Science and Technology news... :: View topic - Why red meat & milk are harmful

Taka · Guest

Finally, a Clue to Explain Why You Should Avoid Red Meat

Several years ago, Professor Ajit Varki of the University
of California, San Diego discovered a molecule called Neu5Gc that
appears in the tissues of every mammal except humans
(Proceedings of the National Academy of Sciences, September
29, 2003). Now he has put together the pieces of a puzzle that
may explain why humans evolved with large brains and why, if we
want to live into old age, we should probably avoid eating meat
from any other mammals (Science, October 31, 2008).
His theory depends on evolution. Living creatures on
earth started as one-celled organisms, progressed to 2 cells, and
eventually to fish and birds. A mutation occurred in progressing
to mammals, who developed the gene to make Neu5Gc.
Mammals progressed to apes and Neanderthals, and as humans
evolved, Neu5Gc added a single oxygen atom to become a
different molecule called Neu5Ac. So Neu5Gc is found in all
mammals and their milks except humans. It is not in fish or birds.
Interestingly, the Neu5Ac molecule explains why humans are the
only mammal to suffer from malaria. The malaria parasite cannot
enter a cell until it grabs onto the Neu5Ac on the surface of human
cells.
Many epidemiological studies show that people who eat
red meat are at increased risk for heart attacks, strokes, at least
17 different cancers, diabetes, autoimmune diseases, arthritis and
asthma. Scientists have blamed saturated fats or burnt fats, but
this does not explain why red meat is linked to all of these
diseases while poultry, fish or saturated fats from plants are
not.
Dr. Varki proposes another theory. When humans ingest
the flesh or milk of any mammal, they absorb Neu5Gc and treat it
the same way as an invading germ, so they make antibodies
against it. This turns on their immunity and keeps it active so it
eventually attacks the host itself, the human body. This is called
chronic inflammation, which can lead to heart attacks, strokes,
cancers and so forth.
Since humans cannot make Neu5Gc, any amount found
in human cells come from the mammals that they have eaten.
Neu5Gc is found in high levels in tumors, with the highest levels
in metastasizing tumors. In our food supply, Dr. Varki found very
high levels of Neu5Gc in beef, pork, lamb and goat, and
moderately high amounts in milk and cheese. Low levels are
found in turkey, duck, chicken and eggs; and negligible amounts
occur in plants and seafood.
I stopped eating meat many years ago, and this report
makes me even more convinced that it should be avoided. I eat
lots of fruits, vegetables, whole grains, beans and nuts, as well
as fish and shellfish. Eggs, long thought to be a harmful high-
cholesterol food, now appear to be a healthful dietary staple.
While poultry appears to be a healthful food according to Dr.
Varki>s theory, I still do not eat it. I do not drink milk and
now plan to limit cheese as well.

Inflammation: More Important than Cholesterol?

At the American Heart Association conference in New
Orleans, researchers from the Jupiter study reported that statin
drugs caused people with normal cholesterol but with high
C-reactive protein levels to suffer 54 percent fewer heart attacks,
48 percent fewer strokes, 46 percent fewer angioplasties or
bypass operations and 20 percent fewer deaths from any cause
than those taking placebos (NEJM November 9, 2008). The
results were so dramatic they made the front page of the New
York Times, Washington Post and many other newspapers.
A C-reactive protein test (CRP) measures inflammation.
Inflammation is caused by anything that keeps your immunity
active such as chronic infections or anything that damages tissue
such as smoking, having high cholesterol or high blood pressure.
Last week I reported a theory to explain why eating mammal meat
causes inflammation and is associated with increased risk for
premature death, cancers and heart attacks. Meat contains a
molecule called Neu5Gc that humans do not have, so the immune
system of humans attacks this protein as if it was an invading
germ and eventually attacks the host itself to destroy the blood
vessels and increase risk for heart attacks and strokes.
Many scientists feel that inflammation is a stronger
predictor of heart attacks than high cholesterol levels. At present,
statins are prescribed to treat people with heart disease or high
cholesterol. This study shows that they prevent heart attacks in
people with high CRP and normal cholesterol levels, presumably
because statins reduce inflammation. About 7 million people in
the US have normal cholesterol and high CRP. Treating them
with a brand-name statin would cost each $116 a month or $9.7
billion a year, and prevent about 28,000 heart attacks, strokes
and cardiovascular deaths each year. Rather than just writing a
prescription, I think doctors should ask why a patient>s CRP is
elevated and try to lower it with lifestyle changes or treatment
of any underlying chronic infection.

SOURCE: http://www.drmirkin.com/public/ezine110908.html

Taka · Guest

Human uptake and incorporation of an immunogenic nonhuman dietary
sialic acid

Pam Tangvoranuntakul*, Pascal Gagneux*, Sandra Diaz*, Muriel Bardor*,
Nissi Varki*, Ajit Varki*,â€ , and Elaine Muchmoreâ€¡

Humans are genetically unable to produce the sialic acid N-
glycolylneuraminic acid (Neu5Gc), because of a mutation that occurred
after our last common ancestor with great apes. Although Neu5Gc is
presumed absent from normal humans, small amounts have been claimed to
exist in human tumors and fetal meconium. We have generated an
antibody with high specificity and avidity for Neu5Gc. Fetal tissues,
normal adult tissues, and breast carcinomas from humans showed
reactivity to this antibody, primarily within secretory epithelia and
blood vessels. The presence of small amounts of Neu5Gc was confirmed
by MS. Absent any known alternate pathway for its synthesis, we
reasoned that these small amounts of Neu5Gc might originate from
exogenous sources. Indeed, human cells fed with Neu5Gc incorporated it
into endogenous glycoproteins. When normal human volunteers ingested
Neu5Gc, a portion was absorbed and eliminated in urine, and small
quantities were incorporated into newly synthesized glycoproteins.
Neu5Gc has never been reported in plants or microbes to our knowledge.
We found that Neu5Gc is rare in poultry and fish, common in milk
products, and enriched in red meats. Furthermore, normal humans have
variable amounts of circulating IgA, IgM, and IgG antibodies against
Neu5Gc, with the highest levels comparable to those of the previously
known anti-Î±-galactose xenoreactive antibodies. This finding
represents an instance wherein humans absorb and metabolically
incorporate a nonhuman dietary component enriched in foods of
mammalian origin, even while generating xenoreactive, and potentially
autoreactive, antibodies against the same molecule. Potential
implications for human diseases are briefly discussed.
http://www.pnas.org/content/100/21/12045.abstract

Nature. 2008 Oct 29.

Incorporation of a non-human glycan mediates human susceptibility to a
bacterial toxin.

