Interesting study.  Now if they will just follow up and tell us how
to
correct it....Something we take like a vitamin?  Something we eat? <<

This study came out about the increased absorption of curcumin when
taken with olive oil or vegetable oil would be a good place to start.
They have shown positive effects with curcumin and that was without
the addition of this enhancing absorption with oil.

"Only curcumin was effective in reducing amyloid plaque burden,
insoluble beta-amyloid peptide (Abeta), and carbonyls"

"In our studies, increasing curcumin solubility with phosphatidyl
choline, olive oil, or stearic acid increases plasma and brain levels
compared with administering
unformulated curcumin powder. Lipidated curcumin formulation resulted
in 11-fold higher levels of curcumin in plasma and 4-fold higher
levels in brain compared to equal doses of curcumin powder or curcumin-
piperine extracts."

Whether this 'lipidated curcumin' is simply curcumin stirred in oil ?

Comparison of systemic availability of curcumin with that of curcumin
formulated with phosphatidylcholine
MARCZYLO Timothy H. (1) ; VERSCHOYLE Richard D. (1) ; COOKE Darren N.
(1) ; MORAZZONI Paolo (2) ; STEWARD William P. (1) ; GESCHER Andreas
J. (1) ; Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Cancer Biomarkers and Prevention Group, Department of Cancer
Studies and Molecular Medicine, University of Leicester, Robert
Kilpatrick Clinical Sciences Building, Leicester Royal Infirmary,
Leicester, LE2 7LX, ROYAUME-UNI
(2) Indena SpA, Viale Ortles 12, 20139 Milan, ITALIE

Abstract
Purpose
Curcumin, a major constituent of the spice turmeric, suppresses
expression of the enzyme cyclooxygenase 2 (Cox-2) and has cancer
chemopreventive properties in rodents. It possesses poor systemic
availability.
We explored whether formulation with phosphatidylcholine
increases the oral bioavailability or affects the metabolite profile
of curcumin.
Methods
Male Wistar rats received 340 mg/kg of either unformulated curcumin
or curcumin formulated with phosphatidylcholine (Meriva) by oral
gavage.
Rats were killed at 15, 30, 60 and 120 min post administration.
Plasma, intestinal mucosa and liver were analysed for the presence of
curcumin and metabolites using HPLC with UV detection.
Identity of curcumin and metabolites was verified by negative ion
electrospray
liquid chromatography/tandem mass spectrometry.
Results
Curcumin, the accompanying curcuminoids desmethoxycurcumin and
bisdesmethoxycurcumin, and the metabolites tetrahydrocurcumin,
hexahydrocurcumin, curcumin glucuronide and curcumin sulfate were
identified in plasma, intestinal mucosa and liver of rats which had
received Meriva.
Peak plasma levels and area under the plasma concentration time curve
(AUC) values for parent curcumin after administration of Meriva were
fivefold higher than the equivalent values seen after unformulated
curcumin.
Similarly, liver levels of curcumin were higher after administration
of Meriva as compared to unformulated curcumin.
In contrast, curcumin concentrations in the gastrointestinal mucosa
after ingestion of Meriva were somewhat lower than those observed
after administration of unformulated curcumin.
Similar observations were made for curcumin metabolites as for parent
compound.
Conclusion
The results suggest that curcumin formulated with phosphatidylcholine
furnishes higher systemic levels of parent agent than unformulated
curcumin.
Revue / Journal Title
Cancer chemotherapy and pharmacology   ISSN 0344-5704   CODEN CCPHDZ
Source / Source
2007, vol. 60, no2, pp. 171-177 [7 page(s) (article)] (25 ref.)

--------

Curcumin structure-function, bioavailability, and efficacy in models
of neuroinflammation and Alzheimer's disease.
Begum AN, Jones MR, Lim GP, Morihara T, Kim P, Heath DD, Rock CL,
Pruitt MA, Yang F, Hudspeth B, Hu S, Faull KF, Teter B, Cole GM,
Frautschy SA.
Department of Medicine, University of California, Los Angeles,
California, USA.

