Alternative, complementary and holistic health care

http://www.mechdir.com/press/catalog/1079/index.html

"18 percent of health care workers have some level of latex allergy"

—————
Excess dietary iron is the root cause for increase in childhood Autism
and allergies
Medical Hypotheses, Volume 61, Issue 2, Pages 220-222
Medical Hypotheses
Abstract
Autism is a profoundly and poorly understood developmental disorder
that impairs a person’s social and communication abilities.
I propose a hypothesis that the excessive dietary iron consumed by
today’s infants is the root cause of increased cases of Autism,
allergies and other childhood diseases. Iron is a powerful immune
system modulator.
Excess iron causes hyperactive immune system.
This hyperactive immune system attacks undigested food peptides.
The chemicals released during these intense allergic reactions can
damage surrounding tissue. Neurodegeneration is caused by combination
of, oxidative stress induced by free iron radicals and intense immune
reactions.
Iron chelators have shown beneficial results in Autism and allergies.

doi:10.1016/S0306-9877(03)00126-9

——————————-

"Loading cells with Fe-D increased their response to latex"

Years ago a guy wondered if his iron overload had anything to do with
his spina .. bifida.

"Up to 73% of children and adolescents with Spina Bifida are
sensitive
to latex"

Iron uptake and release by macrophages is sensitive to propranolol.
Mol Cell Biochem. 2006 Aug;288(1-2):213-7. Epub 2006 May 23.
Komarov AM, Hall JM, Chmielinska JJ, Weglicki WB.
Division of Experimental Medicine, Departments of Biochemistry &
Molecular Biology, The George Washington University Medical Center,
2300 Eye St., NW, Ross Hall, Rm. 441A, Washington, DC 20037,
USA. phy…@gwumc.edu

In this study we have tested the effects of d-propranolol (D-Pro) on
the iron uptake, iron release and oxidative response of iron-loaded
cells
in a cellular model of iron-overload using isolated rat peritoneal
macrophages incubated with iron-dextran (Fe-D).
Pretreatment of macrophages with D-Pro (5-200 microM) prior to Fe-D
exposure decreased the cellular iron content and partially prevented
iron release from latex-activated macrophages.
Release of reactive oxygen species from activated cells was detected
by dichlorodihydrofluorescein (DCDHF, 5 microM) oxidation.
We found that loading cells with Fe-D increased their response to
latex, which was prevented by the lysosomotropic antioxidant agent D-
Pro
(10 microM).

PMID: 16718379

http://www.spinabifidaassociation.org/site/c.liKWL7PLLrF/b.2664425/ap…

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

"Phytic acid reduced cataract by 26 to 44%"

Effect of D-myo-inositol on platelet function and
composition and on cataract development
Biochem Med Metab Biol (1992) 48: 46-55.
JC Ruf, M Ciavatti, T Gustafsson, S Renaud

Diabetes is known to be associated with an increase
in aldose reductase activity, platelet hyperaggregability,
lipid peroxidation, and cataract formation.
A molecule, D-myo-inositol 1,2,6-trisphosphate (PP-56),
derived from phytic acid, could in principle, by supplying
myoinositol to tissues and acting as an antioxidant,
counteract some of the manifestations of diabetes.
Thus, the effects of PP-56 on platelet aggregation,
fatty acids, and polyols were investigated in uncontrolled
streptozotocin-induced diabetes in rat in relation to
cataract and lipid peroxidation.
A decrease in the response of platelet aggregation to
thrombin and ADP (P less than 0.05, P less than 0.001)
and in the level of sorbitol and the ratio
sorbitol/myo-inositol (P less than 0.01) in platelets was
observed in the rats treated by PP-56 for 7-8 weeks.
These beneficial effects were associated with an incidence
of cataract reduced by 26 to 44% (P less than 0.05 to P
less than 0.001) depending on the duration of treatment.
They were also accompanied by a significant lower plasma
level of malondialdehyde (P less than 0.05), and, more
markedly, of conjugated dienes (P less than 0.001) as well
as an increase in platelet lipids of the 20:4(n-6)/20:3(n-6)
ratio, an index of delta 5 desaturase activity.
PP-56 appears to modulate fatty acid desaturases and aldose
reductase in platelets and delay by a few weeks the development
of cataract in this acute model of diabetes.