Byres E, Paton AW, Paton JC, LÃ¶fling JC, Smith DF, Wilce MC, Talbot
UM, Chong DC, Yu H, Huang S, Chen X, Varki NM, Varki A, Rossjohn J,
Beddoe T.
[1] Protein Crystallography Unit and ARC Centre of Excellence for
Structural and Functional Microbial Genomics, Department of
Biochemistry and Molecular Biology, Monash University, Clayton,
Victoria 3800, Australia [2] These authors contributed equally to this
work.

AB(5) toxins comprise an A subunit that corrupts essential eukaryotic
cell functions, and pentameric B subunits that direct target-cell
uptake after binding surface glycans. Subtilase cytotoxin (SubAB) is
an AB(5) toxin secreted by Shiga toxigenic Escherichia coli (STEC),
which causes serious gastrointestinal disease in humans. SubAB causes
haemolytic uraemic syndrome-like pathology in mice through SubA-
mediated cleavage of BiP/GRP78, an essential endoplasmic reticulum
chaperone. Here we show that SubB has a strong preference for glycans
terminating in the sialic acid N-glycolylneuraminic acid (Neu5Gc), a
monosaccharide not synthesized in humans. Structures of SubB-Neu5Gc
complexes revealed the basis for this specificity, and mutagenesis of
key SubB residues abrogated in vitro glycan recognition, cell binding
and cytotoxicity. SubAB specificity for Neu5Gc was confirmed using
mouse tissues with a human-like deficiency of Neu5Gc and human cell
lines fed with Neu5Gc. Despite lack of Neu5Gc biosynthesis in humans,
assimilation of dietary Neu5Gc creates high-affinity receptors on
human gut epithelia and kidney vasculature. This, and the lack of
Neu5Gc-containing body fluid competitors in humans, confers
susceptibility to the gastrointestinal and systemic toxicities of
SubAB. Ironically, foods rich in Neu5Gc are the most common source of
STEC contamination. Thus a bacterial toxin>s receptor is generated by
metabolic incorporation of an exogenous factor derived from food.
PMID: 18971931

Taka · Guest

Glycoconj J. 2008 Sep 7. [Epub ahead of print]

Multiple changes in sialic acid biology during human evolution.

Varki A.
Center for Academic Research and Training in Anthropogeny,
Glycobiology Research and Training Center, Departments of Medicine and
Cellular and Molecular Medicine, University of California, San Diego,
9500 Gilman Dr MC 0687, La Jolla, CA, 92093-0687, USA,

Humans are genetically very similar to "great apes", (chimpanzees,
bonobos, gorillas and orangutans), our closest evolutionary relatives.
We have discovered multiple genetic and biochemical differences
between humans and these other hominids, in relation to sialic acids
and in Siglecs (Sia-recognizing Ig superfamily lectins). An
inactivating mutation in the CMAH gene eliminated human expression of
N-glycolylneuraminic acid (Neu5Gc) a major sialic acid in "great
apes". Additional human-specific changes have been found, affecting at
least 10 of the <60 genes known to be involved in the biology of
sialic acids. There are potential implications for unique features of
humans, as well as for human susceptibility or resistance to disease.
Additionally, metabolic incorporation of Neu5Gc from animal-derived
materials occurs into biotherapeutic molecules and cellular
preparations - and into human tissues from dietary sources,
particularly red meat and milk products. As humans also have varying
and sometime high levels of circulating anti-Neu5Gc antibodies, there
are implications for biotechnology products, and for some human
diseases associated with chronic inflammation.
PMID: 18777136

Trends Mol Med. 2008 Aug;14(8):351-60. Epub 2008 Jul 6.

Sialic acids in human health and disease.

Varki A.
Glycobiology Research and Training Center, Departments of Medicine and
Cellular & Molecular Medicine, University of California at San Diego,
La Jolla, CA 92093-0687, USA.

The surfaces of all vertebrate cells are decorated with a dense and
complex array of sugar chains, which are mostly attached to proteins
and lipids. Most soluble secreted proteins are also similarly
decorated with such glycans. Sialic acids are a diverse family of
sugar units with a nine-carbon backbone that are typically found
attached to the outermost ends of these chains. Given their location
and ubiquitous distribution, sialic acids can mediate or modulate a
wide variety of physiological and pathological processes. This review
considers some examples of their established and newly emerging roles
in aspects of human physiology and disease.
PMID: 18606570

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

Just wondering what the implications of this are for the Kwasniewski>s
diet - perhaps he is right again since the main component of his diet
is the fat, not the lean meat .... There isn>t much Neu5Gc in the
adipose tissue I guess.

Taka

jay · Guest

[quote]high levels of Neu5Gc in beef, pork, lamb and goat,
and moderately high amounts in milk and cheese.
Low levels are found in turkey, duck, chicken and eggs;
and negligible amounts occur in plants and seafood.

in humans, Neu5Gc + oxygen becomes Neu5Ac.
Neu5Gc treated as an invading germ

I eat lots of fruits, vegetables, whole grains, beans and nuts,
as well as fish and shellfish.
[/quote]
Interesting info. Meat, especially red, irritate/inflame my GI.
I too now rely on beans, grains, veggies and fruits.
Occassionally, raw nuts. Even less, boiled chicken. No oils.

Guest

The problem is that the epidemiological evidence does not support this
conclusion, for example:

J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65.

"Intake of total and saturated fat from meat was associated with
statistically significant increases in pancreatic cancer risk but that
from dairy products was not. CONCLUSION: Red and processed meat
intakes were associated with an increased risk of pancreatic cancer.
Fat and saturated fat are not likely to contribute to the underlying
carcinogenic mechanism because the findings for fat from meat and
dairy products differed. Carcinogenic substances related to meat
preparation methods might be responsible for the positive association.
"

As this new report states: "Neu5Gc is a type of glycan, or sugar
molecule, that humans don>t naturally produce, but that can be
incorporated into human tissues as a result of eating red meat. The
body then develops anti-Neu5Gc antibodies – an immune response that
could potentially lead to chronic inflammation, as first suggested in
a 2003 PNAS paper by Varki." Source: http://www.sciencedaily.com/releases/2008/11/081113181428.htm

This is easy to clear up. You just look for markers of inflammation
in those who eat a lot of meat and also dairy eaters who don>t eat
meat (like me), and you compare their markers to vegans. You would
also have to determine if they have AA or Mead acid in their cells,
since "chronic inflammation" is not likely without AA in a person>s
cells. Once this is done, we would have some real evidence to
examine. Right now, it>s conjecture on their part. The HCAs
generated by the meat/PUFA combination, on the other hand, is real and
undeniably dangerous, For example:

Mutat Res. 2002 Sep 30;506-507:9-20. "Comments on the history and
importance of aromatic and heterocyclic amines in public health."
Weisburger JH.

