Anxiety is a normal human response to stress, but in some, it can
develop into a disabling disorder of excessive and
irrational fears, such as obsessive-compulsive disorder, panic
disorder, or posttraumatic stress disorder.
Effective treatments are available and can involve either behavioral
therapy or medications.
Although "it makes intuitive sense that combining these two
treatments
would result in even better results," David Tolin, Ph.D.
notes that has unfortunately not yet been the case and the majority
of
the evidence suggests that combined therapy is no more
effective than behavior therapy alone, and in some cases can even be
less effective.
However, Dr. Tolin is one of the three authors on a meta-analysis
scheduled for publication on June 15th in Biological Psychiatry,
in which they evaluated a potentially important new treatment
paradigm
for anxiety.
Dr. Tolin explains the impetus behind their analysis: "Recently,
several researchers have tried a radically different approach:
instead
of just throwing two effective monotherapies at the problem, they
have
instead looked at medications that specifically target the
biological mechanisms that make psychotherapy work in the first
place."
 John H. Krystal, M.D., Editor of Biological Psychiatry and another
of
the study's authors, adds that "there has now been a sufficient
amount of research in this area to take a step back to look at the
basic research conducted in animals and the initial clinical trials."
This research effort has involved the addition of D-cycloserine, an
old drug long approved by the U.S. Food and Drug Administration for
the treatment of tuberculosis, to exposure-based fear treatment in
animals and humans.
The meta-analysis, a pooling of the published literature on this
approach, provides evidence that D-cycloserine enhances the learning
process in the brain, indicating that, unlike many other medications,
it may improve the effectiveness of behavioral therapy.

There is a caveat, however, as the authors also discovered that
tolerance may develop to this effect. Dr. Krystal comments that, if
so,
"it may be best used before therapy sessions to 'warm up the brain'
and make it more responsive to the treatment sessions rather
than as a daily treatment."

Dr. Tolin makes an additional, important observation regarding this
line of work: "Another very exciting aspect of this work is that it's
one of the few really good examples of translational research in
psychiatry: taking basic science from the laboratory, in this case
animal
studies, and translating that research into useful interventions for
humans." Although additional research is clearly necessitated, this
confirmation of the effectiveness of D-cycloserine is a positive step
forward in improving treatments for individuals suffering with
anxiety
disorders.

Source: Elsevier

-----------------

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/634q5a

Man Is A Herbivore!
http://tinyurl.com/4rq595

Anxiety is a normal human response to stress, but in some, it can
develop into a disabling disorder of excessive and
irrational fears, such as obsessive-compulsive disorder, panic
disorder, or posttraumatic stress disorder.
Effective treatments are available and can involve either behavioral
therapy or medications.
Although "it makes intuitive sense that combining these two
treatments
would result in even better results," David Tolin, Ph.D.
notes that has unfortunately not yet been the case and the majority
of
the evidence suggests that combined therapy is no more
effective than behavior therapy alone, and in some cases can even be
less effective.
However, Dr. Tolin is one of the three authors on a meta-analysis
scheduled for publication on June 15th in Biological Psychiatry,
in which they evaluated a potentially important new treatment
paradigm
for anxiety.
Dr. Tolin explains the impetus behind their analysis: "Recently,
several researchers have tried a radically different approach:
instead
of just throwing two effective monotherapies at the problem, they
have
instead looked at medications that specifically target the
biological mechanisms that make psychotherapy work in the first
place."
 John H. Krystal, M.D., Editor of Biological Psychiatry and another
of
the study's authors, adds that "there has now been a sufficient
amount of research in this area to take a step back to look at the
basic research conducted in animals and the initial clinical trials."
This research effort has involved the addition of D-cycloserine, an
old drug long approved by the U.S. Food and Drug Administration for
the treatment of tuberculosis, to exposure-based fear treatment in
animals and humans.
The meta-analysis, a pooling of the published literature on this
approach, provides evidence that D-cycloserine enhances the learning
process in the brain, indicating that, unlike many other medications,
it may improve the effectiveness of behavioral therapy.

There is a caveat, however, as the authors also discovered that
tolerance may develop to this effect. Dr. Krystal comments that, if
so,
"it may be best used before therapy sessions to 'warm up the brain'
and make it more responsive to the treatment sessions rather
than as a daily treatment."

Dr. Tolin makes an additional, important observation regarding this
line of work: "Another very exciting aspect of this work is that it's
one of the few really good examples of translational research in
psychiatry: taking basic science from the laboratory, in this case
animal
studies, and translating that research into useful interventions for
humans." Although additional research is clearly necessitated, this
confirmation of the effectiveness of D-cycloserine is a positive step
forward in improving treatments for individuals suffering with
anxiety
disorders.

Source: Elsevier

-----------------

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/634q5a

Man Is A Herbivore!
http://tinyurl.com/4rq595

IE: choline .. nicotine .. connection.

What was it that raises those dopamine receptors .. ?

Coincidentally .. choline ..

"The number of lymphocytic dopaminergic receptors increased"

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

So in theory .. vegetable lecithin mixed with maltol would be a remedy
for all of the above .. ?

In theory ..

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

 Risk-Takers May Lack Ability to Limit Brain Chemical

Anti Dementia Drugs Could Aid in Binge Eating Prevention
View Votes
Submitted by staff on Tue, 09/02/2008 - 12:51pm.
From Reuters Health comes the news that binge eaters who have no
control over their binging may in fact be helped by the Alzheimers
drugs menantine, which will not apparently help to reduce the weight
of the patient, but will reduce their binging in both frequency and
severity.

McLean Hospital in Belmont Mass.,told Reuters that the study chief, Dr
Brian Brennan and his team had originally hypothesized that memantine
would reduce the binging and were not suprised by the study's results.

They were however surprised that the drug was not helpful in body
weight reduction.
A study previously done using memantine in just five people showed
that it did reduce both binging as well as body weight.

The binge eater very often will eat massive amounts of food,
completely losing control over their eating, but do not, like the
bulimia patient purge afterwards.
In this study, 16 binge eater took the memantine for twelve weeks and
found that their average number of binges decreased from about five to
one per week, which is a significant decrease.

There was however no effect on the weight,or anxiety or depression.

International Journal of Eating Disorders, September 2008.

---------------------------------

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/4rq595

This stroke study gives evidence of iron being involved.
Iron is now being targeted after a stroke.
Iron comes from the blood spilled in the head during the stroke.
Stroke causes aberrant behavior .. IE: post traumatic stress disorder.

Page last updated at 01:05 GMT, Wednesday, 25 February 2009

Stroke post-traumatic stress risk

Peter Chapman experienced PTSD after a brain haemorrhage
Many stroke sufferers are left with post-traumatic stress disorder
(PTSD), a British study suggests.

More than a third of 105 brain haemorrhage survivors tested positive
for the disorder, with flashbacks and painful memories of their
bleed.

This is a similar level to that found in soldiers returning from war
zones and amongst victims of sexual assault, Neurosurgery journal
reports.

