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Cannabis compound slows lung cancer in mice
Cannabis compound slows lung cancer in mice
Lucky mice.
It seems to speed entry to the criminal "justice" system in humans.
< * w w w .newscientist . com /article/dn11630-cannabis-compound-slows-lung-cancer-in-mice.html>
* tinyurl . com /24k936
Cannabis compound slows lung cancer in mice
The active compound in marijuana, THC, can slow the growth of lung tumours
and reduce the spread of the cancer in mice, a preliminary study reveals.
Human lung cancer tumours grew less than half as fast in mice that
received moderate doses of the compound, the researchers reveal. They hope
that drugs mimicking the apparent anti-cancer effects of
tetrahydrocanabinol (THC) could one day help treat patients. The team
strongly discourage people from self-medicating by smoking marijuana,
noting that doing so could potentially encourage tumour growth.
Ramesh Ganju at the Harvard Cancer Center in Boston, Massachusetts, US,
and colleagues deposited human lung cancer cells under the skin of a dozen
mice and allowed the tumours to grow in the animals for about two weeks.
They then began giving half of these mice daily injections of about 250
micrograms of synthetic THC right next to the tumours for three weeks. A
cannabis cigarette may contain as much as 150 milligrams of THC.
Tumours in the control mice averaged about 0.6 grams in weight by the end
of the five-week trial. By comparison, those in the mice that received THC
weighed just 0.25 grams ? 60% less. Blood blocker
In a separate experiment to test whether THC could slow the spread of
cancer cells (metastasis), the researchers injected human lung cancer
cells into the tail veins of mice to mimic such a spread. The team
immediately started giving half of these animals a daily 250 microgram
injection of THC for three weeks. They found 60% fewer cancerous lesions
in the mice that received THC compared to the control animals.
Ganju believes that THC inhibits cancer growth by blocking the formation
of blood vessels within tumours. Previous tests on human lung cancer cells
in a dish suggested that THC blocked the signalling of a substance known
as epidermal growth factor (EGF). Under normal circumstances, EGF may
promote blood vessel development, Ganju says.
Previous studies have also found that THC can shrink brain tumours.
Nevertheless, experts caution people against smoking marijuana. "I
wouldn't advise that. It could make the cancer grow faster," says Ganju,
noting that THC might encourage the growth of breast cancer. He adds that
that "a lot of work needs to be done" before scientists fully understand
how THC affects tumours.
While some studies have found no link between cannabis use and cancer,
others have concluded that cannabis smoking is "more harmful" than tobacco
because the smoke is inhaled more deeply into the lungs.
Ganju's team presented the new findings this week at the annual meeting of
the American Association for Cancer Research in Los Angeles, California,
US.
--
Phil Stovell, Hampshire, UK
Lucky mice.
It seems to speed entry to the criminal "justice" system in humans.
< * w w w .newscientist . com /article/dn11630-cannabis-compound-slows-lung-cancer-in-mice.html>
* tinyurl . com /24k936
Cannabis compound slows lung cancer in mice
The active compound in marijuana, THC, can slow the growth of lung tumours
and reduce the spread of the cancer in mice, a preliminary study reveals.
Human lung cancer tumours grew less than half as fast in mice that
received moderate doses of the compound, the researchers reveal. They hope
that drugs mimicking the apparent anti-cancer effects of
tetrahydrocanabinol (THC) could one day help treat patients. The team
strongly discourage people from self-medicating by smoking marijuana,
noting that doing so could potentially encourage tumour growth.
Ramesh Ganju at the Harvard Cancer Center in Boston, Massachusetts, US,
and colleagues deposited human lung cancer cells under the skin of a dozen
mice and allowed the tumours to grow in the animals for about two weeks.
They then began giving half of these mice daily injections of about 250
micrograms of synthetic THC right next to the tumours for three weeks. A
cannabis cigarette may contain as much as 150 milligrams of THC.
Tumours in the control mice averaged about 0.6 grams in weight by the end
of the five-week trial. By comparison, those in the mice that received THC
weighed just 0.25 grams ? 60% less. Blood blocker
In a separate experiment to test whether THC could slow the spread of
cancer cells (metastasis), the researchers injected human lung cancer
cells into the tail veins of mice to mimic such a spread. The team
immediately started giving half of these animals a daily 250 microgram
injection of THC for three weeks. They found 60% fewer cancerous lesions
in the mice that received THC compared to the control animals.
Ganju believes that THC inhibits cancer growth by blocking the formation
of blood vessels within tumours. Previous tests on human lung cancer cells
in a dish suggested that THC blocked the signalling of a substance known
as epidermal growth factor (EGF). Under normal circumstances, EGF may
promote blood vessel development, Ganju says.
Previous studies have also found that THC can shrink brain tumours.
Nevertheless, experts caution people against smoking marijuana. "I
wouldn't advise that. It could make the cancer grow faster," says Ganju,
noting that THC might encourage the growth of breast cancer. He adds that
that "a lot of work needs to be done" before scientists fully understand
how THC affects tumours.
While some studies have found no link between cannabis use and cancer,
others have concluded that cannabis smoking is "more harmful" than tobacco
because the smoke is inhaled more deeply into the lungs.
Ganju's team presented the new findings this week at the annual meeting of
the American Association for Cancer Research in Los Angeles, California,
US.
--
Phil Stovell, Hampshire, UK
Re: Cannabis compound slows lung cancer in mice
"Phil Stovell" <phil@stovell.org.uk> wrote in message
news:pan.2007.04.18.14.36.11.259080@stovell.org.uk...
> Lucky mice.
>
> It seems to speed entry to the criminal "justice" system in humans.
>
>
> < * w w w .newscientist . com /article/dn11630-cannabis-compound-slows-lung-cancer-in-mice.html>
> * tinyurl . com /24k936
>
>
> Cannabis compound slows lung cancer in mice
>
> The active compound in marijuana, THC, can slow the growth of lung tumours
> and reduce the spread of the cancer in mice, a preliminary study reveals.
>
> Human lung cancer tumours grew less than half as fast in mice that
> received moderate doses of the compound, the researchers reveal. They hope
> that drugs mimicking the apparent anti-cancer effects of
> tetrahydrocanabinol (THC) could one day help treat patients. The team
> strongly discourage people from self-medicating by smoking marijuana,
> noting that doing so could potentially encourage tumour growth.
>
> Ramesh Ganju at the Harvard Cancer Center in Boston, Massachusetts, US,
> and colleagues deposited human lung cancer cells under the skin of a dozen
> mice and allowed the tumours to grow in the animals for about two weeks.
> They then began giving half of these mice daily injections of about 250
> micrograms of synthetic THC right next to the tumours for three weeks. A
> cannabis cigarette may contain as much as 150 milligrams of THC.
>
> Tumours in the control mice averaged about 0.6 grams in weight by the end
> of the five-week trial. By comparison, those in the mice that received THC
> weighed just 0.25 grams - 60% less. Blood blocker
>
> In a separate experiment to test whether THC could slow the spread of
> cancer cells (metastasis), the researchers injected human lung cancer
> cells into the tail veins of mice to mimic such a spread. The team
> immediately started giving half of these animals a daily 250 microgram
> injection of THC for three weeks. They found 60% fewer cancerous lesions
> in the mice that received THC compared to the control animals.
>
> Ganju believes that THC inhibits cancer growth by blocking the formation
> of blood vessels within tumours. Previous tests on human lung cancer cells
> in a dish suggested that THC blocked the signalling of a substance known
> as epidermal growth factor (EGF). Under normal circumstances, EGF may
> promote blood vessel development, Ganju says.
>
> Previous studies have also found that THC can shrink brain tumours.
> Nevertheless, experts caution people against smoking marijuana. "I
> wouldn't advise that. It could make the cancer grow faster," says Ganju,
> noting that THC might encourage the growth of breast cancer. He adds that
> that "a lot of work needs to be done" before scientists fully understand
> how THC affects tumours.
>
> While some studies have found no link between cannabis use and cancer,
> others have concluded that cannabis smoking is "more harmful" than tobacco
> because the smoke is inhaled more deeply into the lungs.
>
> Ganju's team presented the new findings this week at the annual meeting of
> the American Association for Cancer Research in Los Angeles, California,
> US.
>
> --
> Phil Stovell, Hampshire, UK
>
I found out that it can even bring back the "dead" (grin)
there does seem to be regular studies which suggest it could be helpful in a
few circumstances eg.Cancer, pain, depression and aniexty...
lets hope it really could be used as a basis for a cure for cancer, might
reduce the nonsense notion's of "evil" that prohibitionist hold.. and
finally gain acceptance.
"Phil Stovell" <phil@stovell.org.uk> wrote in message
news:pan.2007.04.18.14.36.11.259080@stovell.org.uk...
> Lucky mice.
>
> It seems to speed entry to the criminal "justice" system in humans.
>
>
> < * w w w .newscientist . com /article/dn11630-cannabis-compound-slows-lung-cancer-in-mice.html>
> * tinyurl . com /24k936
>
>
> Cannabis compound slows lung cancer in mice
>
> The active compound in marijuana, THC, can slow the growth of lung tumours
> and reduce the spread of the cancer in mice, a preliminary study reveals.
>
> Human lung cancer tumours grew less than half as fast in mice that
> received moderate doses of the compound, the researchers reveal. They hope
> that drugs mimicking the apparent anti-cancer effects of
> tetrahydrocanabinol (THC) could one day help treat patients. The team
> strongly discourage people from self-medicating by smoking marijuana,
> noting that doing so could potentially encourage tumour growth.
>
> Ramesh Ganju at the Harvard Cancer Center in Boston, Massachusetts, US,
> and colleagues deposited human lung cancer cells under the skin of a dozen
> mice and allowed the tumours to grow in the animals for about two weeks.
> They then began giving half of these mice daily injections of about 250
> micrograms of synthetic THC right next to the tumours for three weeks. A
> cannabis cigarette may contain as much as 150 milligrams of THC.
>
> Tumours in the control mice averaged about 0.6 grams in weight by the end
> of the five-week trial. By comparison, those in the mice that received THC
> weighed just 0.25 grams - 60% less. Blood blocker
>
> In a separate experiment to test whether THC could slow the spread of
> cancer cells (metastasis), the researchers injected human lung cancer
> cells into the tail veins of mice to mimic such a spread. The team
> immediately started giving half of these animals a daily 250 microgram
> injection of THC for three weeks. They found 60% fewer cancerous lesions
> in the mice that received THC compared to the control animals.
>
> Ganju believes that THC inhibits cancer growth by blocking the formation
> of blood vessels within tumours. Previous tests on human lung cancer cells
> in a dish suggested that THC blocked the signalling of a substance known
> as epidermal growth factor (EGF). Under normal circumstances, EGF may
> promote blood vessel development, Ganju says.
>
> Previous studies have also found that THC can shrink brain tumours.
> Nevertheless, experts caution people against smoking marijuana. "I
> wouldn't advise that. It could make the cancer grow faster," says Ganju,
> noting that THC might encourage the growth of breast cancer. He adds that
> that "a lot of work needs to be done" before scientists fully understand
> how THC affects tumours.
>
> While some studies have found no link between cannabis use and cancer,
> others have concluded that cannabis smoking is "more harmful" than tobacco
> because the smoke is inhaled more deeply into the lungs.
>
> Ganju's team presented the new findings this week at the annual meeting of
> the American Association for Cancer Research in Los Angeles, California,
> US.
>
> --
> Phil Stovell, Hampshire, UK
>
I found out that it can even bring back the "dead" (grin)
there does seem to be regular studies which suggest it could be helpful in a
few circumstances eg.Cancer, pain, depression and aniexty...
lets hope it really could be used as a basis for a cure for cancer, might
reduce the nonsense notion's of "evil" that prohibitionist hold.. and
finally gain acceptance.
Re: Cannabis compound slows lung cancer in mice
Actually Mark I did a quick check of the primary literature and there are at
least 15 conditions, including dementia, atherosclerosis, and diabetes, in
which cannabinoid based interventions offer potential. In regard to this
news item it is consistent with a study released by the American Thoracic
Society sometime ago wherein they found no evidence of increased rates of
lung, head, or neck cancer in pot smokers and they reasoned it is because
of THC impact on cell cycle dynamics. THC and other cannabinoids are known
to inhibit VEGF, which stimulates new blood vessel growth.
"Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
news:5cqVh.3689$VT3.2654@newsfe6-gui.ntli . net ...
>
> "Phil Stovell" <phil@stovell.org.uk> wrote in message
> news:pan.2007.04.18.14.36.11.259080@stovell.org.uk...
> > Lucky mice.
> >
> > It seems to speed entry to the criminal "justice" system in humans.