QUOTE: The carcinogenic risk of aromatic amines in humans was first
discovered when a physician related the occurrence of urinary bladder
cancer to the occupation of his patients. They were employed in the
dyestuff industry, chronically exposed to large amounts of
intermediate arylamines… Epidemiological data suggest that meat eaters
may have a higher risk of breast and colon cancer. HCAs induced cancer
in rats in these organs and also in the prostate and the pancreas. In
addition, there is some evidence that they affect the vascular
system... The amounts of HCAs in cooked foods are small, but other
components in diet such as omega-6-polyunsaturated oils have powerful
promoting effects in target organs of HCAs. On the other hand, the
action of HCAs may be decreased by foods containing antioxidants, such
as vegetables, soy, and tea… Possibly, the carcinogenic effect of HCAs
is accompanied by the presence of reactive oxygen species (ROS), which
are also inhibited by antioxidants.. UNQUOTE.

In the report you cite, we get: "We>ve shown that tumor tissues
contain much more Neu5Gc than is usually found in normal human
tissues," said Varki.

Again, they think that chronic inflammation will occur with a lot of
meat and dairy consumption, but if this is true, why does the evidence
suggest that dairy products have the opposite effect (if you don>t eat
meat too)? These researchers are conjecturing, and they also seem
unaware of evidence they should know about at this point. Let them do
the kinds of studies that the scientific method requires, and then you
can take their claims seriously, but not until then !

jay · Guest

[quote]Again, they think that chronic inflammation will occur with a lot of
meat and dairy consumption, but if this is true, why does the evidence
suggest that dairy products have the opposite effect (if you don>t eat
meat too)?
[/quote]
I am not sure if the following would apply to humans or if the
advantages of butter offset the disadvantages.

Butter feeding enhances TNF-alpha production from macrophages and
lymphocyte adherence in murine small intestinal microvessels.
BACKGROUND AND AIM: Dietary fat is known to modulate immune functions.
Intake of an animal fat-rich diet has been linked to increased risk of
inflammation; however, little is known about how animal fat ingestion
directly affects intestinal immune function. The objective of this
study was to assess the effect of butter feeding on lymphocyte
migration in intestinal mucosa and the changes in adhesion molecules
and cytokines involved in this effect. METHODS: T-lymphocytes isolated
from the spleen were fluorescence-labeled and injected into recipient
mice. Butter was administered into the duodenum, and villus
microvessels of the small intestinal mucosa were observed under an
intravital microscope. mRNA expression of adhesion molecules and
cytokines in the intestinal mucosa were determined by quantitative
PCR. The effect of butter feeding on tumor necrosis factor (TNF)-alpha
mRNA expression of intestinal macrophages was also determined.
RESULTS: Intraluminal butter administration significantly increased
lymphocyte adherence to intestinal microvessels accompanied by
increases in expression levels of adhesion molecules ICAM-1, MAdCAM-1
and VCAM-1. This accumulation was significantly attenuated by anti-
MAdCAM-1 and anti-ICAM-1 antibodies. Butter administration
significantly increased TNF-alpha in the lamina proprial macrophages
but not interleukin-6. Anti-TNF-alpha treatment attenuated the
enhanced expression of adhesion molecules induced by butter
administration. CONCLUSION: T-lymphocyte adherence to microvessels of
the small intestinal mucosa was significantly enhanced after butter
ingestion. This enhancement is due to increase in expression levels of
adhesion molecules of the intestinal mucosa, which is mediated by TNF-
alpha from macrophages in the intestinal lamina propria. PMID: 17914958

ironjustice@aol.com · Guest

On Nov 13, 5:38 pm, Taka <taka0...@gmail.com> wrote:
Finally, a Clue to Explain Why You Should Avoid Red Meat <<

If you look closely .. it doesn>t say it CAUSES cancer .. it says it
is the gas pedal FOR cancer ALREADY there ..

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

[quote]
Several years ago, Professor Ajit Varki of the University
of California, San Diego discovered a molecule called Neu5Gc that
appears in the tissues of every mammal except humans
(Proceedings of the National Academy of Sciences, September
29, 2003). Now he has put together the pieces of a puzzle that
may explain why humans evolved with large brains and why, if we
want to live into old age, we should probably avoid eating meat
from any other mammals (Science, October 31, 2008).
His theory depends on evolution. Living creatures on
earth started as one-celled organisms, progressed to 2 cells, and
eventually to fish and birds. A mutation occurred in progressing
to mammals, who developed the gene to make Neu5Gc.
Mammals progressed to apes and Neanderthals, and as humans
evolved, Neu5Gc added a single oxygen atom to become a
different molecule called Neu5Ac. So Neu5Gc is found in all
mammals and their milks except humans. It is not in fish or birds.
Interestingly, the Neu5Ac molecule explains why humans are the
only mammal to suffer from malaria. The malaria parasite cannot
enter a cell until it grabs onto the Neu5Ac on the surface of human
cells.
Many epidemiological studies show that people who eat
red meat are at increased risk for heart attacks, strokes, at least
17 different cancers, diabetes, autoimmune diseases, arthritis and
asthma. Scientists have blamed saturated fats or burnt fats, but
this does not explain why red meat is linked to all of these
diseases while poultry, fish or saturated fats from plants are
not.
Dr. Varki proposes another theory. When humans ingest
the flesh or milk of any mammal, they absorb Neu5Gc and treat it
the same way as an invading germ, so they make antibodies
against it. This turns on their immunity and keeps it active so it
eventually attacks the host itself, the human body. This is called
chronic inflammation, which can lead to heart attacks, strokes,
cancers and so forth.
Since humans cannot make Neu5Gc, any amount found
in human cells come from the mammals that they have eaten.
Neu5Gc is found in high levels in tumors, with the highest levels
in metastasizing tumors. In our food supply, Dr. Varki found very
high levels of Neu5Gc in beef, pork, lamb and goat, and
moderately high amounts in milk and cheese. Low levels are
found in turkey, duck, chicken and eggs; and negligible amounts
occur in plants and seafood.
I stopped eating meat many years ago, and this report
makes me even more convinced that it should be avoided. I eat
lots of fruits, vegetables, whole grains, beans and nuts, as well
as fish and shellfish. Eggs, long thought to be a harmful high-
cholesterol food, now appear to be a healthful dietary staple.
While poultry appears to be a healthful food according to Dr.
Varki>s theory, I still do not eat it. I do not drink milk and
now plan to limit cheese as well.

Inflammation: More Important than Cholesterol?