Curcumin can reduce inflammation and neurodegeneration, but its
chemical instability and metabolism raise concerns, including whether
the more stable metabolite tetrahydrocurcumin (TC) may mediate
efficacy.
We examined the antioxidant, anti-inflammatory, or anti-amyloidogenic
effects of dietary curcumin and TC, either administered chronically to
aged Tg2576 APPsw mice or acutely to lipopolysaccharide (LPS)-injected
wild-type mice.
Despite dramatically higher drug plasma levels after TC compared with
curcumin gavage, resulting brain levels of parent compounds were
similar, correlating with reduction in LPS-stimulated inducible nitric-
oxide synthase, nitrotyrosine, F2 isoprostanes, and carbonyls.
In both the acute (LPS) and chronic inflammation (Tg2576), TC and
curcumin similarly reduced interleukin-1beta.
Despite these similarities, only curcumin was effective in reducing
amyloid plaque burden, insoluble beta-amyloid peptide (Abeta), and
carbonyls. TC had no impact on plaques or insoluble Abeta, but both
reduced Tris-buffered saline-soluble Abeta and phospho-c-Jun NH(2)-
terminal kinase (JNK).
Curcumin but not TC prevented Abeta aggregation.
The TC metabolite was detected in brain and plasma from mice
chronically fed the parent compound.
These data indicate that the dienone bridge present in curcumin, but
not in TC, is necessary to reduce plaque deposition and protein
oxidation in an Alzheimer's model.
Nevertheless, TC did reduce neuroinflammation and soluble Abeta,
effects that may be attributable to limiting JNK-mediated
transcription.
Because of its favorable safety profile and the involvement of
misfolded proteins, oxidative damage, and inflammation in multiple
chronic degenerative diseases, these data relating curcumin dosing to
the blood and tissue levels required for efficacy should help
translation efforts from multiple successful preclinical models.

PMID: 18417733
PMCID: PMC2527621

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

“However, in humans high oral dosing fails to achieve detectable
plasma levels.  The reported failure to achieve these modest target
levels in humans with oral supplements predicts limited success in
translating to the clinic.  In our studies, increasing curcumin
solubility with phosphatidyl choline, olive oil, or stearic acid
increases plasma and brain levels compared with administering
unformulated curcumin powder. For example, oral gavage of an
optimized
lipidated curcumin formulation (Verdure Sciences, Noblesville,
Indiana) resulted in 11-fold higher levels of curcumin in plasma and
4-
fold higher levels in brain compared to equal doses of curcumin
powder
or curcumin-piperine extracts. A 5 mg curcumin dose delivered by
acute
gavage in this lipid rich formulation (n=5) resulted in 2.15 ± 0.744
µM mouse brain curcumin levels after 3 hrs. After 2 weeks lipidated
formulation at 500 ppm curcumin in chow (n=5) we observed 5.79 ± 1.22
µM mouse brain curcumin, well above the 1-2 µM range of EC50’s for
the
inhibition of iNOS, IL-1ß, PGE2 and isoprostanes. This suggests oral
delivery can achieve our target tissue levels.”

Source: JPET 326:196-208, 2008. Curcumin Structure-Function,
Bioavailability, and Efficacy in Models of Neuroinflammation and
Alzheimer's Disease. Aynun N. Begum, Mychica R. Jones, Giselle P.
Lim,
Takashi Morihara, Peter Kim, Dennis D. Heath, Cheryl L. Rock, Mila A.
Pruitt, Fusheng Yang, Beverly Hudspeth, Shuxin Hu, Kym F. Faull,
Bruce
Teter, Greg M. Cole, and Sally A. Frautschy.  Departments of Medicine
(A.N.B., M.R.J., G.P.L., P.K., F.Y., B.H., S.H., B.T., G.M.C.,
S.A.F.)
and Neurology (G.M.C., S.A.F.) and Psychiatry and Biobehavioral
Sciences and The Semel Institute (K.F.F.), University of California,
Los Angeles, California; Greater Los Angeles Healthcare System,
Geriatric Research Education Clinical Center, Sepulveda, California
(A.N.B., M.R.J., G.P.L., P.K., F.Y., B.H., S.H., B.T., G.M.C.,
S.A.F.); Cancer Prevention and Control Program, Moores UCSD Cancer
Center, University of California San Diego, La Jolla, California
(D.D.H., C.L.R., M.A.P.); and Department of Post-Genomics and
Diseases, Division of Psychiatry and Behavioral Proteomics, Osaka
University Graduate School of Medicine D3, Osaka, Japan (T.M.)

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

 Something we eat ? <<

I wonder what would happen if you added a little .. oil ..