The authors of the study say diagnosing and treating PTSD will aid
recovery.

Subarachnoid haemorrhage affects about 8,000 people in the UK each
year and is a sudden leak of blood over the surface of the brain.

 Doctors do realise this type of stroke is stressful for the patient,
but they do not always ask the patient about anxiety and depression.
Someone needs to

Professor Allan House of the Stroke Association

Although emotional distress following this type of stroke is common,
it is under-recognised, they say, partly because clinicians tend to
focus on physical recovery.

The team from Durham University, the James Cook University Hospital in
Middlesbrough and the Newcastle General Hospital assessed the patients
at three months and again at 13 months after their subarachnoid
haemorrhage using a simple questionnaire.

At both stages, the answers given suggested 37% of the patients had
PTSD.

Traumatic event

The authors say their findings are not surprising, given the nature of
this type of stroke - its sudden, often unexpected and painful onset
in relatively young people, requiring emergency invasive
investigations and surgery.

Add to this having to deal with the fact that they have had a life-
threatening illness, it is understandable why many patients experience
emotional reactions, they say.

Adam Noble and his team say it is relatively easy to spot which stroke
patients are at greatest risk of PTSD by looking for signs of "poor"
coping, such as denial and self-blame.

These patients could be offered pre-emptive treatment, they say.

Mr Noble suggested tailored treatment such as group therapy "and,
where possible, prevention through teaching patients more appropriate
stress-coping strategies after they suffer a stroke".

Professor Allan House of the Stroke Association said: "Doctors do
realise this type of stroke is stressful for the patient, but they do
not always ask the patient about anxiety and depression. Someone needs
to.

"Some patients undoubtedly have PTSD, while others might have
depression or anxiety after a subarachnoid haemorrhage and it is
understandable why."

Peter Chapman, from Hartlepool, suffered a subarachnoid brain
haemorrhage at the age of 45 in 2001.

His PTSD was not picked up until two years after his stroke.

He said: "The first six months were the worst. I was so worried that
it might happen again and I have never shed so many tears in my life.

"If I had been tested and treated for PTSD right from the beginning,
my life would have been 500% better than what it has been, and would
have made the world of difference to my recovery."

-----------------

http://www.dragonsmedicalbulletin.com/b_clinical.html#6

Intracerebral Hemorrhage Patients Might Benefit From Iron Chelation
Treatment?

Abstract: Iron accumulates in the brain and contributes to brain
injury after intracerebral hemorrhage (ICH). The c-Jun-N-terminal
kinase (JNK) signaling pathway mediates cell death after ischemic
stroke, however, the involvement of JNK in ICH is not well known.

This study investigated whether the JNK signaling pathway is
activated
by iron after ICH. Male Sprague-Dawley rats received an infusion of
autologous whole blood (as a model of ICH) or ferrous iron into the
right basal ganglia and control rats had an infusion of saline. Some
ICH rats were treated with either deferoxamine (DFX), an iron
chelator, or vehicle.

Activation of JNK was measured by Western blot analysis and
immunohistochemistry. Free iron in cerebrospinal fluid (CSF) and
behavioral outcomes following ICH were also examined. We found that
activated JNK in the brain were increased after ICH, and an
intracerebral infusion of ferrous iron also upregulated brain
activated JNK. Free iron accumulated in CSF and systemic
administration of DFX after ICH reduces free iron contents in CSF,
suppresses JNK activation and improves ICH-induced neurological
deficits.

Our results demonstrated that the JNK signaling pathway is activated
after ICH and iron may contribute to this activation. DFX reduces
free
iron levels and attenuates activation of JNK suggesting iron
chelation
may be useful therapy for ICH patients.

Wan S, et al. Activation of c-Jun-N-terminal kinase in a rat model of
intracerebral hemorrhage: The role of iron. Neurosci Res. 2009;63(2):
100-5.

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/4rq595

This study would give a bit of credence to the excess oxidation in the
brain
theory in that lithium and maltol are BOTH antioxidants in the body.

"Browning pigment major contributor on exhibiting antioxidant
capacity"

Interactive role of color and antioxidant capacity in caramels
Pi-Jen Tsaia, , , Tzu-Yu Yua, Shyh-Hung Chenb,
Chan-Chiung Liua and Ying-Fang Sunc
aDepartment of Food Science, National Pingtung University
of Technology and Science 1, Hsueh Fu Road,
Nei-Pu Hsiang 91207 Pingtung, Taiwan, ROC
bPublic Health Bureau, Taitung County No. 336,
Bo-Ai Rd., Taitung City. Taitung County 950,
Taiwan, ROC
cDepartment of Biomedical Imaging and Radiological Sciences,
National Yang-Ming University, No. 155, Sec. 2, Linong Street,
Taipei, Taiwan, ROC

Received 26 August 2008;  accepted 11 January 2009.
Available online 20 January 2009.

Abstract
Caramelization, a good source of food color and antioxidant
capacity, depends on pH and sugars.
However, no thorough study regarding the interactive role of the
color and antioxidant capacity in caramel could be found.
In this paper, four sugars (including monosaccharide and
disaccharide) with different concentrations (1-40%) at different
pH (pH 3, 7 and 10) were heated at 90 °C for various durations
(0-42 h).
Results from 240 samples indicated that caramels from
monosaccharide with higher concentration exhibited better
antioxidant capacity at more alkaline condition.
High sugar concentration (40%) may partially overcome the
influence of low pH on monosaccharides or high pH on disaccharide.
Browning intensity (A420) was found to be a good index in monitoring
the antioxidant capacity of caramel. ÄpH may closely reflect the
increase rate of antioxidant capacity, which has not been reported
before.
Further statistic analysis through principal component analysis (PCA)
and structural equation model (SEM) revealed that browning pigment,
the interactive result of sugar concentration and pH, instead of
colorless intermediate, was the major contributor on classifying the
caramels or exhibiting antioxidant capacity.
This is the first paper regarding the representative role of A420
in caramel by confirmatory path analysis.

Keywords: Caramel; Antioxidant capacity; Browning intensity;
PCA; SEM

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

Raving a' loon

Cognitive enhancement drug may also cause addiction
Modafinil's effect on the brain suggests it could be addictive for
some.

Heidi Ledford

A drug used to treat narcolepsy — and often taken to increase
alertness and improve cognitive performance — may have the potential
to become addictive, a small pilot study has shown.

Brain-imaging studies performed on ten men before and after taking the
drug, called modafinil (Provigil), showed that it boosts levels of a
chemical called dopamine, which influences the brain's reward system1.
Drugs of abuse, from tobacco to heroin, also impact dopamine levels,
particularly in an area of the brain called the nucleus accumbens. In
the new study, published on 17 March by the Journal of the American
Medical Association, modafinil also increased dopamine in that
region.

The effect of cognitive-enhancement drugs on the brain is not well
known.GettyIt is an indirect measure of the propensity to trigger
addiction, and patients rarely become dependent upon modafinil, notes
Martha Farah, director of the Center for Cognitive Neuroscience at the
University of Pennsylvania in Philadelphia, who was not involved with
the study. "However, we know that drug dependence is a result of
drugs' effects on the brain's reward system," she says, "and so
finding that modafinil affects this system is also relevant and should
prompt us to look more carefully at the risks of dependence for this
drug."

