Marijuana Prevents Post-Traumatic Symptoms,
By JUDY SIEGEL-ITZKOVICH for Jpost October 05, 2011
Medical marijuana is known to ease pain in cancer patients of all ages and is used for that purpose in Israel and many other countries. Now University of Haifa researchers, working with rodents, have found that administering cannabis after a traumatic experience prevents the development of post-traumatic stress symptoms in a rat model.
They discovered that while the drug does not erase the traumatic experience, it does prevent the development of post-trauma symptoms. If clinical studies show that cannabinoids accomplish the same in humans, they could be boon to Israel, where wars, terror attacks, road accidents and other traumatic events have often occurred, as well as to the rest of the world.
Dr. Irit Akirav of the of the university’s psychology department and colleagues published her findings in the journalNeuropsychopharmacology.
“We found that there is a ‘window of opportunity’ during which administering synthetic marijuana helps deal with symptoms simulating post-traumatic stress disorder [PTSD] in rats,” said Akirav, who led the study. In the study, which she conducted with research student Eti Ganon-Elazar, the researchers set out to examine how administering cannabinoids (synthetic marijuana) affects the development of PTSD-like symptoms in rats, whose physiological reactions to traumatic and stressful events are similar to human reactions.
In the first part of the study, the researchers exposed a group of rats to extreme stress and observed that the rats did indeed display symptoms resembling human PTSD, such as an enhanced startle reflex, impaired extinction learning and disruption of the negative feedback cycle of the stress-influenced HPA axis.
The rats were then divided into four groups. Some were given no marijuana at all; the second group were given a marijuana injection two hours after being exposed to a traumatic event; the third group after 24 hours; and the fourth group after 48 hours.
A week later, the researchers examined the rats and found that the group that had not been given marijuana and the group that got the injection 48 hours after experiencing trauma continued to display PTSD symptoms as well as a high level of anxiety.
By contrast, PTSD symptoms disappeared in the rats that were given marijuana two or 24 hours after experiencing trauma, even though these rats had also developed a high level of anxiety.
“This indicates that the marijuana did not erase the experience of the trauma, but that it specifically prevented the development of post-trauma symptoms in the rat model,” said Akirav, who added that the results suggest there is a particular window of time during which administering marijuana is effective.
Because the human life span is significantly longer than that of rats, the Haifa psychologist explained, one could assume that this window of time would be longer for humans.
The second stage of the study sought to understand the brain mechanism that is put into operation during the administering of marijuana. To do this, they repeated stage one of the experiment, but after the trauma they injected the synthetic marijuana directly into the amygdala area of the brain that is known to be responsible for trauma response. The researchers found that the marijuana blocked development of PTSD symptoms in these cases as well.
From this the researchers were able to conclude that the effect of the marijuana is mediated by a CB1 receptor in the amygdala.
HU LIFE SCIENCES SEMINAR BROUGHT THE BEST Prof. Roger Kornberg of Stanford University, who was awarded the Nobel Prize in Chemistry in 2006, spent five days in Jerusalem recently to direct a “School for Life Sciences” at the Hebrew University of Jerusalem’s Institute for Advanced Studies’ School for Life Sciences that focused on cancer research.
Increased understanding the molecular basis of cancer diseases has significantly improved the ability of doctors to treat certain types of the disease and prolong the life of patients – but many aspects of cancer still remain a mystery. Data gathered by the the Central Bureau of Statistics in Jerusalem indicate that cancer is now the number-one killer in Israel; heart disease used to top the list.
The “school” presented various achievements in cancer research, numerous research challenges, innovative treatment approaches and advanced developments in cancer medication. The classes explained the differences among various types of cancer – why some can be treated, while in others the research is just beginning – and why some types of cancer are more complex than others.
The event has taken place for the past 19 years.
Kornberg, who says the event leads to the sharing of knowledge and can lead to future cooperation, annually comes to HU as a guest professor at the faculty of sciences and as an associate of the biological chemistry department. The 200 participants, most of them Israeli masters and doctoral students, heard more than two dozen lectures by leading cancer researchers from here and abroad. http://nocamels.com/2011/10/marijuana-can-prevents-post-traumatic-symptoms-study-shows/
Study: Cannabis May Relieve Parkinson’s Related PainBy NoCamels Team December 22, 2012
People suffering from Parkinson’s disease often experience random pains. Until recently these pains were not conclusively linked to the disease. However, a recent study conducted at Rabin Medical Center has not only shown that the pain is a symptom of the disease, but also suggests a possible treatment – cannabis.
