- quote -


I suppose this would give a bit of credence to an interaction between
iron and trehalose.

"Trehalose prevented mortality in rats challenged with a lethal dose"

Shock. 2007 Jan;27(1):91-6. Links
The disaccharide trehalose inhibits proinflammatory phenotype
activation in macrophages and prevents mortality in experimental
septic shock.
Minutoli L, Altavilla D, Bitto A, Polito F, Bellocco E, Lagan� G,
Giuliani D, Fiumara T, Magaz� S, Ruggeri P, Guarini S, Squadrito F.
Departments of Clinical and Experimental Medicine and Pharmacology,
University of Messina, Messina, Italy.

Proinflammatory phenotype activation in macrophages (MPhis) after
sepsis orchestrates an inflammatory response leading to multiple organ
dysfunction. Trehalose preserves cell viability during exposure to a
range of environmental stresses. We investigated whether trehalose may
inhibit endotoxin-induced activation of the inflammatory phenotype in
MPhis. Rat peritoneal MPhis were stimulated with 50 microg/mL of
Salmonella enteritidis lipopolysaccharide (LPS). Stimulated MPhis were
coincubated with trehalose (25, 50, and 100 mmol), sucrose (100 mmol),
or RPMI alone. Macrophages cultures were used for Western blot
analysis of extracellular-regulated kinase, c-jun-N terminal kinase,
and inducible nitric oxide synthase; interleukin (IL) 1beta, IL-6, and
tumor necrosis factor alpha (TNF-alpha) gene expression by real-time
reverse transcriptase-polymerase chain reaction, and supernatants for
measuring the release of inflammatory cytokines and nitrite content.
In vitro trehalose significantly blunted LPS-induced extracellular-
regulated kinase (LPS = 21 +/- 6 integrated intensity; LPS + trehalose
100 mmol = 2 +/- 0.3 integrated intensity), c-jun-N terminal kinase
(LPS = 15 +/- 5 integrated intensity; LPS + trehalose 100 mmol = 3.5
+/- 0.9 integrated intensity), and inducible nitric oxide synthase
activation (LPS = 12 +/- 3 integrated intensity; LPS + trehalose 100
mmol = 1 +/- 0.09 integrated intensity), blunted IL-1beta (LPS = 5 +/-
1.9 n-folds/beta-actin; LPS + trehalose 100 mmol = 1.5 +/- 0.8 n-folds/
beta-actin), IL-6 (LPS = 4 +/- 1.5 n-folds/beta-actin; LPS + trehalose
100 mmol = 1.4 +/- 0.5 n-folds/beta-actin), and TNF-alpha (LPS = 4.2
+/- 1.6 n-folds/beta-actin; LPS + trehalose 100 mmol = 1.1 +/- 0.7 n-
folds/beta-actin) gene expression, and markedly reduced the release of
inflammatory cytokines and nitrite content. Furthermore, in vivo
trehalose prevented mortality in rats challenged with a lethal dose
(20 mg/kg; LD90) of LPS (80% survival rate and 70% survival rate 24
and 72 h after LPS injection, respectively) and reduced serum TNF-
alpha. Sucrose did not modified inflammatory phenotype in vitro nor in
vivo protected against endotoxin-induced mortality. Our study suggests
that trehalose inhibits proinflammatory phenotype activation in MPhis
and prevents endotoxin-induced mortality.

PMID: 17172986 [PubMed - indexed for MEDLINE]


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- quote -

- quote -

I suppose this might be WHY iron binding substances .. work.
---------------- "associated with mortality"

Ferritin levels in children with severe sepsis and septic shock
Authors: Garcia, Pedro Celiny Ramos; Longhi, Fernanda; Branco, Ricardo
Garcia1; Piva, Jefferson Pedro; Lacks, Dani; Tasker, Robert Charles1

Source: Acta P�diatrica, Volume 96, Number 12, December 2007 , pp.
1829-1831(3)

Abstract:


Aim: To evaluate serum ferritin level in children with severe sepsis
and septic shock and its association with mortality.

Method: A cohort study of 36 children aged 1 month-16 years with
severe sepsis or septic shock requiring intensive care was conducted.
Serum ferritin levels were measured at the time of diagnosis of sepsis
and a ferritin index (FI = observed serum ferritin divided by the
upper limit of normal ferritin for age and gender) was calculated.

Results: The median age (range) of the children was 6 (2-100) months.
Ferritin was <200 ng/mL in 13 children, 200-500 ng/mL in 11 children
and > 500 ng/mL in 12 children. The mortality associated with these
groups was 23%, 9% and 58%, respectively. A ferritin > 500 ng/mL was
associated with a 3.2 (1.3-7.9) relative risk of death (p = 0.01). FI
of 1.7 was the best cutoff value for identifying those who died. In a
logistic regression analysis, ferritin level and PRISM were
independently associated with mortality.

Conclusions: Ferritin is raised in children with septic shock and high
ferritin level is associated with poorer outcome.
Keywords: Children; Ferritin; Intensive care; Iron metabolism;
Prognosis; Sepsis

Document Type: Research article

DOI: 10.1111/j.1651-2227.2007.00564.x

Affiliations: 1: Department of Paediatrics, School of Clinical
Medicine, University of Cambridge, Cambridge, UK


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- quote -

ferrous[at]paris.com wrote:

- quote -


- quote -


- quote -

HINT: that is why they are not red.

