To: stormcrow
I've put the List on the cloud! Click the link to download the new
2016 Granny Storm Crow's List!
https://1drv.ms/b/s!AkiTiWAuHrKLbx7-n63PHKx_T9I
Just opening the link will show you the List, but you will need to
download it to access the very useful Navigation Index. Click the
"Bookmark" icon if it doesn't automatically show up. No more scrolling
"forever" to get to that study you want! It may take a minute or so
to download- it's over 3,300 pages!
The first section of the List is over 475 pages of links to news
articles, so you won't need a PhD to use the List. Reading a news
article about something first, really makes understanding the actual
medical study much easier!
The second section is devoted to the more recent medical studies and
articles from 2010 to the beginning of August 2016. For people
seriously looking into cannabis and the cannabinoids, this will likely
be the most useful section for a lot of you.
Further down are the older studies that go into detail about some of
the basic questions (how long to hold a hit, storage of cannabis,
effects on hormone levels, etc). The older studies also tend to be
easier to understand, so they are a good place to begin your
education.
At the very bottom is a small mini-dictionary of words you will run
across in the studies. You might even want to print up a copy of it just
as a handy reference until you get used to all of the "Sci-speak"!
And take your Omega 3! It is needed to properly make the CB receptors
that the cannabinoids (like THC and CBD) activate to get you "high",
and also, more importantly, heal you. You want lots of working CB
receptors, and not just for the better "high" that daily use of Omega
3 can bring after a month or two!
And one last thank you to "Old Hippie" (of the "Beyond Chronic" blog)
for his invaluable technical help in getting this List out to all of
you! "Nugs and Hugs" to you, my friend!
I hope you enjoy my List,
Granny
Current
arthritis treatments often have side-effects attributable to active
compounds as well as route of administration. Cannabidiol (CBD)
attenuates inflammation and pain without side-effects, but CBD is
hydrophobic and has poor oral bioavailability. Topical drug application
avoids gastrointestinal administration, first pass metabolism, providing
more constant plasma levels.
METHODS:
This
study examined efficacy of transdermal CBD for reduction in
inflammation and pain, assessing any adverse effects in a rat complete
Freund's adjuvant-induced monoarthritic knee joint model. CBD gels (0.6,
3.1, 6.2 or 62.3 mg/day) were applied for 4 consecutive days after
arthritis induction. Joint circumference and immune cell invasion in
histological sections were measured to indicate level of inflammation.
Paw withdrawal latency (PWL) in response to noxious heat stimulation
determined nociceptive sensitization, and exploratory behaviour
ascertained animal's activity level.
RESULTS:
Measurement
of plasma CBD concentration provided by transdermal absorption revealed
linearity with 0.6-6.2 mg/day doses. Transdermal CBD gel significantly
reduced joint swelling, limb posture scores as a rating of spontaneous
pain, immune cell infiltration and thickening of the synovial membrane
in a dose-dependent manner. PWL recovered to near baseline level.
Immunohistochemical analysis of spinal cord (CGRP, OX42) and dorsal root
ganglia (TNFα) revealed dose-dependent reductions of pro-inflammatory
biomarkers. Results showed 6.2 and 62 mg/day were effective doses.
Exploratory behaviour was not altered by CBD indicating limited effect
on higher brain function.
In
addition to the well-known palliative effects of cannabinoids on some
cancer-associated symptoms, a large body of evidence shows that these
molecules can decrease tumour growth in animal models of cancer. They do
so by modulating key cell signalling pathways involved in the control
of cancer cell proliferation and survival. In addition, cannabinoids
inhibit angiogenesis and decrease metastasis in various tumour types in
laboratory animals. In this review, we discuss the current understanding
of cannabinoids as antitumour agents, focusing on recent discoveries
about their molecular mechanisms of action, including resistance
mechanisms and opportunities for their use in combination therapy. Those
observations have already contributed to the foundation for the
development of the first clinical studies that will analyze the safety
and potential clinical benefit of cannabinoids as anticancer agents.
Preliminary lab studies at the Salk Institute find THC reduces beta amyloid proteins in human neurons
LA JOLLA–Salk Institute scientists have found
preliminary evidence that tetrahydrocannabinol (THC) and other compounds
found in marijuana can promote the cellular removal of amyloid beta, a
toxic protein associated with Alzheimer’s disease.
While these exploratory studies were conducted in neurons grown in
the laboratory, they may offer insight into the role of inflammation in
Alzheimer’s disease and could provide clues to developing novel
therapeutics for the disorder.
“Although other studies have offered evidence that cannabinoids might
be neuroprotective against the symptoms of Alzheimer’s, we believe our
study is the first to demonstrate that cannabinoids affect both
inflammation and amyloid beta accumulation in nerve cells,” says Salk
Professor David Schubert, the senior author of the paper.
Alzheimer’s disease is a progressive brain disorder that leads to
memory loss and can seriously impair a person’s ability to carry out
daily tasks. It affects more than five million Americans according to
the National Institutes of Health, and is a leading cause of death. It
is also the most common cause of dementia and its incidence is expected
to triple during the next 50 years.