Use and abuse
Meanwhile, the results should not prompt those who take modafinil for
medical conditions to discontinue the drug, says study author Nora
Volkow, director of the National Institute on Drug Abuse in Bethesda,
Maryland. Physicians, however, should be aware that addiction is a
possibility and can tell their patients to watch for signs of
dependency, she says.

The US Food and Drug Administration has approved modafinil to treat
narcolepsy and some other sleep disorders, and doctors will sometimes
prescribe the drug off label to treat attention-deficit disorder and
schizophrenia. In recent years, the drug has joined the ranks of
methylphenidate (Ritalin) and amphetamines — drugs which are misused ,
often by students, to improve cognitive function. A recent survey by
Nature found that of those who use drugs to improve focus, 44% have
tried modafinil.

Addiction is a familiar consequence of taking stimulants such as
amphetamines or cocaine and has been found among those who take
methylphenidate as well, although generally only when abnormally high
doses of the drug are taken, or when the drug is administered by
injection rather than orally. But researchers thought modafinil acted
via a different mechanism — one that did not affect the dopamine
system.

"People were saying, 'With Provigil, we don't have to worry'," says
Volkow. "Unfortunately, that is not the case. As of now, all of the
medications that are being used with the expectation of improving
cognitive performance have the potential to produce addiction."

Addictive qualities
Modafinil was thought to promote wakefulness by increasing responses
to brain hormones called orexins. But animal studies showed that
rodents that lack dopamine receptors are unresponsive to the drug, and
in 2006, researchers found that modafinil affects dopamine levels in
the brains of rhesus macaques2.

The animals in these studies were often given high doses of the drug
by injection, whereas humans would take the drug orally and at lower
doses. So Volkow, along with Joanna Fowler of Brookhaven National
Laboratory in Upton, New York, and their colleagues, decided the
effects needed to be analyzed directly in humans.

Volkow and her team administered labelled compounds that bound to free
dopamine receptors and dopamine transporters to ten paid volunteers
before and after the volunteers took modafinil. By imaging these
compounds, the team was able to estimate how many receptors and
transporters in the brain were bound to dopamine after taking the
drug. They found that modafinil blocked dopamine transporters in the
brain, resulting in an increase in dopamine concentration.

The study was performed in only ten subjects, but that is not unusual
for labour-intensive brain-imaging studies, notes Michael Minzenberg,
who studies neurochemical systems at the University of California,
Davis Health System Imaging Research Center. Pilot studies such as
this may not capture the full variation in how individuals within a
population will respond to the drug, he says, but the impact on the
dopamine system is clear.

Still, that dopamine connection may not tell the full story, says
Bertha Madras, professor of psychobiology at Harvard Medical School in
Southborough, Massachusetts. For example, some drugs increase dopamine
levels but have other properties that make them aversive rather than
addictive. "The full spectrum of the pharmacology of the drug is what
drives the abuse potential," she says.

References
Volkow, N. D. et al. JAMA 301, 1148-1154 (2009).
Madras, B. K. et al. J. Pharmacol. Exp. Therapeutics 319, 561-569
(2006).
Published online 17 March 2009 | Nature | doi:10.1038/news.2009.170

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

Choline ..

"Anterior cingulate functioning in attention deficit hyperactivity
disorder (ADHD)"
"Role of Anterior Cingulate Cortex in Parkinson's Disease"
"Fewer D2 receptors in the anterior cingulate cortex in patients with
schizophrenia"
"The anterior cingulate cortex in bipolar disorder "

Brain Abnormality Found in Boys with Attention Deficit Hyperactivity
Disorder
18 March 2009

Researchers trying to uncover the mechanisms that cause attention
deficit hyperactivity disorder (ADHD) and conduct disorder have found
an abnormality in the brains of adolescent boys suffering from the
conditions, but not where they expected to find it.

Boys with either or both of these disorders exhibited a different
pattern of brain activity than normally developing boys when they
played a simple game that sometimes gave them a monetary reward for
correct answers, according to a new study by a University of
Washington research team.

The research focused on two brain areas, the striatum and anterior
cingulate cortex. The striatal region is a network of structures in
the mid brain that motivates people to engage in pleasurable or
rewarding behavior. The anterior cingulate is higher in the brain and
normally activates when an expected reward stops. However, this
process, called extinction, doesn't occur, at least as quickly, in
boys with attention deficit hyperactivity or conduct disorders.
Instead, the striatal region continues to be activated, said Theodore
Beauchaine, a UW associate professor of psychology and senior author
of the paper.

"When children engage in impulsive behavior they are looking to
stimulate themselves and have fun. Children with attention deficit
hyperactivity disorder are always looking to have fun and that is what
gets them in trouble," he said. "A behavior should stop when the
reward stops. When you stop the reward for children with these
disorders, they continue to focus on the reward long afterward and the
anterior cingulate does not appear to become activated."

Attention deficit hyperactivity disorder (ADHD) is one of the most
common mental disorders among children, affecting between 3 and 5
percent of school-age youngsters, or an estimated 2 million.

The researchers used functional magnetic resonance imaging (fMRI) to
compare brain activity in 19 boys with either or both disorders and 11
normally developing boys. The adolescents ranged in age from 12 to 16.

Their brains were scanned while they played the game. The boys looked
at a screen and there was a button under each of their thumbs. When a
light flashed on the left or right side of the screen they were
instructed to press the button on that side. The screen lit up very
fast, up to 100 times a minute. The boys received five cents for each
correct response and could win up to $50. They were not penalized for
wrong answers and their accumulated winnings showed up on the screen.

Each boy had four five-minute blocks of trials. The first and third
trials involved opportunities to earn money. The second and fourth
trials did not involve winning money, but the boys were told to keep
playing the game because the game would change at some point.

Beauchaine said there was no difference in the accuracy or speed – the
behavioral response – between the two groups. But there was a
difference in brain activation. When the non-reward blocks came up the
anterior cingulate lit up for normally developing boys, but those with
either of the disorders, which frequently co-occur, continued to only
show activation in the striatum.

"This shows there is an abnormality, but not in the place we expected
to find it. We expected to find a difference in the way the striatum
functions, but instead found it in anterior cingulate functioning,"
said Beauchaine.