At the American Heart Association conference in New
Orleans, researchers from the Jupiter study reported that statin
drugs caused people with normal cholesterol but with high
C-reactive protein levels to suffer 54 percent fewer heart attacks,
48 percent fewer strokes, 46 percent fewer angioplasties or
bypass operations and 20 percent fewer deaths from any cause
than those taking placebos (NEJM November 9, 2008). The
results were so dramatic they made the front page of the New
York Times, Washington Post and many other newspapers.
A C-reactive protein test (CRP) measures inflammation.
Inflammation is caused by anything that keeps your immunity
active such as chronic infections or anything that damages tissue
such as smoking, having high cholesterol or high blood pressure.
Last week I reported a theory to explain why eating mammal meat
causes inflammation and is associated with increased risk for
premature death, cancers and heart attacks. Meat contains a
molecule called Neu5Gc that humans do not have, so the immune
system of humans attacks this protein as if it was an invading
germ and eventually attacks the host itself to destroy the blood
vessels and increase risk for heart attacks and strokes.
Many scientists feel that inflammation is a stronger
predictor of heart attacks than high cholesterol levels. At present,
statins are prescribed to treat people with heart disease or high
cholesterol. This study shows that they prevent heart attacks in
people with high CRP and normal cholesterol levels, presumably
because statins reduce inflammation. About 7 million people in
the US have normal cholesterol and high CRP. Treating them
with a brand-name statin would cost each $116 a month or $9.7
billion a year, and prevent about 28,000 heart attacks, strokes
and cardiovascular deaths each year. Rather than just writing a
prescription, I think doctors should ask why a patient>s CRP is
elevated and try to lower it with lifestyle changes or treatment
of any underlying chronic infection.

SOURCE:http://www.drmirkin.com/public/ezine110908.html[/quote]

Taka · Guest

Non-human Molecule Absorbed by Eating Red Meat and Dairy Generates an
Immune Response Against the Molecule. (Study by UCSD Researchers)
Link to the article: http://health.ucsd.edu/news/2003/09_29_Varki.html

Non-human Molecule Is Absorbed by Eating Red Meat According to Study
by UCSD Researchers

A non-human, cellular molecule is absorbed into human tissues as a
result of eating red meat and milk products, according to a study by
researchers at the University of California, San Diego (UCSD) School
of Medicine, published online the week of September 29, 2003 in
Proceedings of the National Academy of Sciences. The researchers also
showed that the same foreign molecule generates an immune response
that could potentially lead to inflammation in human tissues.

Several previous studies have linked ingestion of red meat to cancer
and heart disease, and possibly to some disorders involving
inflammation. However, that research has primarily focused on the role
of red-meat saturated fats and on products that arise from cooking.
The UCSD study is the first to investigate human dietary absorption of
a cell-surface molecular sugar called N-glycolylneuraminic acid
(Neu5Gc), which is found in non-human mammals. Not produced in humans,
Neu5Gc occurs naturally in lamb, pork and beef, the so-called “red
meats”. Levels are very low or undetectable in fruits, vegetables,
hen’s eggs, poultry and fish. (see * below)

Conducting laboratory studies with human tissue, followed by tests in
three adult subjects, the UCSD team provided the first proof that
people who ingest Neu5Gc absorb some of it into their tissues. In
addition, they demonstrated that many humans generate an immune
response against the molecule, which the body sees as a foreign
invader.

The study’s senior author, Ajit Varki, M.D., UCSD professor of
medicine and cellular and molecular medicine, and co-director of the
UCSD Glycobiology Research and Training Center, said that although it
is unlikely that the ingestion of Neu5Gc alone would be primarily
responsible for any specific disease, “it is conceivable that gradual
Neu5Gc incorporation into the cells of the body over a lifetime, with
subsequent binding of the circulating antibodies against Neu5Gc (the
immune response), could contribute to the inflammatory processes
involved in various diseases.”

He added that another potential medical barrier related to Neu5Gc
might occur in organ transplantation.

“Over the past decade, the number of patients waiting for organ
transplantation has more than tripled, with little increase in the
number of donor organs. This has led to an exploration of using animal
organs for transplantation into humans, a process called
xenotransplantation,” Varki said. “However, the leading donor
candidate is the pig, an animal in which Neu5Gc happens to be very
common. The current study raises the possibility that human antibodies
against Neu5Gc might recognize the Neu5Gc in the pig organ and
facilitate its rejection.”

In describing the research approach taken by his team, Varki explained
that humans do not produce Neu5Gc because they lack the gene
responsible for its production.** And yet, other researchers have
reported small amounts of Neu5Gc in human cancer tissues.

To verify the existence of Neu5Gc in human cancers, Varki’s
collaborator, Elaine Muchmore, M.D., UCSD professor of medicine and
associate chief of staff for education at the San Diego VA Healthcare
System, developed an antibody that would be attracted by, and bind to
Neu5Gc on tissue samples. The antibody was purified by Pam
Tangvoranuntakul, B.S., the study’s first author and a Ph.D. student
in Varki’s lab.

Working with Nissi Varki, M.D., UCSD professor of pathology and
medicine, Tangvoranuntakul found that the antibody stained not only
human cancers, but also some healthy human tissues. They found that
small amounts of Neu5Gc were present in blood vessels and secretory
cells, such as the mucous membranes. A further chemical analysis by
Sandra Diaz, a Varki research associate, confirmed the presence of
Neu5Gc in human tissue.

Meanwhile, an analysis of healthy human tissue by postdoctoral fellow
Pascal Gagneux, Ph.D., and Tangvoranuntakul determined that most
people had circulating antibodies in the blood that recognized Neu5Gc,
and thus could potentially initiate an inflammatory immune response.

In the absence of any known molecular mechanism that would produce
Neu5Gc in humans, the group reasoned that the small amounts of Neu5Gc
found in human tissue could arise from human ingestion of Neu5Gc in
dietary sources. Postdoctoral fellow Muriel Bardor, Ph.D., showed that
when human cells in culture were exposed to Neu5Gc, they easily
absorbed and incorporated it onto their own surfaces.

However, to study the possibility of dietary absorption, it was
necessary to carry out an ingestion study in healthy people. Because
the researchers were hesitant to give a potentially harmful substance
to humans, Ajit Varki volunteered to be the first subject, followed by
Muchmore and Gagneux.

When the three volunteers drank Neu5Gc purified from pork sources and
dissolved in water, there were no immediate ill effects. An analysis
of the volunteers’ urine, blood, serum (the clear liquid that can be
separated from clotted blood), hair and saliva, both before ingestion
and regularly for several days after, determined that the human body
eliminates most of the Neu5Gc, but retains and metabolically absorbs
small amounts of the foreign sugar. At approximately two days
following ingestion, the Neu5Gc levels were two to three times the
baseline level prior to ingestion. By four to eight days following
ingestion, the levels had dropped nearly to baseline.

The authors cautioned that a causal relationship between Neu5Gc
expression in human tissues with any human disease would be premature
and scientifically speculative at best. Instead, they said their
findings point to the need for population-level analyses of the
presence of Neu5Gc in human tissues in relationship to disease
incidence, and the mechanisms of human incorporation and antibody
response against this sugar.

