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ironjustice@aol.com
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 Posted: Fri Nov 28, 2008 1:46 am Post subject: Re: Pufa Prevents Paranoia |
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On Nov 27, 5:37 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
Evidence based medicine .. IE: decreased receptors in the brain AND
the FACT they smoke four times more than everyone else MEANS .. we
have what is called a PARADOX .. ? <<
Orrr .. it could be just like Parkinson>s .. or what resembles
Parkinson>s .. brain iron accumulation.
In the 61 year old woman her tremors and gait returned to normal when
the iron was EFFECTIVELY targeted by the proper methods.
IF it were to be the same problem iron accumulation one might believe
since the CHOLINE in Parkinson>s was so effective and since this very
same choline is BEING targeted as an effective treatment then one
might think .. based ON .. evidence .. IE: tremors gone and gait
returned to normal .. that the method of targeting POSSIBLE iron in
schizophrenia is not all that far fetched.
Especially when it is already PROVEN iron excess causes schizophrenia.
Clinical trial on the use of cytidine diphosphate choline (CDP-
choline) in Parkinson>s disease.
Cubells JM, Hernando C.
Department of Neurosurgery,
Centro Ramon y Cajal, Madrid, Spain.
Clin Ther 1988;10(6):664-71
Abstract
Thirty patients with Parkinson>s disease, treated with levodopa for
the past few years, concomitantly received 500 mg of cytidine
diphosphate choline (CDP Choline) daily for 30 days. Significant
improvements in some of the neurologic signs and in several
electrophysiologic parameters measuring the traction reflex and the
active contraction were observed. A greater stability of therapeutic
response between doses of levodopa was also seen, although the
incidence of dyskinesia increased. In a second stage of CDP Choline
treatment, also lasting 30 days, the dose of levodopa was reduced by
one-third, and the incidence of dyskinesia dropped to its previous
level, but the therapeutic response remained stable. Addition of CDP
Choline produced significant increases in plasma concentrations of
dopa and homovanillic acid, with no modifications in tyrosine or 3-O-
methyldopa concentrations. A significant increase in the number of
lymphocytic dopaminergic receptors also occurred.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
[quote]
Ok ..
I>ll settle for that ..
Who loves ya.
Tom
Jesus Was A Vegetarian!http://tinyurl.com/634q5a
Man Is A Herbivore!http://tinyurl.com/4rq595
DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk[/quote] |
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ironjustice@aol.com
Guest
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| Posted: Fri Nov 28, 2008 2:14 am Post subject: Re: Pufa Prevents Paranoia |
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On Nov 27, 5:46 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
CDP
Choline produced an increase in lymphocytic dopaminergic receptors <<
NOW that is a good thing ..
THAT is what they are trying to do NOW.
Induce these receptors they find are missing when they cut the brain
out of the skull of your body when you haue shufflel>d off this
mortall coile ..
THAT they dooo by .. ? .. targeting this acetylcholine / choline
connection.
"Concomitantly received cytidine diphosphate choline"
Lecithin is recommended as a BETTER method of choline supplementation
in other brain diseases due to its ability to produce a 5 times
increase of choline and a retention time of 3 times as many hours.
Source Lancet 1977 Jul 9;2(8028):68-9
Title Lecithin consumption raises serum-free-choline levels. Wurtman
RJ, Hirsch
MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its
administration is an effective way of treating tardive dyskinesia.
We found that oral lecithin is considerably more effective in raising
human
serum-choline levels than an equivalent quantity of choline chloride.
30 minutes after ingestion of choline chloride (2-3 g free base),
serum-
choline levels rose by 86% and returned to normal values within 4
hours; 1
hour after lecithin ingestion, these levels rose by 265% and remained
significantly raised for 12 hours.
Lecithin may therefore be the method of choice for accelerating
acetylcholine synthesis by increasing the availability of choline,
its precursor in the blood.
----------------
Source Am J Clin Nutr 1982 Oct;36(4):709-20
Title The use of cholinergic precursors in neuropsychiatric diseases.
Rosenberg
GS, Davis KL.
Preclinical data suggest that cholinergic precursors such as choline
or lecithin, increase levels of acetylcholine in specific brain
structures, and under certain conditions may enhance cholinergic
neurotransmission.
A variety of neuropsychiatric diseases including tardive dyskinesia.
Huntington>s chorea, ataxias, Tourette>s syndrome, schizophrenia,
affective illness, and senile dementia of the Alzheimer type, has been
implicated with a general
underactivity of central cholinergic mechanisms.
Recent studies have investigated the possibility that cholinergic
precursor loading
strategies may provide viable treatments for these disorders of
presumed cholinergic underactivity.
Extensive data demonstrate that the symptoms of tardive dyskinesia can
be reduced by choline or lecithin, whereas investigations in other
disorders have met with mild success, at best, or are still in
preliminary stages.