Laurie

--
Scientifically-credible info on human diet:
http://ecologos.org/ttdd.html
news:alt.food.vegan.science

- quote -



DGDispatch

High Mortality Rate From Septic Shock Due to Candida Infection Due to
Delay in Antimicrobial Therapy: Presented at CCCF


By Pam Harrison


TORONTO, CANADA -- November 5, 2007 -- A large part of the high
mortality rate associated with septic shock in patients with Candida
infections can be attributed to a significant delay in initiation of
appropriate antimicrobial therapy, according to findings from the
Cooperative Antimicrobial therapy of Septic Shock (CATSS) study.


In their study, Faisal Siddiqui, MD, Fellow in Critical Care
Medicine,
University of Manitoba, Winnipeg, Manitoba, Canada, and colleagues
analysed survival in 433 patients with septic shock due to bacterial
infections or candidiasis based on the time it took to administer
effective antimicrobial therapy.


Dr. Siddiqui presented the study results here at the Critical Care
Canada Forum (CCCF).


For their study, the researchers divided time to initiation of
effective antimicrobial therapy from onset of hypotension into
several
different time frames: from 0 to 2 hours; 2 to 6 hours; 6 to 12
hours;
12 to 24 hours; 24 to 72 hours and over 72 hours.


Ninety-nine patients died without ever receiving effective therapy,
while 36 patients received effective antimicrobial therapy before the
onset of septic shock.


The remaining 308 patients were subject to univariate and
multivariate
analysis. On univariate analysis, time to appropriate intervention
was
strongly associated with survival through to hospital discharge in
both the bacterial infection and the candidiasis groups, as was the
APACHE score, the according to the researchers.


"Highly significant, delay-dependent increases in mortality [P <.
0001]
were seen in both groups," Dr. Siddiqui reported.


However, there were marked differences in the distribution of delay
between those with bacterial shock and those with candiasis shock.
For
example, when appropriate antimicrobial therapy was initiated within
0
to 2 hours of hypotension, in-hospital survival rates for both groups
approached 80%.


In-hospital survival rates were also similar for both groups when
antimicrobial therapy was initiated between 2 and 6 hours after
hypotension onset.


Separation in survival rates between those with bacterial shock and
those with candidiasis shock started to occur when treatment was
initiated between 6 and 12 hours after onset of hypotension, where
only about 20% of patients with candidiasis shock survived until
hospital discharge versus about double that for those with bacterial
shock.


A similar pattern was seen between the two groups when treatment was
initiated 12 to 24 hours after hypotension onset, where survival
rates, although low, were still about double those for bacterial
shock
versus those with candidiasis shock. Survival rates were 10% and less
for both groups when treatment was initiated 24 hours and more after
hypotension onset.


However, the median duration of time before appropriate antimicrobial
therapy was initiated was 35.2 hours for those with candidiasis shock
versus 5.5 hours for those with bacterial shock.


Therefore, patients with Candida infections were far less likely to
receive early initiation of appropriate antimicrobial therapy than
those with bacterial shock.


"We all know that with bacterial sepsis, the earlier we initiate
therapy, the better," Dr. Siddiqui said in an interview.


The problem with Candida-associated septic shock is that physicians
tend not to think of fungal causes "right off the bat", he added.
Therefore, antifungal therapy is delayed for 24 to 72 hours in the
majority of patients with Candida.


"We know that we should consider fungal sepsis early in patients who
are immunocompromised as well as those who have been hospitalised for
a long period of time," Dr. Siddiqui said. "But maybe we should also
be considering antifungal therapy early in any patient with septic
shock with the understanding that we would stop therapy if there was
no sign of fungal infection after initial cultures were done."


As the investigators note, mortality for Candida-associated septic
shock exceeds 80% compared with approximately 50% for bacterial
shock.


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- quote -


- quote -

- quote -


Int Immunopharmacol. 2004 Mar;4(3):455-9. Related Articles, Links

Deferoxamine administration in septic animals: improved survival and
altered
apoptotic gene expression.


Messaris E, Antonakis PT, Memos N, Chatzigianni E, Leandros E,
Konstadoulakis
MM.


Laboratory of Surgical Research, First Department of Propaedeutic
Surgery,
Hippocrateion Hospital, Athens Medical School, University of Athens,
Vas Sofias
114, Ano Patisia, Athens 111 41, Greece.


Background: Oxidative damage is one of the major factors that lead to
cell
damage, organ dysfunction and death in sepsis. Thus, an attractive
candidate
for the pharmacologic treatment of the septic syndrome is
desferoxamine (DFX),
an antioxidant iron chelator used for the removal of iron and a
potential free
radical scavenger. Objective: The impact of DFX administration on the
survival
of septic animals. The effect on cell integrity and cycle of vital
organs.
Methods: Sepsis was induced in 40 rats using the cecal ligation and
puncture
method (CLP) and 20 rats randomly received twice subcutaneously DFX
(total
dose: 40 mg/kg). Rats were monitored for 36 h and all vital organs
were
harvested for pathology examination and immunohistochemical detection
of Bax,
Bcl-2, cytochrome c and caspase-8 apoptosis regulating proteins.
Results: Mean
survival in the DFX group was 34.2 h (median 36.0, S.D. 4.4) and 30.2
h (median
36.0, S.D. 9.1) in the control group (p=0.04), while 36 h after follow
up 85%
of the DFX-treated rats and 55% of placebo rats were alive (p=0.04).
Expression
of pro-apoptotic bax protein was significantly increased in the heart,
liver
and kidney of animals in the DFX group compared to the control group.
Conclusions: Treatment with the polymeric iron chelator DFX
significantly
increases survival of septic subjects and alters the expression of
bax, an
apoptosis regulating protein in certain organs (heart, liver and
kidney).


