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Is It What You Eat, Or What Eats It That Makes you Well /Ill? GutMicrobes !!



 
 
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  #1  
Old March 8th, 2010, 04:01 PM posted to alt.support.diet.low-carb
pamela
external usenet poster
 
Posts: 47
Default Is It What You Eat, Or What Eats It That Makes you Well /Ill? GutMicrobes !!

http://www.scientificamerican.com/ar...gut&print=true

SciAm.com

News - March 5, 2010

Genetics in the Gut: Intestinal Microbes Could Drive Obesity and Other
Health Issues


The diversity of germs in the human gut suggests microbiota play a
greater role in health than previously thought, even driving obesity and
other metabolic conditions

By Katherine Harmon

Outnumbering our human cells by about 10 to one, the many minuscule
microbes that live in and on our bodies are a big part of crucial
everyday functions. The lion's share live in the intestinal tract, where
they help fend off bad bacteria and aid in digesting our dinners. But as
scientists use genetics to uncover what microbes are actually present
and what they're doing in there, they are discovering that the bugs play
an even larger role in human health than previously suspected—and
perhaps at times exerting more influence than human genes themselves.

One team of researchers recently completed a catalogue of some 3.3
million human gut microbe genes. Their work, led by Junjie Qin of
BGI–Shenzhen (formerly the Beijing Genomics Institute) and published in
the March 4 edition of Nature, adds to the expanding—but nowhere near
complete—census of species that reside in the intestinal tract.
(Scientific American is part of Nature Publishing Group.)

Another group turned its attention to a particular host gene that seems
to impact these inhabitants of the intestines. They found that in mice,
a loss of one key gene led to a shift in microbiota communities and an
increase in insulin resistance, obesity and other symptoms of metabolic
syndrome (a cluster of these conditions). Their results were published
online March 4 in Science.

The field of gut microbe study has bloomed in the past few years after
decades in the shadows. As the authors of the Science report noted, "The
inability to culture most gut bacteria makes assessment of their causal
role in health and disease technically challenging." But the advance of
genetic sequencing has enabled researchers to make steady progress in
getting to the bottom of these beasties and their role in health. And in
addition to being a quick way to assess these microbial populations,
genomics can also help to elucidate how the two systems—human and
microbe—interact.

Stomach survey
The number of microbes in the human gut was known to be vast, but the
3.3 million microbial genes located in it were a good deal "more than
what we originally expected," says Jun Wang, of BGI and co-author of the
Nature study. The number was especially surprising given that the
microbiota tended to be very similar across the 124 individuals they
sampled in Denmark and Spain.

Previous work had scanned for these microbial genes in the past. The
largest had created about three gigabases (billion base pairs) of
microbial sequences that was trumped by Wang's team, which assembled
more than 576 gigabases.

The hefty catalogue is a "big advance" in the field, says Andrew Gewirtz
of the Department of Pathology and Laboratory Medicine at Emory
University who was not involved in this study. "It really sets in place
a framework for defining—in detail—the microbiome," he says. And as Wang
and his colleagues noted in their study, "To understand and exploit the
impact of the gut microbes on human health and well-being it is
necessary to decipher the content, diversity and functioning of the
microbial gut community."

More than 99 percent of the genes the group found were from bacteria.
"These bacteria have functions, which are essential to our health: They
synthesize vitamins, break down certain compounds—which cannot be
assimilated by our body—[and] play an important role in our immune
system," Wang points out.

Wang's group, which is part of the European Commission–funded MetaHIT
(Metagenomics of the Human Intestinal Tract) consortium, relied on fecal
samples from the 124 individuals. Despite the presumed vastness of
gut-microbe diversity, the researchers found that about 70 percent of
the genetic material in their European sample overlapped with that from
previous studies that examined U.S. and Japanese subjects, suggesting
that, in fact, "the prevalent human microbiome is of a finite and not
overly large size," the researchers concluded.

It is "a very important paper for paving the way for future studies,"
Gewirtz says. "Once you define the baseline you can start looking in
detail at disease."

Wang and his colleagues already had this next step in mind. The samples
for the genetic catalogue came from two groups of obese individuals:
those with inflammatory bowel disease, and a healthy group. The genetic
analysis of the microbial inhabitants of the respective guts "clearly
separates patients from healthy individuals," the researchers concluded
in their paper, suggesting new possibilities for diagnosis and
eventually treatment.

Inflammatory mutations
As the prevalence of metabolic diseases continues to increase across the
U.S. and many other countries, a growing body of research has suggested
that some of these physiological changes might have their roots deep in
the gut—not in the human cells but some of the many microbes there.