Further controlled studies with choline or lecithin using
broader dose ranges, longer durations of treatment, and concomitant
administration of agents which may increase the release of
acetylcholine are warranted
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk |
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ironjustice@aol.com
Guest
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| Posted: Fri Nov 28, 2008 3:19 am Post subject: Re: Pufa Prevents Paranoia |
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On Nov 27, 6:14 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
CDP Choline produced an increase in lymphocytic dopaminergic
receptors <<
The selective á7 nicotinic acetylcholine receptor agonist A-582941
activates immediate early genes in limbic regions of the forebrain:
Differential effects in the juvenile and adult rat
M.S. Thomsena, b, J.D. Mikkelsena, D.B. Timmermanna, D. Petersc, A.
Hay-Schmidtb, H. Martensd and H.H. Hansena, ,
aDepartment of Translational Neurobiology, NeuroSearch A/S,
Pederstrupvej 93, 2750 Ballerup, Denmark
bDepartment of Neuroscience and Pharmacology, University of
Copenhagen, Copenhagen, Denmark
cDepartment of Medicinal Chemistry, NeuroSearch A/S, Ballerup, Denmark
dSynaptic Systems GmbH, Goettingen, Germany
Accepted 30 March 2008. Available online 16 April 2008.
Abstract
Due to the cognitive-enhancing properties of á7 nicotinic
acetylcholine receptor (á7 nAChR) agonists, they have attracted
interest for the treatment of cognitive disturbances in
schizophrenia.
Schizophrenia typically presents in late adolescence or early
adulthood. It is therefore important to study whether á7 nAChR
stimulation activates brain regions involved in cognition in juvenile
as well as adult individuals.
Here, we compared the effects of the novel and selective á7 nAChR
agonist 2-methyl-5-(6-phenyl-pyridazin-3-yl)-octahydro-pyrrolo[3,4-c]
pyrrole (A-582941) in the juvenile and adult rat forebrain using two
markers, activity-regulated cytoskeleton-associated protein (Arc) and
c-Fos, to map neuronal activity.
Acute administration of A-582941 (1, 3, 10 mg/kg) induced a dose-
dependent increase in Arc mRNA expression in the medial prefrontal
cortex (mPFC) and the ventral/lateral orbitofrontal (VO/LO) cortex of
juvenile, but not adult rats.
This effect was mitigated by the á7 nAChR antagonist
methyllycaconitine. A-582941 also increased c-Fos mRNA expression in
the mPFC of juvenile, but not adult rats.
Furthermore, A-582941 increased the number of Arc and c-Fos
immunopositive cells in the mPFC, VO/LO, and shell of the nucleus
accumbens, in both juvenile and adult rats.
The A-582941-induced c-Fos protein expression was significantly
greater in the mPFC and VO/LO of juvenile compared with adult rats.
These data indicate that A-582941-induced á7 nAChR stimulation
activates brain regions critically involved in working memory and
attention.
Furthermore, this effect is more pronounced in juvenile than adult
rats, indicating that the juvenile forebrain is more responsive to á7
nAChR stimulation.
This observation may be relevant in the treatment of juvenile-onset
schizophrenia.
Key words: schizophrenia; nicotinergic; prefrontal cortex; accumbens;
Arc; c-Fos
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
[quote]
NOW that is a good thing ..
THAT is what they are trying to do NOW.
Induce these receptors they find are missing when they cut the brain
out of the skull of your body when you haue shufflel>d off this
mortall coile ..
THAT they dooo by .. ? .. targeting this acetylcholine / choline
connection.
"Concomitantly received cytidine diphosphate choline"
Lecithin is recommended as a BETTER method of choline supplementation
in other brain diseases due to its ability to produce a 5 times
increase of choline and a retention time of 3 times as many hours.
Source Lancet 1977 Jul 9;2(8028):68-9
Title Lecithin consumption raises serum-free-choline levels. Wurtman
RJ, Hirsch
MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its
administration is an effective way of treating tardive dyskinesia.
We found that oral lecithin is considerably more effective in raising
human
serum-choline levels than an equivalent quantity of choline chloride.
30 minutes after ingestion of choline chloride (2-3 g free base),
serum-
choline levels rose by 86% and returned to normal values within 4
hours; 1
hour after lecithin ingestion, these levels rose by 265% and remained
significantly raised for 12 hours.
Lecithin may therefore be the method of choice for accelerating
acetylcholine synthesis by increasing the availability of choline,
its precursor in the blood.
----------------
Source Am J Clin Nutr 1982 Oct;36(4):709-20
Title The use of cholinergic precursors in neuropsychiatric diseases.
Rosenberg
GS, Davis KL.
Preclinical data suggest that cholinergic precursors such as choline
or lecithin, increase levels of acetylcholine in specific brain
structures, and under certain conditions may enhance cholinergic
neurotransmission.
A variety of neuropsychiatric diseases including tardive dyskinesia.
Huntington>s chorea, ataxias, Tourette>s syndrome, schizophrenia,
affective illness, and senile dementia of the Alzheimer type, has been
implicated with a general
underactivity of central cholinergic mechanisms.
Recent studies have investigated the possibility that cholinergic
precursor loading
strategies may provide viable treatments for these disorders of
presumed cholinergic underactivity.
Extensive data demonstrate that the symptoms of tardive dyskinesia can
be reduced by choline or lecithin, whereas investigations in other
disorders have met with mild success, at best, or are still in
preliminary stages.