PMID: 15037222 [PubMed - in process]


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

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- quote -

On Nov 9, 3:12�*am, ironjustice <ironjust...[at]cashette.com> wrote:Green
Tea Proves Powerful Medicine Against Sepsis<<


J Biomed Mater Res. 2003 Jul 1;66A(1):21-8. Related Articles,
Links


The inhibitory activity of serum to prevent bacterial adhesion is
mainly due to
apo-transferrin.


Ardehali R, Shi L, Janatova J, Mohammad SF, Burns GL.


Department of Bioengineering, University of Utah, Salt Lake City,
Utah
84112-9202, USA.


A marked, up to 5-fold, reduction in bacterial adhesion to Tecoflex
polyurethane (PU) surfaces was observed in the presence of bovine/
human serum
or plasma at 0.5% or higher concentrations in the medium. Further
investigation
of the phenomenon resulted in identification, isolation, and
characterization
of the serum component with the ability to significantly reduce
bacterial
adhesion. Upon fractionation of bovine serum by an anion exchange
chromatography, protein pools were made and analyzed by
immunoelectrophoresis
and by polyacrylamide gel electrophoresis in the presence of SDS and
were
examined for their effect on the adhesion of Staphylococcus
epidermidis to PU
surfaces. The pool exhibiting a significant inhibitory effect was
subjected to
further biochemical tests, which resulted in the identification of
transferrin
(Tf) as its predominant protein. Bacterial adhesion studies in the
presence of
purified Tf revealed that holo-Tf (iron-containing form) had no
influence on
bacterial adhesion at any concentration. Only apo-Tf (iron-lacking
form)
exerted the inhibitory effect, in a dose responsive manner at
concentrations of
10 microg/mL or higher. Bacteria remained viable when suspended at the
low
apo-Tf concentrations, sufficient to prevent bacterial adhesion.
Copyright 2003
Wiley Periodicals, Inc.


PMID: 12833427 [PubMed - indexed for MEDLINE]


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- quote -

On Nov 9, 3:12�*am, ironjustice <ironjust...[at]cashette.com> wrote:Green
Tea Proves Powerful Medicine Against Sepsis<<

Crit Care Med 2002 Jul;30(7):1623-1629

Antioxidant protection against iron in children with meningococcal
sepsis.


Festa M, Mumby S, Nadel S, Gutteridge JM, Quinlan GJ
Paediatric Intensive Care Unit, Imperial College School of Medicine at
St
Mary's Hospital (MF, SN), London, UK; and the Unit of Critical Care,
Royal
Brompton and Harefield NHS Trust (SM, JMCG, GJQ), London, UK.


[Record supplied by publisher]


OBJECTIVE: To assess antioxidant protection against iron-catalyzed
reactive
oxygen species in meningococcal sepsis and to establish whether
severity of
illness is related to deficiencies in these antioxidant systems.
DESIGN:
Prospective, controlled study. SETTING: Pediatric intensive care unit
of a
postgraduate teaching hospital. PATIENTS: Twenty children aged 6
months to 15
yrs (median, 5 yrs) with meningococcal septic shock were studied.
Paired
convalescent samples taken 8-10 wks after discharge were available in
nine
children. INTERVENTIONS: Routine management for meningococcal sepsis.
MEASUREMENTS AND MAIN RESULTS: Patients were classified for disease
severity
using the Glasgow Meningococcal Septicaemia Prognostic Score. Paired
acute and
convalescent samples were compared. Transferrin level (1.77 +/- 0.08 g/
L) and
total iron-binding capacity (46.2 +/- 2.0 &mgr;M) were significantly
decreased
in acute patients compared with paired convalescent samples (2.85 +/-
0.10 g/L
and 74.4 +/- 2.5 &mgr;M, respectively; p <.0001). The iron saturation
of
transferrin was significantly increased in acute disease (36.9% +/-
2.5%)
compared with convalescence (18.8% +/- 1.5%; p =.0003). Iron-binding
antioxidant protection was not significantly different in acute (81.4%
+/-
1.7%) and paired convalescent samples (85.6% +/- 2.5%; p =.54).
However,
patients with more severe meningococcal septicemia (GMSPS, > 10; n =
12) had
significantly diminished protection (77.5% +/- 2.4%) compared with
less severe
disease (87.1% +/- 1.6%; p =.0028), and there was a significant
correlation
between disease severity and iron-binding antioxidant protection (R =.
48; p
=.00067) in acute disease. Paired ceruloplasmin levels were available
in six
patients and were decreased in acute disease (0.29 +/- 0.02 g/L)
compared with
convalescence (0.40 +/- 0.04 g/L), although not statistically
significant (p
=.076). However, there was a significant correlation between plasma
ceruloplasmin and disease severity (Pearson product moment
correlation, p
=.038) in the acute patients. Iron-oxidizing antioxidant assays were
performed
in four paired samples and were diminished in acute patients (53.3 +/-
4.4%)
compared with convalescence (67.8 +/- 3.2%; p =.015). Acute samples
demonstrated a significant relationship between iron-oxidizing
antioxidant
protection and both disease severity (r =.30; p =.012) and plasma
ceruloplasmin
levels (r =.48; p =.00067). CONCLUSIONS: Children with meningococcal
septicemia
exhibit abnormal plasma iron chemistry and decreased protection
against
iron-catalyzed oxidative damage. Such deficiencies correlate with
disease
severity.