Emory's Gewirtz and his team tracked the gut microbiota in mice as the
rodents experienced different kinds of metabolic disorders, such as
obesity and insulin resistance. They bred mice with a genetic deficiency
(specifically, the absence of Toll-like receptor 5, or TLR5, which has a
hand in immune response) to see how it might change their microbial gut
communities and metabolic health—and try to understand the order in
which the changes were happening. "It's very much appreciated that
obesity is associated with insulin resistance and type 2 diabetes,"
Gewirtz says. But "which comes first is not entirely clear."

They found that their mice without the TLR5 gene—even when put on
restricted diets—still showed insulin resistance, suggesting that
insulin resistance might lead to obesity rather than the other way
around. But if these mice were allowed to eat as they pleased, they ate
10 percent more than their peers and, by 20 weeks old, had body mass
indexes that were 20 percent higher. Many researchers and public health
officials have blamed the availability (and content) of contemporary
foods, increasingly sedentary lifestyles and human genetics for more
metabolic syndrome cases. But the mouse study suggests that there might
be more to the picture. "The tendency to overeat may be underlain by
changes that are more likely physiological than genetic," Gewirtz says.

Gewirtz and others propose that inflammation—in conjunction with changes
in the gut microbiome—might be driving the cycle. Inflammation can
change the character of the gut microbes, in some cases allowing more
calories to be extracted from food. But, Gewirtz says, "We do not know
which is coming first" if inflammation is changing the microbiota or
vice versa. It is likely, he notes, that whatever kicks off the process,
it will start a sort of feedback loop, where one will increase
accelerates the other.

How much of their findings in mice are likely to translate to humans?
The stomach bacteria in mice are not found in people. But Gewirtz and
his team noted that analogous species live in the human stomach. "We
think it's very plausible" that the findings will carry over to humans,
especially because they "fit with a lot of the ideas" currently
circulating in the research community about insulin resistance and
inflammation, Gewirtz says. His group has already started a new
investigation comparing the human genes and microbial profiles of people
with metabolic syndrome to healthy controls to see if some of the same
correlations in mice appear in humans.

Next genetic steps
Although a fuller grasp of microbial genetics promises to boost wellness
even further, plenty of big unknowns remain. Scientists are still unsure
just how and when these communities of microbes establish themselves in
each person's gut. "Everyone is born sterile," Gewirtz says, noting that
colonization starts during birth but that they do not know when it
reaches relative stability. Regardless of timing, it means that, "the
environment is a big, big factor in determining what someone's
microbiota will be like," he adds.

If gut microbiota do play a large role in diseases such as obesity and
metabolic syndrome, then a recent past change in these communities might
help to explain the expansion of patients—and waistlines—in developed
countries. "The genetics of humans have not changed appreciably in the
last several hundred years," Gewirtz says. "But several changes in the
environment have made it so that the gut microbiota is likely
considerably different than it was 50 years ago."

Wang and his colleagues are already attempting to track the composition
of human gut microbiota back in time to see if this might be the case.
But they have their sights set on even bigger collections of genetic
data. "Our dream is to build a library" of reference genomes, Wang
notes. He hopes to have 10,000 genomes for bacteria within two years.
And, he estimated, as soon as more definitive data about these gut
genetics emerge, microbial-targeted therapeutics will likely be quick to
follow.

  #2  
Old March 8th, 2010, 11:44 PM posted to alt.support.diet.low-carb
[email protected]
external usenet poster
 
Posts: 993
Default Is It What You Eat, Or What Eats It That Makes you Well /Ill? GutMicrobes !!

On Mar 8, 10:01*am, pamela wrote:
http://www.scientificamerican.com/ar...cs-in-the-gut&....

SciAm.com

News - *March 5, 2010

Genetics in the Gut: Intestinal Microbes Could Drive Obesity and Other
Health Issues

The diversity of germs in the human gut suggests microbiota play a
greater role in health than previously thought, even driving obesity and
other metabolic conditions

By Katherine Harmon

Outnumbering our human cells by about 10 to one, the many minuscule
microbes that live in and on our bodies are a big part of crucial
everyday functions. The lion's share live in the intestinal tract, where
they help fend off bad bacteria and aid in digesting our dinners. But as
scientists use genetics to uncover what microbes are actually present
and what they're doing in there, they are discovering that the bugs play
an even larger role in human health than previously suspected and
perhaps at times exerting more influence than human genes themselves.

One team of researchers recently completed a catalogue of some 3.3
million human gut microbe genes. Their work, led by Junjie Qin of
BGI Shenzhen (formerly the Beijing Genomics Institute) and published in
the March 4 edition of Nature, adds to the expanding but nowhere near
complete census of species that reside in the intestinal tract.
(Scientific American is part of Nature Publishing Group.)

