RED MEAT an IRON LADY? --> TMAO (Trimethylamine N-oxide) -&-> CARNITINE -- Rx for Early Retirement or Enterotypes/Microbiota Understandings or Big Pharma--> Rx for mAb's $ (Monoclonal antibodies) $ ?

[randall]

hi


Forget the SODIUM today... beWARE of RED MEAT and CARNITINE.when you
shake that THANG.

Will Jxr go postal?

Or will jxr say the same thing for this as the typical psoriasis
thread warrants?

LIKE.... wouldn't WE KNOW if we dropPed dead each time?

Or does it take a life time? And what is TIME to say an EINSTEIN?

Let's find out..

Did TMAO and RED Meat have any causation for the LOSS of IRON LADY
THATCHER?

http://www.reuters.com/article/2013/04/08/us-thatcher-margaret-profile-idUSBRE9370E820130408
Obituary: Iron Lady Thatcher changed face of Britain
<snip>

or bbc
http://www.bbc.co.uk/news/uk-politics-22067155
Ex-Prime Minister Baroness Thatcher dies, aged 8
<snip>


http://en.wikipedia.org/wiki/Margaret_Thatcher#Illness_and_death


BTW-- red meat does have IRON in it. <w>

If you missed that twist... and $ is the cash for BIG pharma mAb's
and will
obamacare tax RED MEAT next the way Bloomberg went after sugar loaded
soda's?

Yet i've no idea what the iron lady's consumption levels are or were.
Just thought
it was timely to be perfectly honest with you.

Good think i waited a DAY...

But one spin of an ORB... or absorption of TMAO or sugar or ...

OK just the FACTs mam


http://www.nytimes.com/2013/04/08/health/study-points-to-new-culprit-in-heart-disease.html?pagewanted=all
Culprit in Heart Disease Goes Beyond Meat’s Fat

By GINA KOLATA
Published: April 7, 2013

It was breakfast time and the people participating in a study of red
meat and its consequences had hot, sizzling sirloin steaks plopped
down in front of them. The researcher himself bought a George Foreman
grill for the occasion, and the nurse assisting him did the cooking.

For the sake of science, these six men and women ate every last juicy
bite of the 8-ounce steaks. Then they waited to have their blood
drawn.

Dr. Stanley Hazen of the Cleveland Clinic, who led the study, and his
colleagues had accumulated evidence for a surprising new explanation
of why red meat may contribute to heart disease. And they were testing
it with this early morning experiment.

The researchers had come to believe that what damaged hearts was not
just the thick edge of fat on steaks, or the delectable marbling of
their tender interiors. In fact, these scientists suspected that
saturated fat and cholesterol made only a minor contribution to the
increased amount of heart disease seen in red-meat eaters. The real
culprit, they proposed, was a little-studied chemical that is burped
out by bacteria in the intestines after people eat red meat. It is
quickly converted by the liver into yet another little-studied
chemical called TMAO that gets into the blood and increases the risk
of heart disease.

That, at least, was the theory. So the question that morning was:
Would a burst of TMAO show up in people’s blood after they ate steak?
And would the same thing happen to a vegan who had not eaten meat for
at least a year and who consumed the same meal?

The answers were: yes, there was a TMAO burst in the five meat eaters;
and no, the vegan did not have it. And TMAO levels turned out to
predict heart attack risk in humans, the researchers found. The
researchers also found that TMAO actually caused heart disease in
mice. Additional studies with 23 vegetarians and vegans and 51 meat
eaters showed that meat eaters normally had more TMAO in their blood
and that they, unlike those who spurned meat, readily made TMAO after
swallowing pills with carnitine.

“It’s really a beautiful combination of mouse studies and human
studies to tell a story I find quite plausible,” said Dr. Daniel J.
Rader, a heart disease researcher at the University of Pennsylvania
School of Medicine, who was not involved in the research.
http://www.med.upenn.edu/apps/faculty/index.php/g5165284/p17778

Researchers say the work could lead to new treatments for heart
disease — perhaps even an antibiotic to specifically wipe out the
bacterial culprit — and also to a new way to assess heart disease risk
by looking for TMAO in the blood.

Of course, critical questions remain. Would people reduce their heart
attack risk if they lowered their blood TMAO levels? An association
between TMAO levels in the blood and heart disease risk does not
necessarily mean that one causes the other. And which gut bacteria in
particular are the culprits?