PMID: 12130989


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- quote -

- quote -

<<snip> >
Lecithin therapy may be a useful adjuvant therapy in patients with
severe
sepsis.
<<snip> >


Intensive Care Med. 2004 Mar 26 [Epub ahead of print] Related
Articles, Links


Effects of polyenylphosphatidylcholine on cytokines, nitrite/nitrate
levels,
antioxidant activity and lipid peroxidation in rats with sepsis.


Demirbilek S, Ersoy MO, Demirbilek S, Karaman A, Akin M, Bayraktar M,
Bayraktar
N.


Department of Anesthesiology and Reanimation, Medical School of Inonu
University, 44315, Malatya, Turkey.


OBJECTIVES. To determine the effect of pretreatment with
polyenylphosphatidylcholine (lecithin, PPC) on plasma levels of tumor
necrosis
factor (TNF)-alpha, interleukin (IL)-6, IL-10, total nitrite/nitrate
(NOx), and
tissue levels of superoxide dismutase (SOD) and malondialdehyde (MDA)
in septic
rats. DESIGN. Prospective, randomized, controlled animal study.
SETTING.
University laboratory. SUBJECTS. Forty-five Spraque-Dawley rats were
divided
into three groups: group C, sham-operated; group S, sepsis; and group
P, sepsis
pretreated with PPC. INTERVENTIONS. Rats were made septic by cecal
ligation and
puncture (CLP). Group P rats were treated with PPC (100 mg/day orally)
for 10
days before sepsis. Twenty-four hours later CLP, plasma concentrations
of
TNF-alpha, IL-6 and IL-10 and plasma levels of NOx were measured. SOD
and MDA
were determined in liver, lung and heart homogenates. MEASUREMENTS AND
MAIN
RESULTS. All rats in group P survived during the 24-h observation time
after
CLP, whereas survival rate in group S was 66.7% (10/15; P<0.05). PPC
significantly reduced plasma levels of TNF-alpha ( P=0.006), IL-6
( P=0.007),
IL-10 ( P=0.016), NOx ( P<0.001), and tissue levels of MDA ( P<0.001)
in group
P with respect to in group S. Tissue levels of SOD significantly
increased in
group P when compared with group S ( P<0.001). CONCLUSIONS. These
results show
that PPC pretreatment exerts cumulative effects in decreasing the
levels of
cytokines, NOx, and tissue MDA concentrations, with a concomitant
increase in
survival in septic rats. Lecithin therapy may be a useful adjuvant
therapy in
controlling of the excessive production of the inflammatory cytokines
in
patients with severe sepsis. DESCRIPTOR. SIRS/sepsis, experimental
studies


PMID: 15045164 [PubMed - as supplied by publisher]


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


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- quote -

On Nov 9, 3:12�*am, ironjustice <ironjust...[at]cashette.com> wrote:Green
Tea Proves Powerful Medicine Against Sepsis<<


Best Pract Res Clin Haematol 2002 Jun;15(2):411-26

Iron and infection: competition between host and microbes for a
precious
element.


Marx JJ
Eijkman-Winkler Institute for Microbiology,
Infectious Diseases and Inflammation,
University Medical Centre Utrecht,
G04.614,
PO Box 85500, 3508 GA
Utrecht, The Netherlands.


During infection microbes attack host tissues, causing damage to
specific
organs, sepsis or even death.
For proliferation microbes desperately need iron for which they have
to compete
with the host.
Micro-organisms have developed an abundant number of strategies to
acquire iron
from their specific environment and to transport the element to sites
of
incorporation into biologically important molecules.
As part of the non-specific defence mechanisms against infection, the
body
modifies iron metabolism in order to make iron less available for
micro-organisms.
Such processes have a profound effect on the immune system and are
also
expressed in other forms of inflammation.
Microbial iron transport systems are explored as targets for
antibiotic
treatment and vaccines.
In particular, iron chelators, used for the treatment of iron overload
may
become important drugs for fighting bacterial and viral infections.


PMID: 12401315, UI: 22288772


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On Nov 9, 3:12�*am, ironjustice <ironjust...[at]cashette.com> wrote:Green
Tea Proves Powerful Medicine Against Sepsis<<

J R Coll Surg Edinb

2002 Oct;47(5):700-4


The effects of desferrioxamin and vitamin E as supplements to
antibiotics in
the treatment of peritonitis in rats.


Soybir N, Soybir G, Lice H, Dolay K, Ozseker A, Koksoy F
Department of Anesthesiology, Istanbul Memorial Hospital, Istanbul,
Turkey.


[Medline record in process]


AIM:


The aim of the study was to determine the effects of vitamin E and the
iron
chelating agent desferrioxamin (Dfx), supplemented by clindamycin and
gentamycin therapy, on peritonitis caused by caecal ligation of a
puncture
wound in an experimental model.


MATERIALS AND METHODS:


One hundred and twenty Spraque Dawley rats were divided into eight
groups.


Three groups were used as controls; intraperitoneal (i.p.),
subcutaneous (s.c.)
and i.p. and s.c., respectively. Group 4 was treated with Dfx, Group 5
with
vitamin E and Group 6 with antibiotics.


