Major Health Benefits of Medical Cannabis

“The benefits of medical marijuana plant are extensive, pervasive, and long-standing. Because of the way the cannabis impacts the Autonomic Nervous System which develops the breath and relaxes the body, prospective for health and curative characteristics are huge. Some of the major health benefits of medical cannabis are explained below:

Treats Migraines

Cannabis healing has been very effective in the treatment of migraine headaches. Migraine headaches are vascular in source and are often preceded by an air characterized by nausea, flashes of light, faintness or photosensitivity.

Slows Down Tumor Growth

Studies have shown that cannabis help in slow down the facsimile and slow down the production of cancer cells in body. It is also a natural antiemetic, which makes it effectual in plummeting the nausea and vomiting related with chemo and radiation therapies. So taking marijuana slows down the tumor growth too.

Relieves Symptoms of Chronic Diseases

Marijuana is one of the best natural pain relievers that can help sufferers of chronic pain live more relaxed lives. The side effects are often much less severe than the other common pain medications.

Prevents Alzheimer’s

Cannabis reduces the occurrence of depression in Alzheimer’s patients, which can help patients to keep up a higher level of brain function. That is a powerful way to keep patients performance for a longer time after the first onset of Alzheimer’s disease.

Treats Glaucoma

Some strains of this medicinal plant have been shown that, they are potentially decreasing the force that glaucoma can place on the optic nerve; thereby the patients can easily cut the critical condition by smoking or taking the marijuana edibles or medicines.

Prevents Seizures

Seizure is a kind of epilepsy which almost affects more than 2 millions of Americans and 30 millions of people worldwide. Epilepsy is a condition when some of the brain cells become abnormally excitable. People using marijuana to control epilepsy should be alert when there is any removal of any tablets which controls seizures may leave you more susceptible to the patient. Marijuana is no exception. Patients with epilepsy are advised to exercise caution when using oral THC because there is no enough sufficient knowledge about the convulsive or anti-convulsive properties of the single compound.

For ADD and ADHD

Many people who endure with ADD and/or ADHD find that medical cannabis recovers their knack to hub and their level of recital with definite tasks. There are no clinical studies on humans but there are some beginner studies have done on animals that point to less hyperactivity and impulsivity with the use of cannabinoids (the active medicines in cannabis).

Relieve PMS

Millions of women have an illness on Premenstrual Syndrome (PMS). PMS includes the symptoms of headaches, abdominal cramps, bloating and fluid retention. Many women report that they have tried several different medications but none as give any significant relief like Medical Marijuana. Cannabis medicine has shown to give symptomatic relief from all the unpleasant symptoms of PMS.

Calm Those With Tourette’s and OCD

Several psychological disorders have been known to be related with the medical benefits of marijuana as well. Taking weed of prescribed amount on regular basis can slow down the tics for those who are suffering from Tourette’s syndrome and Obsessive Compulsive Disorder (OCD). Yes some of the qualities in marijuana plant help the patient to calm themselves when any creation of intrusive thoughts which produces fear, uneasiness and abnormal behaviors.”

http://www.herbalmission.org/major-health-benefits-of-medical-cannabis.php

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Cluster attacks responsive to recreational cannabis and dronabinol.

Abstract

“Pharmacological preparations of cannabinoid compounds have a variety of therapeutic uses in medicine, including different pain syndromes, but have not been previously reported as beneficial for cluster headache. We present a patient with cluster headache who was refractory to multiple acute and preventive medications but successfully aborted his attacks with recreational marijuana use; subsequent use of dronabinol provided equally effective pain relief. The beneficial effect may be related to the high concentration of cannabinoid receptors in the hypothalamus, which has been implicated as a site of dysfunction in neuroimaging studies of patients with cluster headache.”

http://www.ncbi.nlm.nih.gov/pubmed/19220500

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Cannabis for migraine treatment: the once and future prescription? An historical and scientific review.

Abstract

“Cannabis, or Marijuana, has been used for centuries for both symptomatic and prophylactic treatment of migraine. It was highly esteemed as a headache remedy by the most prominent physicians of the age between 1874 and 1942, remaining part of the Western pharmacopoeia for this indication even into the mid-twentieth century. Current ethnobotanical and anecdotal references continue to refer to its efficacy for this malady, while biochemical studies of THC and anandamide have provided a scientific basis for such treatment. The author believes that controlled clinical trials of Cannabis in acute migraine treatment are warranted.”

http://www.ncbi.nlm.nih.gov/pubmed/9696453

 

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Biochemical changes in endocannabinoid system are expressed in platelets of female but not male migraineurs.