There also are questions about the safety of supplements, like energy
drinks and those used in body building. Such supplements often contain
carnitine, a substance found mostly in red meat.

But the investigators’ extensive experiments in both humans and
animals, published Sunday in Nature Medicine, have persuaded
scientists not connected with the study to seriously consider this new
theory of why red meat eaten too often might be bad for people.

Dr. Frank Sacks, a professor of cardiovascular disease prevention at
the Harvard School of Public Health, called the findings impressive.
“I don’t have any reason to doubt it,” he said, “but it is kind of
amazing.”

Lora Hooper, an associate professor of immunology and microbiology at
the University of Texas Southwestern Medical Center, who follows the
Paleo diet, heavy on meat, exclaimed, “Yikes!”
http://profiles.utsouthwestern.edu/profile/60931/lora-hooper.html
http://www.webmd.com/diet/features/diet-review-the-caveman-paleo-diet

The study does not mean that red meat is entirely bad or that it is
best to avoid it entirely, said Dr. Hazen, the lead researcher. Dr.
Hazen is the chairman of the department of cellular and molecular
medicine at the Lerner Research Institute of the Cleveland Clinic, a
nonprofit academic medical center. Meat contains protein, for example,
and B vitamins, which are both essential for health. But the study’s
findings indicated that the often-noticed association between red meat
consumption and heart disease risk might be related to more than just
the saturated fat and cholesterol in red meats like beef and pork.

Dr. Hazen began his research five years ago with a scientific fishing
expedition. He directs a study of patients who come to the Cleveland
Clinic for evaluations. Over the years, there have been 10,000. All
were at risk for heart disease and agreed to provide blood samples and
to be followed so the researchers would know if any patient had a
heart attack or died of heart disease in the three years after the
first visit. Those samples enabled him to look for small molecules in
the blood to see whether any were associated with heart attacks or
deaths.

That study and a series of additional experiments led to the discovery
that a red meat substance no one had suspected — carnitine — seemed to
be a culprit. Carnitine is found in red meat and gets its name from
the Latin word carnis, the root of carnivore, Dr. Hazen said. It is
also found in other foods, he noted, including fish and chicken and
even dairy products, but in smaller amounts. Red meat, he said, is the
major source, and for many people who eat a lot of red meat, it may be
a concern.

The researchers found that carnitine was not dangerous by itself.
Instead, the problem arose when it was metabolized by bacteria in the
intestines and ended up as TMAO in the blood.

That led to the steak-eating study. It turned out that within a couple
of hours of a regular meat-eater having a steak, TMAO levels in the
blood soared.

But the outcome was quite different when a vegan ate a steak.
Researchers had hypothesized that vegans would not have as many of the
gut bacteria needed to make TMAO, and indeed virtually no TMAO
appeared in the vegan’s blood after he consumed a steak.

“We did not expect to see such a dramatic difference,” Dr. Hazen said.

Then researchers gave meat eaters doses of antibiotics to wipe out
almost all of their gut bacteria. After that, they no longer had TMAO
in their blood either after consuming red meat or carnitine pills.
That meant, he said, that the effect really was because of gut
bacteria.

Researchers then tried to determine whether people with high blood
carnitine or TMAO levels were at higher heart disease risk. They
analyzed blood from more than 2,500 people, asking if carnitine or
TMAO levels predicted heart attacks independently of traditional risk
factors like smoking, high cholesterol and blood pressure. Both
carnitine and TMAO did. But upon further analysis, they discovered
that the effect was solely because of TMAO.

The researchers’ theory, based on their laboratory studies, is that
TMAO enables cholesterol to get into artery walls and also prevents
the body from excreting excess cholesterol.

But what is it about carnitine that bacteria like? The answer, Dr.
Hazen said, is that bacteria use it as a fuel.

He said he worries about carnitine-containing energy drinks. Carnitine
often is added to the drinks on the assumption that is will speed fat
metabolism and increase a person’s energy level, Dr. Hazen said.

Dr. Robert H. Eckel, a professor of medicine at the University of
Colorado and a past president of the American Heart Association,
worried about how carnitine might be affecting body builders and
athletes who often take it because they believe it builds muscle.
http://www.ucdenver.edu/academics/colleges/medicalschool/departments/medicine/EndocrinologyMetabolismDiabetes/faculty_staff/Pages/Eckel.aspx

Those supplements, Dr. Hazen said, “are scary, especially for our
kids.”