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

" Higher levels of acetylcholine"

They’d be protected from .. meningitis .. too ..

Promising New Treatment For Alzheimer’s Suggested Based On Hebrew
University Research
Article Date: 22 Jul 2009 – 0:00 PDT

Research carried out at the Hebrew University of Jerusalem has
resulted in a promising approach to help treat Alzheimer’s disease in
a significant proportion of the population that suffers from a
particularly rapid development of this disease.

In the research at the Silberman Institute of Life Sciences of the
Hebrew University, scientists solved a mystery as to why people who
carried a mutated gene known as BChE-K were prone to more rapid
development of Alzheimer’s than those who had a normal version of the
gene. This mutation appears in about 20 percent of the American and
Israeli populations.

In theory, the carriers of the mutated gene should actually be more
protected from the devastating effects of the disease, since the
mutated protein (the enzyme that is the product of the gene) breaks
down the neurotransmitter acetylcholine at a slower rate than in those
who have the normal gene. The result is that the carriers maintain
higher levels of this neurotransmitter, so they should in principle be
protected from Alzheimer’s disease, in which acetylcholine levels
decrease.

Indeed, these carriers tend to develop the disease later than others,
but when that happens, it progresses more rapidly and does not respond
to medication. Therefore, the bottom line is that carriers of the
mutated gene have a greater risk than others for disease progression.
The reason for this anomalous situation has been a puzzle for a long
time, but the studies by the Hebrew University scientists solved it by
finding the explanation for this increased risk, thereby offering as
well a possible new therapeutic solution.

At the Wolfson Center for Structural Biology at the Hebrew University,
the researchers found that the mutation in the BChE-K gene damages the
very end, or tail, of the resultant mutant enzyme protein. This tail
is the part of BChE which is important for protection from the
Alzheimer’s disease plaques. It does this by interacting with the
Alzheimer’s disease â-amyloid protein and preventing it from
precipitating and forming those brain plaques which are the
neuropathological hallmark of this disease.

To compare the normal protein to the K mutant, the researchers used
synthetic tails of the normal and the K proteins, as well as
engineered human BChE produced in the milk of transgenic goats at a
U.S. company, Pharmathene. The goat- produced protein is prepared at
Pharmathene for the U.S. military as protection from nerve gas
poisoning (a result of earlier research at the Hebrew University). It
was much more stable and efficient than the mutant protein, which
suggests that the BChE-K carriers’ susceptibility to Alzheimer’s could
be substantially improved by treating them with the engineered normal
protein that is produced in the milk of the transgenic goats.

The current study was the last part in the Ph.D. work of Dr. Erez
Podoly, now a post- doctoral fellow with the Nobel laureate Roger
Kornberg at Stanford University. Podoly was the joint student of Prof
Oded Livnah and Prof. Hermona Soreq and won a National Eshkol
fellowship in Biotechnology to perform this work as well as a Kaye
Innovation Award at the Hebrew University. Others who contributed to
this study included Dr, Debbie Shalev and Dr. Ester Bennett from the
Silberman Institute of Life Sciences, Harvey Wilgus from Pharmathene,
and Dr Einor Ben-Assayag and Shani Shenhar- Tsarfati, a Ph.D. student,
both from the Sourasky Medical Center in Tel aviv, where the Israeli
carriers of BChE-K were identified.

The project is patented and is available for licensing by the Yissum
Research Development Company of the Hebrew University of Jerusalem.

An article by the researchers on this work was recently selected as a
Journal of Biological Chemistry (JBC) Paper of the Week and featured
on the cover of the publication.