Source: EurekAlert

----------

Decreased dopamine D2 receptor binding in the anterior cingulate
cortex in schizophrenia.
Arch Gen Psychiatry. 2002 Jan;59(1):25-30.Related Articles, Links
Comment in:
Arch Gen Psychiatry. 2002 Jan;59(1):31-4.
Suhara T, Okubo Y, Yasuno F, Sudo Y, Inoue M, Ichimiya T,
Nakashima Y, Nakayama K, Tanada S, Suzuki K, Halldin C, Farde L.
Division of Advanced Technology for Medical Imaging,
National Institute of Radiological Sciences, 9-1,
Anagawa 4-Chome, Inage-ku, Chiba-shi,
263-8555 Japan. suh...@nirs.go.jp

BACKGROUND:
The clinical efficacy of dopamine D2 receptor antagonism on the
psychotic symptoms of schizophrenia has been widely demonstrated.
However, most in vivo imaging studies have not been able to detect
significant changes in striatal D2 receptors in schizophrenia.
On the other hand, a number of studies have reported abnormalities
in the cerebral cortex of schizophrenia.
The aim of this study was to examine the extrastriatal D2 receptors
of patients with schizophrenia.
METHODS:
Eleven drug-naive male patients with schizophrenia were examined
with positron emission tomography using carbon 11-labeled FLB 457.
Symptoms were assessed using the Brief Psychiatric Rating Scale.
Eighteen healthy controls were used for comparison.
Region-of-interest analysis was performed using the reference tissue
method, and binding potential (BP) was used for the index of dopamine
D2 receptor binding. RESULTS: The BP value was significantly lower,
by about 12.5%, in the anterior cingulate cortex in drug-naive
patients
with schizophrenia than in healthy controls.
A significant negative correlation was observed between BP in the
anterior cingulate cortex and the positive symptom score on Brief
Psychiatric Rating Scale.
CONCLUSIONS:
The lower BP values indicate fewer D2 receptors in the anterior
cingulate cortex in patients with schizophrenia.
Alterations in D2 receptor function in the extrastriatal region may
underlie the positive symptoms of schizophrenia.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

PMID: 11779278

Cerebral Cortex 1992; 2:513-525
© Oxford University Press 1992

--------------------------------------------------------------------------- -----

Attention and Sentence Processing Deficits in Parkinson's
Disease: The Role of Anterior Cingulate Cortex
Murray Grossman, Peter Crino, Martin Reivich,
Matthew B. Stem and Howard I. Hurtig
Department of Neurology, University of Pennsylvania School
of Medicine, and The Graduate Hospital Philadelphia,
Pennsylvania 19104-4283

Correspondence should be addressed to Murray Grossman,
Cognitive Neurology Section, Department of Neurology,
Hospital of the University of Pennsylvania,
3400 Spruce Street, Philadelphia, PA 19104-4283

Parkinson's disease (PD) is a complex neurodegenerative condition
involving a motor disorder that is related to reduced dopaminergic
input to the striatum.
Intellectual deficits are also seen in PD, but the pathophysiology
of these difficulties is poorly understood.
Regional cerebral blood flow (rCBF) was studied in neurologically
intact subjects during the performance of attention-demanding,
sentence processing tasks using positron emission tomography
(PET). T
he results demonstrated significantly increased rCBF in a distributed
set of cerebral regions during the detection of an adjective or a
particular agent in a sentence, including anterior cingulate cortex,
left inferior and middle frontal cortex, left inferior temporo-
occipital
cortex, posterolateral temporal cortex, left caudate, and left
thalamus.
We identified defects in this cerebral network by studying PD
patients
with two PET techniques.
Resting PET studies revealed a significant correlation between
regional cerebral glucose metabolism in anterior cingulate cortex
and deficits in attending to subtle grammatical aspects of sentences.
Studies of PD patients with the PET activation technique revealed
little
change in anterior cingulate and left frontal CBF during performance
of
the adjective detection or agent detection tasks.
These data suggest that a defect in anterior cingulate cortex
contributes
to the cognitive impairments observed in PD.

---------------

Choline, myo-inositol and mood in bipolar disorder: a proton magnetic
resonance spectroscopic imaging study of the anterior cingulate
cortex.
Moore CM, Breeze JL, Gruber SA, Babb SM, Frederick BB,
Villafuerte RA, Stoll AL, Hennen J, Yurgelun-Todd DA, Cohen BM,
Renshaw PF.
Bipolar Disord 2000 Sep;2(3 Pt 2):207-16

This might have something to do with the assault of nurses and doctors
in the hospitals ..

http://www.foxnews.com/story/0,2933,517745,00.html

How cigarettes calm you down

The calming neurological effects of nicotine have been demonstrated in
a group of non-smokers during anger provocation. Scientists writing in
BioMed Central's open access journal Behavioral and Brain Functions
suggest that nicotine may alter the activity of brain areas that are
involved in the inhibition of negative emotions such as anger.

Jean Gehricke led a team of scientists from the University of
California who studied the effect of nicotine patches on the subjects'
tendency to retaliate in response to anger provocation. The subjects
played a computer game and could see a video screen of another player
who they thought to betheir opponent, although, in fact, they were
playing alone. After each round, the victor could give his opponent a
burst of unpleasant noise at a duration and volume set by the winner.
In some of the subjects, nicotine was linked to a reduced tendency to
retaliate, even after provocation by the 'opponent'.

As per Gehricke, "Participants who showed nicotine-induced changes in
anger task performance also showed changes in brain metabolism.
Nicotine-induced reductions in length of retaliation were linked to
changes in brain metabolism in response to nicotine in brain areas
responsible for orienting, planning and processing of emotional
stimuli".

The authors say that their findings support the idea that people of an
angry disposition are more susceptible to nicotine's effects, and are
therefore more likely to become addicted to cigarettes. They conclude,
"Novel behavioral therapys that affect the cortical and limbic brain
areas, like anger management training, may aid smoking cessation
efforts in anger provoking situations that increase withdrawal and
tobacco cravings".

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/4rq595

What PART of NO shteaters on my
threads don't ya understand .. shteater .. ?

http://www.foxnews.com/story/0,2933,517745,00.html

How cigarettes calm you down

The calming neurological effects of nicotine have been demonstrated
in
a group of non-smokers during anger provocation. Scientists writing
in
BioMed Central's open access journal Behavioral and Brain Functions
suggest that nicotine may alter the activity of brain areas that are
involved in the inhibition of negative emotions such as anger.

Jean Gehricke led a team of scientists from the University of
California who studied the effect of nicotine patches on the
subjects'
tendency to retaliate in response to anger provocation. The subjects
played a computer game and could see a video screen of another player
who they thought to betheir opponent, although, in fact, they were
playing alone. After each round, the victor could give his opponent a
burst of unpleasant noise at a duration and volume set by the winner.
In some of the subjects, nicotine was linked to a reduced tendency to
retaliate, even after provocation by the 'opponent'.

As per Gehricke, "Participants who showed nicotine-induced changes in
anger task performance also showed changes in brain metabolism.
Nicotine-induced reductions in length of retaliation were linked to
changes in brain metabolism in response to nicotine in brain areas
responsible for orienting, planning and processing of emotional
stimuli".

The authors say that their findings support the idea that people of
an
angry disposition are more susceptible to nicotine's effects, and are
therefore more likely to become addicted to cigarettes. They
conclude,
"Novel behavioral therapys that affect the cortical and limbic brain
areas, like anger management training, may aid smoking cessation
efforts in anger provoking situations that increase withdrawal and
tobacco cravings".