"Luteolin exposure resulted in 90 percent drop in IL-6 production"

(NaturalNews)
Researchers at the University of Illinois report that a plant
compound
found in abundance in celery and green peppers can disrupt a key
component of the inflammatory response in the brain. The findings
have
implications for research on aging and diseases such as Alzheimer's
and multiple sclerosis.

Inflammation can be a blessing or a blight. It is a critical part of
the body's immune response that in normal circumstances reduces
injury
and promotes healing. When it goes awry, however, the inflammatory
response can lead to serious physical and mental problems.

Inflammation plays a key role in many neurodegenerative diseases and
also is implicated in the cognitive and behavioral impairments seen
in
aging.

The new study looked at luteolin (LOO-tee-OH-lin), a plant flavonoid
known to impede the inflammatory response in several types of cells
outside the central nervous system. The purpose of the study was to
determine if luteolin could also reduce inflammation in the brain,
said animal sciences professor and principal investigator Rodney
Johnson.

"One of the questions we were interested in is whether something like
luteolin, or other bioactive food components, can be used to mitigate
age-associated inflammation and therefore improve cognitive function
and avoid some of the cognitive deficits that occur in aging,"
Johnson
said.

The researchers first studied the effect of luteolin on microglia.
These brain cells are a key component of the immune defense. When
infection occurs anywhere in the body, microglia respond by producing
inflammatory cytokines, chemical messengers that act in the brain to
orchestrate a whole-body response that helps fight the invading
microorganism.

This response is associated with many of the most obvious symptoms of
illness: sleepiness, loss of appetite, fever and lethargy, and
sometimes a temporary diminishment of learning and memory. Neuro-
inflammation can also lead some neurons to self-destruct, with
potentially disastrous consequences if it goes too far.

Graduate research assistant Saebyeol Jang studied the inflammatory
response in microglial cells. She spurred inflammation by exposing
the
cells to lipopolysaccharide (LPS), a component of the cell wall of
many common bacteria.

Those cells that were also exposed to luteolin showed a significantly
diminished inflammatory response. Jang showed that luteolin was
shutting down production of a key cytokine in the inflammatory
pathway, interleukin-6 (IL-6). The effects of luteolin exposure were
dramatic, resulting in as much as a 90 percent drop in IL-6
production
in the LPS-treated cells.

"This was just about as potent an inhibition as anything we had seen
previously," Johnson said.

But how was luteolin inhibiting production of IL-6?

Jang began by looking at a class of proteins involved in
intracellular
signaling, called transcription factors, which bind to specific
"promoter" regions on DNA and increase their transcription into RNA
and translation into proteins.

Using electro-mobility shift assays, which measure the binding of
transcription factors to DNA promoters, Jang eventually determined
that luteolin inhibited IL-6 production by preventing activator
protein-1 (AP-1) from binding the IL-6 promoter.

AP-1 is in turn activated by JNK, an upstream protein kinase. Jang
found that luteolin inhibited JNK phosphorylation in microglial cell
cultures. The failure of the JNK to activate the AP-1 transcription
factor prevented it from binding to the promoter region on the IL-6
gene and transcription came to a halt.

To see if luteolin might have a similar effect in vivo, the
researchers gave mice luteolin-laced drinking water for 21 days
before
injecting the mice with LPS.

Those mice that were fed luteolin had significantly lower levels of
IL-6 in their blood plasma four hours after injection with the LPS.
Luteolin also decreased LPS-induced transcription of IL-6 in the
hippocampus, a brain region that is critical to spatial learning and
memory.

The findings indicate a possible role for luteolin or other bioactive
compounds in treating neuro-inflammation, Johnson said.

"It might be possible to use flavonoids to inhibit JNK and mitigate
inflammatory reactions in the brain," he said. "Inflammatory
cytokines
such as interleukin-6 are very well known to inhibit certain types of
learning and memory that are under the control of the hippocampus,
and
the hippocampus is also very vulnerable to the insults of aging," he
said. "If you had the potential to decrease the production of
inflammatory cytokines in the brain you could potentially limit the
cognitive deficits that result."

The study appeared recently in Proceedings of the National Academy of
Sciences.

Herbalists have known about the cooling properties of celery for
decades and prescribe it for arthritis, hot flashes, and for cooling
down the body on hot summer days.