Source:
Rebecca Zeffert
The Hebrew University of Jerusalem

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

"Excessive hepatic deposition of iron"
"Increases the risk of hepatocellular carcinoma development"
"None of these patients developed hepatocellular carcinoma (HCC)."
"Phlebotomy and Low Iron Diet"

Current Experimental Perspectives on the Clinical
Progression of Alcoholic Liver Disease
Alcoholism: Clinical and Experimental Research
Katja Breitkopf, Laura E. Nagy, Juliane I. Beier,
Sebastian Mueller, Honglei Weng, and Steven Dooley
From the Molecular Alcohol Research in Gastroenterology,
Department of Medicine II, University Hospital Mannheim,
University of Heidelberg, Mannheim, Germany
Correspondence to Reprint requests: Dr. K. Breitkopf,
Molecular Alcohol Research in Gastroenterology,
Department of Medicine II, University Hospital Mannheim,
University of Heidelberg, Theodor-Kutzer-Ufer 1-3,
Mannheim 68167, Germany; Fax: +49 621 3831467;
E-mail: katja.breitk…@medma.uni-heidelberg.de

Review of the corresponding symposium which took place
at the RSA/ISBRA meeting 2008.

Copyright © 2009 Research Society on Alcoholism
KEYWORDS
Steatosis • Steatohepatitis • Liver Fibrosis • HCC
ABSTRACT
Chronic alcohol abuse is an important cause of morbidity
and mortality throughout the world.
Liver damage due to chronic alcohol intoxication initially
leads to accumulation of lipids within the liver and with
ongoing exposure this condition of steatosis may first
progress to an inflammatory stage which leads the way
for fibrogenesis and finally cirrhosis of the liver.
While the earlier stages of the disease are considered
reversible, cirrhotic destruction of the liver architecture
beyond certain limits causes irreversible damage of the
organ and often represents the basis for cancer development.
This review will summarize current knowledge about the
molecular mechanisms underlying the different stages of
alcoholic liver disease (ALD).
Recent observations have led to the identification of
new molecular mechanisms and mediators of ALD.
For example, plasminogen activator inhibitor 1 was shown
to play a central role for steatosis, the anti-inflammatory
adipokine, adiponectin profoundly regulates liver macrophage
function and excessive hepatic deposition of iron is caused
by chronic ethanol intoxication and increases the risk of
hepatocellular carcinoma development.

Received for publication March 2, 2009; accepted May 7, 2009.

DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1530-0277.2009.01015.x About DOI

Early View (Articles online in advance of print)
Published Online: 23 Jul 2009

© 2009 Research Society on Alcoholism
—————–

"None of these patients developed hepatocellular carcinoma (HCC)."

http://cancerres.aacrjournals.org/cg…act/61/24/8697

Clinical Investigations

Normalization of Elevated Hepatic 8-Hydroxy-2′-Deoxyguanosine Levels
in
Chronic Hepatitis C Patients by Phlebotomy and Low Iron Diet1
Junji Kato, Masayoshi Kobune, Tokiko Nakamura, Ganji Kuroiwa, Kohichi
Takada, Rishu Takimoto, Yasuhiro Sato, Koshi Fujikawa, Minoru
Takahashi, Tetsuji Takayama, Tatsuru Ikeda and Yoshiro Niitsu2
Fourth Department of Internal Medicine [J. K., T. N., G. K., K. T., R.
T., Y. S., K. F., M. T., T. T., Y. N.] and Department of Molecular
Medicine [M. K.], Sapporo Medical University School of Medicine, and
Department of Clinical Pathology, Sapporo Medical University Hospital
[T. I.], Sapporo 060-8543, Japan

Accumulation of 8-hydroxy-2′-deoxyguanosine (8-OHdG) in DNA, which may
result from the continuous reactive oxygen species (ROS) generation
associated with chronic inflammation, has been reported in various
human preneoplastic lesions and in cancerous tissues. However, no
direct causative relationship between the 8-OHdG formation and
carcinogenesis has been thus far demonstrated in humans. Directly
proving the causality requires showing that depletion of 8-OHdG levels
in tissue by interfering with ROS generation results in a reduction in
cancer. Chronic hepatitis C virus (HCV) infection is associated with a
high risk of hepatocellular carcinoma (HCC). Several studies on
patients with chronic HCV have shown that hepatic iron overload is
attributable to liver injury and that iron depletion improved serum
aminotransferase levels. Excess iron is known to generate ROS within
cells, which causes mutagenic lesions, such as 8-OHdG. In this study,
therefore, we have evaluated whether therapeutic iron reduction
(phlebotomy and low iron diet) with a long-term follow-up (6 years)
would decrease the hepatic 8-OHdG levels and the risk of HCC
development in patients with chronic HCV. Patients (34) enrolled were
those who had undergone standard IFN therapy but had no sustained
response. Quantitative immunohistochemistry using the KS-400 image
analyzing system and electrochemical detection was used for 8-OHdG
detection. With this treatment, elevated hepatic 8-OHdG levels in
patients with chronic hepatitis C (8.3 ± 4.6/105 dG) significantly
decreased to almost normal levels (2.2 ± 0.9/105 dG; P < 0.001) with
concomitant improvement of hepatitis severity, including fibrosis,
whereas HCV titers were unaffected. None of these patients developed
HCC. Thus, long-term iron reduction therapy in patients with chronic
hepatitis C may potentially lower the risk of progression to HCC.

