Sunday, January 3rd, 2010
Acetaminophen and cannabinoid receptor interactions were the focus of a research article published in the journal of Neuropharmacology in late December 2009. The research demonstrates that the effects of Acetaminophen on pain are mediated through the CB1 receptor. Acetaminophen has previously been shown to elevate the levels of endocannabinoids in the body. Thus increasing the amount of activated cannabinoid receptors, leading to pain relief and anti-inflammatory effects.
Most prescription narcotics such as percocet and vicodin are cut with acetaminophen by pharmaceutical companies. This gives the pain killers more of a “kick.” Without acetaminophen, some pain killers are not nearly as effective. Researchers have been investigating the molecular mechanism for this interaction and the Endocannabinoid System appears to be a big player. Previous research has also shown that there is some “cross talk” between opiate receptors and cannabinoid receptors.
The study investigated the effects of acetaminophen in combination with different pain killers. The authors found that a combination of acetaminophen with gabapentin or morphine produced synergistic pain killing effects in rats. The results may have clinical significance because the effect was observed in rats that are a model of spinal cord injury. Interestingly, this synergistic pain relief disappeared when the rats were given AM251. AM251 blocks the Cannabinoid Type 1 Receptor (CB1R) thus inhibiting CB1R activation.
Given the notable toxicity of acetaminophen, cannabinoids might be a reasonable supplement to accompany current treatments for pain.
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Saturday, January 2nd, 2010
The Journal of Molecular Psychiatry recently published an LTE from a group of researchers who demonstrated that chronic low doses of the cannabinoid WIN55212, resulted in new brain cells or neurons in the hippocampus of old rats. As we age, our ability to make new cells decreases, this may be the cause of many age related disorders. A class of drugs that can restore neurons may be a potential cure for diseases such as Parkinson’s, depression, etc.
The data was simply amazing–3 weeks of treatment resulted in noticeable effects! So this blog includes the figures from the publication, see below. On the left hand side, Figure A shows brain cells stained with red and green. Green, spindle like, staining indicates neuron growth. Pictures A and B show the typical neuron growth in developing brains. As you can see in pictures E and F, chronic administration of a non-psychotropic dose of WIN55212 restores neuron production in older rats, indicated by the green wisps. Note that this green stain is very low in old rats that did not receive the cannabinoid, pictures C and D.
The authors speculate, “Cannabinoid receptor stimulation therapy may thus provide clinical benefit for humans with age-associated memory impairment.”
Lots of molecules can activate cannabinoid receptors, so take your pick. More research is needed to determine which cannabinoids are the best option. None of the plant cannabinoids have not been explored for this effect. This not the first time cannabinoids have been linked to neurogenesis; HU-210 has also demonstrated similar effects.
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Monday, September 7th, 2009
Genetic variations, polymorphisms, or mutations on the gene for the Cannabinoid Type 2 (CB2) Receptor have been linked to osteoporosis, low Bone Mineral Density (BMD), and hand bone strength in case controlled Studies (Yamada 2007, Karsak 2005, and Karsak 2009).
Most cannabinoid research on bone has been conducted in rats and mice. These recent case controlled studies in humans have established a significant association between CB2 gene polymorphisms/mutations to certain bone phenotypes; Mutant CB2 receptors lead to bad bones.
The first study (Karsak 2005) looked at CB1 and CB2 receptor DNA in a sample of French post-menopausal patients and female controls. The authors report that certain changes in CB2 receptor, but not the CB1 receptor, were strongly associated with osteoporosis. The authors claim this is the first study to find a link between the CB2 receptor and a disease in human patients. A study published out of Japan replicated these findings in 2007, in a group of pre and post menopausal women.
Furthermore, it has been speculated that CB2 receptor activation can inhibit atherosclerotic plaques. Atherosclerosis is a late onset disorder, that is inversely correlated to bone mineral density. If your bone density or strength starts decreasing, atherosclerosis progresses. So, CB2 receptor variations could explain the association between the two disorders. THC has already been shown to reduce atherosclerosis in mice by activating the CB2 receptor.
The third study on CB2 genes in humans, examined the role of CB2 DNA or genes on hand bone strength. The author took radio-graphic images and DNA samples from a Chevashian population, an ethnically homogeneous population of people of Bulgaric ancestry that live along the Volga river.
The authors found several recurring, small mutations or SNPs (Small Nucleotide Polymorphisms) were significantly associated certain bone phenotypes. Basically, a less functional form of the CB2 receptor leads to weak hand bone strength.
These studies have showed that the effects of CB2 receptor gene variations have been observed in three different genetic/ethnic backgrounds. Thus supporting a link between the CB2 receptors in humans and bone health. Drugs that activate this receptor are of medical value and importance.
While it appears that cannabinod receptor activation may be positively associated with bone health, no studies have been approved for observing the long term effects of cannabis use/ receptor activation on bone health. An anecdotal answer could be easily derived by comparing different measurements of bone health in long term cannabis users vs. non-users.
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Tuesday, July 21st, 2009
The Journal of Neuroendocrinology published a review last year, which suggests that oral THC may significantly reduce plaque development in diseases associated with obesity, such as atherosclerosis.
Atherosclerosis, a condition of plaque deposits in the lining of the arteries that results from a diet high in cholesterol, is one of the major causes of death in overweight/obesity-related disease. The plaque is created as a by-product of specific cells, called macrophages, when they consume fatty particles. As the plaque gathers, the walls of arteries become stiff and eventually collapse.
The study suggests that THC interacts directly with macrophages and suppresses their plaque-creating abilities through the Cannabinoid Type II receptor (CB2R). Immune cells in our body, such as macrophages, have many more cannabinoid receptors expressed on their surface – this makes them an exceptionally strong target for cannabis-based medicines.
The authors note that oral administration of low doses of THC resulted in significant inhibition of plaque development, an effect that could be reversed by blocking the CB2R.
What does this mean for humans? It is difficult to say without further research. But the results are hopeful. Given the politics surrounding cannabis, it might be a long while before the FDA approves a study in humans on cannabis and atherosclerosis. On the other hand, research such as this shows not only that we have only begun to investigate the healing potential of this remarkable natural compound, but the importance of advocating for a more open environment for future research.
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