Group 7 was treated with vitamin E in combination with antibiotics,
and Group 8
with a combination of antibiotics and Dfx. The rats were studied for
14 days
following treatment, and survivors then humanely dispatched.


Post-mortem examination was undertaken on all the rats studied.


RESULTS:


In the control groups, mortality at 14 days was 66%.


Rats treated with antibiotics alone (Group 5) had a mortality rate of
40%.


Those treated with a combination of antibiotics and vitamin E (Group
7),
however, had a mortality rate of only 14%, and those treated with
antibiotics
and Dfx had a mortality rate of only 7%.


CONCLUSION:


This study suggests that treatment of peritonitis in rats with a
combination of
Dfx and antibiotics has a significant beneficial effect on survival,
in
comparison with treatment with antibiotics alone.


PMID: 12463711, UI: 22351117

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- quote -

<<snip> >
when iron is given during experimental sepsis approximately 60%
mortality,
result.
<<snip> >

Kidney Int. 2004 Jun;65(6):2108-12. Related Articles, Links


Parenteral iron therapy exacerbates experimental sepsis Rapid
Communication.


Zager RA, Johnson AC, Hanson SY.


Department of Medicine, the University of Washington, and the Fred
Hutchinson
Cancer Research Center, Seattle, Washington.


Parenteral iron therapy exacerbates experimental sepsis. Background.
Catalytic
iron can potentiate systemic inflammation via its pro-oxidant
effects.
This
raises the possibility that parenteral iron administration might
exacerbate a
concomitant septic state. This study sought to experimentally test
this
hypothesis. Methods. Male CD-1 mice were subjected to experimental
sepsis via
intraperitoneal injection of heat-killed Escherichia coli+/-
concomitant
intravenous iron sucrose (Venofer; 2 mg). Nonseptic mice +/- iron
therapy
served as controls. Plasma tumor necrosis factor-alpha (TNF-alpha)
levels were
assessed 2 hours postinjections (serving as an inflammatory marker).
Oxidative
stress was gauged in heart or kidney tissue (at either 4 or 24 hours)
by heme
oxygenase-1 (HO-1) mRNA or protein levels. Overall sepsis severity
was
assessed
by morbidity/mortality rates (at 24 hours). Results. Iron alone or
sepsis alone
each induced oxidant stress in heart and kidney (HO-1 mRNA/protein
increases).
When iron and E. coli were coadministered, additive or synergistic
HO-1
mRNA/protein increments resulted. Iron injection alone only slightly
raised
TNF-alpha levels (from 0 to 2.3 pg/mL; P= 0.01). However, iron
approximately
doubled the TNF-alpha increments which arose from the septic state
(1400 -->
2600 pg/mL). Neither sepsis alone, nor iron alone, induced any
mortality and no
mice became moribund (0/24 mice). However, when iron + sepsis were
combined,
approximately 60% of mice either died (5/12) or developed a moribund
(2/12)
state (P= 0.005). Conclusion. Parenteral iron administration can
induce
systemic oxidative stress and modest TNF-alpha release. However, when
iron is
given during experimental sepsis, profound increases in both
processes, and
approximately 60% mortality, result. Given that renal failure
patients
have
decreased antioxidant defenses and intermittently develop bacteremia,
the
potential for parenteral iron therapy to exacerbate clinical sepsis
needs to be
addressed.


PMID: 15149323 [PubMed - in process]


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"High intake of heme iron can lead to high body iron stores "


Dodge Diabetes by Sidestepping Iron
By Kimberly Beauchamp, ND
Healthnotes Newswire (July 20, 2006)-Once again diet is linked to
diabetes risk: Iron from animal sources can now be added to the list
of known culprits, such as excess dietary fat and carbohydrates. Iron
from plant sources, however, does not appear to raise diabetes risk.


Diabetes afflicts nearly one in ten people over the age of 20, says
the National Diabetes Information Clearinghouse. Certain people are
more prone to the disease, particularly those of American Indian,
African American, and Hispanic descent.


A major contributor to heart disease, stroke, high blood pressure,
blindness, and nervous system damage, diabetes is also the leading
cause of kidney failure. Making simple dietary changes like cutting
down on fried foods and eating more vegetables and whole grains may
help prevent diabetes.


The amount of calcium, chromium, magnesium, and iron in the diet
might
also affect a person's chance of developing diabetes. To see what
effect iron intake had on diabetes risk, more than 85,000 healthy
women between ages 34 and 59 provided information about their dietary
habits and supplement use as part of the Nurses' Health Study.


During the course of the 20-year study, 4,599 women developed
diabetes. Study results, published in Diabetes Care, report that non-
heme iron-which comes from plant foods-and iron from supplements
didn't raise the risk of diabetes; however, heme iron-which comes
from
animal products like red meat-greatly increased the risk. Women who
ate the most heme iron increased their risk of developing diabetes by
as much as 28%. Although the main dietary source of heme iron is red
meat, the study found that heme from poultry and fish also increased
diabetes risk.


Studies have shown a connection between high stores of iron in the
body and prediabetes. Acting as a pro-oxidant, iron may cause damage
to the organs and tissues of the body that may eventually lead to
full-
blown diabetes. Because heme iron is more easily absorbed than non-
heme iron, "it is probable that a chronically high intake of heme
iron
can lead to high body iron stores and thus may elevate the risk of
diabetes," the authors said.


How these results will affect the recommendations made to people who
are at risk for diabetes remains to be seen. For now, people without
iron deficiency may be wise to enjoy a diet rich in whole foods,
while
emphasizing plant-based sources of iron.