It has long been known that amyloid beta accumulates within the nerve
cells of the aging brain well before the appearance of Alzheimer’s
disease symptoms and plaques. Amyloid beta is a major component of the
plaque deposits that are a hallmark of the disease. But the precise role
of amyloid beta and the plaques it forms in the disease process remains
unclear. David Schubert, Professor of Salk’s Cellular Neurobiology Laboratory
Click here for a high resolution image
Credit: Salk Institute
In a manuscript published in June 2016’s Aging and Mechanisms of Disease, the Salk team studied nerve cells altered to produce high levels of amyloid beta to mimic aspects of Alzheimer’s disease.
The researchers found that high levels of amyloid beta were
associated with cellular inflammation and higher rates of neuron death.
They demonstrated that exposing the cells to THC reduced amyloid beta
protein levels and eliminated the inflammatory response from the nerve
cells caused by the protein, thereby allowing the nerve cells to
survive.
“Inflammation within the brain is a major component of the damage
associated with Alzheimer’s disease, but it has always been assumed that
this response was coming from immune-like cells in the brain, not the
nerve cells themselves,” says Antonio Currais, a postdoctoral researcher
in Schubert’s laboratory and first author of the paper. “When we were
able to identify the molecular basis of the inflammatory response to
amyloid beta, it became clear that THC-like compounds that the nerve
cells make themselves may be involved in protecting the cells from
dying.”
Brain cells have switches known as receptors that can be activated by
endocannabinoids, a class of lipid molecules made by the body that are
used for intercellular signaling in the brain. The psychoactive effects
of marijuana are caused by THC, a molecule similar in activity to
endocannabinoids that can activate the same receptors. Physical activity
results in the production of endocannabinoids and some studies have
shown that exercise may slow the progression of Alzheimer’s disease.
Schubert emphasized that his team’s findings were conducted in
exploratory laboratory models, and that the use of THC-like compounds as
a therapy would need to be tested in clinical trials.
In separate but related research, his lab found an Alzheimer’s drug
candidate called J147 that also removes amyloid beta from nerve cells
and reduces the inflammatory response in both nerve cells and the brain.
It was the study of J147 that led the scientists to discover that
endocannabinoids are involved in the removal of amyloid beta and the
reduction of inflammation.
Other authors on the paper include Oswald Quehenberger and Aaron Armando at the University of California, San Diego; and Pamela Maher and Daniel Daughtery at the Salk Institute.
The study was supported by the National Institutes of Health, The Burns Foundation and The Bundy Foundation.
Alzheimer’s
Disease patients benefited from marijuana, Israeli researchers report.
Above, Julianne Moore in 2015’s ‘Still Alice’.
Adding marijuana to the treatment of Alzheimer’s Disease “is safe
and a promising treatment option”, Israeli researchers conclude, in the
latest study on the burgeoning practice.
Alzheimer’s Disease is a devastating and fatal degenerative
neurological disease affecting more than five million Americans today.
One in three seniors will die with Alzheimer’s or another dementia, and
Alzheimer’s is the sixth leading cause of death in the nation, costing
America about $203 billion in 2013.
Past studies
indicate the active ingredients in cannabis can provide palliative
relief to Alzheimer’s patients with dementia — calming them down and
allowing them to sleep. Cell studies also indicate cannabis’ active
ingredients could prevent the onset and progression of Alzheimer’s, by
interrupting the cycle of beta-amyloid plaque creation thought to cause
Alzheimer’s Disease.
Researchers at the Abarbanel Mental Health Center and the Sackler
Faculty of Medicine at Tel-Aviv University, in Israel, along with the
Department of Psychology, at Bar-Ilan University conducted one of the
first clinical studies of cannabis on human Alzheimer’s patients.
The main active ingredient in cannabis “tetrahydrocannabinol (THC) is
a potential treatment for Alzheimer’s disease (AD)” researchers wrote.
They wanted to measure the safety and efficacy of giving a medical
cannabis oil containing THC as an add-on to existing Alzheimer’s drugs.
Their goal: relieving the terrifying behavioral and psychological
symptoms of dementia.
Eleven patients were recruited into an open-label, month-long trial.
Ten patients finished the trial, and researchers reported “significant
reduction” in mental illness severity, especially with regard to
delusions, agitation/aggression, irritability, apathy, sleep, and
caregiver distress.
“Adding [medical cannabis oil] to [Alzheimer’s Disease] patients’
pharmacotherapy is safe and a promising treatment option,” researchers
concluded.
Read: “Safety
and Efficacy of Medical Cannabis Oil for Behavioral and Psychological
Symptoms of Dementia: An-Open Label, Add-On, Pilot Study” Smell the Truth editor David Downs is the author ofThe Medical Marijuana Guidebook, out in paperback this February (Whitman Publishing).
For people suffering from chronic pain, treatment options are generally limited. You can take prescription painkillers
such as Vicodin or Oxycotin, but while they might alleviate your
discomfort, they are also addictive and dangerous. And as the U.S.
continues to struggle with rising rates of opiate addiction, the search is on for a safer alternative. Cannabis appears to be a good candidate.