Further controlled studies with choline or lecithin using
broader dose ranges, longer durations of treatment, and concomitant
administration of agents which may increase the release of
acetylcholine are warranted
Who loves ya.
Tom
Jesus Was A Vegetarian!http://tinyurl.com/634q5a
Man Is A Herbivore!http://tinyurl.com/4rq595
DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk[/quote] |
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ironjustice@aol.com
Guest
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| Posted: Fri Nov 28, 2008 3:40 am Post subject: Re: Pufa Prevents Paranoia |
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|
On Nov 27, 7:19 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
CDP Choline produced an increase in lymphocytic dopaminergic
receptors <<
Coincidentally .. choline .. stands in for nicotine ..
"Nicotine, choline, and PNU-282987"
Involvement of 7 Nicotinic Acetylcholine Receptors in Gene Expression
of Dopamine Biosynthetic Enzymes in Rat Brain
Vol. 303, Issue 3, 896-903, December 2002
Lidia Serova and Esther L. Sabban
Department of Biochemistry and Molecular Biology, New York Medical
College, Valhalla, New York
Abstract
Brain dopaminergic systems are critical in mediating the physiological
responses to nicotine.
The effects of several concentrations of nicotine (0.08, 0.17, or 0.33
mg/kg body weight) and involvement of 7 nicotinic acetylcholine
receptors (nAChRs) in gene expression of key enzymes in dopamine
biosynthesis were evaluated in the ventral tegmental area (VTA) and
substantia nigra (SN), cell bodies of the mesocorticolimbic and
nigrostriatal pathways.
Nicotine elicited a dose-dependent elevation of mRNA for tyrosine
hydroxylase (TH), the rate-limiting enzyme in dopamine biosynthesis in
VTA and SN.
The VTA was more sensitive to lower concentrations of nicotine with
maximal response observed with the lowest dose of nicotine.
Nicotine also elevated mRNA levels of GTP cyclohydrolase I (GTPCH),
rate limiting in biosynthesis of TH>s essential cofactor
tetrahydrobiopterin in both dopaminergic locations.
The changes in TH and GTPCH mRNAs were correlated.
Pretreatment with the 7 nAChR antagonist methyllycaconitine prevented
the nicotine-induced rise in TH or GTPCH mRNA in VTA and SN.
Administration of 7 nAChR agonist 3-[2,4-dimethoxybenzilidene]
anabaseine at 1 to 10 mg/kg or (E,E-3-(cinnamylidene)anabaseine at 0.3
to 1 mg/kg increased TH mRNA in VTA and SN, but not in peripheral
catecholaminergic cells.
Thus, agonists of 7 nAChRs have therapeutic potential for increasing
TH gene expression in dopaminergic regions without some of nicotine>s
disadvantages, such as its harmful effects on the cardiovascular
system.
The findings indicate that nicotine may regulate dopamine biosynthesis
by alterations in gene expression of TH and its cofactor.
The 7 nAChRs are involved in mediating these effects of nicotine.
-------------------
Choline .. stands in for nicotine ..
"Nicotine, choline, and PNU-282987"
"We found that nicotine, choline, and PNU-282987
(a specific ¦Á7 nAChR agonist) decreased excess lung water
and lung vascular permeability, and reduced protein
concentration in the bronchoalveolar lavage(BAL).
Deficiency of ¦Á7 nAChR resulted in a 2-fold increase in
excess lung water and lung vascular permeability."
AJRCMB Articles in Press.
Published on April 12, 2007 as doi:10.1165/rcmb.2006-0240OC
ABSTRACT
New evidence indicates that neural mechanisms can downregulate
acute inflammation.
In these studies, we tested the potential role of the ¦Á7 nicotinic
acetylcholine receptor (¦Á7 nAChR) in a rodent model of
acid-induced acute lung injury.
We first determined that the ¦Á7 nAChR was expressed by
alveolar macrophages and lung epithelial cells.
Then, using an acid-induced acute lung injury mouse model,
we found that nicotine, choline, and PNU-282987
(a specific ¦Á7 nAChR agonist) decreased excess lung water
and lung vascular permeability, and reduced protein
concentration in the bronchoalveolar lavage(BAL).
Deficiency of ¦Á7 nAChR resulted in a 2-fold increase in
excess lung water and lung vascular permeability.
The reduction of proinflammatory cytokines (MIP-2 and
TNF-¦Á) in the BAL with nicotine probably resulted from
the suppression of NF-¦ÊB activation in alveolar macrophages.
The beneficial effect of nicotine was also tested in
rat model of acid-induced acute lung injury in which BAL
protein and RAGE, a marker of type I cell injury, were
reduced by nicotine treatment.
These results indicate that activation of ¦Á7 nAChR may
provide a new therapeutic pathway for the treatment of
acute lung injury.
-----------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
[quote]On Nov 27, 6:14 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
CDP Choline produced an increase in lymphocytic dopaminergic
receptors
The selective ¨¢7 nicotinic acetylcholine receptor agonist A-582941
activates immediate early genes in limbic regions of the forebrain:
Differential effects in the juvenile and adult rat
M.S. Thomsena, b, J.D. Mikkelsena, D.B. Timmermanna, D. Petersc, A.