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/4rq595

"The alpha7 nAChR-selective agonist choline promoted dopamine release
in vitro and in vivo"

That would be vegetable lecithin ..

alpha7 and non-alpha7 nicotinic acetylcholine receptors modulate
dopamine release in vitro and in vivo in the rat prefrontal cortex.
Eur J Neurosci. 2009 Feb;29(3):539-50. Epub 2009 Jan 28.
Livingstone PD, Srinivasan J, Kew JN, Dawson LA, Gotti C,
Moretti M, Shoaib M, Wonnacott S.
Department of Biology & Biochemistry, University of Bath, Bath, UK.

Nicotine enhances attentional and working memory aspects of
executive function in the prefrontal cortex (PFC) where dopamine
plays a major role.
Here, we have determined the nicotinic acetylcholine receptor
(nAChR) subtypes that can modulate dopamine release in rat
PFC using subtype-selective drugs.
Nicotine and 5-Iodo-A-85380 (beta2* selective) elicited [(3)H]
dopamine release from both PFC and striatal prisms in vitro and
dopamine overflow from medial PFC in vivo.
Blockade by dihydro-beta-erythroidine supports the participation
of beta2* nAChRs.
However, insensitivity of nicotine-evoked [(3)H]dopamine release
to alpha-conotoxin-MII in PFC prisms suggests no involvement
of alpha6beta2* nAChRs, in contrast to the striatum, and this
distinction is supported by immunoprecipitation of nAChR
subunits from these tissues.
The alpha7 nAChR-selective agonists choline and Compound A
also promoted dopamine release from PFC in vitro and in vivo,
and their effects were enhanced by the alpha7 nAChR-selective
allosteric potentiator PNU-120596 and blocked by specific
antagonists.
DNQX and MK801 inhibited [(3)H]dopamine release evoked by
choline and PNU-120596, suggesting crosstalk between alpha7
nAChRs, glutamate and dopamine in the PFC.
In vivo, systemic (but not local) administration of PNU-120596,
in the absence of agonist, facilitated dopamine overflow in the
medial PFC, consistent with the activation of extracortical
alpha7 nAChRs by endogenous acetylcholine or choline.
These data establish that both beta2* and alpha7 nAChRs can
modulate dopamine release in the PFC in vitro and in vivo.
Through their distinct actions on dopamine release, these nAChR
subtypes could contribute to executive function, making them
specific therapeutic targets for conditions such as schizophrenia
and attention deficit hyperactivity disorder.

PMID: 19187266
---------

This article clearly shows in the plant .. maltol a sugar  .. is
ESSENTIAL for the breakdown of dopamine .. it keeps the dopamine
THERE .. / prevents the breakdown.

Effect of maltol on the oxidation of DL-DOPA, dopamine, N-
acetyldopamine (NADA), and norepinephrine by mushroom tyrosinase.
Pigment Cell Res. 1997 Jun;10(3):139-49.
Kahn V, Ben-Shalom N.
Department of Food Science, Agricultural Research Organization,
Volcani Center, Bet Dagan, Israel.

Maltol (3-hydroxy-2-methyl-4H-pyran-4-one) appears to inhibit the
rate
of oxidation of DL-DOPA, dopamine, NADA and epinephrine by tyrosinase
when assayed spectrophotometrically but not when assayed
polarographically.
Maltol has an effect on the spectrum of product(s) formed when each
catecholamine was oxidized by tyrosinase showing that maltol hastens
the disappearance of the quinones, possibly by conjugating with them.
Indeed, at relatively high concentrations, maltol prevented the
conversion of DL-DOPA, dopamine, and norepinephrine to their
corresponding melanins via tyrosinase.

PMID: : 9266600

---------------------------------------------------------
This would evidence the use of lecithin simple vegetable lecithin
due to its efficient choline absorption.
Nicotine and choline and acetylcholine are called alpha7 nAChR
agonists.

"Efficacy of alpha7 nAChR agonists across a range of cognitive
processes ranging from pre-attentive to attentive states and
working and recognition memory provides a solid basis for their
pro-cognitive effects"

"Acetylcholine, nicotine, and choline were effective"
"These agonists were also effective"

A Cog in Cognition: How the alpha7 nicotinic acetylcholine receptor
is geared towards improving cognitive deficits.
Leiser SC, Bowlby MR, Comery TA, Dunlop J
Pharmacol Ther 2009 Apr 4.

Cognition, memory, and attention and arousal have been linked to
Nicotinic acetylcholine receptors (nAChR).
Thus it is not surprising that nAChRs have been strongly implicated
as therapeutic targets for treating cognitive deficits in disorders
such as schizophrenia and Alzheimer's disease (AD).
In particular the alpha7 (alpha7) nAChR has been closely linked with
normalization of P50 auditory evoked potential (AEP) gating deficits,
and to a lesser extent improvements in prepulse inhibition (PPI) of
the acoustic startle response.
These two brain phenomena can be considered as pre-attentive,
occurring while sensory information is being processed, and are
important endophenotypes in schizophrenia with deficits likely
contributing to the cognitive fragmentation associated with the
disease.
In addition alpha7 nAChRs have been implicated in attention, in
particular under high attentional demand, and in more demanding
working memory tasks such as long delays in delayed matching
tasks.
Efficacy of alpha7 nAChR agonists across a range of cognitive
processes ranging from pre-attentive to attentive states and working
and
recognition memory provides a solid basis for their pro-cognitive
effects.
This review will focus on the recent work highlighting the role of
alpha7 in cognition and cognitive processes.

Pharmacology & therapeutics [Pharmacol Ther]

------------

"Nicotinic therapies may be useful for treating cognitive deficits"
"Adjunctive nicotinic therapies"

That would be a .. smoke.

Interaction between nicotinic and dopaminergic therapies on cognition
in a chronic Parkinson model.
Decamp E, Schneider JS
Brain Res 2009 Jan 27.

While levodopa therapy for PD may effectively relieve motor
symptoms, many of the cognitive deficits experienced by PD
patients (and in animal models of PD) are not effectively
managed by this treatment.
In contrast, previous work has shown positive effects of
nicotinic therapies on cognition in PD models.
The present study evaluated the effects of levodopa, nicotine
and the nicotinic acetylcholine receptor agonist SIB-1553A
alone and in combination on cognition in a non-human primate
model of early PD.
Three adult male Rhesus monkeys, previously administered
low doses of the neurotoxin MPTP over several months to
produce cognitive deficits, were trained to perform a modified
spatial delayed response task in which the attentional
demands of the task were manipulated by varying the
duration of the cue presentation while keeping the memory
demands of the task low and constant.
Task performance was assessed after administration of
levodopa, nicotine ditartrate, or SIB-1553A and after
administration of drug combinations.
Animals performed normally when task attentional load
was low (i.e., with long cue durations) but performance
was significantly impaired on short cue duration trials.
Levodopa further impaired performance on short cue
duration trials and induced a deficit on long cue duration
trials.
Nicotine and SIB-1553A improved performance on short
cue trials and when co-administered with levodopa,
counteracted levodopa-induced deficits.
These results confirm that nicotinic therapies may be
useful for treating cognitive deficits associated with PD
and suggest that negative effects of levodopa on cognition
may be amenable to correction with adjunctive nicotinic
therapies.