“50 to 80 percent of Parkinson’s patients suffer from pain that could not be treated properly,” says Professor Ruth Djaldetti, senior neurologist and Head of the Movement Disorder Clinic, who conducted the research. “In light of the study’s results, we could treat the pain efficiently and improve the patient’s quality of life.”
According to Djaldetti, the results of the study support the approach that patients suffering from this type of pain might be able to find relief by treatment with cannabis. Despite the promising results, Djaldetti says that further research should be done on the subject, so that in the future, medical treatment can be adjusted according to individual gene-mapping.
The study was published in the European Journal of Pain.
Effects of homologues and analogues of palmitoylethanolamide upon the inactivation of the endocannabinoid anandamideSweden, 2001
Doctors: Jonsson KO Vandevoorde S Lambert DM Tiger G Fowler CJ
School: Umea University
Ailments: Endocannabinoid System
Study: Clinical Study, OTHERS
1. The ability of a series of homologues and analogues of palmitoylethanolamide to inhibit the uptake and fatty acid amidohydrolase (FAAH)-catalysed hydrolysis of [(3)H]-anandamide ([(3)H]-AEA) has been investigated. 2. Palmitoylethanolamide and homologues with chain lengths from 12 – 18 carbon atoms inhibited rat brain [(3)H]-AEA metabolism with pI(50) values of approximately 5. Homologues with chain lengths < or = eight carbon atoms gave < 20% inhibition at 100 microM. 3. R-palmitoyl-(2-methyl)ethanolamide, palmitoylisopropylamide and oleoylethanolamide inhibited [(3)H]-AEA metabolism with pI(50) values of 5.39 (competitive inhibition), 4.89 (mixed type inhibition) and 5.33 (mixed type inhibition), respectively. 4. With the exception of oleoylethanolamide, the compounds did not produce dramatic inhibition of [(3)H]-WIN 55,212-2 binding to human CB(2) receptors expressed on CHO cells. Palmitoylethanolamide, palmitoylisopropylamide and R-palmitoyl-(2-methyl)ethanolamide had modest effects upon [(3)H]-CP 55,940 binding to human CB(1) receptors expressed on CHO cells. 5. Most of the compounds had little effect upon the uptake of [(3)H]-AEA into C6 and/or RBL-2H3 cells. However, palmitoylcyclohexamide (100 microM) and palmitoylisopropylamide (30 and 100 microM) produced more inhibition of [(3)H]-AEA uptake than expected to result from inhibition of [(3)H]-AEA metabolism alone. 6. In intact C6 cells, palmitoylisopropylamide and oleoylethanolamide inhibited formation of [(3)H]-ethanolamine from [(3)H]-AEA to a similar extent as AM404, whereas palmitoylethanolamide, palmitoylcyclohexamide and R-palmitoyl-(2-methyl)ethanolamide were less effective. 7. These data provide useful information upon the ability of palmitoylethanolamide analogues to act as ‘entourage’ compounds. Palmitoylisopropylamide may prove useful as a template for design of compounds that reduce the cellular accumulation and metabolism of AEA without affecting either CB(1) or CB(2) receptors. External Article: http://www.ncbi.nlm.nih.gov/pubmed/11498512
Characterization of palmitoylethanolamide transport in mouse Neuro-2a neuroblastoma and rat RBL-2H3 basophilic leukaemia cells: comparison with anandamide
Doctors: Jacobsson SO Fowler CJ
School: Umea University
Ailments: Cancer Treatment
Study: Clinical Study, BOTH
In the present study, the pharmacological and functional properties of PEA and AEA uptake have been investigated in mouse Neuro-2a neuroblastoma and, for comparison, in rat RBL-2H3 basophilic leukaemia cells. Saturable uptake of PEA and AEA into both cell lines were demonstrated with apparent K(M) values of 28 microM (PEA) and 10 microM (AEA) in Neuro-2a cells, and 30 microM (PEA) and 9.3 microM (AEA) in RBL-2H3 cells. Both PEA and AEA uptake showed temperature-dependence but only the AEA uptake was sensitive to treatment with Pronase and phenylmethylsulfonyl fluoride. The AEA uptake was inhibited by AM404, 2-arachidonoylglycerol (2-AG), R1- and S1-methanandamide, arachidonic acid and olvanil with similar