Hay-Schmidtb, H. Martensd and H.H. Hansena, ,
aDepartment of Translational Neurobiology, NeuroSearch A/S,
Pederstrupvej 93, 2750 Ballerup, Denmark
bDepartment of Neuroscience and Pharmacology, University of
Copenhagen, Copenhagen, Denmark
cDepartment of Medicinal Chemistry, NeuroSearch A/S, Ballerup, Denmark
dSynaptic Systems GmbH, Goettingen, Germany
Accepted 30 March 2008. Available online 16 April 2008.
Abstract
Due to the cognitive-enhancing properties of ¨¢7 nicotinic
acetylcholine receptor (¨¢7 nAChR) agonists, they have attracted
interest for the treatment of cognitive disturbances in
schizophrenia.
Schizophrenia typically presents in late adolescence or early
adulthood. It is therefore important to study whether ¨¢7 nAChR
stimulation activates brain regions involved in cognition in juvenile
as well as adult individuals.
Here, we compared the effects of the novel and selective ¨¢7 nAChR
agonist 2-methyl-5-(6-phenyl-pyridazin-3-yl)-octahydro-pyrrolo[3,4-c]
pyrrole (A-582941) in the juvenile and adult rat forebrain using two
markers, activity-regulated cytoskeleton-associated protein (Arc) and
c-Fos, to map neuronal activity.
Acute administration of A-582941 (1, 3, 10 mg/kg) induced a dose-
dependent increase in Arc mRNA expression in the medial prefrontal
cortex (mPFC) and the ventral/lateral orbitofrontal (VO/LO) cortex of
juvenile, but not adult rats.
This effect was mitigated by the ¨¢7 nAChR antagonist
methyllycaconitine. A-582941 also increased c-Fos mRNA expression in
the mPFC of juvenile, but not adult rats.
Furthermore, A-582941 increased the number of Arc and c-Fos
immunopositive cells in the mPFC, VO/LO, and shell of the nucleus
accumbens, in both juvenile and adult rats.
The A-582941-induced c-Fos protein expression was significantly
greater in the mPFC and VO/LO of juvenile compared with adult rats.
These data indicate that A-582941-induced ¨¢7 nAChR stimulation
activates brain regions critically involved in working memory and
attention.
Furthermore, this effect is more pronounced in juvenile than adult
rats, indicating that the juvenile forebrain is more responsive to ¨¢7
nAChR stimulation.
This observation may be relevant in the treatment of juvenile-onset
schizophrenia.
Key words: schizophrenia; nicotinergic; prefrontal cortex; accumbens;
Arc; c-Fos
Who loves ya.
Tom
Jesus Was A Vegetarian!http://tinyurl.com/634q5a
Man Is A Herbivore!http://tinyurl.com/4rq595
DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
NOW that is a good thing ..
THAT is what they are trying to do NOW.
Induce these receptors they find are missing when they cut the brain
out of the skull of your body when you haue shufflel>d off this
mortall coile ..
THAT they dooo by .. ? .. targeting this acetylcholine / choline
connection.
"Concomitantly received cytidine diphosphate choline"
Lecithin is recommended as a BETTER method of choline supplementation
in other brain diseases due to its ability to produce a 5 times
increase of choline and a retention time of 3 times as many hours.
Source Lancet 1977 Jul 9;2(8028):68-9
Title Lecithin consumption raises serum-free-choline levels. Wurtman
RJ, Hirsch
MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its
administration is an effective way of treating tardive dyskinesia.
We found that oral lecithin is considerably more effective in raising
human
serum-choline levels than an equivalent quantity of choline chloride.
30 minutes after ingestion of choline chloride (2-3 g free base),
serum-
choline levels rose by 86% and returned to normal values within 4
hours; 1
hour after lecithin ingestion, these levels rose by 265% and remained
significantly raised for 12 hours.
Lecithin may therefore be the method of choice for accelerating
acetylcholine synthesis by increasing the availability of choline,
its precursor in the blood.
----------------
Source Am J Clin Nutr 1982 Oct;36(4):709-20
Title The use of cholinergic precursors in neuropsychiatric diseases.
Rosenberg
GS, Davis KL.
Preclinical data suggest that cholinergic precursors such as choline
or lecithin, increase levels of acetylcholine in specific brain
structures, and under certain conditions may enhance cholinergic
neurotransmission.
A variety of neuropsychiatric diseases including tardive dyskinesia.
Huntington>s chorea, ataxias, Tourette>s syndrome, schizophrenia,
affective illness, and senile dementia of the Alzheimer type, has been
implicated with a general
underactivity of central cholinergic mechanisms.
Recent studies have investigated the possibility that cholinergic
precursor loading
strategies may provide viable treatments for these disorders of
presumed cholinergic underactivity.
Extensive data demonstrate that the symptoms of tardive dyskinesia can
be reduced by choline or lecithin, whereas investigations in other
disorders have met with mild success, at best, or are still in
preliminary stages.
Further controlled studies with choline or lecithin using
broader dose ranges, longer durations of treatment, and concomitant
administration of agents which may increase the release of
acetylcholine are warranted
Who loves ya.