> >
> >
> >
< * w w w .newscientist . com /article/dn11630-cannabis-compound-slows-lung-ca
ncer-in-mice.html>
> > * tinyurl . com /24k936
> >
> >
> > Cannabis compound slows lung cancer in mice
> >
> > The active compound in marijuana, THC, can slow the growth of lung
tumours
> > and reduce the spread of the cancer in mice, a preliminary study
reveals.
> >
> > Human lung cancer tumours grew less than half as fast in mice that
> > received moderate doses of the compound, the researchers reveal. They
hope
> > that drugs mimicking the apparent anti-cancer effects of
> > tetrahydrocanabinol (THC) could one day help treat patients. The team
> > strongly discourage people from self-medicating by smoking marijuana,
> > noting that doing so could potentially encourage tumour growth.
> >
> > Ramesh Ganju at the Harvard Cancer Center in Boston, Massachusetts, US,
> > and colleagues deposited human lung cancer cells under the skin of a
dozen
> > mice and allowed the tumours to grow in the animals for about two weeks.
> > They then began giving half of these mice daily injections of about 250
> > micrograms of synthetic THC right next to the tumours for three weeks. A
> > cannabis cigarette may contain as much as 150 milligrams of THC.
> >
> > Tumours in the control mice averaged about 0.6 grams in weight by the
end
> > of the five-week trial. By comparison, those in the mice that received
THC
> > weighed just 0.25 grams - 60% less. Blood blocker
> >
> > In a separate experiment to test whether THC could slow the spread of
> > cancer cells (metastasis), the researchers injected human lung cancer
> > cells into the tail veins of mice to mimic such a spread. The team
> > immediately started giving half of these animals a daily 250 microgram
> > injection of THC for three weeks. They found 60% fewer cancerous lesions
> > in the mice that received THC compared to the control animals.
> >
> > Ganju believes that THC inhibits cancer growth by blocking the formation
> > of blood vessels within tumours. Previous tests on human lung cancer
cells
> > in a dish suggested that THC blocked the signalling of a substance known
> > as epidermal growth factor (EGF). Under normal circumstances, EGF may
> > promote blood vessel development, Ganju says.
> >
> > Previous studies have also found that THC can shrink brain tumours.
> > Nevertheless, experts caution people against smoking marijuana. "I
> > wouldn't advise that. It could make the cancer grow faster," says Ganju,
> > noting that THC might encourage the growth of breast cancer. He adds
that
> > that "a lot of work needs to be done" before scientists fully understand
> > how THC affects tumours.
> >
> > While some studies have found no link between cannabis use and cancer,
> > others have concluded that cannabis smoking is "more harmful" than
tobacco
> > because the smoke is inhaled more deeply into the lungs.
> >
> > Ganju's team presented the new findings this week at the annual meeting
of
> > the American Association for Cancer Research in Los Angeles, California,
> > US.
> >
> > --
> > Phil Stovell, Hampshire, UK
> >
>
> I found out that it can even bring back the "dead" (grin)
>
> there does seem to be regular studies which suggest it could be helpful in
a
> few circumstances eg.Cancer, pain, depression and aniexty...
>
> lets hope it really could be used as a basis for a cure for cancer, might
> reduce the nonsense notion's of "evil" that prohibitionist hold.. and
> finally gain acceptance.
>
>
Actually Mark I did a quick check of the primary literature and there are at
least 15 conditions, including dementia, atherosclerosis, and diabetes, in
which cannabinoid based interventions offer potential. In regard to this
news item it is consistent with a study released by the American Thoracic
Society sometime ago wherein they found no evidence of increased rates of
lung, head, or neck cancer in pot smokers and they reasoned it is because
of THC impact on cell cycle dynamics. THC and other cannabinoids are known
to inhibit VEGF, which stimulates new blood vessel growth.
"Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
news:5cqVh.3689$VT3.2654@newsfe6-gui.ntli . net ...
>
> "Phil Stovell" <phil@stovell.org.uk> wrote in message
> news:pan.2007.04.18.14.36.11.259080@stovell.org.uk...
> > Lucky mice.
> >
> > It seems to speed entry to the criminal "justice" system in humans.
> >
> >
> >
< * w w w .newscientist . com /article/dn11630-cannabis-compound-slows-lung-ca
ncer-in-mice.html>
> > * tinyurl . com /24k936
> >
> >
> > Cannabis compound slows lung cancer in mice
> >
> > The active compound in marijuana, THC, can slow the growth of lung
tumours
> > and reduce the spread of the cancer in mice, a preliminary study
reveals.
> >
> > Human lung cancer tumours grew less than half as fast in mice that
> > received moderate doses of the compound, the researchers reveal. They
hope
> > that drugs mimicking the apparent anti-cancer effects of
> > tetrahydrocanabinol (THC) could one day help treat patients. The team
> > strongly discourage people from self-medicating by smoking marijuana,
> > noting that doing so could potentially encourage tumour growth.
> >
> > Ramesh Ganju at the Harvard Cancer Center in Boston, Massachusetts, US,
> > and colleagues deposited human lung cancer cells under the skin of a
dozen
> > mice and allowed the tumours to grow in the animals for about two weeks.
> > They then began giving half of these mice daily injections of about 250
> > micrograms of synthetic THC right next to the tumours for three weeks. A
> > cannabis cigarette may contain as much as 150 milligrams of THC.
> >
> > Tumours in the control mice averaged about 0.6 grams in weight by the
end
> > of the five-week trial. By comparison, those in the mice that received
THC
> > weighed just 0.25 grams - 60% less. Blood blocker
> >
> > In a separate experiment to test whether THC could slow the spread of
> > cancer cells (metastasis), the researchers injected human lung cancer
> > cells into the tail veins of mice to mimic such a spread. The team
> > immediately started giving half of these animals a daily 250 microgram
> > injection of THC for three weeks. They found 60% fewer cancerous lesions
> > in the mice that received THC compared to the control animals.
> >
> > Ganju believes that THC inhibits cancer growth by blocking the formation
> > of blood vessels within tumours. Previous tests on human lung cancer
cells
> > in a dish suggested that THC blocked the signalling of a substance known
> > as epidermal growth factor (EGF). Under normal circumstances, EGF may
> > promote blood vessel development, Ganju says.
> >
> > Previous studies have also found that THC can shrink brain tumours.
> > Nevertheless, experts caution people against smoking marijuana. "I
> > wouldn't advise that. It could make the cancer grow faster," says Ganju,
> > noting that THC might encourage the growth of breast cancer. He adds
that
> > that "a lot of work needs to be done" before scientists fully understand
> > how THC affects tumours.
> >
> > While some studies have found no link between cannabis use and cancer,
> > others have concluded that cannabis smoking is "more harmful" than
tobacco
> > because the smoke is inhaled more deeply into the lungs.
> >
> > Ganju's team presented the new findings this week at the annual meeting
of
> > the American Association for Cancer Research in Los Angeles, California,
> > US.
> >
> > --
> > Phil Stovell, Hampshire, UK
> >
>
> I found out that it can even bring back the "dead" (grin)
>
> there does seem to be regular studies which suggest it could be helpful in
a
> few circumstances eg.Cancer, pain, depression and aniexty...
>
> lets hope it really could be used as a basis for a cure for cancer, might
> reduce the nonsense notion's of "evil" that prohibitionist hold.. and
> finally gain acceptance.
>
>
Re: Cannabis compound slows lung cancer in mice
>>
>> >
>>
>> I found out that it can even bring back the "dead" (grin)
>>
>> there does seem to be regular studies which suggest it could be helpful
>> in
> a
>> few circumstances eg.Cancer, pain, depression and aniexty...
>>
>> lets hope it really could be used as a basis for a cure for cancer,
>> might
>> reduce the nonsense notion's of "evil" that prohibitionist hold.. and
>> finally gain acceptance.
"John H." <bingblat@goaway . com .au> wrote in message
news:46283e76@quokka.wn . com .au...
> Actually Mark I did a quick check of the primary literature and there are
> at
> least 15 conditions, including dementia, atherosclerosis, and diabetes, in
> which cannabinoid based interventions offer potential. In regard to this
> news item it is consistent with a study released by the American Thoracic
> Society sometime ago wherein they found no evidence of increased rates of
> lung, head, or neck cancer in pot smokers and they reasoned it is because
> of THC impact on cell cycle dynamics. THC and other cannabinoids are known
> to inhibit VEGF, which stimulates new blood vessel growth.
> "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
(I reordered the above, i was told earlier that post should be posted after
the original otherwise it "troll like" behaviour. Don't get me wrong i don't
mind but i guess we should try and follow neticate where possible..I'm sure
i've broken loads of rules without realising).
I was being a little sarcastic(i believe in it's theroputic nature), I know
there are lots of medical conditions cannabis can help with.. I guess i
should have deatailed more...thanks for pointing this out though...I think
most people who've read my previous mails, over the last couple of months,
to this group will know i'm a fan, but I only know what i have read(I'm no
expert). I try to research at sites that have some credability but i can
only go on their data..
However I would suggest that cannabis makes you "feel good" and would reduce
how much people notice their illness's, people may think it helps and it
does but it isn't making them "better" more masking their illness..other
drugs would do the same job due to their "painkiller" nature...I could be
wrong(if i am i'm sure you'll tell me and explain why?), and to be fair, it
dosn't matter to me as the end result is the person feels "better". I just
like to cover all the bases..
Here's one website which details quite a few illness which cannabis is
reported to help..
* w w w .pacifier . com /~alive/index_se_cmu.htm
I just think we need to be careful about syaing that cannabis is a
"medicinal wonder", it's still early days with regards to reaserch. The
"prohibition" people would move quickly to turn that aginst us in the event
cannabis is proven not to help.. . it may harm further, the drugs reputation..
>>
>> >
>>
>> I found out that it can even bring back the "dead" (grin)
>>
>> there does seem to be regular studies which suggest it could be helpful
>> in
> a
>> few circumstances eg.Cancer, pain, depression and aniexty...
>>
>> lets hope it really could be used as a basis for a cure for cancer,
>> might
>> reduce the nonsense notion's of "evil" that prohibitionist hold.. and
>> finally gain acceptance.
"John H." <bingblat@goaway . com .au> wrote in message
news:46283e76@quokka.wn . com .au...
> Actually Mark I did a quick check of the primary literature and there are
> at
> least 15 conditions, including dementia, atherosclerosis, and diabetes, in
> which cannabinoid based interventions offer potential. In regard to this
> news item it is consistent with a study released by the American Thoracic
> Society sometime ago wherein they found no evidence of increased rates of
> lung, head, or neck cancer in pot smokers and they reasoned it is because
> of THC impact on cell cycle dynamics. THC and other cannabinoids are known
> to inhibit VEGF, which stimulates new blood vessel growth.
> "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
(I reordered the above, i was told earlier that post should be posted after
the original otherwise it "troll like" behaviour. Don't get me wrong i don't
mind but i guess we should try and follow neticate where possible..I'm sure
i've broken loads of rules without realising).
I was being a little sarcastic(i believe in it's theroputic nature), I know
there are lots of medical conditions cannabis can help with.. I guess i
should have deatailed more...thanks for pointing this out though...I think
most people who've read my previous mails, over the last couple of months,
to this group will know i'm a fan, but I only know what i have read(I'm no
expert). I try to research at sites that have some credability but i can
only go on their data..
However I would suggest that cannabis makes you "feel good" and would reduce
how much people notice their illness's, people may think it helps and it
does but it isn't making them "better" more masking their illness..other
drugs would do the same job due to their "painkiller" nature...I could be
wrong(if i am i'm sure you'll tell me and explain why?), and to be fair, it
dosn't matter to me as the end result is the person feels "better". I just
like to cover all the bases..
Here's one website which details quite a few illness which cannabis is
reported to help..
* w w w .pacifier . com /~alive/index_se_cmu.htm
I just think we need to be careful about syaing that cannabis is a
"medicinal wonder", it's still early days with regards to reaserch. The
"prohibition" people would move quickly to turn that aginst us in the event
cannabis is proven not to help.. . it may harm further, the drugs reputation..
Re: Cannabis compound slows lung cancer in mice
Hey Mark,
I wasn't specifically commenting on your post. Lately I've been going
through the primary literature to investigate the therapeutic potential of
cannabinoids. The studies I mentioned have little if anything to do with how
people feel, the vast majority relate to cellular and clinical based studies
where biological markers are utilised to measure effect. On the basis of the
current research there is no other plant that offers so much therapeutic
potential. However, smoking is bad. Need vaporisers.