Another group turned its attention to a particular host gene that seems
to impact these inhabitants of the intestines. They found that in mice,
a loss of one key gene led to a shift in microbiota communities and an
increase in insulin resistance, obesity and other symptoms of metabolic
syndrome (a cluster of these conditions). Their results were published
online March 4 in Science.

The field of gut microbe study has bloomed in the past few years after
decades in the shadows. As the authors of the Science report noted, "The
inability to culture most gut bacteria makes assessment of their causal
role in health and disease technically challenging." But the advance of
genetic sequencing has enabled researchers to make steady progress in
getting to the bottom of these beasties and their role in health. And in
addition to being a quick way to assess these microbial populations,
genomics can also help to elucidate how the two systems human and
microbe interact.

Stomach survey
The number of microbes in the human gut was known to be vast, but the
3.3 million microbial genes located in it were a good deal "more than
what we originally expected," says Jun Wang, of BGI and co-author of the
Nature study. The number was especially surprising given that the
microbiota tended to be very similar across the 124 individuals they
sampled in Denmark and Spain.

Previous work had scanned for these microbial genes in the past. The
largest had created about three gigabases (billion base pairs) of
microbial sequences that was trumped by Wang's team, which assembled
more than 576 gigabases.

The hefty catalogue is a "big advance" in the field, says Andrew Gewirtz
of the Department of Pathology and Laboratory Medicine at Emory
University who was not involved in this study. "It really sets in place
a framework for defining in detail the microbiome," he says. And as Wang
and his colleagues noted in their study, "To understand and exploit the
impact of the gut microbes on human health and well-being it is
necessary to decipher the content, diversity and functioning of the
microbial gut community."

More than 99 percent of the genes the group found were from bacteria.
"These bacteria have functions, which are essential to our health: They
synthesize vitamins, break down certain compounds which cannot be
assimilated by our body [and] play an important role in our immune
system," Wang points out.

Wang's group, which is part of the European Commission funded MetaHIT
(Metagenomics of the Human Intestinal Tract) consortium, relied on fecal
samples from the 124 individuals. Despite the presumed vastness of
gut-microbe diversity, the researchers found that about 70 percent of
the genetic material in their European sample overlapped with that from
previous studies that examined U.S. and Japanese subjects, suggesting
that, in fact, "the prevalent human microbiome is of a finite and not
overly large size," the researchers concluded.

It is "a very important paper for paving the way for future studies,"
Gewirtz says. "Once you define the baseline you can start looking in
detail at disease."

Wang and his colleagues already had this next step in mind. The samples
for the genetic catalogue came from two groups of obese individuals:
those with inflammatory bowel disease, and a healthy group. The genetic
analysis of the microbial inhabitants of the respective guts "clearly
separates patients from healthy individuals," the researchers concluded
in their paper, suggesting new possibilities for diagnosis and
eventually treatment.

Inflammatory mutations
As the prevalence of metabolic diseases continues to increase across the
U.S. and many other countries, a growing body of research has suggested
that some of these physiological changes might have their roots deep in
the gut not in the human cells but some of the many microbes there.

Emory's Gewirtz and his team tracked the gut microbiota in mice as the
rodents experienced different kinds of metabolic disorders, such as
obesity and insulin resistance. They bred mice with a genetic deficiency
(specifically, the absence of Toll-like receptor 5, or TLR5, which has a
hand in immune response) to see how it might change their microbial gut
communities and metabolic health and try to understand the order in
which the changes were happening. "It's very much appreciated that
obesity is associated with insulin resistance and type 2 diabetes,"
Gewirtz says. But "which comes first is not entirely clear."

They found that their mice without the TLR5 gene even when put on
restricted diets still showed insulin resistance, suggesting that
insulin resistance might lead to obesity rather than the other way
around. But if these mice were allowed to eat as they pleased, they ate
10 percent more than their peers and, by 20 weeks old, had body mass
indexes that were 20 percent higher. Many researchers and public health
officials have blamed the availability (and content) of contemporary
foods, increasingly sedentary lifestyles and human genetics for more
metabolic syndrome cases. But the mouse study suggests that there might
be more to the picture. "The tendency to overeat may be underlain by
changes that are more likely physiological than genetic," Gewirtz says.