Dr. Hazen, though, has taken his findings to heart. He used to eat red
meat several times a week, about 12 ounces at a time. Now, he said, he
eats it once every two weeks and has no more than 4 to 6 ounces at a
time.

“I am not a vegan,” Dr. Hazen said. “I like a good steak.”
<snip>

http://en.wikipedia.org/wiki/Trimethylamine_N-oxide

http://en.wikipedia.org/wiki/Trimethylamine_N-oxide#Health_issues
Health issues
Recent studies show that high levels of TMAO increase the risks of
cardiovascular disease. The consumption of red meat appears to be
linked with people having higher TMAO levels in their bodies
<snip>

The abstract for the above:

http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3145.html
Intestinal microbiota metabolism of L-carnitine, a nutrient in red
meat, promotes atherosclerosis

Robert A Koeth, Zeneng Wang, Bruce S Levison, Jennifer A Buffa,
Elin Org, Brendan T Sheehy, Earl B Britt, Xiaoming Fu, Yuping Wu,
Lin Li, Jonathan D Smith, Joseph A DiDonato, Jun Chen, Hongzhe Li,
Gary D Wu, James D Lewis, Manya Warrier, J Mark Brown, Ronald M
Krauss, W H Wilson Tang, Frederic D Bushman, Aldons J Lusis &
Stanley L Hazen

Abstract
Intestinal microbiota metabolism of choline and phosphatidylcholine
produces trimethylamine (TMA), which is further metabolized to a
proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate
here that metabolism by intestinal microbiota of dietary L-carnitine,
a trimethylamine abundant in red meat, also produces TMAO and
accelerates atherosclerosis in mice. Omnivorous human subjects
produced more TMAO than did vegans or vegetarians following ingestion
of L-carnitine through a microbiota-dependent mechanism. The presence
of specific bacterial taxa in human feces was associated with both
plasma TMAO concentration and dietary status. Plasma L-carnitine
levels in subjects undergoing cardiac evaluation (n = 2,595) predicted
increased risks for both prevalent cardiovascular disease (CVD) and
incident major adverse cardiac events (myocardial infarction, stroke
or death), but only among subjects with concurrently high TMAO levels.
Chronic dietary L-carnitine supplementation in mice altered cecal
microbial composition, markedly enhanced synthesis of TMA and TMAO,
and increased atherosclerosis, but this did not occur if intestinal
microbiota was concurrently suppressed. In mice with an intact
intestinal microbiota, dietary supplementation with TMAO or either
carnitine or choline reduced in vivo reverse cholesterol transport.
Intestinal microbiota may thus contribute to the well-established link
between high levels of red meat consumption and CVD risk.
<snip>

4 hits - Koeth R[Author]
http://www.ncbi.nlm.nih.gov/pubmed/?term=koeth+R%5BAuthor%5D

242 hits - Hazen SL[Author]
http://www.ncbi.nlm.nih.gov/pubmed/?term=Hazen+SL%5BAuthor%5D

tmao -695 hits
http://www.ncbi.nlm.nih.gov/pubmed/?term=tmao

#2 of 695

http://www.ncbi.nlm.nih.gov/pubmed/23518648
J Med Microbiol. 2013 Mar 21.
Phospholipid catabolism by gut microbiota and the risk of
cardiovascular disease.

Sitaraman R.

Source
TERI University.

Abstract
Trimethylamine N-oxide, derived from dietary choline, has been
identified as a possible marker of the risk of developing
cardiovascular disease (CVD). Studies in mice indicate that TMAO can
also be produced by the action of gut microflora on dietary choline,
but the actual microbial effectors of this transformation remain
unknown. Phospholipid catabolism by the microflora can, in principle,
serve as a source of choline, and genomic data indicate that major
commensals of the human gut encode several putative phospholipases/
glycerophosphoryl diester phosphodiesterases of unknown specificity
and function. It is therefore highly likely that these enzymes,
especially phosopholipase D, of gut microbiota (and pathogens) could
contribute to the total choline load in the host on a chronic basis,
increasing the risk of developing CVD.