Tom
Jesus Was A Vegetarian!http://tinyurl.com/634q5a
Man Is A Herbivore!http://tinyurl.com/4rq595
DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk- Hide quoted text -
- Show quoted text -[/quote] |
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Guest
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| Posted: Fri Nov 28, 2008 4:19 am Post subject: Re: Pufa Prevents Paranoia |
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"Fatty acids again shown to aid children with behavior problems
Researchers reported last year that supplementation with essential
fatty acids can dramatically accelerate learning and reduce behavior
problems in children with developmental coordination disorder (see"
Hmmm, wonder if it affects those similar problems caused by low iron,
which is the world>s number one health problem. |
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Guest
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| Posted: Fri Nov 28, 2008 4:22 am Post subject: Re: Pufa Prevents Paranoia |
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This is why fish oil is being tried for psycotic folk.
In which response we got:
"snip"
Hmmm, seems some people would be helped with the fish oil in their
paranoia more then others. |
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ironjustice@aol.com
Guest
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| Posted: Fri Nov 28, 2008 5:35 am Post subject: Re: Pufa Prevents Paranoia |
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On Nov 27, 7:40 pm, "ironjust...@aol.com" <ironjust...@aol.com>
wrote:choline .. stands in for nicotine ..<<
Genetics of Smoking and Schizophrenia
Page Range: 43 - 59
DOI: 10.1300/J374v03n03_05
Copyright Year: 2007
Contributors: Sherry Leonard PhD, Departments of Psychiatry and
Pharmacology, University of Colorado at Denver and Health Sciences
Center, Aurora, CO, 80045, sherry_leonard@uchsc.edu
Sharon Mexal PhD, The Institute for Behavioral Genetics, Boulder, CO
Robert Freedman MD, Departments of Psychiatry and Pharmacology,
University of Colorado at Denver, and Health Sciences Center, Veterans
Affairs Medical Research Service, Denver, CO
Abstract:
Schizophrenia is a common mental illness with a high prevalence of
smoking. More than 80% of schizophrenics smoke compared to 25% of the
general population. Both schizophrenia and tobacco use have strong
genetic components, which may overlap. It has been suggested that
smoking in schizophrenia may be a form of self-medication in an
attempt to treat an underlying biological pathology. Smoking
normalizes auditory evoked potential and eye tracking deficits in
schizophrenia, as well as improving cognitive function. Nicotine acts
through a family of nicotinic receptors with either high or low
affinity for nicotine. The loci for several of these receptors have
been genetically linked to both smoking and to schizophrenia. Smoking
changes gene expression for more than 200 genes in human hippocampus,
and differentially normalizes aberrant gene expression in
schizophrenia. The 7* nicotinic receptor, linked to schizophrenia and
smoking, has been implicated in sensory processing deficits and is
important for cognition and protection from neurotoxicity. Nicotine,
however, has multiple health risks and desensitizes the receptor. A
Phase I trial of DMXB-A, an 7* agonist, shows improvement in both P50
gating and in cognition, suggesting that further development of
nicotinic cholinergic drugs is a promising direction in schizophrenia
research. doi:10.1300/J374v03n03_05
Journal Title:
Journal of Dual Diagnosis:
research and practice in substance abuse comorbidity
Volume: 3 Issue: 3/4
ISSN: 1550-4263 Pub Date: 11/1/2007 -----------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
[quote]On Nov 27, 7:19 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
CDP Choline produced an increase in lymphocytic dopaminergic
receptors
Coincidentally .. choline .. stands in for nicotine ..
"Nicotine, choline, and PNU-282987"
Involvement of 7 Nicotinic Acetylcholine Receptors in Gene Expression
of Dopamine Biosynthetic Enzymes in Rat Brain
Vol. 303, Issue 3, 896-903, December 2002
Lidia Serova and Esther L. Sabban
Department of Biochemistry and Molecular Biology, New York Medical
College, Valhalla, New York
Abstract
Brain dopaminergic systems are critical in mediating the physiological
responses to nicotine.
The effects of several concentrations of nicotine (0.08, 0.17, or 0.33
mg/kg body weight) and involvement of 7 nicotinic acetylcholine
receptors (nAChRs) in gene expression of key enzymes in dopamine
biosynthesis were evaluated in the ventral tegmental area (VTA) and
substantia nigra (SN), cell bodies of the mesocorticolimbic and
nigrostriatal pathways.
Nicotine elicited a dose-dependent elevation of mRNA for tyrosine
hydroxylase (TH), the rate-limiting enzyme in dopamine biosynthesis in
VTA and SN.
The VTA was more sensitive to lower concentrations of nicotine with
maximal response observed with the lowest dose of nicotine.
Nicotine also elevated mRNA levels of GTP cyclohydrolase I (GTPCH),
rate limiting in biosynthesis of TH>s essential cofactor
tetrahydrobiopterin in both dopaminergic locations.
The changes in TH and GTPCH mRNAs were correlated.
Pretreatment with the 7 nAChR antagonist methyllycaconitine prevented
the nicotine-induced rise in TH or GTPCH mRNA in VTA and SN.