News Source:

University of Illinois at Urbana-Champaign (2008, May 23). Plant
Flavonoid In Celery And Green Peppers Found To Reduce Inflammatory
Response in the Brain
(http://www.uiuc.edu/)

About the author
Leslee Dru Browning is a 6th generation Medical Herbalist &
Nutritionist from the ancestral line of Patty Bartlett Sessions;
Pioneer Mid-Wife & Herbalist. Leslee practiced Medical Herbalism and
Nutritional Healing for over 25 years and specialized in Cancer
Wellness along with Chronic Illness. She now devotes her career to
teaching people, through her writing, about Natural Healing from An
Herbal Perspective.

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

Source: Johns Hopkins Medical Institutions     Released: Fri
23-Sep-2005, 08:45 ET
Key Protein Linked to Transverse Myelitis and Multiple Sclerosis
Libraries
Medical News   Keywords
JOHNS HOPKINS IL-6 TRANSVERSE MYELITIS MULTIPLE SCLEROSIS

Hopkins researchers have discovered a single molecule that is a cause
of an autoimmune disease in the central nervous system, called
transverse myelitis (TM), that is related to multiple sclerosis.

Newswise - Hopkins researchers have discovered a single molecule that
is a cause of an autoimmune disease in the central nervous system,
called transverse myelitis (TM), that is related to multiple
sclerosis.

In a study published in the October issue of The Journal of Clinical
Investigation, psychiatrist Adam Kaplin, M.D., Ph.D., an assistant
professor at The Johns Hopkins University School of Medicine, and
neurologist Douglas Kerr, M.D., Ph.D., also an assistant professor at
Hopkins, showed that the levels of the protein, IL-6, are
dramatically
elevated in the spinal fluid of transverse myelitis (TM) patients.

Although the majority of TM patients suffer a single attack, 15
percent to 30 percent of patients go on to develop full-blown MS. TM
evolves rapidly and without warning and usually results in permanent
impairment, including weakness of the legs and arms, bowel and
bladder
dysfunction, pain and paralysis.

IL-6 is a chemical messenger that cells of the immune system use to
communicate with one another. One of the cell types injured by high
levels of IL-6 includes oligodendrocytes, which help produce the
protective myelin sheath coating around nerve cells. The findings
offer one possible mechanism responsible for demyelinating disorders,
such as TM and MS, and may aid in the development of effective
therapies against these disorders, the researchers say.

"This is the first time a single culprit has been identified as
causing a CNS autoimmune disease," said Kaplin.

The researchers began investigating the protein IL-6 when they became
aware that TM patients suffered from memory impairment and
depression.
IL-6 has been implicated in mood and concentration disorders.

"This discovery is a success story that begins with listening
carefully to what patients are telling us about their suffering and
then collaborating across disciplines to open up new avenues of
investigation," said Kaplin.

"TM is related to other autoimmune disorders of the nervous system,
including Guillain-Barré syndrome, MS and acute disseminated
encephalomyelitis.
This study may give us a foothold in understanding all of these
disorders and how they are linked together.
The benefit is, therefore, not only to those who are paralyzed by TM,
but to those who have disabilities due to a variety of autoimmune
disorders. We are actively using these findings to aid in developing
future diagnostic, prognostic and therapeutic advancements," said
Kerr, director of the Johns Hopkins Transverse Myelitis Center, the
only center devoted to TM in the world.

Researchers analyzed 42 inflammatory proteins in the cerebrospinal
fluid of both TM and healthy patients. They found that IL-6 was
consistently elevated in TM patients' spinal fluid. Further, the
level
of IL-6 directly correlated with the severity of paralysis.

Using cell culture and animal studies, the researchers confirmed that
elevated IL-6 levels were directly injurious to the spinal cord. They
showed that spinal fluid from TM patients induced death of spinal
cord
cells when cultured in a dish and that IL-6, when infused in adult
rats, induced paralysis. Under the microscope, tissue from IL-6-
infused rats showed demyelination and injury of axons, pathology that
was nearly identical to that seen in human patients with TM.

Kerr and Kaplin also deduced that the reason IL-6 elevations injure
only the spinal cord and not other regions of the nervous system was
because distinct regions of the nervous system have different
responses to IL-6. They concluded that these different types of
responses might be a part of why different autoimmune disorders of
the
nervous system affect distinct regions and cause distinct symptoms.