(Diabetes Care 2006;29:1370-6)


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


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

"My article is new . 2007"

But not as new as those posted since 2006 showing that iron is
controlled in humans and that iron in excess is a most often genetic
disorder. So the real case in diabetes is to know how iron level
control which is normal is not always so and how genetically this is the
case.

Three of same posted by your very hand recently and others by myself.

Jesus ate a mediterranean diet.

- quote -


Your article is old. 2004
My article is new . 2007
Try to keep .. up .

"Heme iron showed a statistically significant association with risk."

Relative risk increased as heme iron consumption increased.
Consumed meat increased risk by 28%.
The group who ate 2.25 mg or more of meat a day had a 52% greater risk
than the group who ate less than .75 mg of meat per day.
Meat- eaters underwent phlebotomy to lower their blood iron to that of
the vegetarian group.
Steady-state plasma glucose concentrations were 41% lower after
phlebotomy / Fe depletion.


http://www.townsendletter.com/May2007/shorts0507.htm

Iron Intake, Meat, and Type 2 Diabetes
Consumption of heme iron found in animal products, particularly red
meat, is associated with increased insulin resistance and diabetes
risk in men and women. Unlike iron found in dried fruit, kelp, some
whole grains, and brewer's yeast, heme iron from red meat, fish, and
poultry is highly bioavailable and readily stored in the body.
Epidemiological studies, cited by Swapnil Rajpathak and colleagues at
Harvard Medical School, have associated high iron stores with an
increased risk of cardiovascular disease, metabolic syndrome,
gestational diabetes, and type 2 diabetes. Different hypotheses have
been proposed for this relationship. Increased oxidative stress due
to
iron's action as a catalyst in the formation of hydroxyl radicals is
one possible factor. Also, high iron levels may slow the liver's
extraction of insulin from the bloodstream. A third explanation is
that iron deposits in pancreatic b-cells may hamper insulin
secretion.


A prospective cohort study, conducted within the Nurses' Health
Study,
reported "no association between total, dietary, supplemental, or
non-
heme iron intake and the risk of diabetes" among women. Heme iron,
however, showed a statistically significant association with diabetes
risk. Rajpathak and colleagues reported that relative risk increased
as consumption increased, after controlling for age, body mass index
(BMI), and other risk factors. The group of women who consumed the
most meat increased their risk of diabetes by 28%. When not
controlling for other diabetic risk factors, the group of women who
ate 2.25 mg or more of meat a day had a 52% greater risk of
developing
diabetes than the group who ate less than .75 mg of meat per day.
Another study by Harvard researchers found that women who eat bacon,
hot dogs, and sausage frequently have a greater risk of developing
diabetes than meat-eaters who stick to beef, lamb, and/or pork.


A third Harvard study looked at the relationship of iron intake and
diabetes among men. As in the women's study, total iron intake was
not
associated with type 2 diabetes. This study, however, found that only
heme iron from red meat was associated with an increased risk:
"...the
association may have been confounded by other components of red meat
intake because heme-iron intake from sources other than red meat
(e.g., fish, chicken, and egg) was not associated with the risk of
type 2 diabetes."


A 2001 study involving 30 lacto-ovo vegetarians and 30 meat-eaters
reported a correlation between insulin resistance and body iron
stores, as measured by serum ferritin concentrations. The vegetarians
had eaten eggs but no meat within the previous five years. Meat-
eaters
had eaten animal muscle at least once a day for five years before the
study. All sixty participants were lean, glucose-tolerant, and had
normal blood pressure. Nancy W. Hua and co-authors reported, "Lacto-
ovo vegetarians were more insulin-sensitive than meat-eaters, with a
steady-state plasma glucose (mmol/l) of 4.1 (95% CI 3.5, 5.0) v. 6.9
(95% CI 5.2, 7.5) for meat-eaters (P=0.0028)." Six of the male meat-
eaters also underwent phlebotomy to lower their blood iron
concentration range to that of the vegetarian group. Steady-state
plasma glucose concentrations were 41% lower after phlebotomy
(P=0.0008), "indicating enhancement of insulin-stimulated glucose
disposal following Fe depletion."


Hua NW, Stoohs RA, Facchini FS. Low iron status and enhanced insulin
sensitivity in lacto-ovo vegetarians. British Journal of Nutrition.
2001;86:515-519.


Jiang R, Ma J, Ascherio A, et al. Dietary iron intake and blood
donations in relation to risk of type 2 diabetes in men: A
prospective
cohort study. American Journal of Clinical Nutrition. 2004;79:70-75.
Available at: www.ajcn.org/cgi/reprint/79/1/70. Accessed February 8,
2007.


Rajpathak S, Ma J, Manson J, et al. Iron intake and the risk of type
2
diabetes in women. Diabetes Care. June 2006;29(6):1370-1376.
Available
at: http://www.hu.usp.br/plotufo/testo%2...2009%.2006.pdf.
Accessed February 8, 2007.
(April 2007: Try this link: http://care.diabetesjournals.org/cgi.../29/6/1370.pdf
88KB .pdf)


Schulze MB, Manson JE, Willett WC, Hu FB. Processed meat intake and
incidence of type 2 diabetes in younger and middle-aged women.
(Abstract) Diabetologia. November 2003. Available at:
www.springerlink.com/content/5m0a47bn3y3tmvd7/. Accessed February 8,
2007.