The study was supported by grants to Varki from the National
Institutes of Health (NIH) and the G. Harold and Leila Y. Mathers
Charitable Foundation. Some human studies were done in the UCSD
General Clinical Research Center, which is also supported by the NIH.

##

* Sialic Acid and Neu5Gc content of common food items

Food Neu5Gc intake if eaten at daily recommended servings Total
micrograms
Cod 27
Salmon 810
Tuna 27
Chicken 27
Turkey 27
Duck 27
Milk (cow, 2%) 711
Milk (cow, raw) 711
Butter 45
Cheese (cow) 600
Lamb 4,860
Pork 5,130
Cheese (goat) 5,544
Beef 11,610
Beef, lean portion 9,720
Beef fat 10,260

**

In the late 1990s, the first example of a complete genetic and
biochemical difference between humans and apes was reported by a group
led by Ajit Varki, M.D., working closely with Elaine Muchmore, M.D.
They showed that humans are different from chimpanzees and other great
apes in not having the enzyme responsible for producing Neu5Gc, which
is also found on the cell surfaces of other non-human mammals. The
group showed that this biochemical difference was due to a human-
specific mutation in the gene encoding the enzyme CMP-Neu5Ac
hydroxylase (CMAH), which is responsible for synthesizing Neu5Gc in
apes and other mammals.

SOURCE: http://www.vegsandiego.com/veg/101/Non-human_Molecule_Absorbed_by_Eating_Red

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

This article shows it is also present in beef fat in substantial
amounts so the Kwasniewski diet doesn>t exclude it. Dairy products
are not that rich source though. The human antibodies against Neu5Gc
are of the IgG class, same as the antibodies in different so called
food intolerancies (not allergies, those are of the IgE class). Some
IgG classes (IgG4) could be even protective against inflammation.
Since there is no TLR receptor specific for this molecule it could be
well tolerated if encountered from young childhood. The real
problems are the molecules targeted by the innate immunity and
recognized by the TLR class receptors such as LPS/endotoxin and
unmethylated CpG DNAs. And the Mammoths also carried Neu5Gc I guess
so the Varki>s hypothesis may be flawed - perhaps he developed very
sensitive antibodies for distinguishing Neu5Gc from Neu5Ac and wanted
to build his career on them ...

Taka

Taka · Guest

On Nov 23, 9:03 pm, Kofi <k...@anon.un> wrote:
[quote]however, in rural New Guinea, worm infestation doesn¹t
lessen the asthma rate;
[/quote]
So if you followed strictly the scientific method this negates the
helminths hypothesis. I would like to see whether there is a refined
vegetable oil supply to the rural New Guinea ... The worms cause
anemia thus lowering iron and possibly the LTC leukotrienes with it,
then we have the PGE2-induced TREGs. Now what would trigger the IgG4
class specifically?

Taka

Kofi · Guest

[quote]Several previous studies have linked ingestion of red meat to cancer
and heart disease, and possibly to some disorders involving
inflammation. However, that research has primarily focused on the role
of red-meat saturated fats and on products that arise from cooking.
[/quote]
Red meat contains heme, which is rich in iron, so it oxidizes the lining
of the gut as it>s absorbed (leading to colon cancer). Red meat also
has a curious habit of raising insulin without affecting blood sugar
thus making western countries taller and more cancer-prone. You>ve also
got the collagen content to deal with and that>s a much more likely
explanation for why someone gets arthritis while eating red meat -
antibodies to collagen.

However, it>s interesting to note not the disease risks but overall
longevity. This has been a point of contention. Meat consumption per
se doesn>t reduce one>s life span. I don>t remember what red meat
consumption does to lifespan - I>m sure someone here will point it out -
but given the high Neu5Gc in some non-red meats this wash on longevity
would seem to run counter to the Neu5Gc hypothesis - although, as
someone who is autoimmune, I freely admit I may well make anti-Neu5Gc
antibodies now and that could explain some of my symptoms.

[quote]The UCSD study is the first to investigate human dietary absorption of
a cell-surface molecular sugar called N-glycolylneuraminic acid
(Neu5Gc), which is found in non-human mammals. Not produced in humans,
Neu5Gc occurs naturally in lamb, pork and beef, the so-called ³red
meats². Levels are very low or undetectable in fruits, vegetables,
hen¹s eggs, poultry and fish. (see * below)

Conducting laboratory studies with human tissue, followed by tests in
three adult subjects, the UCSD team provided the first proof that
people who ingest Neu5Gc absorb some of it into their tissues. In
addition, they demonstrated that many humans generate an immune
response against the molecule, which the body sees as a foreign
invader.

The study¹s senior author, Ajit Varki, M.D., UCSD professor of
medicine and cellular and molecular medicine, and co-director of the
UCSD Glycobiology Research and Training Center, said that although it
is unlikely that the ingestion of Neu5Gc alone would be primarily
responsible for any specific disease, ³it is conceivable that gradual
Neu5Gc incorporation into the cells of the body over a lifetime, with
subsequent binding of the circulating antibodies against Neu5Gc (the
immune response), could contribute to the inflammatory processes
involved in various diseases.²
[/quote]
Just as you need someone who understands history to run a country and
regulate financial markets (note how this excludes Phil Gramm and George
Bush), you need people who understand human evolution - ALL of human
evolution - to study changes in modern diet.

We evolved with helminths living in our gut and regulating our immune
responses. Taka>s point on IgG4 (of which modern humans are deficient)
hits the mark. IgG4 prevents mast cells from degranulating and it>s
upregulated by helminths; that>s just one of the beneficial things
helminths do to block autoimmunity. Gluten/gliadin isn>t native to the
human body either and Celiac is a mostly modern problem. We might as
well as blame wheat for causing Celiac (which, basically, it does - but
the point is it>s probably not sufficient to do it, just necessary). We
probably get these diseases because of dysregulation of the gut.
Changes in helminths, H. pylori, Bacteroides fragilis and other
symbionts now missing or threatened by modern diet and modern medicine
could entirely account for any adverse reaction to Neu5Gc. Add T. suis
to a population and they might never develop an inflammatory reaction
against Neu5Gc.

Remember that atherosclerosis is a disease of low regulatory T-cells
(Tregs). You can make all the dietary links to it you wish but as long
as everyone in your study population lacks Treg-boosting helminths you
haven>t ruled out the hypothesis that missing helminths are causing the
cardiovascular disease and that the dietary reactions are irrelevant in
a "healthy" population.

Regarding milk in the Neu5Gc hypothesis, most milk-drinkers are drinking
cow>s milk. This has casein, another target for antibodies. Since
everyone drinking milk in the survey is probably drinking cow>s milk,
how does this validate the Neu5Gc hypothesis?