Brain research [Brain Res]
------------------

"Acetylcholine, nicotine, and choline were effective"
"These agonists were also effective"

Synaptic potentials mediated by alpha 7
nicotinic acetylcholine receptors in sup
J Neurosci (2002) 22: 29-37.
GI Hatton, QZ Yang

Cocaine: Perceived as a reward by the brain?
May 19th, 2009 Cocaine is one of the oldest drugs known to humans, and
its abuse has become widespread since the end of the 19th century. At
the same time, we know rather little about its effects on the human
brain or the mechanisms that lead to cocaine addiction. The latest
article by Dr. Marco Leyton, of the Montreal Neurological Institute
(MNI), McGill University and the McGill University Health Centre,
which was published in the journal Biological Psychiatry on May 15,
2009, not only demonstrates a link between cocaine and the reward
circuits in the brain but also associates the susceptibility to
addiction with these mechanisms.

Ads by Google
Cedars Treatment Center - An Affordable & Effective Addiction
Treatment Center.Call 866.716.2006 - www.CedarsCobblehill.com

Teen With a Drug Problem? - New Addiction Program in Calgary Youth and
Family-Based Therapy - www.hullservices.ca

The results of this study show that sniffing cocaine triggers high
levels of dopamine secretion in a central region of the brain called
the striatum. Dopamine is known to play a critical role in the brain's
response to reward as well as in its response to addictive drugs.

This study was carried out in ten non-addicted users of cocaine, all
of whom sniffed cocaine on one test day and placebo powder on another.
Participants underwent blood tests before and after taking the drug,
and dopamine release in the brain was measured using PET scans.

"The ability of cocaine to activate dopamine release varies markedly
from person to person. Our study suggests that this is related to how
much of the drug the person consumed in the past," explained Dr.
Leyton. The more cocaine someone has used in his or her lifetime, the
more the brain will secrete dopamine during subsequent cocaine use.
"It's possible therefore that the intensity of the reward-circuit
response is related to increased susceptibility to addiction," stated
Dr. Leyton.

Although the relationship between the intensity of dopamine secretion
and the frequency of drug use has been demonstrated, researchers still
do not fully understand its mechanism of action. Is it the repeated
stimulation of the reward circuit that leads to addiction, or is it an
inherent sensitivity to addiction that leads to the increased
secretion of dopamine? This question is not easy to answer, especially
since other factors come into play, such as other aspects of the
subject's personal history.

Whatever the answer, the relationship between dopamine and cocaine
means that this hormone could be a potential target for treatment
against addiction. More research is required before treatments are
available, but this study opens a new door in this direction.

Source: McGill University Health Centre (news : web)

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

NO shteaters on my threads .. shteater ..

I've repeatedly told you shteaters to stay off my threads ..

DOOO .. it shteater ..

DOOOOO .. it ..

http://www.foxnews.com/story/0,2933,517745,00.html

How cigarettes calm you down

The calming neurological effects of nicotine have been demonstrated
in a group of non-smokers during anger provocation. Scientists
writing
in BioMed Central's open access journal Behavioral and Brain
Functions
suggest that nicotine may alter the activity of brain areas that are
involved in the inhibition of negative emotions such as anger.

Jean Gehricke led a team of scientists from the University of
California who studied the effect of nicotine patches on the
subjects'
tendency to retaliate in response to anger provocation. The subjects
played a computer game and could see a video screen of another player
who they thought to betheir opponent, although, in fact, they were
playing alone. After each round, the victor could give his opponent a
burst of unpleasant noise at a duration and volume set by the winner.
In some of the subjects, nicotine was linked to a reduced tendency to
retaliate, even after provocation by the 'opponent'.

As per Gehricke, "Participants who showed nicotine-induced changes in
anger task performance also showed changes in brain metabolism.
Nicotine-induced reductions in length of retaliation were linked to
changes in brain metabolism in response to nicotine in brain areas
responsible for orienting, planning and processing of emotional
stimuli".

The authors say that their findings support the idea that people of
an angry disposition are more susceptible to nicotine's effects, and
are
therefore more likely to become addicted to cigarettes. They
conclude,
"Novel behavioral therapys that affect the cortical and limbic brain
areas, like anger management training, may aid smoking cessation
efforts in anger provoking situations that increase withdrawal and
tobacco cravings".

dopamine <<

Cocaine: Perceived as a reward by the brain?
May 19th, 2009 Cocaine is one of the oldest drugs known to humans,
and
its abuse has become widespread since the end of the 19th century. At
the same time, we know rather little about its effects on the human
brain or the mechanisms that lead to cocaine addiction. The latest
article by Dr. Marco Leyton, of the Montreal Neurological Institute
(MNI), McGill University and the McGill University Health Centre,
which was published in the journal Biological Psychiatry on May 15,
2009, not only demonstrates a link between cocaine and the reward
circuits in the brain but also associates the susceptibility to
addiction with these mechanisms.

Ads by Google
Cedars Treatment Center - An Affordable & Effective Addiction
Treatment Center.Call 866.716.2006 - www.CedarsCobblehill.com

Teen With a Drug Problem? - New Addiction Program in Calgary Youth
and
Family-Based Therapy - www.hullservices.ca

The results of this study show that sniffing cocaine triggers high
levels of dopamine secretion in a central region of the brain called
the striatum. Dopamine is known to play a critical role in the
brain's
response to reward as well as in its response to addictive drugs.

This study was carried out in ten non-addicted users of cocaine, all
of whom sniffed cocaine on one test day and placebo powder on
another.
Participants underwent blood tests before and after taking the drug,
and dopamine release in the brain was measured using PET scans.

"The ability of cocaine to activate dopamine release varies markedly
from person to person. Our study suggests that this is related to how
much of the drug the person consumed in the past," explained Dr.
Leyton. The more cocaine someone has used in his or her lifetime, the
more the brain will secrete dopamine during subsequent cocaine use.
"It's possible therefore that the intensity of the reward-circuit
response is related to increased susceptibility to addiction," stated
Dr. Leyton.

Although the relationship between the intensity of dopamine secretion
and the frequency of drug use has been demonstrated, researchers
still
do not fully understand its mechanism of action. Is it the repeated
stimulation of the reward circuit that leads to addiction, or is it
an
inherent sensitivity to addiction that leads to the increased
secretion of dopamine? This question is not easy to answer,
especially
since other factors come into play, such as other aspects of the
subject's personal history.

Whatever the answer, the relationship between dopamine and cocaine
means that this hormone could be a potential target for treatment
against addiction. More research is required before treatments are
available, but this study opens a new door in this direction.