I was very surprised at the wide range of possible uses but this one really
takes the cake(THC better than current drugs):
6/03/2007 11:34PM
Mol. Pharmaceutics, 3 (6), 773 -777, 2006. 10.1021/mp060066m
S1543-8384(06)00066-9
Web Release Date: August 9, 2006
Copyright © 2006 American Chemical Society
A Molecular Link between the Active Component of Marijuana and Alzheimer's
Disease Pathology
Lisa M. Eubanks, Claude J. Rogers, Albert E. Beuscher IV, George F. Koob,
Arthur J. Olson, Tobin J. Dickerson, and Kim D. Janda*
Departments of Chemistry, Immunology, and Molecular Biology, Molecular and
Integrated Neurosciences Department, The Skaggs Institute for Chemical
Biology, and Worm Institute for Research and Medicine, The Scripps Research
Institute, 10550 North Torrey Pines Road, La Jolla, California 92037
Received June 11, 2006
Abstract:
Alzheimer's disease is the leading cause of dementia among the elderly, and
with the ever-increasing size of this population, cases of Alzheimer's
disease are expected to triple over the next 50 years. Consequently, the
development of treatments that slow or halt the disease progression have
become imperative to both improve the quality of life for patients and
reduce the health care costs attributable to Alzheimer's disease. Here, we
demonstrate that the active component of marijuana, 9-tetrahydrocannabinol
(THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well
as prevents AChE-induced amyloid -peptide (A) aggregation, the key
pathological marker of Alzheimer's disease. Computational modeling of the
THC-AChE interaction revealed that THC binds in the peripheral anionic site
of AChE, the critical region involved in amyloidgenesis. Compared to
currently approved drugs prescribed for the treatment of Alzheimer's
disease, THC is a considerably superior inhibitor of A aggregation, and this
study provides a previously unrecognized molecular mechanism through which
cannabinoid molecules may directly impact the progression of this
debilitating disease.
Keywords: Cannabinoids; Alzheimer's disease; acetylcholinesterase
And this one from a while back:
Article:
Cannabidiol and (2)D 9 -tetrahydrocannabinol are
neuroprotective antioxidants
Authors: A. J. HAMPSON* ? ,M.GRIMALDI ? ,J.AXELROD*, AND D. WINK §
Journal:
Proc. Natl. Acad. Sci. USA
Vol. 95, pp. 8268-8273, July 1998
Medical Sciences
Location:
n\ni
Cannabidiol and ()9-tetrahydrocannabinol are neuroprotective antioxidants
Date obtained: 17/02/2000
Web Page:
Date Read: 19/02/2000
Date to Review: 31/12/2000
Keywords:
Printed:
Notes:
ABSTRACT
The neuroprotective actions of cannabidiol and other cannabinoids were
examined in rat cortical neuron cultures exposed to toxic levels of the
excitatory neurotrans-mitter glutamate. Glutamate toxicity was reduced by
both cannabidiol, a nonpsychoactive constituent of marijuana, and the
psychotropic cannabinoid (2)D 9 -tetrahydrocannabinol (THC). Cannabinoids
protected equally well against neuro-toxicity mediated by
N-methyl-D-aspartate receptors, 2-ami-no-
3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid recep-tors, or kainate
receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown to
be calcium dependent; this study demonstrates that
2-amino-3-(4-butyl-3-hydroxyisox-azol- 5-yl)propionic acidykainate
receptor-type neurotoxicity is also calcium-dependent, partly mediated by
voltage sensi-tive calcium channels. The neuroprotection observed with
cannabidiol and THC was unaffected by cannabinoid receptor antagonist,
indicating it to be cannabinoid receptor indepen-dent. Previous studies have
shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol,
THC and several synthetic cannabinoids all were demonstrated to be
antioxi-dants by cyclic voltametry. Cannabidiol and THC also were shown to
prevent hydroperoxide-induced oxidative damage as well as or better than
other antioxidants in a chemical (Fenton reaction) system and neuronal
cultures. Cannabidiol was more protective against glutamate neurotoxicity
than either ascorbate or a-tocopherol, indicating it to be a potent
anti-oxidant. These data also suggest that the naturally occurring,
nonpsychotropic cannabinoid, cannabidiol, may be a poten-tially useful
therapeutic agent for the treatment of oxidative neurological disorders such
as cerebral ischemia.
Extracts
These results suggest that cannabidiol protects simi-shown). These results
suggest that cannabidiol protects simi-larly, regardless of whether toxicity
is mediated by NMDA,AMPA, or kainate receptors.
AMPAyKainate Toxicity Is Calcium Dependent.
Increasedcalcium influx is known to be a key factor in NMDAr-induced cell
death (4), but its role in AMPA and kainate toxicity is less clear. It has
been suggested that AMPAykainate receptors may not directly allow entry of
sufficient calcium to kill cells. However, AMPAykainate receptors f lux
large amounts of sodium, which can depolarize cell membranes. Such
depolar-ization may activate both voltage-sensitive calcium channels (21)
and facilitate NMDAr activation (22, 23). In this way, AMPAykainate receptor
stimulation may lead indirectly to accumulation of toxic intracellular
calcium levels.
--
cannabinoid HU-211 all donated electrons at a similar poten-tial as the
antioxidant BHT. Anandamide (arachidonyl-ethanolamide), which is not a
cannabinoid in structure but is an endogenous ligand for the cannabinoid
receptor, did not undergo oxidation in this assay (Fig. 4A). Three other
canna-binoids, cannabinol, nabilone, and levanantrodol, also were tested,
and they, too, exhibited oxidation profiles similar to cannabidiol and THC
(data not shown).
The ability of cannabinoids to be oxidized readily suggests that they may
possess antioxidant properties comparable to BHT
--
unaffected by cannabinoid receptor antagonist. This suggests that
cannabinoids may have potentially useful therapeutic effects that are
independent of psychoactivity-inducing can-nabinoid receptors (12) and so
are not necessarily accompa-nied by psychotropic side effects.
-
Cannabidiol blocked glutamate toxicity in cortical neurons with equal
potency regardless of whether the insult was mediated by NMDAr, AMPA
receptors, or kainate receptors. This suggests that either cannabinoids
antagonize all three glutamate receptors with the same affinity, or, more
likely, their site of action is downstream of initial receptor activation
--
Neurotoxic concentrations of glutamate induce mas-sive calcium influx
through NMDAr (4) that ultimately kills the cell. This study has
demonstrated that the toxic effects of glutamate are also calcium-dependent
when mediated by AMPAykainate receptors. Both EDTA (a calcium chelator) and
voltage-sensitive calcium channel inhibitors reduced in-dicate that many
cannabinoids exert a considerable protective antioxidant effect in neuronal
cultures. The similarity of the voltamagrams observed with cannabidiol,
HU-211, and several other cannabinoids also suggests that the reported
antioxidant effect of HU-211 is not a feature unique to this atypical
cannabinoid, (as previously implied; e.g., ref. 11) but, rather, a common
property of classical cannabinoid structures. The potency of cannabidiol as
an antioxidant was examined by comparing it on an equimolar basis with other
commonly used antioxidants. Cannabidiol protected neurons to a greater
degree than either of the dietary antioxidants, a-tocopherol or ascorbate.
As in the Fenton reaction system, cannabidiol protected neurons with
comparable efficacy to the potent antioxidant BHT. The similar antioxidant
abilities of canna-bidiol and BHT in this chemical system and their
comparable protection in neuronal cultures implies that cannabidiol
neu-roprotection is caused by an antioxidant effect.
The antioxidative properties of cannabinoids suggest a therapeutic use as
neuroprotective agents, and the particular properties of cannabidiol make it
a good candidate for such development. Although cannabidiol was similar in
neuropro-tective capacity to BHT, cannabidiol has no known tumor-promoting
effects [unlike BHT (25, 26)]. The lack of psycho-activity
--
Furthermore, the ability of can-nabidiol to protect against neuronal injury
without inhibiting NMDAr may reduce the occurrence of toxicity or side
effects associated with NMDAr antagonists (27). Previous studies have
indicated that cannabidiol is not toxic, even when chron-ically administered
to humans (28) or given in large acute doses [700 mgyday (29)]. In vivo
studies to examine the efficacy of cannabidiol as a treatment for
experimentally induced isch-emic stroke are currently in progress.
Project:
"Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
news:FM0Wh.4452$kb4.566@newsfe1-win.ntli . net ...
>
> >>
> >> >
> >>
> >> I found out that it can even bring back the "dead" (grin)
> >>
> >> there does seem to be regular studies which suggest it could be helpful
> >> in
> > a
> >> few circumstances eg.Cancer, pain, depression and aniexty...
> >>
> >> lets hope it really could be used as a basis for a cure for cancer,
> >> might
> >> reduce the nonsense notion's of "evil" that prohibitionist hold.. and
> >> finally gain acceptance.
>
> "John H." <bingblat@goaway . com .au> wrote in message
> news:46283e76@quokka.wn . com .au...
> > Actually Mark I did a quick check of the primary literature and there
are
> > at
> > least 15 conditions, including dementia, atherosclerosis, and diabetes,
in
> > which cannabinoid based interventions offer potential. In regard to this
> > news item it is consistent with a study released by the American
Thoracic
> > Society sometime ago wherein they found no evidence of increased rates
of
> > lung, head, or neck cancer in pot smokers and they reasoned it is
because
> > of THC impact on cell cycle dynamics. THC and other cannabinoids are
known
> > to inhibit VEGF, which stimulates new blood vessel growth.
> > "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
>
> (I reordered the above, i was told earlier that post should be posted
after
> the original otherwise it "troll like" behaviour. Don't get me wrong i
don't
> mind but i guess we should try and follow neticate where possible..I'm
sure
> i've broken loads of rules without realising).
>
> I was being a little sarcastic(i believe in it's theroputic nature), I
know
> there are lots of medical conditions cannabis can help with.. I guess i
> should have deatailed more...thanks for pointing this out though...I think
> most people who've read my previous mails, over the last couple of months,
> to this group will know i'm a fan, but I only know what i have read(I'm no
> expert). I try to research at sites that have some credability but i can
> only go on their data..
>
> However I would suggest that cannabis makes you "feel good" and would
reduce
> how much people notice their illness's, people may think it helps and it
> does but it isn't making them "better" more masking their illness..other
> drugs would do the same job due to their "painkiller" nature...I could be
> wrong(if i am i'm sure you'll tell me and explain why?), and to be fair,
it
> dosn't matter to me as the end result is the person feels "better". I just
> like to cover all the bases..
>
> Here's one website which details quite a few illness which cannabis is
> reported to help..
>
> * w w w .pacifier . com /~alive/index_se_cmu.htm
>
> I just think we need to be careful about syaing that cannabis is a
> "medicinal wonder", it's still early days with regards to reaserch. The
> "prohibition" people would move quickly to turn that aginst us in the
event
> cannabis is proven not to help.. . it may harm further, the drugs
reputation..
>
>
Hey Mark,
I wasn't specifically commenting on your post. Lately I've been going
through the primary literature to investigate the therapeutic potential of
cannabinoids. The studies I mentioned have little if anything to do with how
people feel, the vast majority relate to cellular and clinical based studies
where biological markers are utilised to measure effect. On the basis of the
current research there is no other plant that offers so much therapeutic
potential. However, smoking is bad. Need vaporisers.
I was very surprised at the wide range of possible uses but this one really
takes the cake(THC better than current drugs):
6/03/2007 11:34PM
Mol. Pharmaceutics, 3 (6), 773 -777, 2006. 10.1021/mp060066m
S1543-8384(06)00066-9
Web Release Date: August 9, 2006
Copyright © 2006 American Chemical Society
A Molecular Link between the Active Component of Marijuana and Alzheimer's
Disease Pathology
Lisa M. Eubanks, Claude J. Rogers, Albert E. Beuscher IV, George F. Koob,
Arthur J. Olson, Tobin J. Dickerson, and Kim D. Janda*
Departments of Chemistry, Immunology, and Molecular Biology, Molecular and
Integrated Neurosciences Department, The Skaggs Institute for Chemical
Biology, and Worm Institute for Research and Medicine, The Scripps Research
Institute, 10550 North Torrey Pines Road, La Jolla, California 92037
Received June 11, 2006
Abstract:
Alzheimer's disease is the leading cause of dementia among the elderly, and
with the ever-increasing size of this population, cases of Alzheimer's
disease are expected to triple over the next 50 years. Consequently, the
development of treatments that slow or halt the disease progression have
become imperative to both improve the quality of life for patients and
reduce the health care costs attributable to Alzheimer's disease. Here, we
demonstrate that the active component of marijuana, 9-tetrahydrocannabinol
(THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well
as prevents AChE-induced amyloid -peptide (A) aggregation, the key
pathological marker of Alzheimer's disease. Computational modeling of the
THC-AChE interaction revealed that THC binds in the peripheral anionic site
of AChE, the critical region involved in amyloidgenesis. Compared to
currently approved drugs prescribed for the treatment of Alzheimer's
disease, THC is a considerably superior inhibitor of A aggregation, and this
study provides a previously unrecognized molecular mechanism through which
cannabinoid molecules may directly impact the progression of this
debilitating disease.