Administration of 7 nAChR agonist 3-[2,4-dimethoxybenzilidene]
anabaseine at 1 to 10 mg/kg or (E,E-3-(cinnamylidene)anabaseine at 0.3
to 1 mg/kg increased TH mRNA in VTA and SN, but not in peripheral
catecholaminergic cells.
Thus, agonists of 7 nAChRs have therapeutic potential for increasing
TH gene expression in dopaminergic regions without some of nicotine>s
disadvantages, such as its harmful effects on the cardiovascular
system.
The findings indicate that nicotine may regulate dopamine biosynthesis
by alterations in gene expression of TH and its cofactor.
The 7 nAChRs are involved in mediating these effects of nicotine.
-------------------
Choline .. stands in for nicotine ..
"Nicotine, choline, and PNU-282987"
"We found that nicotine, choline, and PNU-282987
(a specific ¦Á7 nAChR agonist) decreased excess lung water
and lung vascular permeability, and reduced protein
concentration in the bronchoalveolar lavage(BAL).
Deficiency of ¦Á7 nAChR resulted in a 2-fold increase in
excess lung water and lung vascular permeability."
AJRCMB Articles in Press.
Published on April 12, 2007 as doi:10.1165/rcmb.2006-0240OC
ABSTRACT
New evidence indicates that neural mechanisms can downregulate
acute inflammation.
In these studies, we tested the potential role of the ¦Á7 nicotinic
acetylcholine receptor (¦Á7 nAChR) in a rodent model of
acid-induced acute lung injury.
We first determined that the ¦Á7 nAChR was expressed by
alveolar macrophages and lung epithelial cells.
Then, using an acid-induced acute lung injury mouse model,
we found that nicotine, choline, and PNU-282987
(a specific ¦Á7 nAChR agonist) decreased excess lung water
and lung vascular permeability, and reduced protein
concentration in the bronchoalveolar lavage(BAL).
Deficiency of ¦Á7 nAChR resulted in a 2-fold increase in
excess lung water and lung vascular permeability.
The reduction of proinflammatory cytokines (MIP-2 and
TNF-¦Á) in the BAL with nicotine probably resulted from
the suppression of NF-¦ÊB activation in alveolar macrophages.
The beneficial effect of nicotine was also tested in
rat model of acid-induced acute lung injury in which BAL
protein and RAGE, a marker of type I cell injury, were
reduced by nicotine treatment.
These results indicate that activation of ¦Á7 nAChR may
provide a new therapeutic pathway for the treatment of
acute lung injury.
-----------------
Who loves ya.
Tom
Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
Man Is A Herbivore!http://tinyurl.com/a3cc3
DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
On Nov 27, 6:14 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
CDP Choline produced an increase in lymphocytic dopaminergic
receptors
The selective ¨¢7 nicotinic acetylcholine receptor agonist A-582941
activates immediate early genes in limbic regions of the forebrain:
Differential effects in the juvenile and adult rat
M.S. Thomsena, b, J.D. Mikkelsena, D.B. Timmermanna, D. Petersc, A.
Hay-Schmidtb, H. Martensd and H.H. Hansena, ,
aDepartment of Translational Neurobiology, NeuroSearch A/S,
Pederstrupvej 93, 2750 Ballerup, Denmark
bDepartment of Neuroscience and Pharmacology, University of
Copenhagen, Copenhagen, Denmark
cDepartment of Medicinal Chemistry, NeuroSearch A/S, Ballerup, Denmark
dSynaptic Systems GmbH, Goettingen, Germany
Accepted 30 March 2008. Available online 16 April 2008.
Abstract
Due to the cognitive-enhancing properties of ¨¢7 nicotinic
acetylcholine receptor (¨¢7 nAChR) agonists, they have attracted
interest for the treatment of cognitive disturbances in
schizophrenia.
Schizophrenia typically presents in late adolescence or early
adulthood. It is therefore important to study whether ¨¢7 nAChR
stimulation activates brain regions involved in cognition in juvenile
as well as adult individuals.
Here, we compared the effects of the novel and selective ¨¢7 nAChR
agonist 2-methyl-5-(6-phenyl-pyridazin-3-yl)-octahydro-pyrrolo[3,4-c]
pyrrole (A-582941) in the juvenile and adult rat forebrain using two
markers, activity-regulated cytoskeleton-associated protein (Arc) and
c-Fos, to map neuronal activity.
Acute administration of A-582941 (1, 3, 10 mg/kg) induced a dose-
dependent increase in Arc mRNA expression in the medial prefrontal
cortex (mPFC) and the ventral/lateral orbitofrontal (VO/LO) cortex of
juvenile, but not adult rats.
This effect was mitigated by the ¨¢7 nAChR antagonist
methyllycaconitine. A-582941 also increased c-Fos mRNA expression in
the mPFC of juvenile, but not adult rats.
Furthermore, A-582941 increased the number of Arc and c-Fos
immunopositive cells in the mPFC, VO/LO, and shell of the nucleus
accumbens, in both juvenile and adult rats.
The A-582941-induced c-Fos protein expression was significantly
greater in the mPFC and VO/LO of juvenile compared with adult rats.