I would like to point out that both milk and red meat are opioid ligands
(as are rice and wheat). If these substances pass through a leaky gut
(like one hit with sugar and antibiotics), they>re gonna bind to opiate
receptors and screw up immune responses, nervous system signals and any
other system relying on opiates/endocannabinoids. This isn>t even a
factor in the hypothesis under discussion. To rule out this effect with
milk you>d have to look at milk-drinking populations that rely entirely
on goat or camel milk - and as far as I know, all those have water
quality issues and thus a population with extensive helminth exposure.

I would also like to point out that mast cell-degranulation is a factor
in many autoimmune diseases that has largely been overlooked and it>s
never been ruled out satisfactorily. For instance, mast cell
degranulation occurs in male-pattern baldness. Everyone talks about
androgens but no one talks about its autoimmune aspects. Well, the
modern Japanese populace didn>t start going bald until they moved from
rural areas into cities - where the water would be purified of
helminths. It>s possible - given the way antibodies are passed from
mother to son - that, like autism, this autoimmune problem took time to
build and only did so in conjunction with dietary changes or various
toxic exposures. (We know for sure that certain men go bald in Japan
from antibiotic exposure and/or loss of soy in their diet; gut bacteria
process soy into equol which then binds to DHT.) No one>s yet examined
baldness in a population totally immersed in G.I. helminths so the
changes in T-cells and mast cells seen in baldness can>t be isolated
from helminths.

For that matter, Tregs have unique antiviral capacities. We don>t know
if our responses to, say, herpesviruses - which are known to interfere
with the IL-10 pathway - have been affected by this change in helminths.

We also haven>t even discussed the epidemic of vitamin D3-deficiency.
Lack of sun exposure (which, yes, is problematic viz. skin aging and
cancer) has produced record low vitamin D3 levels and that affects
everything in the human body including the immune response. I>d gainsay
people with lower D3 levels are more likely per se to have food
intolerances - so is it the fault of Neu5Gc or a fluorescent
lighting/sunscreen nation?

[quote]³Over the past decade, the number of patients waiting for organ
transplantation has more than tripled, with little increase in the
number of donor organs. This has led to an exploration of using animal
organs for transplantation into humans, a process called
xenotransplantation,² Varki said. ³However, the leading donor
candidate is the pig, an animal in which Neu5Gc happens to be very
common. The current study raises the possibility that human antibodies
against Neu5Gc might recognize the Neu5Gc in the pig organ and
facilitate its rejection.²
[/quote]
So what? Engineer pigs to express purely human immune markers in their
cells. You have to do that in the first place anyway...

[quote]----------------------------

This article shows it is also present in beef fat in substantial
amounts so the Kwasniewski diet doesn>t exclude it. Dairy products
are not that rich source though. The human antibodies against Neu5Gc
are of the IgG class, same as the antibodies in different so called
food intolerances (not allergies, those are of the IgE class). Some
IgG classes (IgG4) could be even protective against inflammation.
Since there is no TLR receptor specific for this molecule it could be
well tolerated if encountered from young childhood. The real
problems are the molecules targeted by the innate immunity and
recognized by the TLR class receptors such as LPS/endotoxin and
unmethylated CpG DNAs. And the Mammoths also carried Neu5Gc I guess
so the Varki>s hypothesis may be flawed - perhaps he developed very
sensitive antibodies for distinguishing Neu5Gc from Neu5Ac and wanted
to build his career on them ...
[/quote]
Notes

there is an inverse relationship between parasitic infection (especially
worms/helminths) and allergy; as parasitic infections dropped on the
Pacific island of Mauke, allergies increased proportionately; one theory
is that when freed of parasitic targets, the immune system has time on
its hands and turns on innocuous allergens; the body¹s Y-shaped IgG
antibodies usually target bacteria and viruses by latching directly on
to target proteins and recruiting immune cells; parasites activate a
different mechanism - Y-shaped IgE antibodies - which attach their tails
to the surface of mast cells; mast cells are found wherever the body
comes into contact with the outside world and thus multicellular
parasites - mucous membranes of the eyes, nose, and throat, and in the
lining of the lungs and gut; once the initial IgE response is complete,
each mast cell has 100,000 to 500,000 Y-shaped antibodies protruding
from its surface with outstretched arms; usually within two weeks of
worm infestation, the immune system is primed and each mast cell
contains a thousand or more large, globular granules; a worm protein
sticks to the arms of two adjacent IgE antibodies and sets off a
reaction causing the mast cell to burst and spew its granules (mast cell
degranulation) of histamines and other inflammatory chemicals that
infiltrate local tissues; this causes itching; blood vessels dilate and
leak; tissues swell and mucus production increases; this response may
prevent worms from infiltrating further through the skin; other cells
are attracted to dump toxins on the parasites; intestinal worms, on the
other hand, come in through the mouth and attack the GI tract; in this
case, an inflamed gut producing fluid and mucus causes in diarrheamaybe
to flush out worms before they can attach; some worms can also spend
part of their life cycle in the human lung (like schistosomiasis); this
may trigger coughing and sneezing; this responses are all more acute to
newcomers in the tropics when first exposed to parasites; some worms do
get through though mostly the system works to protect people; in the
absence of helminths, IgE antibodies can zero in on airborne allergens
(causing asthma or hayfever) or ingested foods instead; worm infested
rats have weak allergy responsesl their IgE antibodies are tied up
fighting worms; however, in rural New Guinea, worm infestation doesn¹t
lessen the asthma rate; there¹s an IgG antibody that competes with IgE;
this G antibody (IgG4) grabs the worm protein before it bumps into the E
antibody attached to a mast cell and this prevents the mast cell
degranulation; IgG4 (1-2%) is the rarest of the IgG¹s; IgG1 targets
viruses and bacteria and is the most common; in people with parasites,
IgG4 jumpts to 18%
<http://www.discover.com/issues/sep-93/features/ofparasitesandpo264/>

the hygiene hypothesis was advanced in 1989 by David Strachan of the
London School of Hygiene and Tropical Medicine; the immune system
expects a dirty environment and when it isn¹t living in one it becomes
hyperactive; Gabonese children with worm infestations have fewer
allergies (and more IL-10, which blocks inflammatory signals among
immune cells); children treated for worms became much more sensitive to
dust mites; Alan Brown of Britain>s University of Nottingham has treated
his hayfever with intestinal hookworms (NECATOR AMERICANUS); they cause
anemia and require overeating; Joel Weinstock (once at the University of
Iowa, now Tufts) used pig whipworms (Trichuris suis; TSO from Ovamed) to
treat ulcerative colitis <http://www.cosmosmagazine.com/node/695>

Kofi · Guest

In article
<6b295818-3a57-46b5-adef-c0a286c80336@h5g2000yqh.googlegroups.com>,
Taka <taka0038@gmail.com> wrote:

[quote]On Nov 23, 9:03 pm, Kofi <k...@anon.un> wrote:
however, in rural New Guinea, worm infestation doesn¹t
lessen the asthma rate;

So if you followed strictly the scientific method this negates the
helminths hypothesis.
[/quote]
What aspect?