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

"Methionine and choline-deficient diet-induced steatohepatitis"

Pro-oxidant-mediated hepatic fibrosis and effects of
antioxidant intervention in murine dietary steatohepatitis.
Int J Mol Med. 2009 Aug;24(2):171-80.
Phung N, Pera N, Farrell G, Leclercq I, Hou JY, George J.
Storr Liver Unit, Westmead Millennium Institute,
University of Sydney at Westmead Hospital,
Westmead, NSW 2145, Australia.

The mechanistic significance of oxidative stress to
fibrogenesis in the methionine and choline-deficient
(MCD) diet-induced model of steatohepatitis was
evaluated by antioxidant intervention, using either
vitamin E or L-2-oxothiazolidine-4-carboxylate (OTC),
a cysteine precursor that promotes glutathione synthesis.
Significant depletion of hepatic reduced glutathione (GSH)
and elevation of thiobarbituric acid reactive substances
(TBARS) occurred from week 3 in association with hepatic
injury in mice fed the MCD diet.
Hepatic stellate cell (HSC) activation and increased
collagen alpha1(I) mRNA expression, together with
morphologic fibrosis were evident from week 5.
Vitamin E repleted GSH, reduced TBARS, steatosis,
inflammation, HSC activation and collagen alpha1(I) mRNA
expression, and ameliorated fibrosis.
Vitamin E did not effect the expression of either profibrogenic
cytokines (transforming growth factor-beta 1, connective tissue
growth factor) or matrix remodeling enzymes (tissue inhibitor
of metalloproteinase-1 and -2, matrix metalloproteinase-2 and -13).
Despite repletion of hepatic GSH in OTC-supplemented mice, the
initial benefit in the reduction of hepatic TBARS and inhibition
of collagen alpha1(I) mRNA expression at week 5, failed to protect
these mice from hepatic injury or fibrosis at later time points.
Oxidative stress or products of lipid peroxidation mediate HSC
activation and collagen gene expression directly in the MCD model
of steatohepatitis.
Vitamin E but not glutathione augmentation can interrupt this
pathogenic process.

PMID: 19578790

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

It is when we are thinking and doing things that are kind, just, and
right, that we become healthier (hungrier) than ever.

"The lot is cast into the lap,  but its every decision is from the
LORD." (Proverbs 16:33)

Amen.

A Spirit-guided exegesis of Proverbs 16:33 …

http://groups.google.com/group/sci.med.cardiology/msg/085dcffcafb7e4e2?

Nothing happens by chance because everything happens only as GOD
allows it (Ecclesiastes 9:11):

http://groups.google.com/group/sci.med.cardiology/msg/21527d1832960109?

Sign that GOD can easily unleash an H5N1 Pandemic at any time:

http://groups.google.com/group/sci.med.cardiology/msg/a4581567229974c0?

What we are teaching to prepare folks in our local communities for the
probable eventuality of a deadlier Pan-Flu:

http://www.youtube.com/watch?v=jfmkax1wbRU

How to not be fearful:

Trust the truth, Who is Jesus !!!

http://T3WiJ.com

May dear neighbors, friends, and brethren have a blessedly wonderful
2009th year since the birth of our LORD Jesus Christ as our Messiah,
the Son of Man …

… by being hungrier:

http://groups.google.com/group/sci.med.cardiology/msg/f891e617d10bd689?

Hunger is wonderful ! ! !

It’s how we know the answer to the question "What does Jesus
want?" (WDJW):

http://WDJW.net

Yes, hunger is our knowledge of good versus evil that Adam and Eve
paid for with their and our immortal lives:

http://groups.google.com/group/sci.med.cardiology/msg/52a3db8576495806?