These data indicate that A-582941-induced ¨¢7 nAChR stimulation
activates brain regions critically involved in working memory and
attention.
Furthermore, this effect is more pronounced in juvenile than adult
rats, indicating that the juvenile forebrain is more responsive to ¨¢7
nAChR stimulation.
This observation may be relevant in the treatment of juvenile-onset
schizophrenia.
Key words: schizophrenia; nicotinergic; prefrontal cortex; accumbens;
Arc; c-Fos
Who loves ya.
Tom
Jesus Was A Vegetarian!http://tinyurl.com/634q5a
Man Is A Herbivore!http://tinyurl.com/4rq595
DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
NOW that is a good thing ..
THAT is what they are trying to do NOW.
Induce these receptors they find are missing when they cut the brain
out of the skull of your body when you haue shufflel>d off this
mortall coile ..
THAT they dooo by .. ? .. targeting this acetylcholine / choline
connection.
"Concomitantly received cytidine diphosphate choline"
Lecithin is recommended as a BETTER method of choline supplementation
in other brain diseases due to its ability to produce a 5 times
increase of choline and a retention time of 3 times as many hours.
Source Lancet 1977 Jul 9;2(8028):68-9
Title Lecithin consumption raises serum-free-choline levels. Wurtman
RJ, Hirsch
MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its
administration is an effective way of treating tardive dyskinesia.
We found that oral lecithin is considerably more effective in raising
human
serum-choline levels than an equivalent quantity of choline chloride.
30 minutes after ingestion of choline chloride (2-3 g free base),
serum-
choline levels rose by 86% and returned to normal values within 4
hours; 1
hour after lecithin ingestion, these levels rose by 265% and remained
significantly raised for 12 hours.
Lecithin may therefore be the method of choice for accelerating
acetylcholine synthesis by increasing the availability of choline,
its precursor in the blood.
----------------
Source Am J Clin Nutr 1982 Oct;36(4):709-20
Title The use of cholinergic precursors in neuropsychiatric diseases.
Rosenberg
GS, Davis KL.
Preclinical data suggest that cholinergic precursors such as choline
or lecithin, increase levels of acetylcholine in specific brain
structures, and under certain conditions may enhance cholinergic
neurotransmission.
A variety of neuropsychiatric diseases including tardive dyskinesia.
Huntington>s chorea, ataxias, Tourette>s syndrome, schizophrenia,
affective illness, and senile dementia of the Alzheimer type, has been
implicated with a general
underactivity of central cholinergic mechanisms.
Recent studies have investigated the possibility that cholinergic
precursor loading
strategies may provide viable treatments for these disorders of
presumed cholinergic underactivity.
Extensive data demonstrate that the symptoms of tardive dyskinesia can
be reduced by choline or lecithin, whereas investigations in other
disorders have met with mild success, at best, or are still in
preliminary
...
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Matti Narkia
Guest
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| Posted: Fri Nov 28, 2008 6:42 am Post subject: Re: Pufa Prevents Paranoia |
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marcia wrote:
[quote]On Nov 27, 12:09 am, ironjustice <ironjust...@cashette.com> wrote:
"With or without the omega-3 fatty acid alpha-linolenic acid"
Jesus Was A Vegetarian!http://tinyurl.com/634q5a
Vegetarians should get their Omega-3 fatty acids from Flax seed oil.
Taking fish oil would break their dietary rules.
[/quote]
Freshly ground flaxseeds are probably healthier option for them than
flaxseed oil. Walnuts are also a good choice. But because of the
conversion problem, perhaps they should also consider taking
vegetarian DHA capsules prepared from algae.
--
Matti Narkia
http://ma.gnolia.com/groups/Nutrition |
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Guest
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| Posted: Fri Nov 28, 2008 7:26 am Post subject: Re: Pufa Prevents Paranoia |
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"This somewhat explains the four times the rate of cigarette smoking in
schizophrenia.
This somewhat explains the four times the rate of cigarette smoking in
schizophrenia.
"Substantiates 7 nicotinic acetylcholine receptor in schizophrenia"
Not according to what the abstract you posted said:
"Recent studies indicate an association of the neuronal 7 nicotinic
acetylcholine receptor (7 AChR) with several aspects of schizophrenia,
and decreased levels of this receptor in postmortem brains of
schizophrenic patients have been reported. In view of that and in"
More not less receptors should be associated with increased smoking. |
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Guest
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| Posted: Fri Nov 28, 2008 7:28 am Post subject: Re: Pufa Prevents Paranoia |
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This is why fish oil is being tried for psycotic folk.
In which response we got:
"snip"
Hmmm, seems some people would be helped with the fish oil in their
paranoia more then others. |
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Guest
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| Posted: Fri Nov 28, 2008 7:32 am Post subject: Re: Pufa Prevents Paranoia |
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"Fatty acids again shown to aid children with behavior problems
Researchers reported last year that supplementation with essential
fatty acids can dramatically accelerate learning and reduce behavior
problems in children with developmental coordination disorder (see"
Hmmm, wonder if it affects those similar problems caused by low iron,
which is the world>s number one health problem.