Abstract

“The endogenous cannabinoid anandamide (AEA) plays important roles in modulating pain. Head pain is an almost universal human experience, yet primary headache disorders, such as migraine without aura (MoA) or episodic tension-type headache (ETTH), can represent a serious threat to well-being when frequent and disabling. We assessed the discriminating role of endocannabinoids among patients with ETTH or MoA, and control subjects. We measured the activity of AEA hydrolase and AEA transporter, and the level of cannabinoid receptors in peripheral platelets from MoA, ETTH and healthy controls. Sixty-nine headache patients and 36 controls were selected. Diagnosis of headache type was made according to the International Headache Society criteria. We observed significant sex differences concerning AEA membrane transporter and fatty acid amide hydrolase activity in all groups. An increase in the activity of AEA hydrolase and AEA transporter was found in female but not male migraineurs. Cannabinoid receptors were the same in all groups. Here we show that the endocannabinoid system in human platelets is altered in female but not male migraneurs. Our results suggest that in migraineur women an increased AEA degradation by platelets, and hence a reduced concentration of AEA in blood, might reduce the pain threshold and possibly explain the prevalence of migraine in women. The involvement of the endocannabinoid system in migraine is new and broadens our knowledge of this widespread and multifactorial disease.”

http://www.ncbi.nlm.nih.gov/pubmed/16472333

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Endocannabinoids in platelets of chronic migraine patients and medication-overuse headache patients: relation with serotonin levels.

Abstract

“BACKGROUND:

Chronic migraine (CM) and medication-overuse headaches (MOH) are well-recognized disabling conditions affecting a significant portion of the headache population attending centers specialized in treating headaches. A dysfunctioning of the serotonergic system has been demonstrated in MOH and CM patients. Here we report on our assessment of the dysfunctioning of the endocannabinoid system as a potential underlying factor in pathogenic mechanisms involved in CM and MOH.

METHOD:

To test the hypothesis of an impairment in the endocannabinoid system in patients with MOH and CM and to assess its relationship with any disruption of the serotonergic system, we determined the levels of the two main endogenous cannabinoids, anandamide (AEA) and 2-acylglycerol (2-AG), in platelets of 20 CM patients, 20 MOH patients and 20 control subjects and also measured the platelet serotonin levels in the same patients.

RESULTS:

We found that 2-AG and AEA levels were significantly lower in MOH patients and CM patients than in the control subjects, without significant differences between the two patient groups. Serotonin levels were also strongly reduced in the two patient groups and were correlated with 2-AG levels, with higher values for MOH patients.

CONCLUSION:

These data support the potential involvement of a dysfunctioning of the endocannabinoid and serotonergic systems in the pathology of CM and MOH. These systems appear to be mutually related and able to contribute to the chronification of both CM and MOH.”

http://www.ncbi.nlm.nih.gov/pubmed/18004553

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Acute Reduction of Anandamide-Hydrolase (FAAH) Activity is Coupled With a Reduction of Nociceptive Pathways Facilitation in Medication-Overuse Headache Subjects After Withdrawal Treatment.

Abstract

“Objectives.- We investigated (1) a possible relationship between the functional activity of the endocannabinoid system and the facilitation of pain processing in migraineurs with medication-overuse headache, and (2) the effect of withdrawal treatment on both. Background.- The endocannabinoid system antinociception effect includes prevention of nociceptive pathways sensitization. The sensitization of the pain pathways has been demonstrated to be pivotal in the development and maintenance of chronic form of migraine, including medication-overuse headache. Methods.- We used the temporal summation threshold of the nociceptive withdrawal reflex to explore the spinal cord pain processing, and the platelet activity of the enzyme fatty acid amide hydrolase to detect the functional state of the endocannabinoid system in 27 medication-overuse headache subjects before and 10 and 60 days after a standard withdrawal treatment and compared results with those of 14 controls. Results.- A significantly reduced temporal summation threshold and increased related pain sensation was found in subjects before withdrawal treatment when compared with controls. A significant fatty acid amide hydrolase activity reduction coupled with a significant improvement (reduction) in facilitation of spinal cord pain processing (increase in temporal summation threshold and reduction in related pain sensation) was found in medication-overuse headache subjects at both 10 and 60 days after withdrawal treatment when compared with medication-overuse headache subjects before withdrawal treatment. Conclusions.- We demonstrated a marked facilitation in spinal cord pain processing in medication-overuse headache before withdrawal treatment when compared with controls. Furthermore, the acute reduction of the fatty acid amide hydrolase activity coupled with a reduction of the facilitation in pain processing immediately (10 days) after withdrawal treatment and its persistence 60 days after withdrawal treatment could represent the consequence of a mechanism devoted to acutely reduce the degradation of endocannabinoids and aimed to increase the activity of the endocannabinoid system that results in an antinociceptive effect.”