PMID: 23518648


14 of 695 have : carnitine
http://www.ncbi.nlm.nih.gov/pubmed/?term=tmao+carnitine

Useing : trimethylamine-N-oxide - 851 hits
http://www.ncbi.nlm.nih.gov/pubmed/?term=trimethylamine-N-oxide

#6 of 851

http://www.ncbi.nlm.nih.gov/pubmed/23364764
Pathology: At the heart of the problem.
Willyard C.
Nature. 2013 Jan 31;493(7434):S10-1. doi: 10.1038/493S10a. No abstract
available.
PMID: 23364764

Maybe with an abstract this IRON hoopLA would be for Willyard instead
of the above authors?

OK..

seven hits in the P NG for Lora Hooper
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=lora+hooper&start=0&hl=en&

And with a background in microbiota maybe Hooper will tackle this
stroke of genius?

http://www.ncbi.nlm.nih.gov/pubmed/?term=Hooper+LV%5BAuthor%5D

18 of 53 have keyword: microbiota
http://www.ncbi.nlm.nih.gov/pubmed/?term=Hooper+LV%5BAuthor%5D+microbiota


Hooper with Dr. GALLO at ucsd last year on skin and gut

4 of 53 or 2 of 18

http://www.ncbi.nlm.nih.gov/pubmed/22728527
Nat Rev Immunol. 2012 Jun 25;12(7):503-16. doi: 10.1038/nri3228.
Epithelial antimicrobial defence of the skin and intestine.

Gallo RL, Hooper LV.

Source
Division of Dermatology, Department of Medicine, University of
California-San Diego, San Diego, California 92093, USA.
rga...@ucsd.edu

Abstract
Surface tissues of the body such as the skin and intestinal tract are
in direct contact with the external environment and are thus
continuously exposed to large numbers of microorganisms. To cope with
the substantial microbial exposure, epithelial surfaces produce a
diverse arsenal of antimicrobial proteins that directly kill or
inhibit the growth of microorganisms. In this Review, we highlight new
advances in our understanding of how epithelial antimicrobial proteins
protect against pathogens and contribute to microbiota-host
homeostasis at the skin and gut mucosae. Further, we discuss recent
insights into the regulatory mechanisms that control antimicrobial
protein expression. Finally, we consider how impaired antimicrobial
protein expression and function can contribute to disease.

PMID: 22728527
PMCID: PMC3563335
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22728527/
nice figure
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563335/figure/F1/


And is it the HOT ZONE for all Autoimmunity?

Larry Smarr found he had crohn's before his Doctor via a lactoferrin
test and
a subsequent 3D image er er ER Figure of his colon... LOL

And then self quantification meant sense to him.. and NOT ME..

I knew already.. LOL

OK>

Tired of tooting me horn... or corn...

What is

Just run it all ready..

OK... back off id squid.. we lost an iron lady today...


92 hits : lactoferrin + crohn's -pubmed
http://www.ncbi.nlm.nih.gov/pubmed/?term=lactoferrin+crohn's

#4 of 92 looks interesting

http://www.ncbi.nlm.nih.gov/pubmed/22347830
Gastroenterol Hepatol (N Y). 2012 Jan;8(1):29-38.
Mucosal healing in inflammatory bowel disease-a true paradigm of
success?

Dave M, Loftus EV Jr.

Source
Division of Gastroenterology and Hepatology at Mayo Clinic in
Rochester, Minnesota, USA.

Abstract
Mucosal healing is gaining more acceptance as a measure of disease
activity in Crohn's disease and ulcerative colitis, and it is also
gaining acceptance as an endpoint in clinical trials. Recent
publications have correlated achievement of mucosal healing with good
outcomes. Currently, there is no validated definition of what
constitutes mucosal healing in inflammatory bowel disease. In clinical
trials of ulcerative colitis, mucosal healing has been achieved with 5-
aminosalicylates, corticosteroids, azathioprine, and infliximab. For
Crohn's disease, mucosal healing has been achieved with
corticosteroids, infliximab, and adalimumab, and mucosal healing has
been maintained with infliximab. Achievement of long-term mucosal
healing has been associated with a decreased risk of colectomy and
colorectal cancer in ulcerative colitis patients, a decreased need for
cortico-steroid treatment in Crohn's disease patients, and a trend
toward a decreased need for hospitalization in Crohn's disease
patients. Unfortunately, assessment of mucosal healing requires
regular use of endoscopy, which is associated with increased costs,
patient discomfort, and side effects. Biomarkers such as fecal
calprotec-tin, fecal lactoferrin, serum C-reactive protein, and fecal
S1 00A1 2 have been shown to correlate with disease activity in
ulcerative colitis and Crohn's disease; in the future, these
biomarkers might be used as surrogate markers for mucosal healing.
Newer clinical trials are incorporating mucosal healing as an endpoint
for evaluation of efficacy. However, before mucosal healing will be
sufficient to guide therapy, clinicians need a standard definition of
mucosal healing and a consistently used, prospectively validated scale
with good interobserver agreement.