Keywords: Cannabinoids; Alzheimer's disease; acetylcholinesterase
And this one from a while back:
Article:
Cannabidiol and (2)D 9 -tetrahydrocannabinol are
neuroprotective antioxidants
Authors: A. J. HAMPSON* ? ,M.GRIMALDI ? ,J.AXELROD*, AND D. WINK §
Journal:
Proc. Natl. Acad. Sci. USA
Vol. 95, pp. 8268-8273, July 1998
Medical Sciences
Location:
n\ni
Cannabidiol and ()9-tetrahydrocannabinol are neuroprotective antioxidants
Date obtained: 17/02/2000
Web Page:
Date Read: 19/02/2000
Date to Review: 31/12/2000
Keywords:
Printed:
Notes:
ABSTRACT
The neuroprotective actions of cannabidiol and other cannabinoids were
examined in rat cortical neuron cultures exposed to toxic levels of the
excitatory neurotrans-mitter glutamate. Glutamate toxicity was reduced by
both cannabidiol, a nonpsychoactive constituent of marijuana, and the
psychotropic cannabinoid (2)D 9 -tetrahydrocannabinol (THC). Cannabinoids
protected equally well against neuro-toxicity mediated by
N-methyl-D-aspartate receptors, 2-ami-no-
3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid recep-tors, or kainate
receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown to
be calcium dependent; this study demonstrates that
2-amino-3-(4-butyl-3-hydroxyisox-azol- 5-yl)propionic acidykainate
receptor-type neurotoxicity is also calcium-dependent, partly mediated by
voltage sensi-tive calcium channels. The neuroprotection observed with
cannabidiol and THC was unaffected by cannabinoid receptor antagonist,
indicating it to be cannabinoid receptor indepen-dent. Previous studies have
shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol,
THC and several synthetic cannabinoids all were demonstrated to be
antioxi-dants by cyclic voltametry. Cannabidiol and THC also were shown to
prevent hydroperoxide-induced oxidative damage as well as or better than
other antioxidants in a chemical (Fenton reaction) system and neuronal
cultures. Cannabidiol was more protective against glutamate neurotoxicity
than either ascorbate or a-tocopherol, indicating it to be a potent
anti-oxidant. These data also suggest that the naturally occurring,
nonpsychotropic cannabinoid, cannabidiol, may be a poten-tially useful
therapeutic agent for the treatment of oxidative neurological disorders such
as cerebral ischemia.
Extracts
These results suggest that cannabidiol protects simi-shown). These results
suggest that cannabidiol protects simi-larly, regardless of whether toxicity
is mediated by NMDA,AMPA, or kainate receptors.
AMPAyKainate Toxicity Is Calcium Dependent.
Increasedcalcium influx is known to be a key factor in NMDAr-induced cell
death (4), but its role in AMPA and kainate toxicity is less clear. It has
been suggested that AMPAykainate receptors may not directly allow entry of
sufficient calcium to kill cells. However, AMPAykainate receptors f lux
large amounts of sodium, which can depolarize cell membranes. Such
depolar-ization may activate both voltage-sensitive calcium channels (21)
and facilitate NMDAr activation (22, 23). In this way, AMPAykainate receptor
stimulation may lead indirectly to accumulation of toxic intracellular
calcium levels.
--
cannabinoid HU-211 all donated electrons at a similar poten-tial as the
antioxidant BHT. Anandamide (arachidonyl-ethanolamide), which is not a
cannabinoid in structure but is an endogenous ligand for the cannabinoid
receptor, did not undergo oxidation in this assay (Fig. 4A). Three other
canna-binoids, cannabinol, nabilone, and levanantrodol, also were tested,
and they, too, exhibited oxidation profiles similar to cannabidiol and THC
(data not shown).
The ability of cannabinoids to be oxidized readily suggests that they may
possess antioxidant properties comparable to BHT
--
unaffected by cannabinoid receptor antagonist. This suggests that
cannabinoids may have potentially useful therapeutic effects that are
independent of psychoactivity-inducing can-nabinoid receptors (12) and so
are not necessarily accompa-nied by psychotropic side effects.
-
Cannabidiol blocked glutamate toxicity in cortical neurons with equal
potency regardless of whether the insult was mediated by NMDAr, AMPA
receptors, or kainate receptors. This suggests that either cannabinoids
antagonize all three glutamate receptors with the same affinity, or, more
likely, their site of action is downstream of initial receptor activation
--
Neurotoxic concentrations of glutamate induce mas-sive calcium influx
through NMDAr (4) that ultimately kills the cell. This study has
demonstrated that the toxic effects of glutamate are also calcium-dependent
when mediated by AMPAykainate receptors. Both EDTA (a calcium chelator) and
voltage-sensitive calcium channel inhibitors reduced in-dicate that many
cannabinoids exert a considerable protective antioxidant effect in neuronal
cultures. The similarity of the voltamagrams observed with cannabidiol,
HU-211, and several other cannabinoids also suggests that the reported
antioxidant effect of HU-211 is not a feature unique to this atypical
cannabinoid, (as previously implied; e.g., ref. 11) but, rather, a common
property of classical cannabinoid structures. The potency of cannabidiol as
an antioxidant was examined by comparing it on an equimolar basis with other
commonly used antioxidants. Cannabidiol protected neurons to a greater
degree than either of the dietary antioxidants, a-tocopherol or ascorbate.
As in the Fenton reaction system, cannabidiol protected neurons with
comparable efficacy to the potent antioxidant BHT. The similar antioxidant
abilities of canna-bidiol and BHT in this chemical system and their
comparable protection in neuronal cultures implies that cannabidiol
neu-roprotection is caused by an antioxidant effect.
The antioxidative properties of cannabinoids suggest a therapeutic use as
neuroprotective agents, and the particular properties of cannabidiol make it
a good candidate for such development. Although cannabidiol was similar in
neuropro-tective capacity to BHT, cannabidiol has no known tumor-promoting
effects [unlike BHT (25, 26)]. The lack of psycho-activity
--
Furthermore, the ability of can-nabidiol to protect against neuronal injury
without inhibiting NMDAr may reduce the occurrence of toxicity or side
effects associated with NMDAr antagonists (27). Previous studies have
indicated that cannabidiol is not toxic, even when chron-ically administered
to humans (28) or given in large acute doses [700 mgyday (29)]. In vivo
studies to examine the efficacy of cannabidiol as a treatment for
experimentally induced isch-emic stroke are currently in progress.
Project:
"Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
news:FM0Wh.4452$kb4.566@newsfe1-win.ntli . net ...
>
> >>
> >> >
> >>
> >> I found out that it can even bring back the "dead" (grin)
> >>
> >> there does seem to be regular studies which suggest it could be helpful
> >> in
> > a
> >> few circumstances eg.Cancer, pain, depression and aniexty...
> >>
> >> lets hope it really could be used as a basis for a cure for cancer,
> >> might
> >> reduce the nonsense notion's of "evil" that prohibitionist hold.. and
> >> finally gain acceptance.
>
> "John H." <bingblat@goaway . com .au> wrote in message
> news:46283e76@quokka.wn . com .au...
> > Actually Mark I did a quick check of the primary literature and there
are
> > at
> > least 15 conditions, including dementia, atherosclerosis, and diabetes,
in
> > which cannabinoid based interventions offer potential. In regard to this
> > news item it is consistent with a study released by the American
Thoracic
> > Society sometime ago wherein they found no evidence of increased rates
of
> > lung, head, or neck cancer in pot smokers and they reasoned it is
because
> > of THC impact on cell cycle dynamics. THC and other cannabinoids are
known
> > to inhibit VEGF, which stimulates new blood vessel growth.
> > "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
>
> (I reordered the above, i was told earlier that post should be posted
after
> the original otherwise it "troll like" behaviour. Don't get me wrong i
don't
> mind but i guess we should try and follow neticate where possible..I'm
sure
> i've broken loads of rules without realising).
>
> I was being a little sarcastic(i believe in it's theroputic nature), I
know
> there are lots of medical conditions cannabis can help with.. I guess i
> should have deatailed more...thanks for pointing this out though...I think
> most people who've read my previous mails, over the last couple of months,
> to this group will know i'm a fan, but I only know what i have read(I'm no
> expert). I try to research at sites that have some credability but i can
> only go on their data..
>
> However I would suggest that cannabis makes you "feel good" and would
reduce
> how much people notice their illness's, people may think it helps and it
> does but it isn't making them "better" more masking their illness..other
> drugs would do the same job due to their "painkiller" nature...I could be
> wrong(if i am i'm sure you'll tell me and explain why?), and to be fair,
it
> dosn't matter to me as the end result is the person feels "better". I just
> like to cover all the bases..
>
> Here's one website which details quite a few illness which cannabis is
> reported to help..
>
> * w w w .pacifier . com /~alive/index_se_cmu.htm
>
> I just think we need to be careful about syaing that cannabis is a
> "medicinal wonder", it's still early days with regards to reaserch. The
> "prohibition" people would move quickly to turn that aginst us in the
event
> cannabis is proven not to help.. . it may harm further, the drugs
reputation..
>
>
Re: Cannabis compound slows lung cancer in mice
"John H." <bingblat@goaway . com .au> wrote in message
news:4628b034@quokka.wn . com .au...
> Hey Mark,
>
> I wasn't specifically commenting on your post. Lately I've been going
> through the primary literature to investigate the therapeutic potential of
> cannabinoids. The studies I mentioned have little if anything to do with
> how
> people feel, the vast majority relate to cellular and clinical based
> studies
> where biological markers are utilised to measure effect
Thats a great point! cannabis is curing not just masking then...
. On the basis of the
> current research there is no other plant that offers so much therapeutic
> potential. However, smoking is bad. Need vaporisers.
Smoking is not good for you agreed, would it be possible for THC to actually
block the harmful effects of smoking, assuming you already smoked cigs??
you list some really bad conditions below, i'm glad cannabis is beging to be
proven to help.. . it may well make people reassess their feeling about the
plant, it hard to hate the plant that provides a potential cure for so many
of societies worst illnesses...
> I was very surprised at the wide range of possible uses but this one
> really
> takes the cake(THC better than current drugs):
> 6/03/2007 11:34PM
>
>
> Mol. Pharmaceutics, 3 (6), 773 -777, 2006. 10.1021/mp060066m
> S1543-8384(06)00066-9
>
> Web Release Date: August 9, 2006
>
> Copyright © 2006 American Chemical Society
>
> A Molecular Link between the Active Component of Marijuana and Alzheimer's
> Disease Pathology
>
> Lisa M. Eubanks, Claude J. Rogers, Albert E. Beuscher IV, George F. Koob,
> Arthur J. Olson, Tobin J. Dickerson, and Kim D. Janda*
>
> Departments of Chemistry, Immunology, and Molecular Biology, Molecular and
> Integrated Neurosciences Department, The Skaggs Institute for Chemical
> Biology, and Worm Institute for Research and Medicine, The Scripps
> Research
> Institute, 10550 North Torrey Pines Road, La Jolla, California 92037
>
> Received June 11, 2006
>
> Abstract:
>
> Alzheimer's disease is the leading cause of dementia among the elderly,
> and
> with the ever-increasing size of this population, cases of Alzheimer's
> disease are expected to triple over the next 50 years. Consequently, the
> development of treatments that slow or halt the disease progression have
> become imperative to both improve the quality of life for patients and
> reduce the health care costs attributable to Alzheimer's disease. Here, we
> demonstrate that the active component of marijuana, 9-tetrahydrocannabinol
> (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as
> well
> as prevents AChE-induced amyloid -peptide (A) aggregation, the key
> pathological marker of Alzheimer's disease. Computational modeling of the
> THC-AChE interaction revealed that THC binds in the peripheral anionic
> site
> of AChE, the critical region involved in amyloidgenesis. Compared to
> currently approved drugs prescribed for the treatment of Alzheimer's
> disease, THC is a considerably superior inhibitor of A aggregation, and
> this
> study provides a previously unrecognized molecular mechanism through which
> cannabinoid molecules may directly impact the progression of this
> debilitating disease.