"When we started, we knew nothing about the bad players in this drama
in the spinal cord of CNS autoimmune diseases - it was a classic
murder mystery and we set out together to find out 'who done it',"
said Kaplin. "We've answered who could have done it, and how, and
where."

Funding for this study was provided by the National Institutes of
Health. Other investigators involved in this study, conducted solely
at Hopkins, were Deepa M. Deshpande, M.S.; Erick Scott, B.S.; Chitra
Krishnan, M.S.; Jessica S. Carmen, B.S.; Irina Shats, M.S.; Tara
Martinez, B.S.; Jennifer Drummond, B.S.; Sonny Dike, M.D.; Mickail
Pletnikov, M.D., Ph.D.; Sanjay C. Keswani, M.B.; Timothy H. Moran,
Ph.D.; Carlos A. Pardo, M.D., and Peter A. Calabresi, M.D.

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

© 2005 Newswise.  All Rights Reserved.

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

if they will just follow up and tell us how to
correct it....Something we take like a vitamin?  Something we eat?- <<

Something ALREADY eaten.

Age-related iron accumulation occurs when we eat meat.

"Lacto-ovo vegetarians had body Fe stores of 35 and 72 for meat-eaters
"

Iron builds increasingly overwhelming finally the bodies ability to
keep i 'in check' .
Iron spills / body cannot bind up / store the iron causing oxidation
and it destroys the antioxidants in the body.

Free radical / oxidation / rust theory of ageing.

This study was recently published.

They have found by keeping the iron levels at those levels found in a
vegetarian leads to a 300% decrease in cancer recurrance.

This is the study below.

It gives credence to my contention the accumulated iron levels prove
man to be a herbivore.

One cannot argue a food which kills an animal / us is a 'natural' food
for that animal / you.

Iron stores tested in vegetarians versus meateaters found twice as
much iron in a meat eater on average than a vegetarian. "35 versus
72"
-----------------

"Overall, 75% of new cancers occurred in patients with mean ferritin
levels > 57 ng/mL."

"These results almost seem to be too good to be true."

Reducing Iron Stores by Phlebotomy Lowers Cancer Risk in Older Men

Jul 08 - Cancer incidence and mortality in
older men may be reduced by repeated phlebotomy to lower serum
ferritin levels, according to findings published online on July 8 in
the Journal of the National Cancer Institute.

Observational studies suggest that lower body iron stores may protect
against malignancy by reducing iron-induced oxidative stress, Dr. Leo
R. Zacharski and his associates note.

To test this possibility, Dr. Zacharski, at the White River Junction
Veterans Affairs Medical Center, Vermont, and his group conducted an
ad hoc analysis of data from a VA study in which patients with
peripheral arterial disease were assigned to repeated blood
collections (n = 636) or to a control group (n = 641), originally for
prevention of atherosclerotic complications .

The population was 99% male, mean age 67 years, with mean ferritin
levels at baseline of 122 ng/mL. Phlebotomy was scheduled every
6months to maintain ferritin levels between 25 and 60 ng/mL. During a
mean follow-up of 4.5 years, there were 60 new visceral malignancies
in the control patients and 38 in the iron-reduction patients (p =
0.023).

The risk of new malignancy (hazard ratio 0.65, p = 0.036) was
significantly lower in the phlebotomy group. Among patients who did
develop cancer, cancer-specific mortality (HR 0.39, p = 0.003) and
all- cause mortality (HR 0.49, p = 0.009) were lower in the
phlebotomy
group.

Overall, 75% of new cancers occurred in patients with mean ferritin
levels > 57 ng/mL.

These findings do not pertain to younger patients without vascular
disease, women, or African Americans, whose ferritin levels are
higher than those of Caucasians, the investigators say. Instead,
"these observations provide incentive for future studies and insight
into optimal clinical trial design."

Dr. Zacharski's team suggests "there may be a need to redefine the
normal range for the serum ferritin level based on associated disease
risk." They also call for re-evaluation of the policy of routinely
administering iron to anemic cancer patients.

In a related editorial, Dr. Mads Melbye, at Statens Serum Institut in
Copenhagen and colleagues suggest that "these results almost seem to
be too good to be true."

While recommending that "all possibilities for bias must be carefully
examined" and that "the results have to be interpreted with caution,"
the editorialists also support more research on this topic.