potencies for the two cell types. PEA, up to a concentration of 100 microM, did not affect AEA uptake in either cell line. AEA, 2-AG, arachidonic acid, R1-methanandamide, (9)-THC, and cannabidiol inhibited PEA transport in both cell lines. The non-steroidal anti-inflammatory drug indomethacin inhibited the AEA uptake but had very weak effects on the uptake of PEA. From these data, it can be concluded that PEA is transported in to cells both by passive diffusion and by a facilitated transport that is pharmacologically distinguishable from AEA uptake. External Article: http://www.ncbi.nlm.nih.gov/pubmed/11309246
The effects of short-chain fatty acids on human colon cancer cell phenotype are associated with histone hyperacetylationUSA, 2002
Doctors: Brian F. Hinnebusch Shufen Meng James T. Wu Sonia Y. Archer Richard A. Hodin
School: Harvard Medical School
Ailments: Colon Disease
Study: Clinical Study, OTHERS
We sought to determine the effects of a variety of the SCFA on colon carcinoma cell growth, differentiation and apoptosis. HT-29 or HCT-116 (wild-type and p21-deleted) cells were treated with physiologically relevant concentrations of various SCFA, and histone acetylation state was assayed by acid-urea-triton-X gel electrophoresis and immunoblotting. Growth and apoptotic effects were studied by flow cytometry, and differentiation effects were assessed using transient transfections and Northern blotting. Propionate (C3) and valerate (C5) caused growth arrest and differentiation in human colon carcinoma cells. The magnitude of their effects was associated with a lesser degree of histone hyperacetylation compared with butyrate. Acetate (C2) and caproate (C6), in contrast, did not cause histone hyperacetylation and also had no appreciable effects on cell growth or differentiation. SCFA-induced transactivation of the differentiation marker gene, intestinal alkaline phosphatase (IAP), was blocked by histone deacetylase (HDAC), further supporting the critical link between SCFA and histones. Butyrate also significantly increased apoptosis, whereas the other SCFA studied did not. The growth arrest induced by the SCFA was characterized by an increase in the expression of the p21 cell-cycle inhibitor and down-regulation of cyclin B1 (CB1). In p21-deleted HCT-116 colon cancer cells, the SCFA did not alter the rate of proliferation. These data suggest that the antiproliferative, apoptotic and differentiating properties of the various SCFA are linked to the degree of induced histone hyperacetylation. Furthermore, SCFA-mediated growth arrest in colon carcinoma cells requires the p21 gene. External Article: http://www.ncbi.nlm.nih.gov/pubmed/11983830
If you live in a US state or country that permits medicinal or recreational (“adult use”) cannabis, CBD-rich strains and oils are available at most marijuana dispensaries or you can grow your own varieties yourself (depending on state law).
The legal availability of CBD in other US states is often challenged, but what is certain is that natural cannabinoids found in hemp are specifically exempt from the Controlled Substances Act. Since natural cannabinoids are found in all hemp products, and hemp products are found on grocery store shelves nationwide, hemp oils would appear to be the easiest, legal manner in which to obtain CBD.
Products made from hemp are found in retail stores nationwide, thanks to a federal exemption to the definition of “marijuana”. Since 1937, the federal statue controlling “marijuana” has excluded the mature stalks, fiber, oil, and any other preparation of the mature stalks of Cannabis sativa L., commonly known as “hemp”, from the definition of “marijuana.” When the Hemp Industries Association defended hemp’s exempt status in 2004, the DEA declined to challenge this ruling, which is why there continues to be a wide variety of hemp products on the market today. Walk into many retail and grocery stores and you will find hemp protein powder, hemp seeds, hemp clothing, and hemp oil.
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