http://www.ncbi.nlm.nih.gov/pubmed/22670561

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Anandamide Is Able to Inhibit Trigeminal Neurons Using an in Vivo Model of Trigeminovascular-Mediated Nociception

Abstract

“Arachidonylethanolamide (anandamide, AEA) is believed to be the endogenous ligand of the cannabinoid CB(1) and CB(2) receptors. CB(1) receptors have been found localized on fibers in the spinal trigeminal tract and spinal trigeminal nucleus caudalis. Known behavioral effects of anandamide are antinociception, catalepsy, hypothermia, and depression of motor activity, similar to Delta(9)-tetrahydocannanbinol, the psychoactive constituent of cannabis. It may be a possible therapeutic target for migraine. In this study, we looked at the possible role of the CB(1) receptor in the trigeminovascular system, using intravital microscopy to study the effects of anandamide against various vasodilator agents. Anandamide was able to inhibit dural blood vessel dilation brought about by electrical stimulation by 50%, calcitonin gene-related peptide (CGRP) by 30%, capsaicin by 45%, and nitric oxide by 40%. CGRP(8-37) was also able to attenuate nitric oxide (NO)-induced dilation by 50%. The anandamide inhibition was reversed by the CB(1) receptor antagonist AM251. Anandamide also reduced the blood pressure changes caused by CGRP injection, this effect was not reversed by AM251. It would seem that anandamide acts both presynaptically, to prevent CGRP release from trigeminal sensory fibers, and postsynaptically to inhibit the CGRP-induced NO release in the smooth muscle of dural arteries. CB(1) receptors seem to be involved in the NO/CGRP relationship that exists in causing headache and dural blood vessel dilation. It also seems that some of the blood pressure changes caused by anandamide are mediated by a noncannabinoid receptor, as AM251 was unable to reverse these effects. It can be suggested that anandamide is tonically released to play some form of modulatory role in the trigeminovascular system.

The known behavioral effects of anandamide are similar to that of Δ9-tetrahydrocannabinol, the psychoactive constituent of cannabis, being antinociception, catalepsy, hypothermia, and depression of motor activity (Dewey, 1986; Adams et al., 1998). Although there is a history of anecdotal evidence suggesting the use of cannabinoids is effective at reducing headache and providing other pain relief, its potential as an acute migraine treatment and even preventive has never been scientifically studied in animal studies or clinical trial (Russo, 1998). However, one anonymous standardized survey found that of those using cannabis medicinally, over 10% were using it to relieve headache or migraine (Schnelle et al., 1999). Although many aspects of the study are open to debate, such as the highly selected nature of patient group, it is nevertheless an interesting observation.”

http://jpet.aspetjournals.org/content/309/1/56.long

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Cannabinoid (CB1) Receptor Activation Inhibits Trigeminovascular Neurons