>
> Keywords: Cannabinoids; Alzheimer's disease; acetylcholinesterase
>
>
>
> And this one from a while back:
>
> Article:
> Cannabidiol and (2)D 9 -tetrahydrocannabinol are
> neuroprotective antioxidants
> Authors: A. J. HAMPSON* ? ,M.GRIMALDI ? ,J.AXELROD*, AND D. WINK §
> Journal:
> Proc. Natl. Acad. Sci. USA
> Vol. 95, pp. 8268-8273, July 1998
> Medical Sciences
> Location:
> n\ni
> Cannabidiol and ()9-tetrahydrocannabinol are neuroprotective antioxidants
> Date obtained: 17/02/2000
> Web Page:
> Date Read: 19/02/2000
> Date to Review: 31/12/2000
> Keywords:
> Printed:
> Notes:
> ABSTRACT
>
> The neuroprotective actions of cannabidiol and other cannabinoids were
> examined in rat cortical neuron cultures exposed to toxic levels of the
> excitatory neurotrans-mitter glutamate. Glutamate toxicity was reduced by
> both cannabidiol, a nonpsychoactive constituent of marijuana, and the
> psychotropic cannabinoid (2)D 9 -tetrahydrocannabinol (THC). Cannabinoids
> protected equally well against neuro-toxicity mediated by
> N-methyl-D-aspartate receptors, 2-ami-no-
> 3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid recep-tors, or kainate
> receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown
> to
> be calcium dependent; this study demonstrates that
> 2-amino-3-(4-butyl-3-hydroxyisox-azol- 5-yl)propionic acidykainate
> receptor-type neurotoxicity is also calcium-dependent, partly mediated by
> voltage sensi-tive calcium channels. The neuroprotection observed with
> cannabidiol and THC was unaffected by cannabinoid receptor antagonist,
> indicating it to be cannabinoid receptor indepen-dent. Previous studies
> have
> shown that glutamate toxicity may be prevented by antioxidants.
> Cannabidiol,
> THC and several synthetic cannabinoids all were demonstrated to be
> antioxi-dants by cyclic voltametry. Cannabidiol and THC also were shown to
> prevent hydroperoxide-induced oxidative damage as well as or better than
> other antioxidants in a chemical (Fenton reaction) system and neuronal
> cultures. Cannabidiol was more protective against glutamate neurotoxicity
> than either ascorbate or a-tocopherol, indicating it to be a potent
> anti-oxidant. These data also suggest that the naturally occurring,
> nonpsychotropic cannabinoid, cannabidiol, may be a poten-tially useful
> therapeutic agent for the treatment of oxidative neurological disorders
> such
> as cerebral ischemia.
>
> Extracts
>
> These results suggest that cannabidiol protects simi-shown). These results
> suggest that cannabidiol protects simi-larly, regardless of whether
> toxicity
> is mediated by NMDA,AMPA, or kainate receptors.
> AMPAyKainate Toxicity Is Calcium Dependent.
>
> Increasedcalcium influx is known to be a key factor in NMDAr-induced cell
> death (4), but its role in AMPA and kainate toxicity is less clear. It has
> been suggested that AMPAykainate receptors may not directly allow entry of
> sufficient calcium to kill cells. However, AMPAykainate receptors f lux
> large amounts of sodium, which can depolarize cell membranes. Such
> depolar-ization may activate both voltage-sensitive calcium channels (21)
> and facilitate NMDAr activation (22, 23). In this way, AMPAykainate
> receptor
> stimulation may lead indirectly to accumulation of toxic intracellular
> calcium levels.
> --
> cannabinoid HU-211 all donated electrons at a similar poten-tial as the
> antioxidant BHT. Anandamide (arachidonyl-ethanolamide), which is not a
> cannabinoid in structure but is an endogenous ligand for the cannabinoid
> receptor, did not undergo oxidation in this assay (Fig. 4A). Three other
> canna-binoids, cannabinol, nabilone, and levanantrodol, also were tested,
> and they, too, exhibited oxidation profiles similar to cannabidiol and THC
> (data not shown).
> The ability of cannabinoids to be oxidized readily suggests that they may
> possess antioxidant properties comparable to BHT
> --
> unaffected by cannabinoid receptor antagonist. This suggests that
> cannabinoids may have potentially useful therapeutic effects that are
> independent of psychoactivity-inducing can-nabinoid receptors (12) and so
> are not necessarily accompa-nied by psychotropic side effects.
> -
> Cannabidiol blocked glutamate toxicity in cortical neurons with equal
> potency regardless of whether the insult was mediated by NMDAr, AMPA
> receptors, or kainate receptors. This suggests that either cannabinoids
> antagonize all three glutamate receptors with the same affinity, or, more
> likely, their site of action is downstream of initial receptor activation
> --
> Neurotoxic concentrations of glutamate induce mas-sive calcium influx
> through NMDAr (4) that ultimately kills the cell. This study has
> demonstrated that the toxic effects of glutamate are also
> calcium-dependent
> when mediated by AMPAykainate receptors. Both EDTA (a calcium chelator)
> and
> voltage-sensitive calcium channel inhibitors reduced in-dicate that many
> cannabinoids exert a considerable protective antioxidant effect in
> neuronal
> cultures. The similarity of the voltamagrams observed with cannabidiol,
> HU-211, and several other cannabinoids also suggests that the reported
> antioxidant effect of HU-211 is not a feature unique to this atypical
> cannabinoid, (as previously implied; e.g., ref. 11) but, rather, a common
> property of classical cannabinoid structures. The potency of cannabidiol
> as
> an antioxidant was examined by comparing it on an equimolar basis with
> other
> commonly used antioxidants. Cannabidiol protected neurons to a greater
> degree than either of the dietary antioxidants, a-tocopherol or ascorbate.
> As in the Fenton reaction system, cannabidiol protected neurons with
> comparable efficacy to the potent antioxidant BHT. The similar antioxidant
> abilities of canna-bidiol and BHT in this chemical system and their
> comparable protection in neuronal cultures implies that cannabidiol
> neu-roprotection is caused by an antioxidant effect.
> The antioxidative properties of cannabinoids suggest a therapeutic use as
> neuroprotective agents, and the particular properties of cannabidiol make
> it
> a good candidate for such development. Although cannabidiol was similar in
> neuropro-tective capacity to BHT, cannabidiol has no known tumor-promoting
> effects [unlike BHT (25, 26)]. The lack of psycho-activity
> --
> Furthermore, the ability of can-nabidiol to protect against neuronal
> injury
> without inhibiting NMDAr may reduce the occurrence of toxicity or side
> effects associated with NMDAr antagonists (27). Previous studies have
> indicated that cannabidiol is not toxic, even when chron-ically
> administered
> to humans (28) or given in large acute doses [700 mgyday (29)]. In vivo
> studies to examine the efficacy of cannabidiol as a treatment for
> experimentally induced isch-emic stroke are currently in progress.
> Project:
>
>
>
>
>
>
> "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
> news:FM0Wh.4452$kb4.566@newsfe1-win.ntli . net ...
>>
>> >>
>> >> >
>> >>
>> >> I found out that it can even bring back the "dead" (grin)
>> >>
>> >> there does seem to be regular studies which suggest it could be
>> >> helpful
>> >> in
>> > a
>> >> few circumstances eg.Cancer, pain, depression and aniexty...
>> >>
>> >> lets hope it really could be used as a basis for a cure for cancer,
>> >> might
>> >> reduce the nonsense notion's of "evil" that prohibitionist hold.. and
>> >> finally gain acceptance.
>>
>> "John H." <bingblat@goaway . com .au> wrote in message
>> news:46283e76@quokka.wn . com .au...
>> > Actually Mark I did a quick check of the primary literature and there
> are
>> > at
>> > least 15 conditions, including dementia, atherosclerosis, and diabetes,
> in
>> > which cannabinoid based interventions offer potential. In regard to
>> > this
>> > news item it is consistent with a study released by the American
> Thoracic
>> > Society sometime ago wherein they found no evidence of increased rates
> of
>> > lung, head, or neck cancer in pot smokers and they reasoned it is
> because
>> > of THC impact on cell cycle dynamics. THC and other cannabinoids are
> known
>> > to inhibit VEGF, which stimulates new blood vessel growth.
>> > "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
>>
>> (I reordered the above, i was told earlier that post should be posted
> after
>> the original otherwise it "troll like" behaviour. Don't get me wrong i
> don't
>> mind but i guess we should try and follow neticate where possible..I'm
> sure
>> i've broken loads of rules without realising).
>>
>> I was being a little sarcastic(i believe in it's theroputic nature), I
> know
>> there are lots of medical conditions cannabis can help with.. I guess i
>> should have deatailed more...thanks for pointing this out though...I
>> think
>> most people who've read my previous mails, over the last couple of
>> months,
>> to this group will know i'm a fan, but I only know what i have read(I'm
>> no
>> expert). I try to research at sites that have some credability but i can
>> only go on their data..
>>
>> However I would suggest that cannabis makes you "feel good" and would
> reduce
>> how much people notice their illness's, people may think it helps and it
>> does but it isn't making them "better" more masking their illness..other
>> drugs would do the same job due to their "painkiller" nature...I could be
>> wrong(if i am i'm sure you'll tell me and explain why?), and to be fair,
> it
>> dosn't matter to me as the end result is the person feels "better". I
>> just
>> like to cover all the bases..
>>
>> Here's one website which details quite a few illness which cannabis is
>> reported to help..
>>
>> * w w w .pacifier . com /~alive/index_se_cmu.htm
>>
>> I just think we need to be careful about syaing that cannabis is a
>> "medicinal wonder", it's still early days with regards to reaserch. The
>> "prohibition" people would move quickly to turn that aginst us in the
> event
>> cannabis is proven not to help.. . it may harm further, the drugs
> reputation..
>>
>>
>
>
"John H." <bingblat@goaway . com .au> wrote in message
news:4628b034@quokka.wn . com .au...
> Hey Mark,
>
> I wasn't specifically commenting on your post. Lately I've been going
> through the primary literature to investigate the therapeutic potential of
> cannabinoids. The studies I mentioned have little if anything to do with
> how
> people feel, the vast majority relate to cellular and clinical based
> studies
> where biological markers are utilised to measure effect
Thats a great point! cannabis is curing not just masking then...
. On the basis of the
> current research there is no other plant that offers so much therapeutic
> potential. However, smoking is bad. Need vaporisers.
Smoking is not good for you agreed, would it be possible for THC to actually
block the harmful effects of smoking, assuming you already smoked cigs??
you list some really bad conditions below, i'm glad cannabis is beging to be
proven to help.. . it may well make people reassess their feeling about the
plant, it hard to hate the plant that provides a potential cure for so many
of societies worst illnesses...
> I was very surprised at the wide range of possible uses but this one
> really
> takes the cake(THC better than current drugs):
> 6/03/2007 11:34PM
>
>
> Mol. Pharmaceutics, 3 (6), 773 -777, 2006. 10.1021/mp060066m
> S1543-8384(06)00066-9
>
> Web Release Date: August 9, 2006
>
> Copyright © 2006 American Chemical Society
>
> A Molecular Link between the Active Component of Marijuana and Alzheimer's
> Disease Pathology
>
> Lisa M. Eubanks, Claude J. Rogers, Albert E. Beuscher IV, George F. Koob,
> Arthur J. Olson, Tobin J. Dickerson, and Kim D. Janda*
>
> Departments of Chemistry, Immunology, and Molecular Biology, Molecular and
> Integrated Neurosciences Department, The Skaggs Institute for Chemical
> Biology, and Worm Institute for Research and Medicine, The Scripps
> Research
> Institute, 10550 North Torrey Pines Road, La Jolla, California 92037
>
> Received June 11, 2006
>
> Abstract:
>
> Alzheimer's disease is the leading cause of dementia among the elderly,
> and
> with the ever-increasing size of this population, cases of Alzheimer's
> disease are expected to triple over the next 50 years. Consequently, the
> development of treatments that slow or halt the disease progression have
> become imperative to both improve the quality of life for patients and
> reduce the health care costs attributable to Alzheimer's disease. Here, we
> demonstrate that the active component of marijuana, 9-tetrahydrocannabinol
> (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as
> well
> as prevents AChE-induced amyloid -peptide (A) aggregation, the key
> pathological marker of Alzheimer's disease. Computational modeling of the
> THC-AChE interaction revealed that THC binds in the peripheral anionic
> site
> of AChE, the critical region involved in amyloidgenesis. Compared to
> currently approved drugs prescribed for the treatment of Alzheimer's
> disease, THC is a considerably superior inhibitor of A aggregation, and
> this
> study provides a previously unrecognized molecular mechanism through which
> cannabinoid molecules may directly impact the progression of this
> debilitating disease.