Source: McGill University Health Centre (news : web)

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

    Reply    Reply to author    Forward       Rate this post:  Text
for clearing space

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Please update your nickname on the subscription settings page before
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ironjustice    View profile
  More options Apr 27, 12:25 pm

Newsgroups: soc.support.depression.manic, alt.support.attn-deficit,
sci.med, misc.health.alternative, sci.med.nutrition
From: ironjustice <ironjust...@rock.com>
Date: Mon, 27 Apr 2009 12:25:43 -0700 (PDT)
Local: Mon, Apr 27 2009 12:25 pm
Subject: Re: Dopamine Theory Aberrant Behavior.
Reply | Reply to author | Forward | Print | Individual message | Show
original | Report this message | Find messages by this author
On Apr 24, 3:18 pm, ironjustice <ironjust...@cashette.com>
wrote::"Multiple addictive, impulsive and compulsive behavioral
propensities, such as severe alcoholism,cocaine, heroin, marijuana
and
nicotine use,
glucose bingeing,  pathological gambling, sex addiction, ADHD,
Tourette's Syndrome, autism, chronic violence, posttraumatic stress
disorder,
schizoid/avoidant cluster, conduct disorder and antisocial
behavior." <<

"The alpha7 nAChR-selective agonist choline promoted dopamine release
in vitro and in vivo"

That would be vegetable lecithin ..

alpha7 and non-alpha7 nicotinic acetylcholine receptors modulate
dopamine release in vitro and in vivo in the rat prefrontal cortex.
Eur J Neurosci. 2009 Feb;29(3):539-50. Epub 2009 Jan 28.
Livingstone PD, Srinivasan J, Kew JN, Dawson LA, Gotti C,
Moretti M, Shoaib M, Wonnacott S.
Department of Biology & Biochemistry, University of Bath, Bath, UK.

Nicotine enhances attentional and working memory aspects of
executive function in the prefrontal cortex (PFC) where dopamine
plays a major role.
Here, we have determined the nicotinic acetylcholine receptor
(nAChR) subtypes that can modulate dopamine release in rat
PFC using subtype-selective drugs.
Nicotine and 5-Iodo-A-85380 (beta2* selective) elicited [(3)H]
dopamine release from both PFC and striatal prisms in vitro and
dopamine overflow from medial PFC in vivo.
Blockade by dihydro-beta-erythroidine supports the participation
of beta2* nAChRs.
However, insensitivity of nicotine-evoked [(3)H]dopamine release
to alpha-conotoxin-MII in PFC prisms suggests no involvement
of alpha6beta2* nAChRs, in contrast to the striatum, and this
distinction is supported by immunoprecipitation of nAChR
subunits from these tissues.
The alpha7 nAChR-selective agonists choline and Compound A
also promoted dopamine release from PFC in vitro and in vivo,
and their effects were enhanced by the alpha7 nAChR-selective
allosteric potentiator PNU-120596 and blocked by specific
antagonists.
DNQX and MK801 inhibited [(3)H]dopamine release evoked by
choline and PNU-120596, suggesting crosstalk between alpha7
nAChRs, glutamate and dopamine in the PFC.
In vivo, systemic (but not local) administration of PNU-120596,
in the absence of agonist, facilitated dopamine overflow in the
medial PFC, consistent with the activation of extracortical
alpha7 nAChRs by endogenous acetylcholine or choline.
These data establish that both beta2* and alpha7 nAChRs can
modulate dopamine release in the PFC in vitro and in vivo.
Through their distinct actions on dopamine release, these nAChR
subtypes could contribute to executive function, making them
specific therapeutic targets for conditions such as schizophrenia
and attention deficit hyperactivity disorder.

PMID: 19187266
---------

This article clearly shows in the plant .. maltol a sugar  .. is
ESSENTIAL for the breakdown of dopamine .. it keeps the dopamine
THERE .. / prevents the breakdown.

Effect of maltol on the oxidation of DL-DOPA, dopamine, N-
acetyldopamine (NADA), and norepinephrine by mushroom tyrosinase.
Pigment Cell Res. 1997 Jun;10(3):139-49.
Kahn V, Ben-Shalom N.
Department of Food Science, Agricultural Research Organization,
Volcani Center, Bet Dagan, Israel.

Maltol (3-hydroxy-2-methyl-4H-pyran-4-one) appears to inhibit the
rate
of oxidation of DL-DOPA, dopamine, NADA and epinephrine by tyrosinase
when assayed spectrophotometrically but not when assayed
polarographically.
Maltol has an effect on the spectrum of product(s) formed when each
catecholamine was oxidized by tyrosinase showing that maltol hastens
the disappearance of the quinones, possibly by conjugating with them.
Indeed, at relatively high concentrations, maltol prevented the
conversion of DL-DOPA, dopamine, and norepinephrine to their
corresponding melanins via tyrosinase.

PMID: : 9266600

---------------------------------------------------------
This would evidence the use of lecithin simple vegetable lecithin
due to its efficient choline absorption.
Nicotine and choline and acetylcholine are called alpha7 nAChR
agonists.

In response the usual, yawn, potty mouth nonsense.

You shteaters were told NO shteaters on my threads .. shteater ..

You were told that many times shteater ..

I've specifically told you shteaters to stay off my threads ..

That is because you disease ridden mutated dysfunctional freaks
have a propensity for abnormal behavior .. like .. eating sht for
example ..

Soooo .. shteaters are not allowed to post ..

You shteaters are to go to
alt.shteating.mutated.disease.ridden.freaks ..

DOOO .. it shteater ..

DOOOOO .. it ..

http://www.foxnews.com/story/0,2933,517745,00.html

How cigarettes calm you down

The calming neurological effects of nicotine have been demonstrated
in a group of non-smokers during anger provocation. Scientists
writing
in BioMed Central's open access journal Behavioral and Brain
Functions
suggest that nicotine may alter the activity of brain areas that are
involved in the inhibition of negative emotions such as anger.

Jean Gehricke led a team of scientists from the University of
California who studied the effect of nicotine patches on the
subjects'
tendency to retaliate in response to anger provocation. The subjects
played a computer game and could see a video screen of another player
who they thought to betheir opponent, although, in fact, they were
playing alone. After each round, the victor could give his opponent a
burst of unpleasant noise at a duration and volume set by the winner.
In some of the subjects, nicotine was linked to a reduced tendency to
retaliate, even after provocation by the 'opponent'.

As per Gehricke, "Participants who showed nicotine-induced changes in
anger task performance also showed changes in brain metabolism.
Nicotine-induced reductions in length of retaliation were linked to
changes in brain metabolism in response to nicotine in brain areas
responsible for orienting, planning and processing of emotional
stimuli".

The authors say that their findings support the idea that people of
an angry disposition are more susceptible to nicotine's effects, and
are
therefore more likely to become addicted to cigarettes. They
conclude,
"Novel behavioral therapys that affect the cortical and limbic brain
areas, like anger management training, may aid smoking cessation
efforts in anger provoking situations that increase withdrawal and
tobacco cravings".

dopamine <<

Cocaine: Perceived as a reward by the brain?
May 19th, 2009 Cocaine is one of the oldest drugs known to humans,
and
its abuse has become widespread since the end of the 19th century. At
the same time, we know rather little about its effects on the human
brain or the mechanisms that lead to cocaine addiction. The latest
article by Dr. Marco Leyton, of the Montreal Neurological Institute
(MNI), McGill University and the McGill University Health Centre,
which was published in the journal Biological Psychiatry on May 15,
2009, not only demonstrates a link between cocaine and the reward
circuits in the brain but also associates the susceptibility to
addiction with these mechanisms.