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


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



- quote -

On Nov 13, 6:37 am, ferr...[at]paris.com wrote:The body controls heme
iron intake at the gut.<<

You are .. mistaken.

"High intake of heme iron can lead to high body iron stores "


Dodge Diabetes by Sidestepping Iron
By Kimberly Beauchamp, ND
Healthnotes Newswire (July 20, 2006)-Once again diet is linked to
diabetes risk: Iron from animal sources can now be added to the list
of known culprits, such as excess dietary fat and carbohydrates. Iron
from plant sources, however, does not appear to raise diabetes risk.


Diabetes afflicts nearly one in ten people over the age of 20, says
the National Diabetes Information Clearinghouse. Certain people are
more prone to the disease, particularly those of American Indian,
African American, and Hispanic descent.


A major contributor to heart disease, stroke, high blood pressure,
blindness, and nervous system damage, diabetes is also the leading
cause of kidney failure. Making simple dietary changes like cutting
down on fried foods and eating more vegetables and whole grains may
help prevent diabetes.


The amount of calcium, chromium, magnesium, and iron in the diet
might
also affect a person's chance of developing diabetes. To see what
effect iron intake had on diabetes risk, more than 85,000 healthy
women between ages 34 and 59 provided information about their dietary
habits and supplement use as part of the Nurses' Health Study.


During the course of the 20-year study, 4,599 women developed
diabetes. Study results, published in Diabetes Care, report that non-
heme iron-which comes from plant foods-and iron from supplements
didn't raise the risk of diabetes; however, heme iron-which comes
from
animal products like red meat-greatly increased the risk. Women who
ate the most heme iron increased their risk of developing diabetes by
as much as 28%. Although the main dietary source of heme iron is red
meat, the study found that heme from poultry and fish also increased
diabetes risk.


Studies have shown a connection between high stores of iron in the
body and prediabetes. Acting as a pro-oxidant, iron may cause damage
to the organs and tissues of the body that may eventually lead to
full-
blown diabetes. Because heme iron is more easily absorbed than non-
heme iron, "it is probable that a chronically high intake of heme
iron
can lead to high body iron stores and thus may elevate the risk of
diabetes," the authors said.


How these results will affect the recommendations made to people who
are at risk for diabetes remains to be seen. For now, people without
iron deficiency may be wise to enjoy a diet rich in whole foods,
while
emphasizing plant-based sources of iron.


(Diabetes Care 2006;29:1370-6)


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


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

'Dietary iron intake and blood donations in relation to risk of type 2
diabetes'

Am J Clin Nutr. 2004 Jan;79(1)

"Conclusions: Heme-iron intake from red meat sources is positively^
associated with the risk of type 2 diabetes. Total iron intake,^
heme-iron intake from non-red meat sources, and blood^ donations are
not related to the risk of type 2 diabetes.^"

So it is something about red meat other then heme iron persey, such as
saturated fat a well known risk factor. Other meats ok, total iron and
giving blood did not affect risk level even though iron levels might be
lower.

Other studies confirm the red meat as risk factor along with deli type
meats both of which are high in saturated fats.

The body controls heme iron intake at the gut.

Jesus ate a mediterranean diet.

- quote -

<<snip> >
when iron is given during experimental sepsis approximately 60%
mortality,
result.
<<snip> >

Kidney Int. 2004 Jun;65(6):2108-12. Related Articles, Links


Parenteral iron therapy exacerbates experimental sepsis Rapid
Communication.


Zager RA, Johnson AC, Hanson SY.


Department of Medicine, the University of Washington, and the Fred
Hutchinson
Cancer Research Center, Seattle, Washington.


Parenteral iron therapy exacerbates experimental sepsis. Background.
Catalytic
iron can potentiate systemic inflammation via its pro-oxidant effects.
This
raises the possibility that parenteral iron administration might
exacerbate a
concomitant septic state. This study sought to experimentally test
this
hypothesis. Methods. Male CD-1 mice were subjected to experimental
sepsis via
intraperitoneal injection of heat-killed Escherichia coli+/-
concomitant
intravenous iron sucrose (Venofer; 2 mg). Nonseptic mice +/- iron
therapy
served as controls. Plasma tumor necrosis factor-alpha (TNF-alpha)
levels were
assessed 2 hours postinjections (serving as an inflammatory marker).
Oxidative
stress was gauged in heart or kidney tissue (at either 4 or 24 hours)
by heme
oxygenase-1 (HO-1) mRNA or protein levels. Overall sepsis severity was
assessed
by morbidity/mortality rates (at 24 hours). Results. Iron alone or
sepsis alone
each induced oxidant stress in heart and kidney (HO-1 mRNA/protein
increases).
When iron and E. coli were coadministered, additive or synergistic
HO-1
mRNA/protein increments resulted. Iron injection alone only slightly
raised
TNF-alpha levels (from 0 to 2.3 pg/mL; P= 0.01). However, iron
approximately
doubled the TNF-alpha increments which arose from the septic state
(1400 -->
2600 pg/mL). Neither sepsis alone, nor iron alone, induced any
mortality and no
mice became moribund (0/24 mice). However, when iron + sepsis were
combined,
approximately 60% of mice either died (5/12) or developed a moribund
(2/12)
state (P= 0.005). Conclusion. Parenteral iron administration can
induce
systemic oxidative stress and modest TNF-alpha release. However, when
iron is
given during experimental sepsis, profound increases in both
processes, and
approximately 60% mortality, result. Given that renal failure patients
have
decreased antioxidant defenses and intermittently develop bacteremia,
the
potential for parenteral iron therapy to exacerbate clinical sepsis
needs to be
addressed.