>
> Keywords: Cannabinoids; Alzheimer's disease; acetylcholinesterase
>
>
>
> And this one from a while back:
>
> Article:
> Cannabidiol and (2)D 9 -tetrahydrocannabinol are
> neuroprotective antioxidants
> Authors: A. J. HAMPSON* ? ,M.GRIMALDI ? ,J.AXELROD*, AND D. WINK §
> Journal:
> Proc. Natl. Acad. Sci. USA
> Vol. 95, pp. 8268-8273, July 1998
> Medical Sciences
> Location:
> n\ni
> Cannabidiol and ()9-tetrahydrocannabinol are neuroprotective antioxidants
> Date obtained: 17/02/2000
> Web Page:
> Date Read: 19/02/2000
> Date to Review: 31/12/2000
> Keywords:
> Printed:
> Notes:
> ABSTRACT
>
> The neuroprotective actions of cannabidiol and other cannabinoids were
> examined in rat cortical neuron cultures exposed to toxic levels of the
> excitatory neurotrans-mitter glutamate. Glutamate toxicity was reduced by
> both cannabidiol, a nonpsychoactive constituent of marijuana, and the
> psychotropic cannabinoid (2)D 9 -tetrahydrocannabinol (THC). Cannabinoids
> protected equally well against neuro-toxicity mediated by
> N-methyl-D-aspartate receptors, 2-ami-no-
> 3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid recep-tors, or kainate
> receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown
> to
> be calcium dependent; this study demonstrates that
> 2-amino-3-(4-butyl-3-hydroxyisox-azol- 5-yl)propionic acidykainate
> receptor-type neurotoxicity is also calcium-dependent, partly mediated by
> voltage sensi-tive calcium channels. The neuroprotection observed with
> cannabidiol and THC was unaffected by cannabinoid receptor antagonist,
> indicating it to be cannabinoid receptor indepen-dent. Previous studies
> have
> shown that glutamate toxicity may be prevented by antioxidants.
> Cannabidiol,
> THC and several synthetic cannabinoids all were demonstrated to be
> antioxi-dants by cyclic voltametry. Cannabidiol and THC also were shown to
> prevent hydroperoxide-induced oxidative damage as well as or better than
> other antioxidants in a chemical (Fenton reaction) system and neuronal
> cultures. Cannabidiol was more protective against glutamate neurotoxicity
> than either ascorbate or a-tocopherol, indicating it to be a potent
> anti-oxidant. These data also suggest that the naturally occurring,
> nonpsychotropic cannabinoid, cannabidiol, may be a poten-tially useful
> therapeutic agent for the treatment of oxidative neurological disorders
> such
> as cerebral ischemia.
>
> Extracts
>
> These results suggest that cannabidiol protects simi-shown). These results
> suggest that cannabidiol protects simi-larly, regardless of whether
> toxicity
> is mediated by NMDA,AMPA, or kainate receptors.
> AMPAyKainate Toxicity Is Calcium Dependent.
>
> Increasedcalcium influx is known to be a key factor in NMDAr-induced cell
> death (4), but its role in AMPA and kainate toxicity is less clear. It has
> been suggested that AMPAykainate receptors may not directly allow entry of
> sufficient calcium to kill cells. However, AMPAykainate receptors f lux
> large amounts of sodium, which can depolarize cell membranes. Such
> depolar-ization may activate both voltage-sensitive calcium channels (21)
> and facilitate NMDAr activation (22, 23). In this way, AMPAykainate
> receptor
> stimulation may lead indirectly to accumulation of toxic intracellular
> calcium levels.
> --
> cannabinoid HU-211 all donated electrons at a similar poten-tial as the
> antioxidant BHT. Anandamide (arachidonyl-ethanolamide), which is not a
> cannabinoid in structure but is an endogenous ligand for the cannabinoid
> receptor, did not undergo oxidation in this assay (Fig. 4A). Three other
> canna-binoids, cannabinol, nabilone, and levanantrodol, also were tested,
> and they, too, exhibited oxidation profiles similar to cannabidiol and THC
> (data not shown).
> The ability of cannabinoids to be oxidized readily suggests that they may
> possess antioxidant properties comparable to BHT
> --
> unaffected by cannabinoid receptor antagonist. This suggests that
> cannabinoids may have potentially useful therapeutic effects that are
> independent of psychoactivity-inducing can-nabinoid receptors (12) and so
> are not necessarily accompa-nied by psychotropic side effects.
> -
> Cannabidiol blocked glutamate toxicity in cortical neurons with equal
> potency regardless of whether the insult was mediated by NMDAr, AMPA
> receptors, or kainate receptors. This suggests that either cannabinoids
> antagonize all three glutamate receptors with the same affinity, or, more
> likely, their site of action is downstream of initial receptor activation
> --
> Neurotoxic concentrations of glutamate induce mas-sive calcium influx
> through NMDAr (4) that ultimately kills the cell. This study has
> demonstrated that the toxic effects of glutamate are also
> calcium-dependent
> when mediated by AMPAykainate receptors. Both EDTA (a calcium chelator)
> and
> voltage-sensitive calcium channel inhibitors reduced in-dicate that many
> cannabinoids exert a considerable protective antioxidant effect in
> neuronal
> cultures. The similarity of the voltamagrams observed with cannabidiol,
> HU-211, and several other cannabinoids also suggests that the reported
> antioxidant effect of HU-211 is not a feature unique to this atypical
> cannabinoid, (as previously implied; e.g., ref. 11) but, rather, a common
> property of classical cannabinoid structures. The potency of cannabidiol
> as
> an antioxidant was examined by comparing it on an equimolar basis with
> other
> commonly used antioxidants. Cannabidiol protected neurons to a greater
> degree than either of the dietary antioxidants, a-tocopherol or ascorbate.
> As in the Fenton reaction system, cannabidiol protected neurons with
> comparable efficacy to the potent antioxidant BHT. The similar antioxidant
> abilities of canna-bidiol and BHT in this chemical system and their
> comparable protection in neuronal cultures implies that cannabidiol
> neu-roprotection is caused by an antioxidant effect.
> The antioxidative properties of cannabinoids suggest a therapeutic use as
> neuroprotective agents, and the particular properties of cannabidiol make
> it
> a good candidate for such development. Although cannabidiol was similar in
> neuropro-tective capacity to BHT, cannabidiol has no known tumor-promoting
> effects [unlike BHT (25, 26)]. The lack of psycho-activity
> --
> Furthermore, the ability of can-nabidiol to protect against neuronal
> injury
> without inhibiting NMDAr may reduce the occurrence of toxicity or side
> effects associated with NMDAr antagonists (27). Previous studies have
> indicated that cannabidiol is not toxic, even when chron-ically
> administered
> to humans (28) or given in large acute doses [700 mgyday (29)]. In vivo
> studies to examine the efficacy of cannabidiol as a treatment for
> experimentally induced isch-emic stroke are currently in progress.
> Project:
>
>
>
>
>
>
> "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
> news:FM0Wh.4452$kb4.566@newsfe1-win.ntli . net ...
>>
>> >>
>> >> >
>> >>
>> >> I found out that it can even bring back the "dead" (grin)
>> >>
>> >> there does seem to be regular studies which suggest it could be
>> >> helpful
>> >> in
>> > a
>> >> few circumstances eg.Cancer, pain, depression and aniexty...
>> >>
>> >> lets hope it really could be used as a basis for a cure for cancer,
>> >> might
>> >> reduce the nonsense notion's of "evil" that prohibitionist hold.. and
>> >> finally gain acceptance.
>>
>> "John H." <bingblat@goaway . com .au> wrote in message
>> news:46283e76@quokka.wn . com .au...
>> > Actually Mark I did a quick check of the primary literature and there
> are
>> > at
>> > least 15 conditions, including dementia, atherosclerosis, and diabetes,
> in
>> > which cannabinoid based interventions offer potential. In regard to
>> > this
>> > news item it is consistent with a study released by the American
> Thoracic
>> > Society sometime ago wherein they found no evidence of increased rates
> of
>> > lung, head, or neck cancer in pot smokers and they reasoned it is
> because
>> > of THC impact on cell cycle dynamics. THC and other cannabinoids are
> known
>> > to inhibit VEGF, which stimulates new blood vessel growth.
>> > "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
>>
>> (I reordered the above, i was told earlier that post should be posted
> after
>> the original otherwise it "troll like" behaviour. Don't get me wrong i
> don't
>> mind but i guess we should try and follow neticate where possible..I'm
> sure
>> i've broken loads of rules without realising).
>>
>> I was being a little sarcastic(i believe in it's theroputic nature), I
> know
>> there are lots of medical conditions cannabis can help with.. I guess i
>> should have deatailed more...thanks for pointing this out though...I
>> think
>> most people who've read my previous mails, over the last couple of
>> months,
>> to this group will know i'm a fan, but I only know what i have read(I'm
>> no
>> expert). I try to research at sites that have some credability but i can
>> only go on their data..
>>
>> However I would suggest that cannabis makes you "feel good" and would
> reduce
>> how much people notice their illness's, people may think it helps and it
>> does but it isn't making them "better" more masking their illness..other
>> drugs would do the same job due to their "painkiller" nature...I could be
>> wrong(if i am i'm sure you'll tell me and explain why?), and to be fair,
> it
>> dosn't matter to me as the end result is the person feels "better". I
>> just
>> like to cover all the bases..
>>
>> Here's one website which details quite a few illness which cannabis is
>> reported to help..
>>
>> * w w w .pacifier . com /~alive/index_se_cmu.htm
>>
>> I just think we need to be careful about syaing that cannabis is a
>> "medicinal wonder", it's still early days with regards to reaserch. The
>> "prohibition" people would move quickly to turn that aginst us in the
> event
>> cannabis is proven not to help.. . it may harm further, the drugs
> reputation..
>>
>>
>
>
Re: Cannabis compound slows lung cancer in mice
Smoking:
I previously mentioned that report from the A Thoracic society. In fact if
smoking marijuana was a major or even minor cause of respiratory pathologies
it should be all over the literature by now. Given our current understanding
it is reasonable to assume that cannabinoids have anti cancer properties and
so may confer some protection from cig smoking; especially given the potent
antioxidant and anti inflammatory functions of cannabinoids; both of which
are known to help prevent cancers. There might be some small protection. Put
it this way: if you smoke cigarettes smoking cannabis is probably better cig
smoking alone.
A recent report from the American
"Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
news:l96Wh.18501$N94.7941@newsfe4-gui.ntli . net ...
>
> "John H." <bingblat@goaway . com .au> wrote in message
> news:4628b034@quokka.wn . com .au...
> > Hey Mark,
> >
> > I wasn't specifically commenting on your post. Lately I've been going
> > through the primary literature to investigate the therapeutic potential
of
> > cannabinoids. The studies I mentioned have little if anything to do with
> > how
> > people feel, the vast majority relate to cellular and clinical based
> > studies
> > where biological markers are utilised to measure effect
>
>
> Thats a great point! cannabis is curing not just masking then...
>
>
> . On the basis of the
> > current research there is no other plant that offers so much therapeutic
> > potential. However, smoking is bad. Need vaporisers.
>
> Smoking is not good for you agreed, would it be possible for THC to
actually
> block the harmful effects of smoking, assuming you already smoked cigs??
>
> you list some really bad conditions below, i'm glad cannabis is beging to
be
> proven to help.. . it may well make people reassess their feeling about the
> plant, it hard to hate the plant that provides a potential cure for so
many
> of societies worst illnesses...
>
> > I was very surprised at the wide range of possible uses but this one
> > really
> > takes the cake(THC better than current drugs):
> > 6/03/2007 11:34PM
> >
> >
> > Mol. Pharmaceutics, 3 (6), 773 -777, 2006. 10.1021/mp060066m
> > S1543-8384(06)00066-9
> >
> > Web Release Date: August 9, 2006
> >
> > Copyright © 2006 American Chemical Society
> >
> > A Molecular Link between the Active Component of Marijuana and
Alzheimer's
> > Disease Pathology
> >
> > Lisa M. Eubanks, Claude J. Rogers, Albert E. Beuscher IV, George F.
Koob,
> > Arthur J. Olson, Tobin J. Dickerson, and Kim D. Janda*
> >
> > Departments of Chemistry, Immunology, and Molecular Biology, Molecular
and
> > Integrated Neurosciences Department, The Skaggs Institute for Chemical
> > Biology, and Worm Institute for Research and Medicine, The Scripps
> > Research
> > Institute, 10550 North Torrey Pines Road, La Jolla, California 92037
> >
> > Received June 11, 2006
> >
> > Abstract:
> >
> > Alzheimer's disease is the leading cause of dementia among the elderly,
> > and
> > with the ever-increasing size of this population, cases of Alzheimer's
> > disease are expected to triple over the next 50 years. Consequently, the
> > development of treatments that slow or halt the disease progression have
> > become imperative to both improve the quality of life for patients and
> > reduce the health care costs attributable to Alzheimer's disease. Here,
we
> > demonstrate that the active component of marijuana,
9-tetrahydrocannabinol
> > (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as
> > well
> > as prevents AChE-induced amyloid -peptide (A) aggregation, the key
> > pathological marker of Alzheimer's disease. Computational modeling of
the
> > THC-AChE interaction revealed that THC binds in the peripheral anionic
> > site
> > of AChE, the critical region involved in amyloidgenesis. Compared to
> > currently approved drugs prescribed for the treatment of Alzheimer's
> > disease, THC is a considerably superior inhibitor of A aggregation, and
> > this
> > study provides a previously unrecognized molecular mechanism through
which
> > cannabinoid molecules may directly impact the progression of this
> > debilitating disease.