Ads by Google
Cedars Treatment Center - An Affordable & Effective Addiction
Treatment Center.Call 866.716.2006 - www.CedarsCobblehill.com

Teen With a Drug Problem? - New Addiction Program in Calgary Youth
and
Family-Based Therapy - www.hullservices.ca

The results of this study show that sniffing cocaine triggers high
levels of dopamine secretion in a central region of the brain called
the striatum. Dopamine is known to play a critical role in the
brain's
response to reward as well as in its response to addictive drugs.

This study was carried out in ten non-addicted users of cocaine, all
of whom sniffed cocaine on one test day and placebo powder on
another.
Participants underwent blood tests before and after taking the drug,
and dopamine release in the brain was measured using PET scans.

"The ability of cocaine to activate dopamine release varies markedly
from person to person. Our study suggests that this is related to how
much of the drug the person consumed in the past," explained Dr.
Leyton. The more cocaine someone has used in his or her lifetime, the
more the brain will secrete dopamine during subsequent cocaine use.
"It's possible therefore that the intensity of the reward-circuit
response is related to increased susceptibility to addiction," stated
Dr. Leyton.

Although the relationship between the intensity of dopamine secretion
and the frequency of drug use has been demonstrated, researchers
still
do not fully understand its mechanism of action. Is it the repeated
stimulation of the reward circuit that leads to addiction, or is it
an
inherent sensitivity to addiction that leads to the increased
secretion of dopamine? This question is not easy to answer,
especially
since other factors come into play, such as other aspects of the
subject's personal history.

Whatever the answer, the relationship between dopamine and cocaine
means that this hormone could be a potential target for treatment
against addiction. More research is required before treatments are
available, but this study opens a new door in this direction.

Source: McGill University Health Centre (news : web)

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

    Reply    Reply to author    Forward       Rate this post:  Text
for clearing space

You must Sign in before you can post messages.
To post a message you must first join this group.
Please update your nickname on the subscription settings page before
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ironjustice    View profile
  More options Apr 27, 12:25 pm

Newsgroups: soc.support.depression.manic, alt.support.attn-deficit,
sci.med, misc.health.alternative, sci.med.nutrition
From: ironjustice <ironjust...@rock.com>
Date: Mon, 27 Apr 2009 12:25:43 -0700 (PDT)
Local: Mon, Apr 27 2009 12:25 pm
Subject: Re: Dopamine Theory Aberrant Behavior.
Reply | Reply to author | Forward | Print | Individual message | Show
original | Report this message | Find messages by this author
On Apr 24, 3:18 pm, ironjustice <ironjust...@cashette.com>
wrote::"Multiple addictive, impulsive and compulsive behavioral
propensities, such as severe alcoholism,cocaine, heroin, marijuana
and
nicotine use,
glucose bingeing,  pathological gambling, sex addiction, ADHD,
Tourette's Syndrome, autism, chronic violence, posttraumatic stress
disorder,
schizoid/avoidant cluster, conduct disorder and antisocial
behavior." <<

"The alpha7 nAChR-selective agonist choline promoted dopamine release
in vitro and in vivo"

That would be vegetable lecithin ..

alpha7 and non-alpha7 nicotinic acetylcholine receptors modulate
dopamine release in vitro and in vivo in the rat prefrontal cortex.
Eur J Neurosci. 2009 Feb;29(3):539-50. Epub 2009 Jan 28.
Livingstone PD, Srinivasan J, Kew JN, Dawson LA, Gotti C,
Moretti M, Shoaib M, Wonnacott S.
Department of Biology & Biochemistry, University of Bath, Bath, UK.

Nicotine enhances attentional and working memory aspects of
executive function in the prefrontal cortex (PFC) where dopamine
plays a major role.
Here, we have determined the nicotinic acetylcholine receptor
(nAChR) subtypes that can modulate dopamine release in rat
PFC using subtype-selective drugs.
Nicotine and 5-Iodo-A-85380 (beta2* selective) elicited [(3)H]
dopamine release from both PFC and striatal prisms in vitro and
dopamine overflow from medial PFC in vivo.
Blockade by dihydro-beta-erythroidine supports the participation
of beta2* nAChRs.
However, insensitivity of nicotine-evoked [(3)H]dopamine release
to alpha-conotoxin-MII in PFC prisms suggests no involvement
of alpha6beta2* nAChRs, in contrast to the striatum, and this
distinction is supported by immunoprecipitation of nAChR
subunits from these tissues.
The alpha7 nAChR-selective agonists choline and Compound A
also promoted dopamine release from PFC in vitro and in vivo,
and their effects were enhanced by the alpha7 nAChR-selective
allosteric potentiator PNU-120596 and blocked by specific
antagonists.
DNQX and MK801 inhibited [(3)H]dopamine release evoked by
choline and PNU-120596, suggesting crosstalk between alpha7
nAChRs, glutamate and dopamine in the PFC.
In vivo, systemic (but not local) administration of PNU-120596,
in the absence of agonist, facilitated dopamine overflow in the
medial PFC, consistent with the activation of extracortical
alpha7 nAChRs by endogenous acetylcholine or choline.
These data establish that both beta2* and alpha7 nAChRs can
modulate dopamine release in the PFC in vitro and in vivo.
Through their distinct actions on dopamine release, these nAChR
subtypes could contribute to executive function, making them
specific therapeutic targets for conditions such as schizophrenia
and attention deficit hyperactivity disorder.

PMID: 19187266
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This article clearly shows in the plant .. maltol a sugar  .. is
ESSENTIAL for the breakdown of dopamine .. it keeps the dopamine
THERE .. / prevents the breakdown.

Effect of maltol on the oxidation of DL-DOPA, dopamine, N-
acetyldopamine (NADA), and norepinephrine by mushroom tyrosinase.
Pigment Cell Res. 1997 Jun;10(3):139-49.
Kahn V, Ben-Shalom N.
Department of Food Science, Agricultural Research Organization,
Volcani Center, Bet Dagan, Israel.

Maltol (3-hydroxy-2-methyl-4H-pyran-4-one) appears to inhibit the
rate
of oxidation of DL-DOPA, dopamine, NADA and epinephrine by tyrosinase
when assayed spectrophotometrically but not when assayed
polarographically.
Maltol has an effect on the spectrum of product(s) formed when each
catecholamine was oxidized by tyrosinase showing that maltol hastens
the disappearance of the quinones, possibly by conjugating with them.
Indeed, at relatively high concentrations, maltol prevented the
conversion of DL-DOPA, dopamine, and norepinephrine to their
corresponding melanins via tyrosinase.