PMID: 22347830 [PubMed]
PMCID: PMC3277196
Free PMC Article


And there you go and here i am.

Can't we beat the gut trip and not dePend on Queen mAb's?

There is a time phrasing?

http://en.wikipedia.org/wiki/Queen_Mab#Mercutio.27s_speech_.28in_the_adapted_prose_version.29

[...] time out of mind...


OK..

Once they nail the marker's the usage of queen mAb is automatic unless
we find the
enterotypes or THE GUT BUG to save the DAY>

But is the bug simply a ratio and/or lost of usage say B. Fragilis
slows or stops Tp53 (p53)
from working correctly and you develop cancer etc.


#1 of 92

http://www.ncbi.nlm.nih.gov/pubmed/22813730
J Clin Pathol. 2012 Nov;65(11):981-5. doi: 10.1136/
jclinpath-2012-200901. Epub 2012 Jul 19.
Faecal markers of gastrointestinal inflammation.

Sherwood RA.

Source
Clinical Biochemistry, King's College Hospital, London, UK.
roy.sh...@nhs.net

Abstract
Gastrointestinal (GI) symptoms including abdominal pain, bloating and
diarrhoea are a relatively common reason for consulting a physician.
They may be due to inflammatory bowel disease (inflammatory bowel
disease; Crohn's disease, ulcerative colitis and indeterminate
colitis), malignancy (colorectal cancer), infectious colitis or
irritable bowel syndrome (IBS). Differentiation between these involves
the use of clinical, radiological, endoscopic and serological
techniques, which are invasive or involve exposure to radiation.
Serological markers include C-reactive protein, erythrocyte
sedimentation rate and antibodies (perinuclear antineutrophil
cytoplasm antibody and anti-Saccharomyces cerevisiae antibody). Faecal
markers that can aid in distinguishing inflammatory disorders from non-
inflammatory conditions are non-invasive and generally acceptable to
the patient. As IBS accounts for up to 50% of cases presenting to the
GI clinic and is a diagnosis of exclusion (Rome III criteria), any
test that can reliably distinguish IBS from organic disease could
speed diagnosis and reduce endoscopy waiting times. Faecal
calprotectin, lactoferrin, M2-PK and S100A12 will be reviewed.

PMID: 22813730


ONE hit of 92 has : keyword::: microbiome

http://www.ncbi.nlm.nih.gov/pubmed/?term=lactoferrin+crohn's+microbiota

#1 of 1

PMID: 22687960

So... with the rise of the microbiome we should hop on pop already.

Queen mAb is outa MIND to my WHEY of thinking... LOL

http://en.wikipedia.org/wiki/Monoclonal_antibody


And the dalai Lama does NOT eat red meat iirc.

Who else?

Well Einstein stopped but didn't supplement with copper ..
So he only lasted a YEAR...

But he gave MORE then most will ever GET?

Who else is a vegan or non red meat eater off the top of my head?


How about that guy who lived in the Del Mar Castle?

I forgot his name.

Oh well..


oh... almost forgot.

http://en.wikipedia.org/wiki/Just_the_facts,_ma%27am#.22Just_the_facts.2C_ma.27am.22
"Just the facts, ma'am"
While "Just the facts, ma'am" has come to be known as Dragnet's
catchphrase (it has been copied and parodied many times by other
productions), it was never actually uttered by Joe Friday. The closest
lines were "All we want are the facts, ma'am" and "All we know are the
facts, ma'am".[8] The "Just the facts, ma'am" phrase did, however,
appear in the parody St. George and the Dragonet, a 1953 short audio
satire by Stan Freberg (see below).
<snip>


Isn't it funny how the FACTs change day by day?

http://www.enotes.com/shakespeare-quotes/time-out-joint
Hamlet:
Let us go in together,
And still your fingers on your lips, I pray.
The time is out of joint—O cursèd spite,
That ever I was born to set it right!
Nay, come, let's go together.


randall.. and they say... nevermind