I stated worm infestations would probably lower immune reactions to
innocuous molecules in the food supply. Worm infestation rates are
still inversely proportional to allergies, M.S., lupus, etc. on a
population basis.

[quote]I would like to see whether there is a refined
vegetable oil supply to the rural New Guinea ... The worms cause
anemia thus lowering iron and possibly the LTC leukotrienes with it,
then we have the PGE2-induced TREGs. Now what would trigger the IgG4
class specifically?
[/quote]
The worm studies I>ve seen show elevated PGE2 / LTB with infection.
It>s probably a strategy the helminths use to survive and avoid the
immune system. That would be consistent with elevated Treg function.

You>ll have to sketch out the IgG4 connection a little more before I can
comment on it.

Microbes Infect. 2006 Mar;8(3):873-9. Epub 2006 Jan 18.

The filarial parasite Onchocerca volvulus generates the lipid mediator
prostaglandin E(2).

Brattig NW, Schwohl A, Rickert R, Buttner DW.
Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse
74, D-20359 Hamburg, Germany.

Prostaglandins exhibit regulatory effects on the vascular and immune
system. Prostaglandin E(2) (PGE(2)) modulates T helper (Th) cell and
effector cell functional reactivity, thereby promoting Th2 responses. We
found significant expression of PGE(2) in male and female Onchocerca
volvulus. Using immunohistology, PGE(2) was predominantly detected in
the hypodermis of adult O. volvulus, the metabolically most active
tissue of the filaria. In contrast, the muscles were PGE(2)-negative and
the epithelia of intestine and uterus and male genital tract showed only
weak staining. Oocytes were well labeled whereas embryos and sperms did
not react. Less pronounced PGE(2) staining was observed in some dermal
microfilariae. The expression of PGE(2) was found independent of
antifilarial (ivermectin) as well as anti-endobacterial (doxycycline)
treatment of O. volvulus-infected patients. PGE(2) was also demonstrated
in extracts of adult worms by high-performance liquid
chromatography-mass spectrometry. Release of PGE(2) from live or
moribund filariae can affect the host s metabolism and immune response
in favor of the filarial parasite.

PMID: 16513382

Infect Immun. 2002 Jul;70(7):3656-64.

Chronic helminth infection induces alternatively activated macrophages
expressing high levels of CCR5 with low interleukin-12 production and
Th2-biasing ability.

Rodriguez-Sosa M, Satoskar AR, Calderon R, Gomez-Garcia L, Saavedra R,
Bojalil R, Terrazas LI.
Department of Immunology, Instituto Nacional de Cardiologia Ignacio
Chavez, D.F. Mexico 14080, Mexico.

Helminth infections induce Th2-type biased immune responses. Although
the mechanisms involved in this phenomenon are not yet clearly defined,
antigen-presenting cells (APC) could play an important role in this
process. Here, we have used peritoneal macrophages (F4/80+) recruited at
different times after challenge with Taenia crassiceps as APC and tested
their ability to regulate Th1/Th2 differentiation. Macrophages from
acute infections produced high levels of interleukin-12 (IL-12) and
nitric oxide (NO), paralleled with low levels of IL-6 and prostaglandin
E(2) (PGE(2)) and with the ability to induce strong antigen-specific
CD4+ T-cell proliferation in response to nonrelated antigens. In
contrast, macrophages from chronic infections produced higher levels of
IL-6 and PGE(2) and had suppressed production of IL-12 and NO,
associated with a poor ability to induce antigen-specific proliferation
in CD4+ T cells. Failure to induce proliferation was not due to a
deficient expression of accessory molecules, since major
histocompatibility complex class II, CD40, and B7-2 were up-regulated,
together with CD23 and CCR5 as infection progressed. These macrophages
from chronic infections were able to bias CD4+ T cells to produce IL-4
but not gamma interferon (IFN-gamma), contrary to macrophages from acute
infections. Blockade of B7-2 and IL-6 and inhibition of PGE(2) failed to
restore the proliferative response in CD4+ T cells. Furthermore, studies
using STAT6(-/-) mice revealed that STAT6-mediated signaling was
essential for the expansion of these alternatively activated
macrophages. These data demonstrate that helminth infections can induce
different macrophage populations that have Th2-biasing properties.

Publication Types:
* Research Support, Non-U.S. Gov>t

PMID: 12065507

Taka · Guest

On Nov 24, 3:07 am, Kofi <k...@anon.un> wrote:
[quote]The worm studies I>ve seen show elevated PGE2 / LTB with infection.
It>s probably a strategy the helminths use to survive and avoid the
immune system. That would be consistent with elevated Treg function.
[/quote]
Yes, that is the effect of PGE2 but not LTBs. The leukotrienes are
destructive inducing among others metaloproteinases which melt away
the parasites. E.g. cysteinyl leukotrienes are produced when the body
mistakes pollen for the parasites and damage the mucous membranes.
Prostaglandins come later in the immune response to clean out the mess
caused by leukotrienes and rebuild the damaged tissue IMHO.

Taka

None · Guest

Kofi <kofi@anon.un> wrote in news:kofi-FA7AE4.06032523112008
@news.west.earthlink.net:

[quote]It>s possible - given the way antibodies are passed from
mother to son - that, like autism, this autoimmune problem took time to
build and only did so in conjunction with dietary changes or various
toxic exposures. (We know for sure that certain men go bald in Japan
from antibiotic exposure and/or loss of soy in their diet; gut bacteria
process soy into equol which then binds to DHT.)
[/quote]
Can you elaborate further on the antibiotic/hairloss link? Is it simply
because that this class of drugs destroys the helminths in the gut?

Thanks in advance.

Kofi · Guest

In article <Xns9B5F8C2722787None@69.16.185.250>, None <--@nowhre.inv>
wrote:

[quote]Kofi <kofi@anon.un> wrote in news:kofi-FA7AE4.06032523112008
@news.west.earthlink.net:

It>s possible - given the way antibodies are passed from
mother to son - that, like autism, this autoimmune problem took time to
build and only did so in conjunction with dietary changes or various
toxic exposures. (We know for sure that certain men go bald in Japan
from antibiotic exposure and/or loss of soy in their diet; gut bacteria
process soy into equol which then binds to DHT.)