> >
> > Keywords: Cannabinoids; Alzheimer's disease; acetylcholinesterase
> >
> >
> >
> > And this one from a while back:
> >
> > Article:
> > Cannabidiol and (2)D 9 -tetrahydrocannabinol are
> > neuroprotective antioxidants
> > Authors: A. J. HAMPSON* ? ,M.GRIMALDI ? ,J.AXELROD*, AND D. WINK §
> > Journal:
> > Proc. Natl. Acad. Sci. USA
> > Vol. 95, pp. 8268-8273, July 1998
> > Medical Sciences
> > Location:
> > n\ni
> > Cannabidiol and ()9-tetrahydrocannabinol are neuroprotective
antioxidants
> > Date obtained: 17/02/2000
> > Web Page:
> > Date Read: 19/02/2000
> > Date to Review: 31/12/2000
> > Keywords:
> > Printed:
> > Notes:
> > ABSTRACT
> >
> > The neuroprotective actions of cannabidiol and other cannabinoids were
> > examined in rat cortical neuron cultures exposed to toxic levels of the
> > excitatory neurotrans-mitter glutamate. Glutamate toxicity was reduced
by
> > both cannabidiol, a nonpsychoactive constituent of marijuana, and the
> > psychotropic cannabinoid (2)D 9 -tetrahydrocannabinol (THC).
Cannabinoids
> > protected equally well against neuro-toxicity mediated by
> > N-methyl-D-aspartate receptors, 2-ami-no-
> > 3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid recep-tors, or kainate
> > receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown
> > to
> > be calcium dependent; this study demonstrates that
> > 2-amino-3-(4-butyl-3-hydroxyisox-azol- 5-yl)propionic acidykainate
> > receptor-type neurotoxicity is also calcium-dependent, partly mediated
by
> > voltage sensi-tive calcium channels. The neuroprotection observed with
> > cannabidiol and THC was unaffected by cannabinoid receptor antagonist,
> > indicating it to be cannabinoid receptor indepen-dent. Previous studies
> > have
> > shown that glutamate toxicity may be prevented by antioxidants.
> > Cannabidiol,
> > THC and several synthetic cannabinoids all were demonstrated to be
> > antioxi-dants by cyclic voltametry. Cannabidiol and THC also were shown
to
> > prevent hydroperoxide-induced oxidative damage as well as or better than
> > other antioxidants in a chemical (Fenton reaction) system and neuronal
> > cultures. Cannabidiol was more protective against glutamate
neurotoxicity
> > than either ascorbate or a-tocopherol, indicating it to be a potent
> > anti-oxidant. These data also suggest that the naturally occurring,
> > nonpsychotropic cannabinoid, cannabidiol, may be a poten-tially useful
> > therapeutic agent for the treatment of oxidative neurological disorders
> > such
> > as cerebral ischemia.
> >
> > Extracts
> >
> > These results suggest that cannabidiol protects simi-shown). These
results
> > suggest that cannabidiol protects simi-larly, regardless of whether
> > toxicity
> > is mediated by NMDA,AMPA, or kainate receptors.
> > AMPAyKainate Toxicity Is Calcium Dependent.
> >
> > Increasedcalcium influx is known to be a key factor in NMDAr-induced
cell
> > death (4), but its role in AMPA and kainate toxicity is less clear. It
has
> > been suggested that AMPAykainate receptors may not directly allow entry
of
> > sufficient calcium to kill cells. However, AMPAykainate receptors f lux
> > large amounts of sodium, which can depolarize cell membranes. Such
> > depolar-ization may activate both voltage-sensitive calcium channels
(21)
> > and facilitate NMDAr activation (22, 23). In this way, AMPAykainate
> > receptor
> > stimulation may lead indirectly to accumulation of toxic intracellular
> > calcium levels.
> > --
> > cannabinoid HU-211 all donated electrons at a similar poten-tial as the
> > antioxidant BHT. Anandamide (arachidonyl-ethanolamide), which is not a
> > cannabinoid in structure but is an endogenous ligand for the cannabinoid
> > receptor, did not undergo oxidation in this assay (Fig. 4A). Three other
> > canna-binoids, cannabinol, nabilone, and levanantrodol, also were
tested,
> > and they, too, exhibited oxidation profiles similar to cannabidiol and
THC
> > (data not shown).
> > The ability of cannabinoids to be oxidized readily suggests that they
may
> > possess antioxidant properties comparable to BHT
> > --
> > unaffected by cannabinoid receptor antagonist. This suggests that
> > cannabinoids may have potentially useful therapeutic effects that are
> > independent of psychoactivity-inducing can-nabinoid receptors (12) and
so
> > are not necessarily accompa-nied by psychotropic side effects.
> > -
> > Cannabidiol blocked glutamate toxicity in cortical neurons with equal
> > potency regardless of whether the insult was mediated by NMDAr, AMPA
> > receptors, or kainate receptors. This suggests that either cannabinoids
> > antagonize all three glutamate receptors with the same affinity, or,
more
> > likely, their site of action is downstream of initial receptor
activation
> > --
> > Neurotoxic concentrations of glutamate induce mas-sive calcium influx
> > through NMDAr (4) that ultimately kills the cell. This study has
> > demonstrated that the toxic effects of glutamate are also
> > calcium-dependent
> > when mediated by AMPAykainate receptors. Both EDTA (a calcium chelator)
> > and
> > voltage-sensitive calcium channel inhibitors reduced in-dicate that many
> > cannabinoids exert a considerable protective antioxidant effect in
> > neuronal
> > cultures. The similarity of the voltamagrams observed with cannabidiol,
> > HU-211, and several other cannabinoids also suggests that the reported
> > antioxidant effect of HU-211 is not a feature unique to this atypical
> > cannabinoid, (as previously implied; e.g., ref. 11) but, rather, a
common
> > property of classical cannabinoid structures. The potency of cannabidiol
> > as
> > an antioxidant was examined by comparing it on an equimolar basis with
> > other
> > commonly used antioxidants. Cannabidiol protected neurons to a greater
> > degree than either of the dietary antioxidants, a-tocopherol or
ascorbate.
> > As in the Fenton reaction system, cannabidiol protected neurons with
> > comparable efficacy to the potent antioxidant BHT. The similar
antioxidant
> > abilities of canna-bidiol and BHT in this chemical system and their
> > comparable protection in neuronal cultures implies that cannabidiol
> > neu-roprotection is caused by an antioxidant effect.
> > The antioxidative properties of cannabinoids suggest a therapeutic use
as
> > neuroprotective agents, and the particular properties of cannabidiol
make
> > it
> > a good candidate for such development. Although cannabidiol was similar
in
> > neuropro-tective capacity to BHT, cannabidiol has no known
tumor-promoting
> > effects [unlike BHT (25, 26)]. The lack of psycho-activity
> > --
> > Furthermore, the ability of can-nabidiol to protect against neuronal
> > injury
> > without inhibiting NMDAr may reduce the occurrence of toxicity or side
> > effects associated with NMDAr antagonists (27). Previous studies have
> > indicated that cannabidiol is not toxic, even when chron-ically
> > administered
> > to humans (28) or given in large acute doses [700 mgyday (29)]. In vivo
> > studies to examine the efficacy of cannabidiol as a treatment for
> > experimentally induced isch-emic stroke are currently in progress.
> > Project:
> >
> >
> >
> >
> >
> >
> > "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
> > news:FM0Wh.4452$kb4.566@newsfe1-win.ntli . net ...
> >>
> >> >>
> >> >> >
> >> >>
> >> >> I found out that it can even bring back the "dead" (grin)
> >> >>
> >> >> there does seem to be regular studies which suggest it could be
> >> >> helpful
> >> >> in
> >> > a
> >> >> few circumstances eg.Cancer, pain, depression and aniexty...
> >> >>
> >> >> lets hope it really could be used as a basis for a cure for cancer,
> >> >> might
> >> >> reduce the nonsense notion's of "evil" that prohibitionist hold..
and
> >> >> finally gain acceptance.
> >>
> >> "John H." <bingblat@goaway . com .au> wrote in message
> >> news:46283e76@quokka.wn . com .au...
> >> > Actually Mark I did a quick check of the primary literature and there
> > are
> >> > at
> >> > least 15 conditions, including dementia, atherosclerosis, and
diabetes,
> > in
> >> > which cannabinoid based interventions offer potential. In regard to
> >> > this
> >> > news item it is consistent with a study released by the American
> > Thoracic
> >> > Society sometime ago wherein they found no evidence of increased
rates
> > of
> >> > lung, head, or neck cancer in pot smokers and they reasoned it is
> > because
> >> > of THC impact on cell cycle dynamics. THC and other cannabinoids are
> > known
> >> > to inhibit VEGF, which stimulates new blood vessel growth.
> >> > "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
> >>
> >> (I reordered the above, i was told earlier that post should be posted
> > after
> >> the original otherwise it "troll like" behaviour. Don't get me wrong i
> > don't
> >> mind but i guess we should try and follow neticate where possible..I'm
> > sure
> >> i've broken loads of rules without realising).
> >>
> >> I was being a little sarcastic(i believe in it's theroputic nature), I
> > know
> >> there are lots of medical conditions cannabis can help with.. I guess i
> >> should have deatailed more...thanks for pointing this out though...I
> >> think
> >> most people who've read my previous mails, over the last couple of
> >> months,
> >> to this group will know i'm a fan, but I only know what i have read(I'm
> >> no
> >> expert). I try to research at sites that have some credability but i
can
> >> only go on their data..
> >>
> >> However I would suggest that cannabis makes you "feel good" and would
> > reduce
> >> how much people notice their illness's, people may think it helps and
it
> >> does but it isn't making them "better" more masking their
illness..other
> >> drugs would do the same job due to their "painkiller" nature...I could
be
> >> wrong(if i am i'm sure you'll tell me and explain why?), and to be
fair,
> > it
> >> dosn't matter to me as the end result is the person feels "better". I
> >> just
> >> like to cover all the bases..
> >>
> >> Here's one website which details quite a few illness which cannabis is
> >> reported to help..
> >>
> >> * w w w .pacifier . com /~alive/index_se_cmu.htm
> >>
> >> I just think we need to be careful about syaing that cannabis is a
> >> "medicinal wonder", it's still early days with regards to reaserch. The
> >> "prohibition" people would move quickly to turn that aginst us in the
> > event
> >> cannabis is proven not to help.. . it may harm further, the drugs
> > reputation..
> >>
> >>
> >
> >
>
>
Smoking:
I previously mentioned that report from the A Thoracic society. In fact if
smoking marijuana was a major or even minor cause of respiratory pathologies
it should be all over the literature by now. Given our current understanding
it is reasonable to assume that cannabinoids have anti cancer properties and
so may confer some protection from cig smoking; especially given the potent
antioxidant and anti inflammatory functions of cannabinoids; both of which
are known to help prevent cancers. There might be some small protection. Put
it this way: if you smoke cigarettes smoking cannabis is probably better cig
smoking alone.
A recent report from the American
"Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
news:l96Wh.18501$N94.7941@newsfe4-gui.ntli . net ...
>
> "John H." <bingblat@goaway . com .au> wrote in message
> news:4628b034@quokka.wn . com .au...
> > Hey Mark,
> >
> > I wasn't specifically commenting on your post. Lately I've been going
> > through the primary literature to investigate the therapeutic potential
of
> > cannabinoids. The studies I mentioned have little if anything to do with
> > how
> > people feel, the vast majority relate to cellular and clinical based
> > studies
> > where biological markers are utilised to measure effect
>
>
> Thats a great point! cannabis is curing not just masking then...
>
>
> . On the basis of the
> > current research there is no other plant that offers so much therapeutic
> > potential. However, smoking is bad. Need vaporisers.
>
> Smoking is not good for you agreed, would it be possible for THC to
actually
> block the harmful effects of smoking, assuming you already smoked cigs??
>
> you list some really bad conditions below, i'm glad cannabis is beging to
be
> proven to help.. . it may well make people reassess their feeling about the
> plant, it hard to hate the plant that provides a potential cure for so
many
> of societies worst illnesses...