Hunger is the physical "hearts burning within us" feeling that unlocks
the 4 mysteries of the "Road to Emmaus" adventure described in Luke
24:

http://groups.google.com/group/sci.med.cardiology/msg/386f56c2f6d0b154?

Moreover, being hungrier is the key to being Jesus’ disciples:

http://groups.google.com/group/sci.med.cardiology/msg/bd20d7c4fe878897?

Being physically hungrier is how we will physically recognize Jesus
when He physically returns for us to meet Him physically in the air:

http://groups.google.com/group/sci.med.cardiology/msg/ffa6609710ea9587?

"Blessed are you who hunger NOW…

… for you will be satisfied." — LORD Jesus Christ (Luke 6:21)

Amen.

Here is a Spirit-guided exegesis of Luke 6:21 given in hopes of
promoting much greater understanding:

http://groups.google.com/group/sci.med.cardiology/msg/cc2aa8f8a4d41360?

Jesus is LORD, forever !!!

http://JiL4ever.net

Be hungrier, which is truly healthier for mind, body, and soul:

http://groups.google.com/group/sci.med.cardiology/msg/991d4e30704307e7?

Marana tha

Prayerfully in the awesome name of our Messiah, LORD Jesus Christ,

Andrew <><
—
Andrew B. Chung, MD/PhD
Board-certified Cardiologist
and Author of "Be Hungry"
http://NetCabal.com
"Don’t be left behind as were Cleopas and Simon …
… —————–> be hungry ! ! !"

http://groups.google.com/group/sci.med.cardiology/msg/9642aafa0aad16eb?

Only the truth can cure the "hunger is starvation" delusion:
http://groups.google.com/group/sci.med.cardiology/msg/74281ab7d7ce78de?

Posted this morning at Electric Politics, an interview on health care
reform with Wendell Potter. Until recently Wendell was Vice President
for Public Affairs at Cigna, one of the largest health insurance
corporations. But Wendell had a conversion experience and now puts his
considerable talents and energy into the struggle for genuine reform.
He’s recently testified before the Senate, was on Bill Moyers two
weeks ago, has been interviewed by Amy Goodman, and generally has been
rearranging the battlefield! At Electric Politics he further explores
some of his original ideas.

If you find this podcast useful and interesting please feel free to
redistribute the link.

http://www.electricpolitics.com/podcast/2009/07/health_not_profits_1….

"Loading cells with Fe-D increased their response to latex"

Years ago a guy wondered if his iron overload had anything to do with
his
spina .. bifida.

"Up to 73% of children and adolescents with Spina Bifida are sensitive
to latex"

Iron uptake and release by macrophages is sensitive to propranolol.
Mol Cell Biochem. 2006 Aug;288(1-2):213-7. Epub 2006 May 23.
Komarov AM, Hall JM, Chmielinska JJ, Weglicki WB.
Division of Experimental Medicine, Departments of Biochemistry &
Molecular Biology, The George Washington University Medical Center,
2300 Eye St., NW, Ross Hall, Rm. 441A, Washington, DC 20037,
USA. phy…@gwumc.edu

In this study we have tested the effects of d-propranolol (D-Pro) on
the iron uptake, iron release and oxidative response of iron-loaded
cells
in a cellular model of iron-overload using isolated rat peritoneal
macrophages incubated with iron-dextran (Fe-D).
Pretreatment of macrophages with D-Pro (5-200 microM) prior to Fe-D
exposure decreased the cellular iron content and partially prevented
iron release from latex-activated macrophages.
Release of reactive oxygen species from activated cells was detected
by dichlorodihydrofluorescein (DCDHF, 5 microM) oxidation.
We found that loading cells with Fe-D increased their response to
latex, which was prevented by the lysosomotropic antioxidant agent D-
Pro
(10 microM).

PMID: 16718379

http://www.spinabifidaassociation.org/site/c.liKWL7PLLrF/b.2664425/ap…

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

Using jdrew63…@aol.com

http://groups.google.com/groups/profile?enc_user=mjG-gxIAAAAcoQ2KLl1V…

39225 messages.

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mark.probert @_replaced.for.your.security