A new study
published in the Journal of Pain found that chronic pain patients who
used marijuana for one year had reduced discomfort, improved quality of
life, and experienced no increased risk of serious side effects. McGill
University researchers analyzed reports from 216 cannabis users and 215
non-users, finding that pot is effective at treating pain.
"[W]e
noted significant improvements in pain intensity and the physical
dimension of quality of life over one year among the cannabis users
compared to controls," the researchers wrote.
"There was also significant improvement among cannabis users in
measures of the sensory component of pain, symptom distress, and total
mood disturbance compared to controls."
This
isn't the first study to look at the effects of marijuana on pain. In
2009, the National Association of Boards of Pharmacy announced that
cannabis could help with "multiple pain syndromes," including
neuropathic (burning), mechanical (aching), and inflammatory (acute,
sharp) pain. Not only is the substance an effective analgesic, but it
also carries "minimal physical dependence" with limited drug
interactions, the organization wrote.
What's more, a review of cannabis trials published in the British Journal of Clinical Pharmacology
concluded that "it is reasonable to consider cannabinoids as a
treatment option for the management of chronic neuropathic pain with
evidence of efficacy in other types of chronic pain such as fibromyalgia
and rheumatoid arthritis as well."
And a 2013 study published in the Clinical Journal of Pain
found that "cannabinergic pain medicines have been shown to be modestly
effective and safe treatments in patients with a variety of chronic
pain conditions," leading researchers to conclude that incorporating
medical cannabis into pain medicine education "seems warranted and
continuing clinical research and empiric treatment trials are
appropriate."
The
takeaway here is something that might seem obvious to regular marijuana
users: pot is good for pain. But it's not just good, it's safe. Even
over-the-counter medication such as Tylenol carries risk of overdose
if you take too much, threatening to damage your liver. Cannabis, on
the other hand, has no serious side effects, and numerous studies have
demonstrated that it is similarly effective at treating various types of
pain.
What's remarkable about this potential health benefit is what it could mean in the context of America's heroin epidemic. According to the National Institute on Drug Abuse, abuse of painkillers directly correlates with the rise of heroin addiction
in the U.S. If a person becomes addicted to prescription pain
medication, there is a strong chance that they could transition to
cheaper, more potent drugs such as heroin.
But
in states where pain patients have access to medical marijuana, the
rate of fatal drug overdose is reduced, suggesting that pot is something
of an "anti-gateway drug."
By legalizing marijuana and allowing people to manage their pain with
cannabis, we could effectively stop the cycle and help patients who
might benefit from a safe and non-addictive alternative to pills.
ImportanceOpioid analgesic overdose mortality continues to rise in the
United States, driven by increases in prescribing for chronic pain.
Because chronic pain is a major indication for medical cannabis, laws
that establish access to medical cannabis may change overdose mortality
related to opioid analgesics in states that have enacted them. ObjectiveTo determine the association between the presence of state medical cannabis laws and opioid analgesic overdose mortality. Design, Setting, and ParticipantsA time-series analysis was conducted of medical cannabis laws
and state-level death certificate data in the United States from 1999 to
2010; all 50 states were included. ExposuresPresence of a law establishing a medical cannabis program in the state. Main Outcomes and MeasuresAge-adjusted opioid analgesic overdose death rate per 100 000
population in each state. Regression models were developed including
state and year fixed effects, the presence of 3 different policies
regarding opioid analgesics, and the state-specific unemployment rate. ResultsThree states (California, Oregon, and Washington) had medical
cannabis laws effective prior to 1999. Ten states (Alaska, Colorado,
Hawaii, Maine, Michigan, Montana, Nevada, New Mexico, Rhode Island, and
Vermont) enacted medical cannabis laws between 1999 and 2010. States
with medical cannabis laws had a 24.8% lower mean annual opioid overdose
mortality rate (95% CI, −37.5% to −9.5%; P = .003) compared with
states without medical cannabis laws. Examination of the association
between medical cannabis laws and opioid analgesic overdose mortality in
each year after implementation of the law showed that such laws were
associated with a lower rate of overdose mortality that generally
strengthened over time: year 1 (−19.9%; 95% CI, −30.6% to −7.7%; P = .002), year 2 (−25.2%; 95% CI, −40.6% to −5.9%; P = .01), year 3 (−23.6%; 95% CI, −41.1% to −1.0%; P = .04), year 4 (−20.2%; 95% CI, −33.6% to −4.0%; P = .02), year 5 (−33.7%; 95% CI, −50.9% to −10.4%; P = .008), and year 6 (−33.3%; 95% CI, −44.7% to −19.6%; P < .001). In secondary analyses, the findings remained similar. Conclusions and Relevance
Medical cannabis laws are associated with significantly lower
state-level opioid overdose mortality rates. Further investigation is
required to determine how medical cannabis laws may interact with
policies aimed at preventing opioid analgesic overdose.
Adding marijuana to the treatment of Alzheimer’s Disease “is safe
and a promising treatment option”, Israeli researchers conclude, in the
latest study on the burgeoning practice.
