people will experience different results. These results are dependent on the environment and surroundings that they are in when they consume THC, the people that are around them, as well as their state of mind or mood before consumption.

 

Intense feelings of happiness and joy are quite common, with uncontrollable bursts of laughter being quite common. Feelings of paranoia and worry are also quite common, though they are not as intense as the feelings created by other, more dramatic drugs.

 

The reality is that the effects of Marijuana are not identical within each individual, and though we certainly don’t encourage experimentation or consumption, it is impossible for us to state with any level of certainty the effects of Marijuana on each unique individual.

 

http://www.healthadel.com/what-happens-to-your-body-when-smoking-marijuana/

 

 

 

I think for the uninitiated smoker of MM, the above effects could be a little fearsome,  for someone in the midst of severe withdrawal it could be devastating,  even for someone who is accustomed to the effects of MM the effect of using it with a  compromised nervous system could spell disaster.

 

 


 

 

I think the psychoactive nature of MM makes it a really bad choice for anyone not accustomed to its effects.  For some users, the "pleasurable" effects of MM may mask the symptoms of BW, but I hope no one decides to try it outside of a prescription based on what they read on the internet.

 

There is no cure for what we have, we just have to wait and hope it gets better.

 

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Sorry..I may have missed where it commented on THC raising Glutamate?  Can you show me the source of that again?  Thanks for your help.
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Sorry..I may have missed where it commented on THC raising Glutamate?  Can you show me the source of that again?  Thanks for your help.

 

 

Abstract

 

Cannabinoid modulation of prefrontal cortex and hippocampus neuronal functioning has been correlated to the disruptive action of marijuana on memory tasks. This study investigates the effects of Δ9-tetrahydrocannabinol (Δ9-THC) on dopamine, glutamate and GABA levels in vivo by brain microdialysis in the prefrontal cortex. Δ9-THC (1 mg/kg, i.v.) significantly increased extracellular dopamine and glutamate levels and decreased GABA levels. These effects were prevented by the cannabinoid antagonist SR141716A (1 mg/kg, i.v.), which per se was ineffective. These results suggest that Δ9-THC disrupt the normal interplay between neurotransmitters in this area and may bear relevance in understanding neuronal mechanisms underlying cannabinoid-induced cognitive deficits.

 

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6SYR-46WVXNG-D&_user=10&_coverDate=09%2F06%2F2002&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1566521767&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=455f7bbe8eb32d6be73f9a1983bfdfe0&searchtype=a

 

 

 

The effects of the principal psychoactive component of marijuana, Δ9-tetrahydrocannabinol (Δ9-THC), on endogenous extracellular glutamate levels in primary cultures of rat cerebral cortex neurons were investigated. Locally applied Δ9-THC (0.03, 3, 300, and 1,000 nM) concentration-dependently increased basal extracellular glutamate levels (+18% ± 11%, +54% ± 10%, +90% ± 14%, +149% ± 33% vs. basal). The facilitatory effects of Δ9-THC (3 and 300 nM) on cortical glutamate were fully counteracted in the presence of the selective CB1 receptor antagonist SR141716A (10 nM) and by replacement of the normal Krebs-Ringer bicarbonate buffer with a low-Ca2+ (0.2 mM) medium. Δ9-THC application also induced an enhancement in K+-evoked glutamate levels. These findings suggest that an increase in cortical glutamatergic transmission mediated by local CB1 receptor activation may underlie some of the psychoactive and behavioral effects of acute marijuana consumption. © 2002 Wiley-Liss, Inc.

 

http://onlinelibrary.wiley.com/doi/10.1002/jnr.10242/abstract

 

 

 

 

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