Furthermore, they write, "a cautious standpoint toward iron
supplementation where no proper indication exists is perhaps
advisable."

J Natl Cancer Inst 2008;100.

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

Decreased Cancer Risk After Iron Reduction in Patients With
Peripheral
Arterial Disease: Results From a Randomized Trial.
Zacharski LR, Chow BK, Howes PS, Shamayeva G, Baron JA, Dalman RL,
Malenka DJ, Ozaki CK, Lavori PW

J Natl Cancer Inst 2008 Jul 8.

Background
Excess iron has been implicated in cancer risk through increased
iron- catalyzed free radical-mediated oxidative stress.
Methods
A multicenter randomized, controlled, single-blinded clinical trial
(VA Cooperative Study #410) tested the hypothesis that reducing iron
stores by phlebotomy would influence vascular outcomes in patients
with peripheral arterial disease.
Patients without a visceral malignancy in the last 5 years (n = 1277)
were randomly assigned to control (n = 641) or iron reduction (n =
636).
Occurrence of new visceral malignancy and cause-specific mortality
data were collected prospectively.
Cancer and mortality outcomes in the two arms were compared using
intent-to-treat analysis with a Cox proportional hazards regression
model.
Statistical tests were two-sided.
Results
Patients were followed up for an average of 4.5 years.
Ferritin levels were similar in both groups at baseline but were
lower in iron reduction patients than control patients across all 6-
month visits (mean = 79.7 ng/mL, 95% confidence interval [CI] = 73.8
to 85.5 ng/mL vs 122.5 ng/mL, 95% CI = 115.5 to 129.5 ng/mL; P < .
001).
Risk of new visceral malignancy was lower in the iron reduction group
than in the control group (38 vs 60, hazard ratio [HR] = 0.65, 95% CI
= 0.43 to 0.97; P = .036), and, among patients with new cancers,
those
in the iron reduction group had lower cancer-specific and all-cause
mortality (HR = 0.39, 95% CI = 0.21 to 0.72; P = .003; and HR = 0.49,
95% CI = 0.29 to 0.83; P = .009, respectively) than those in the
control group.
Mean ferritin levels across all 6-monthly visits were similar in
patients in the iron reduction and control groups who developed
cancer but were lower among all patients who did not develop cancer
than among those who did (76.4 ng/mL, 95% CI = 71.4 to 81.4 ng/mL, vs
127.1 ng/mL, 95% CI = 71.2 to 183.0 ng/mL; P = .017).
Conclusions
Iron reduction was associated with lower cancer risk and mortality.
Further studies are needed to define the role of body iron in cancer
risk.
Journal of the National Cancer Institute [J Natl Cancer Inst]

---------------------------------------------------------------------------­­­-----
Br J Nutr 2001 Oct;86(4):515-9

Low iron status and enhanced insulin sensitivity in lacto-ovo
vegetarians.

   Hua NW, Stoohs RA, Facchini FS

  Department of Medicine, Division of Nephrology, San Francisco
General
  Hospital, San Francisco, CA, USA.

  [Medline record in process]

  The efficacy of insulin in stimulating whole-body glucose disposal
  (insulin sensitivity) was quantified using direct methodology in
  thirty lacto-ovo vegetarians and in thirty meat-eaters. All
subjects
  were adult, lean (BMI <23 kg/m2), healthy and glucose tolerant.
  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; respectively. In addition, lacto-ovo
  vegetarians had lower body Fe stores, as indicated by a serum
ferritin
  concentration (mg/l) of 35 (95 % CI 21, 49) compared with 72 (95 %
CI
  45, 100) for meat-eaters To test whether or not Fe status might
  modulate insulin sensitivity, body Fe was lowered by phlebotomy in
six
  male meat-eaters to levels similar to that seen in vegetarians,
with a
  resultant approximately 40 % enhancement of insulin-mediated
glucose
  disposal Our results demonstrate that lacto-ovo vegetarians are
more
  insulin sensitive and have lower Fe stores than meat-eaters. In
  addition, it seems that reduced insulin sensitivity in meat-eaters
is
  amenable to improvement by reducing body Fe. The latter finding is
in
  agreement with results from animal studies where, no matter how
  induced, Fe depletion consistently enhanced glucose disposal.

  PMID: 11591239, UI: 21475355

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

http://tinyurl.com/5cjd97

This study shows the effects of the different types of eating on the
body.

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