Gewirtz and others propose that inflammation in conjunction with changes
in the gut microbiome might be driving the cycle. Inflammation can
change the character of the gut microbes, in some cases allowing more
calories to be extracted from food. But, Gewirtz says, "We do not know
which is coming first" if inflammation is changing the microbiota or
vice versa. It is likely, he notes, that whatever kicks off the process,
it will start a sort of feedback loop, where one will increase
accelerates the other.

How much of their findings in mice are likely to translate to humans?
The stomach bacteria in mice are not found in people. But Gewirtz and
his team noted that analogous species live in the human stomach. "We
think it's very plausible" that the findings will carry over to humans,
especially because they "fit with a lot of the ideas" currently
circulating in the research community about insulin resistance and
inflammation, Gewirtz says. His group has already started a new
investigation comparing the human genes and microbial profiles of people
with metabolic syndrome to healthy controls to see if some of the same
correlations in mice appear in humans.

Next genetic steps
Although a fuller grasp of microbial genetics promises to boost wellness
even further, plenty of big unknowns remain. Scientists are still unsure
just how and when these communities of microbes establish themselves in
each person's gut. "Everyone is born sterile," Gewirtz says, noting that
colonization starts during birth but that they do not know when it
reaches relative stability. Regardless of timing, it means that, "the
environment is a big, big factor in determining what someone's
microbiota will be like," he adds.

If gut microbiota do play a large role in diseases such as obesity and
metabolic syndrome, then a recent past change in these communities might
help to explain the expansion of patients and waistlines in developed
countries. "The genetics of humans have not changed appreciably in the
last several hundred years," Gewirtz says. "But several changes in the
environment have made it so that the gut microbiota is likely
considerably different than it was 50 years ago."

Wang and his colleagues are already attempting to track the composition
of human gut microbiota back in time to see if this might be the case.
But they have their sights set on even bigger collections of genetic
data. "Our dream is to build a library" of reference genomes, Wang
notes. He hopes to have 10,000 genomes for bacteria within two years.
And, he estimated, as soon as more definitive data about these gut
genetics emerge, microbial-targeted therapeutics will likely be quick to
follow.


This left me wondering. Broad spectrum antibiotics knock out many of
these microbiota, which is why patients on them for any extended
length of time are told to take acidophilous to restore some friendly
bacteria. So, if some of the microbiota are indeed evil and causing
obesity or whatever, one would think some patients might suddenly see
an improvement after taking a course of one of these antibiotics.
Yes? I suppose it's possible that the evil ones are resistant to
whatever antibiotics, but you would think that with all the
antibiotics they have pumped into at least some people, someone would
have suddenly been cured of obesity by accident.
  #3  
Old March 8th, 2010, 11:55 PM posted to alt.support.diet.low-carb
Doug Freyburger
external usenet poster
 
Posts: 1,866
Default Is It What You Eat, Or What Eats It That Makes you Well /Ill? Gut Microbes !!

wrote:

This left me wondering. Broad spectrum antibiotics knock out many of
these microbiota, which is why patients on them for any extended
length of time are told to take acidophilous to restore some friendly
bacteria. So, if some of the microbiota are indeed evil and causing
obesity or whatever, one would think some patients might suddenly see
an improvement after taking a course of one of these antibiotics.
Yes? I suppose it's possible that the evil ones are resistant to
whatever antibiotics, but you would think that with all the
antibiotics they have pumped into at least some people, someone would
have suddenly been cured of obesity by accident.


Dr Atkins put a lot of effort into fighting candidia because he wondered
the opposite - What if the good bacteria stabilize metabolism and
killing them off is one of the main underlying causes of the obesity
epidemic? Certainly the obesity epidemic happened after widespread use
(and likely over use) of antibiotics.

It's easy to blame other societal changes like super-sized fast food
portions and a stress on low fat to the exclusion of any other dieting
plan. It's easy to ignore the effect that antibiotics driven changes in
intestinal bacteria has. But how to measure the effect of the bacteria?

The reason I am not all that worried about it is the comment that
everyone is born sterile (incidentally - I don't believe that). If it's
true then we all get innoculated with all of those types of bacteria
early in our lives. If we get them early they have to be all over the
place so we muct be innoculated constantly not just when we are infants.
  #4  
Old March 9th, 2010, 12:02 AM posted to alt.support.diet.low-carb
Bill who putters
external usenet poster
 
Posts: 10
Default Is It What You Eat, Or What Eats It That Makes you Well /Ill? Gut Microbes !!

In article ,
Doug Freyburger wrote:


The reason I am not all that worried about it is the comment that
everyone is born sterile (incidentally - I don't believe that).


Last I looked we are born between Feces and Urine.

--
Bill Garden in shade zone 5 S Jersey USA
http://www.globalissues.org/article/75/world-military-spending

 




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