In response:
"You have been told not to post to my threads dioxin boy .."
Sooo, it seems low iron is indeed the cause of cognitive problems. Try
an increase in the fish oil, which might help the paranoia too. |
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Guest
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| Posted: Fri Nov 28, 2008 8:50 pm Post subject: Re: Pufa Prevents Paranoia |
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" Evidence based medicine .. IE: decreased receptors in the brain AND
the FACT they smoke four times more than everyone else MEANS .. we
have what is called a PARADOX .. ? <<
Orrr .. it could be just like Parkinson>s .. or what resembles
Parkinson>s .. brain iron accumulation.
In the 61 year old woman her tremors and gait returned to normal when
the iron was EFFECTIVELY targeted by the proper methods."
No, the numbers of recptors do not fit thelevel of smoking, the
relationship is backwards of what it should be given your guess.
Low iron is part of the development of Parkinson>s, you were given the
research to show it. You are only guessing. Guesses are fine but in
the end science holds sway. |
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Guest
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| Posted: Fri Nov 28, 2008 9:00 pm Post subject: Re: Pufa Prevents Paranoia |
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More not less receptors should be associated with increased smoking.
<<
"They smoke four times more .. pal ..
They don>t smoke four times more .. ?
They will BEG you for a smoke .. it is that .. bad .."
As is common of almost all former patients of mental hospitals and not
just with the diagnosis in question. How do you know they will "beg",
personal experience?
"Now .. what were you saying about your .. opinion as to the efficacy of
nicotine in schizophrenia .. ?
Evidence based medicine .. IE: decreased receptors in the brain AND the
FACT they smoke four times more than everyone else MEANS .. we have what
is called a PARADOX .. ?
Ok ..
I>ll settle for that .."
Translation, the evidence does not fit the preassumed guess so call it a
"paradox" and keep the guess. |
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ironjustice
Guest
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| Posted: Sun Nov 30, 2008 1:15 am Post subject: Re: Pufa Prevents Paranoia |
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On Nov 28, 7:00 am, mo...@otr.com wrote:
Translation, the evidence does not fit the preassumed guess so call
it a
"paradox" and keep the guess. <<
Orr .. you try to figure out why this .. PROVEN .. scientific ..
'guess' IS .. wrong .. ?
WHAT makes them sooo .. different from say .. Parkinson>s and THEIR
reaction to nicotine .. ?
Do Parkinson>s .. bi-polar .. Alzheimer>s SHARE the same disregulation
of receptors .. and IF there IS a receptor 'problem' what IS it that
causes the receptor problem.
The oxidative stress theory of iron accumulation can fit here.
Iron excess has been proven already to cause schizophrenia,
Juvenile schizophrenia seems to be treatable and / or curable but when
they have progressed to an older age they say it is not curable.
ADHD in children in China were found to have ONLY iron and ascorbate
as the defining difference whether they contracted ADHD or .. not.
One may consider the GRADUAL increase of disability 'could' be related
to the GRADUAL increase of iron / age related iron accumulation /
oxidative stress.
IF the receptors CAN be regenerated / IE: 61 year old Parkinsons'
patient walking and talking .. then these findings of lower or higher
receptors could be easily made redundant / who cares they grow back.
Simple field studies of extreme targeting by low iron diet and iron
elimination therapy / IE: phlebotomy as in the case of the dancing 61
year old woman .. with .. Parkinsons' ..
-----------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk |
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ironjustice
Guest
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| Posted: Sun Nov 30, 2008 1:29 am Post subject: Re: Pufa Prevents Paranoia |
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On Nov 28, 7:00 am, mo...@otr.com wrote:As is common of almost all
former patients of mental hospitals and not
just with the diagnosis in question. How do you know they will
"beg",
personal experience? <<
You should maybe highlight the post when you decide to respond to a
thread a person might miss one or two of your .. gems.
Smoking IS .. common .. ?
I may have to think real hard to remember what these OTHER mental
illnesses might BE that would put one in a mental hospital ..
And as to my personal experiences with schizophrenia .. what>s it
to .. ya ..
You would have a .. problem .. if .. I do have personal experience
with schizophrenia .. ?
Heh .. heh ..
Panhandler on the corner .. ?
Myself .. ?
A buddy .. ?
My .. mom .. ?
Which ONE of those do you disapprove of my .. personal experience .. ?
Just to see who and when one discriminates or reacts differently ..
to .. there .. buddy .. -----------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
[quote] More not less receptors should be associated with increased smoking.
"They smoke four times more .. pal ..
They don>t smoke four times more .. ?
They will BEG you for a smoke .. it is that .. bad .."
As is common of almost all former patients of mental hospitals and not
just with the diagnosis in question. How do you know they will "beg",
personal experience?
"Now .. what were you saying about your .. opinion as to the efficacy of
nicotine in schizophrenia .. ?
Evidence based medicine .. IE: decreased receptors in the brain AND the
FACT they smoke four times more than everyone else MEANS .. we have what
is called a PARADOX .. ?
Ok ..
I>ll settle for that .."
Translation, the evidence does not fit the preassumed guess so call it a
"paradox" and keep the guess.[/quote] |
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