>
> > I was very surprised at the wide range of possible uses but this one
> > really
> > takes the cake(THC better than current drugs):
> > 6/03/2007 11:34PM
> >
> >
> > Mol. Pharmaceutics, 3 (6), 773 -777, 2006. 10.1021/mp060066m
> > S1543-8384(06)00066-9
> >
> > Web Release Date: August 9, 2006
> >
> > Copyright © 2006 American Chemical Society
> >
> > A Molecular Link between the Active Component of Marijuana and
Alzheimer's
> > Disease Pathology
> >
> > Lisa M. Eubanks, Claude J. Rogers, Albert E. Beuscher IV, George F.
Koob,
> > Arthur J. Olson, Tobin J. Dickerson, and Kim D. Janda*
> >
> > Departments of Chemistry, Immunology, and Molecular Biology, Molecular
and
> > Integrated Neurosciences Department, The Skaggs Institute for Chemical
> > Biology, and Worm Institute for Research and Medicine, The Scripps
> > Research
> > Institute, 10550 North Torrey Pines Road, La Jolla, California 92037
> >
> > Received June 11, 2006
> >
> > Abstract:
> >
> > Alzheimer's disease is the leading cause of dementia among the elderly,
> > and
> > with the ever-increasing size of this population, cases of Alzheimer's
> > disease are expected to triple over the next 50 years. Consequently, the
> > development of treatments that slow or halt the disease progression have
> > become imperative to both improve the quality of life for patients and
> > reduce the health care costs attributable to Alzheimer's disease. Here,
we
> > demonstrate that the active component of marijuana,
9-tetrahydrocannabinol
> > (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as
> > well
> > as prevents AChE-induced amyloid -peptide (A) aggregation, the key
> > pathological marker of Alzheimer's disease. Computational modeling of
the
> > THC-AChE interaction revealed that THC binds in the peripheral anionic
> > site
> > of AChE, the critical region involved in amyloidgenesis. Compared to
> > currently approved drugs prescribed for the treatment of Alzheimer's
> > disease, THC is a considerably superior inhibitor of A aggregation, and
> > this
> > study provides a previously unrecognized molecular mechanism through
which
> > cannabinoid molecules may directly impact the progression of this
> > debilitating disease.
> >
> > Keywords: Cannabinoids; Alzheimer's disease; acetylcholinesterase
> >
> >
> >
> > And this one from a while back:
> >
> > Article:
> > Cannabidiol and (2)D 9 -tetrahydrocannabinol are
> > neuroprotective antioxidants
> > Authors: A. J. HAMPSON* ? ,M.GRIMALDI ? ,J.AXELROD*, AND D. WINK §
> > Journal:
> > Proc. Natl. Acad. Sci. USA
> > Vol. 95, pp. 8268-8273, July 1998
> > Medical Sciences
> > Location:
> > n\ni
> > Cannabidiol and ()9-tetrahydrocannabinol are neuroprotective
antioxidants
> > Date obtained: 17/02/2000
> > Web Page:
> > Date Read: 19/02/2000
> > Date to Review: 31/12/2000
> > Keywords:
> > Printed:
> > Notes:
> > ABSTRACT
> >
> > The neuroprotective actions of cannabidiol and other cannabinoids were
> > examined in rat cortical neuron cultures exposed to toxic levels of the
> > excitatory neurotrans-mitter glutamate. Glutamate toxicity was reduced
by
> > both cannabidiol, a nonpsychoactive constituent of marijuana, and the
> > psychotropic cannabinoid (2)D 9 -tetrahydrocannabinol (THC).
Cannabinoids
> > protected equally well against neuro-toxicity mediated by
> > N-methyl-D-aspartate receptors, 2-ami-no-
> > 3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid recep-tors, or kainate
> > receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown
> > to
> > be calcium dependent; this study demonstrates that
> > 2-amino-3-(4-butyl-3-hydroxyisox-azol- 5-yl)propionic acidykainate
> > receptor-type neurotoxicity is also calcium-dependent, partly mediated
by
> > voltage sensi-tive calcium channels. The neuroprotection observed with
> > cannabidiol and THC was unaffected by cannabinoid receptor antagonist,
> > indicating it to be cannabinoid receptor indepen-dent. Previous studies
> > have
> > shown that glutamate toxicity may be prevented by antioxidants.
> > Cannabidiol,
> > THC and several synthetic cannabinoids all were demonstrated to be
> > antioxi-dants by cyclic voltametry. Cannabidiol and THC also were shown
to
> > prevent hydroperoxide-induced oxidative damage as well as or better than
> > other antioxidants in a chemical (Fenton reaction) system and neuronal
> > cultures. Cannabidiol was more protective against glutamate
neurotoxicity
> > than either ascorbate or a-tocopherol, indicating it to be a potent
> > anti-oxidant. These data also suggest that the naturally occurring,
> > nonpsychotropic cannabinoid, cannabidiol, may be a poten-tially useful
> > therapeutic agent for the treatment of oxidative neurological disorders
> > such
> > as cerebral ischemia.
> >
> > Extracts
> >
> > These results suggest that cannabidiol protects simi-shown). These
results
> > suggest that cannabidiol protects simi-larly, regardless of whether
> > toxicity
> > is mediated by NMDA,AMPA, or kainate receptors.
> > AMPAyKainate Toxicity Is Calcium Dependent.
> >
> > Increasedcalcium influx is known to be a key factor in NMDAr-induced
cell
> > death (4), but its role in AMPA and kainate toxicity is less clear. It
has
> > been suggested that AMPAykainate receptors may not directly allow entry
of
> > sufficient calcium to kill cells. However, AMPAykainate receptors f lux
> > large amounts of sodium, which can depolarize cell membranes. Such
> > depolar-ization may activate both voltage-sensitive calcium channels
(21)
> > and facilitate NMDAr activation (22, 23). In this way, AMPAykainate
> > receptor
> > stimulation may lead indirectly to accumulation of toxic intracellular
> > calcium levels.
> > --
> > cannabinoid HU-211 all donated electrons at a similar poten-tial as the
> > antioxidant BHT. Anandamide (arachidonyl-ethanolamide), which is not a
> > cannabinoid in structure but is an endogenous ligand for the cannabinoid
> > receptor, did not undergo oxidation in this assay (Fig. 4A). Three other
> > canna-binoids, cannabinol, nabilone, and levanantrodol, also were
tested,
> > and they, too, exhibited oxidation profiles similar to cannabidiol and
THC
> > (data not shown).
> > The ability of cannabinoids to be oxidized readily suggests that they
may
> > possess antioxidant properties comparable to BHT
> > --
> > unaffected by cannabinoid receptor antagonist. This suggests that
> > cannabinoids may have potentially useful therapeutic effects that are
> > independent of psychoactivity-inducing can-nabinoid receptors (12) and
so
> > are not necessarily accompa-nied by psychotropic side effects.
> > -
> > Cannabidiol blocked glutamate toxicity in cortical neurons with equal
> > potency regardless of whether the insult was mediated by NMDAr, AMPA
> > receptors, or kainate receptors. This suggests that either cannabinoids
> > antagonize all three glutamate receptors with the same affinity, or,
more
> > likely, their site of action is downstream of initial receptor
activation
> > --
> > Neurotoxic concentrations of glutamate induce mas-sive calcium influx
> > through NMDAr (4) that ultimately kills the cell. This study has
> > demonstrated that the toxic effects of glutamate are also
> > calcium-dependent
> > when mediated by AMPAykainate receptors. Both EDTA (a calcium chelator)
> > and
> > voltage-sensitive calcium channel inhibitors reduced in-dicate that many
> > cannabinoids exert a considerable protective antioxidant effect in
> > neuronal
> > cultures. The similarity of the voltamagrams observed with cannabidiol,
> > HU-211, and several other cannabinoids also suggests that the reported
> > antioxidant effect of HU-211 is not a feature unique to this atypical
> > cannabinoid, (as previously implied; e.g., ref. 11) but, rather, a
common
> > property of classical cannabinoid structures. The potency of cannabidiol
> > as
> > an antioxidant was examined by comparing it on an equimolar basis with
> > other
> > commonly used antioxidants. Cannabidiol protected neurons to a greater
> > degree than either of the dietary antioxidants, a-tocopherol or
ascorbate.
> > As in the Fenton reaction system, cannabidiol protected neurons with
> > comparable efficacy to the potent antioxidant BHT. The similar
antioxidant
> > abilities of canna-bidiol and BHT in this chemical system and their
> > comparable protection in neuronal cultures implies that cannabidiol
> > neu-roprotection is caused by an antioxidant effect.
> > The antioxidative properties of cannabinoids suggest a therapeutic use
as
> > neuroprotective agents, and the particular properties of cannabidiol
make
> > it
> > a good candidate for such development. Although cannabidiol was similar
in
> > neuropro-tective capacity to BHT, cannabidiol has no known
tumor-promoting
> > effects [unlike BHT (25, 26)]. The lack of psycho-activity
> > --
> > Furthermore, the ability of can-nabidiol to protect against neuronal
> > injury
> > without inhibiting NMDAr may reduce the occurrence of toxicity or side
> > effects associated with NMDAr antagonists (27). Previous studies have
> > indicated that cannabidiol is not toxic, even when chron-ically
> > administered
> > to humans (28) or given in large acute doses [700 mgyday (29)]. In vivo
> > studies to examine the efficacy of cannabidiol as a treatment for
> > experimentally induced isch-emic stroke are currently in progress.
> > Project:
> >
> >
> >
> >
> >
> >
> > "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
> > news:FM0Wh.4452$kb4.566@newsfe1-win.ntli . net ...
> >>
> >> >>
> >> >> >
> >> >>
> >> >> I found out that it can even bring back the "dead" (grin)
> >> >>
> >> >> there does seem to be regular studies which suggest it could be
> >> >> helpful
> >> >> in
> >> > a
> >> >> few circumstances eg.Cancer, pain, depression and aniexty...
> >> >>
> >> >> lets hope it really could be used as a basis for a cure for cancer,
> >> >> might
> >> >> reduce the nonsense notion's of "evil" that prohibitionist hold..
and
> >> >> finally gain acceptance.
> >>
> >> "John H." <bingblat@goaway . com .au> wrote in message
> >> news:46283e76@quokka.wn . com .au...
> >> > Actually Mark I did a quick check of the primary literature and there
> > are
> >> > at
> >> > least 15 conditions, including dementia, atherosclerosis, and
diabetes,
> > in
> >> > which cannabinoid based interventions offer potential. In regard to
> >> > this
> >> > news item it is consistent with a study released by the American
> > Thoracic
> >> > Society sometime ago wherein they found no evidence of increased
rates
> > of
> >> > lung, head, or neck cancer in pot smokers and they reasoned it is
> > because
> >> > of THC impact on cell cycle dynamics. THC and other cannabinoids are
> > known
> >> > to inhibit VEGF, which stimulates new blood vessel growth.
> >> > "Mark Whiteley" <mark.whiteley53@ntlworld . com > wrote in message
> >>
> >> (I reordered the above, i was told earlier that post should be posted
> > after
> >> the original otherwise it "troll like" behaviour. Don't get me wrong i
> > don't
> >> mind but i guess we should try and follow neticate where possible..I'm
> > sure
> >> i've broken loads of rules without realising).
> >>
> >> I was being a little sarcastic(i believe in it's theroputic nature), I
> > know
> >> there are lots of medical conditions cannabis can help with.. I guess i
> >> should have deatailed more...thanks for pointing this out though...I
> >> think
> >> most people who've read my previous mails, over the last couple of
> >> months,
> >> to this group will know i'm a fan, but I only know what i have read(I'm
> >> no
> >> expert). I try to research at sites that have some credability but i
can
> >> only go on their data..
> >>
> >> However I would suggest that cannabis makes you "feel good" and would
> > reduce
> >> how much people notice their illness's, people may think it helps and
it
> >> does but it isn't making them "better" more masking their
illness..other
> >> drugs would do the same job due to their "painkiller" nature...I could
be
> >> wrong(if i am i'm sure you'll tell me and explain why?), and to be
fair,
> > it
> >> dosn't matter to me as the end result is the person feels "better". I
> >> just
> >> like to cover all the bases..
> >>
> >> Here's one website which details quite a few illness which cannabis is
> >> reported to help..
> >>
> >> * w w w .pacifier . com /~alive/index_se_cmu.htm
> >>
> >> I just think we need to be careful about syaing that cannabis is a
> >> "medicinal wonder", it's still early days with regards to reaserch. The
> >> "prohibition" people would move quickly to turn that aginst us in the
> > event
> >> cannabis is proven not to help.. . it may harm further, the drugs
> > reputation..
> >>
> >>
> >
> >
>
>