PMID: 15149323 [PubMed - in process]




Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


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



- quote -

- quote -

You are .. mistaken.

"High intake of heme iron can lead to high body iron stores "


Dodge Diabetes by Sidestepping Iron
By Kimberly Beauchamp, ND
Healthnotes Newswire (July 20, 2006)-Once again diet is linked to
diabetes risk: Iron from animal sources can now be added to the list
of known culprits, such as excess dietary fat and carbohydrates. Iron
from plant sources, however, does not appear to raise diabetes risk.


Diabetes afflicts nearly one in ten people over the age of 20, says
the National Diabetes Information Clearinghouse. Certain people are
more prone to the disease, particularly those of American Indian,
African American, and Hispanic descent.


A major contributor to heart disease, stroke, high blood pressure,
blindness, and nervous system damage, diabetes is also the leading
cause of kidney failure. Making simple dietary changes like cutting
down on fried foods and eating more vegetables and whole grains may
help prevent diabetes.


The amount of calcium, chromium, magnesium, and iron in the diet
might
also affect a person's chance of developing diabetes. To see what
effect iron intake had on diabetes risk, more than 85,000 healthy
women between ages 34 and 59 provided information about their dietary
habits and supplement use as part of the Nurses' Health Study.


During the course of the 20-year study, 4,599 women developed
diabetes. Study results, published in Diabetes Care, report that non-
heme iron-which comes from plant foods-and iron from supplements
didn't raise the risk of diabetes; however, heme iron-which comes
from
animal products like red meat-greatly increased the risk. Women who
ate the most heme iron increased their risk of developing diabetes by
as much as 28%. Although the main dietary source of heme iron is red
meat, the study found that heme from poultry and fish also increased
diabetes risk.


Studies have shown a connection between high stores of iron in the
body and prediabetes. Acting as a pro-oxidant, iron may cause damage
to the organs and tissues of the body that may eventually lead to
full-
blown diabetes. Because heme iron is more easily absorbed than non-
heme iron, "it is probable that a chronically high intake of heme
iron
can lead to high body iron stores and thus may elevate the risk of
diabetes," the authors said.


How these results will affect the recommendations made to people who
are at risk for diabetes remains to be seen. For now, people without
iron deficiency may be wise to enjoy a diet rich in whole foods,
while
emphasizing plant-based sources of iron.


(Diabetes Care 2006;29:1370-6)


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


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

"women between ages 34 and 59 provided information about their dietary
habits and supplement use as part of the Nurses' Health Study."

This long term study has been used for many research projects. In
addition to the one at hand another showed:

1. only red meat but not other animal protein sources had higher
diabetes risk.

2. total iron was not correleated with risk of diabetes.

3. blood donations which might reduce iron stores did not change risk of
diabetes.

A hand full of studies now have also shown the red meat risk factor. If
it is red but not other meat sources then one must look to what about
red meat might be an associated factor. Saturated fat is the answer.
Lean non red meats do not have an elevated risk level.

God bless.

- quote -

You are .. mistaken.

"High intake of heme iron can lead to high body iron stores "

Dodge Diabetes by Sidestepping Iron
By Kimberly Beauchamp, ND
Healthnotes Newswire (July 20, 2006)-Once again diet is linked to
diabetes risk: Iron from animal sources can now be added to the list
of known culprits, such as excess dietary fat and carbohydrates. Iron
from plant sources, however, does not appear to raise diabetes risk.

Diabetes afflicts nearly one in ten people over the age of 20, says
the National Diabetes Information Clearinghouse. Certain people are
more prone to the disease, particularly those of American Indian,
African American, and Hispanic descent.

A major contributor to heart disease, stroke, high blood pressure,
blindness, and nervous system damage, diabetes is also the leading
cause of kidney failure. Making simple dietary changes like cutting
down on fried foods and eating more vegetables and whole grains may
help prevent diabetes.

The amount of calcium, chromium, magnesium, and iron in the diet might
also affect a person's chance of developing diabetes. To see what
effect iron intake had on diabetes risk, more than 85,000 healthy
women between ages 34 and 59 provided information about their dietary
habits and supplement use as part of the Nurses' Health Study.

During the course of the 20-year study, 4,599 women developed
diabetes. Study results, published in Diabetes Care, report that non-
heme iron-which comes from plant foods-and iron from supplements
didn't raise the risk of diabetes; however, heme iron-which comes from
animal products like red meat-greatly increased the risk. Women who
ate the most heme iron increased their risk of developing diabetes by
as much as 28%. Although the main dietary source of heme iron is red
meat, the study found that heme from poultry and fish also increased
diabetes risk.

Studies have shown a connection between high stores of iron in the
body and prediabetes. Acting as a pro-oxidant, iron may cause damage
to the organs and tissues of the body that may eventually lead to full-
blown diabetes. Because heme iron is more easily absorbed than non-
heme iron, "it is probable that a chronically high intake of heme iron
can lead to high body iron stores and thus may elevate the risk of
diabetes," the authors said.

How these results will affect the recommendations made to people who
are at risk for diabetes remains to be seen. For now, people without
iron deficiency may be wise to enjoy a diet rich in whole foods, while
emphasizing plant-based sources of iron.

(Diabetes Care 2006;29:1370-6)


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


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