Can you elaborate further on the antibiotic/hairloss link? Is it simply
because that this class of drugs destroys the helminths in the gut?
[/quote]
Certain gut bacteria in certain Japanese men process soy into a DHT
inhibitor, equol. Antibiotics kill those bacteria and destroy the
protection soy offers them. There>s no data per se linking helminths
and hair loss yet.

Taka · Guest

Mystery of the meat-eaters' molecule

Not so rare: a molecule absorbed by eating red meat has been linked to
inflammation and auto-immune illnesses
Our inability to produce a chemical present in every other primate may
be linked to a series of chronic diseases. Roger Highfield explains
more.

What does it mean to be human? For most people, it all comes down to
that extraordinary object between our ears, and how it blesses us with
language, laughter and logic. But not for Ajit Varki, a doctor-cum-
scientist who works in California.

For him, being human is also about a single chemical that separates us
from our closest relatives, and which could be linked to many of our
most debilitating illnesses.

The story began in 1984, when Prof Varki was working at the University
of California, San Diego. When treating a woman with bone-marrow
failure, he injected her with horse serum. The treatment carried the
risk of a side effect called "serum sickness", in which the patient>s
immune system launches an attack on a molecule present in the serum
called Neu5Gc.

Sure enough, her skin erupted with an itchy red rash. Investigating
further, Prof Varki found that Neu5Gc was foreign to humans, even
though we carry a very similar version of the same molecule - which
may be one reason why animal-to-human organ and tissue transplants do
not work well.

But in recent years, he has come to believe that the implications of
this molecular difference are much wider. He has built up a range of
evidence that potentially links Neu5Gc, a so-called sialic acid, to
chronic disease.

This is because the animal version is absorbed by humans as a result
of eating red meat and milk products, and there is evidence that the
body views it as an invader.

Eating these foods could trigger inflammation and, over the long term,
heart disease, certain cancers and auto-immune illnesses. Prof Varki
stresses, however, that "we have not proven any link to disease, just
suggested that it is something to explore".

This sialic acid plays a number of roles: it helps us recognise cells
and helps cells stick together (this stickiness is also exploited by
microbes, which latch on to the sugary molecule to invade our cells).
It also helps regulate our immune response, which may influence the
progression of diseases and even play a part in human evolution.

The first evidence that this particular molecule is of unique
importance to humans came a decade ago. Prof Varki>s team, along with
Prof Elaine Muchmore, also of the University of California, studied
blood from chimps, bonobos, gorillas, orangutans and humans.

They found that we are the only primates whose bodies do not produce
Neu5Gc - although further research established that our Neanderthal
cousins were missing this version of the sugar acid, too.

Instead, human (and Neanderthal) cells bristle with a sugar called
Neu5Ac. The two molecules are identical, apart from one little detail:
the ape molecule has a single extra oxygen atom. Because of the many
different jobs this sugar does throughout the body, this one atom was
the first example found of a fundamental genetic and biochemical
difference between humans and our closest relatives.

Profs Muchmore and Varki then found out why this oxygen atom is
missing: our molecule is the precursor of the animal version. Unlike
chimpanzees and other great apes, humans lack a particular version of
an enzyme that converts Neu5Ac (or, to give it its full name, N-
acetylneuraminic acid) into Neu5Gc. This tiny change could potentially
explain some of the more unusual differences between humans and apes.

Chimpanzees do not seem to suffer from heart disease, cancers,
rheumatoid arthritis or bronchial asthma - common conditions in
humans. Nor do they get sick from the human malaria parasite, which
uses sialic acid to latch on to our blood cells.

In recent studies, Prof Varki>s team has found tantalising evidence
that this mysterious molecule could be exerting a wider effect on our
health, through the substances we eat.

After testing a range of foods, they found the highest levels of
Neu5Gc in red meat: up to 11,600 micrograms could be absorbed from the
recommended daily serving of beef, 5,100 from pork and 4,900 from
lamb. The level in goat>s cheese was 5,500, but fell to around 700 in
milk and salmon. Cod, tuna, turkey and duck were in the twenties.

Given that food is broken down in the stomach, did eating animal
tissue present the same dangers of provoking an immune attack as
transplanting it? Following that great scientific tradition of self-
experimentation, Profs Varki, Muchmore and Pascal Gagneux ate pure
Neu5Gc to see what would happen.

Not only did the foreign sugar show up in the body soon after eating,
but tests also revealed that many people carry antibodies that react
to Neu5Gc - a protective immune response, but one which could trigger
damaging inflammation.

Prof Varki>s colleague - and wife - Prof Nissi Varki then found that
small amounts of Neu5Gc were present in normal human tissue, probably
as a result of long-term consumption. And as well as food, many
biotherapeutic products made in animal cells and/or using animal
materials were also contaminated with Neu5Gc.

This raised the fascinating possibility that anti-Neu5Gc antibodies
are involved in auto-immunity. Auto-immune diseases, such as type-1 or
juvenile diabetes and some types of arthritis, occur when the body
mistakenly attacks healthy tissue.

Because the animal version of the sugar is so similar to the human
one, the latter could be caught in the friendly fire directed by the
immune system. Chronic inflammation is also linked with cancer;
intriguingly, the team found that Neu5Gc was concentrated in tumours,
particularly those that spread throughout the body. This could aid
detection of such diseases, by getting scientists to look for the
animal acid rather than the tumours themselves.

Some of this might sound familiar: several previous studies have
linked ingestion of red meat to cancer and heart disease, and possibly
to some other disorders involving inflammation, such as arthritis and
lupus. But these focused mostly on the role of saturated fats, and on
products that arise from cooking.

Prof Varki, however, believes that his little molecular difference
could also be to blame: Neu5Gc elicits an immune reaction that might
contribute to a whole spectrum of human-specific diseases. Although
they have not proven this yet, the evidence is sufficiently compelling
for his team to start work on ways to eliminate Neu5Gc from the body.

But the question remains: why are humans unique among primates in not
producing Neu5Gc?

By studying the mutations in the enzyme that makes this molecular
difference between apes and humans, Prof Varki, along with Prof
Naoyuki Takahata of the Graduate University for Advanced Studies in
Kanagawa, Japan, estimates that the genetic change first appeared up
to three million years ago, which coincides with the emergence of Homo
erectus, the first of our ancestors to venture out of Africa.

At the time, life was nasty, brutish and short: any subtle but chronic
effects of this foreign sugar would not be felt until old age, and
Homo erectus did not survive that long.

If the mutation that kept us producing Neu5Ac rather than Neu5Gc
helped shrug off a particular disease, it would have spread rapidly
through the population. It is ironic that what may have protected our
ancestors then could be responsible for much of the pain of their long-
lived descendants.

SOURCE: http://www.telegraph.co.uk/scienceandtechnology/science/sciencenews/3346666/Mystery-of-the-meat-eaters%27-molecule.html


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