Abstract

“Migraine is a common and disabling neurological disorder that involves activation or the perception of activation of the trigeminovascular system. Cannabinoid (CB) receptors are present in brain and have been suggested to be antinociceptive. Here we determined the effect of cannabinoid receptor activation on neurons with trigeminovascular nociceptive input in the rat. Neurons in the trigeminocervical complex (TCC) were studied using extracellular electrophysiological techniques. Responses to both dural electrical stimulation and cutaneous facial receptive field activation of the ophthalmic division of the trigeminal nerve and the effect of cannabinoid agonists and antagonists were studied. Nonselective CB receptor activation with R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2, 3-de]-1,4-benzoxazin-yl]-(1-naphthalenyl) (WIN55,212; 1 mg kg(-1)) inhibited neuronal responses to A-(by 52%) and C-fiber (by 44%) afferents, an effect blocked by the CB(1) receptor antagonist SR141716 [N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide; 3 mg kg(-1)] but not the CB2 receptor antagonist AM630 (6-iodopravadoline; 3 mg kg(-1)). Anandamide (10 mg kg(-1)) was able to inhibit both A- and C-fiber-elicited TCC firing, only after transient receptor potential vanilloid 1 receptor inhibition. Activation of cannabinoid receptors had no effect on cutaneous receptive fields when recorded from TCC neurons. The data show that manipulation of CB1 receptors can affect the responses of trigeminal neurons with A- and C-fiber inputs from the dura mater. This may be a direct effect on neurons in the TCC itself or an effect in discrete areas of the brain that innervate these neurons. The data suggest that CB receptors may have therapeutic potential in migraine, cluster headache, or other primary headaches, although the potential hazards of psychoactive side effects that accompany cannabinoid treatments may be complex to overcome.”

“In conclusion, activation of CB1 receptors is able to inhibit trigeminal neurons with A-fiber and C-fiber input in the TCC in response to activation of the ophthalmic division of the trigeminal nerve. Anandamide was only able to inhibit neurons with A-fiber inputs after inhibition of the TRPV1 receptor, highlighting the dual agonist properties of anandamide in the brain. These results support an involvement of the cannabinoid CB1 receptor and TRPV1 receptors in trigeminal neuronal firing, helping to further understand the pathophysiology of the trigeminovascular system and indicate potential directions for the development of new therapeutic agents, notwithstanding the potential difficulties of the psychoactive side effects accompanying cannabinoid treatments.”

http://jpet.aspetjournals.org/content/320/1/64.long

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Degradation of endocannabinoids in chronic migraine and medication overuse headache.

Abstract

“Chronic migraine (CM) is frequently associated with medication overuse headache (MOH). The endocannabinoid system plays a role in modulating pain including headache and is involved in the common neurobiological mechanism underlying drug addiction and reward system. Anandamide (AEA) and 2-arachidonoylglycerol are the most biologically active endocannabinoids, which bind to both central and peripheral cannabinoid receptors. The level of AEA in the extracellular space is controlled by cellular uptake via a specific AEA membrane transporter (AMT), followed by intracellular degradation by the enzyme AEA hydrolase (fatty acid amide hydrolase, FAAH). AMT and FAAH have also been characterized in human platelets. We assayed the activity of AMT and of FAAH in platelets isolated from four groups of subjects: MOH, CM without MOH, episodic migraine and controls. AMT and FAAH were significantly reduced in CM and MOH, compared to either controls or episodic migraine group. This latter finding was observed in both males and females with CM and MOH. Changes observed in the biochemical mechanisms degrading endogenous cannabinoids may reflect an adaptative behaviour induced by chronic headache and/or drug overuse.”

http://www.ncbi.nlm.nih.gov/pubmed/18358734

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Alterations of the endocannabinoid system in an animal model of migraine: evaluation in cerebral areas of rat.

Abstract

“Endocannabinoids are involved in the modulation of pain and hyperalgesia. In this study we investigated the role of the endocannabinoid system in the migraine model based on nitroglycerin-induced hyperalgesia in the rat. Male rats were injected with nitroglycerin (10 mg/kg, i.p.) or vehicle and sacrificed 4 h later. The medulla, the mesencephalon and the hypothalamus were dissected out and utilized for the evaluation of activity of fatty acid amide hydrolase (that degrades the endocannabinoid anandamide), monoacylglycerol lipase (that degrades the endocannabinoid 2-arachidonoylglycerol), and binding sites specific for cannabinoid (CB) receptors. The findings obtained show that nitroglycerin-induced hyperalgesia is associated with increased activity of both hydrolases and increased density of CB binding sites in the mesencephalon. In the hypothalamus we observed an increase in the activity of fatty acid amide hydrolase associated with an increase in density of CB binding sites, while in the medulla only the activity of fatty acid amide hydrolase was increased. Anandamide also proved effective in preventing nitroglycerin-induced activation (c-Fos) of neurons in the nucleus trigeminalis caudalis. These data strongly support the involvement of the endocannabinoid system in the modulation of nitroglycerin-induced hyperalgesia, and, possibly, in the pathophysiological mechanisms of migraine.”

http://www.ncbi.nlm.nih.gov/pubmed/19515121

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