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Reply | Forward Message #488 of 555 |

Hi!

I cleared on these test vials of the following bacterias and this gene - With me they were autoimmune, and even with V's Rainbow LED Litebox, took me an hour.  This alone makes this significant.  It would have taken way longer than 4 hours without, but when you consider what this does to a person, it's a small price to pay. 

More than 1/3rd of our nation is looking for answers.  This is very interesting to me.

Mice inoculated with a combination of B. theta and an archaean bacteria, Bacteroides thetaiotaomicron ( B. theta) and Methanobrevibacter smithii ( M. smithii), extracted much more calories ... and supress protein FIAF  (see below)  which ordinarily prevents the body from storing fat.

Also, See below- The research team has also identified a gene in the Ad-36 virus, called E4Orfl, that seems to play a key role in switching on the fat accumulation process in infected animals.

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Fat Factors

http://www.nytimes.com/2006/08/13/magazine/13obesity.html?pagewanted=2

Published: August 13, 2006

 

Of the trillions and trillions of cells in a typical human body — at least 10 times as many cells in a single individual as there are stars in the Milky Way — only about 1 in 10 is human. The other 90 percent are microbial. These microbes — a term that encompasses all forms of microscopic organisms, including bacteria, fungi, protozoa and a form of life called archaea — exist everywhere. They are found in the ears, nose, mouth, vagina, anus, as well as every inch of skin, especially the armpits, the groin and between the toes. The vast majority are in the gut, which harbors 10 trillion to 100 trillion of them. “Microbes colonize our body surfaces from the moment of our birth,” Gordon said. “They are with us throughout our lives, and at the moment of our death they consume us.”

How should we be fighting the obesity epidemic?

Known collectively as the gut microflora (or microbiota, a term Gordon prefers because it derives from the Greek word bios, for “life”), these microbes have a Star Trek analogue, he says: the Borg Collective, a community of cybernetically enhanced humanoids with functions so intertwined that they operate as a single intelligence, sort of like an ant colony. In its Borglike way, the microflora assumes an extraordinary array of functions on our behalf — functions that we couldn’t manage on our own. It helps create the capillaries that line and nourish the intestines. It produces vitamins, in particular thiamine, pyroxidine and vitamin K. It provides the enzymes necessary to metabolize cholesterol and bile acid. It digests complex plant polysaccharides, the fiber found in grains, fruits and vegetables that would otherwise be indigestible.

And it helps extract calories from the food we eat and helps store those calories in fat cells for later use — which gives them, in effect, a role in determining whether our diets will make us fat or thin.

In the womb, humans are free of microbes. Colonization begins during the journey down the birth canal, which is riddled with bacteria, some of which make their way onto the newborn’s skin. From that moment on, every mother’s kiss, every swaddling blanket, carries on it more microbes, which are introduced into the baby’s system.

By about the age of 2, most of a person’s microbial community is established, and it looks much like any other person’s microbial community. But in the same way that it takes only a small percentage of our genome to make each of us unique, modest differences in our microflora may make a big difference from one person to another. It’s not clear what accounts for individual variations. Some guts may be innately more hospitable to certain microbes, either because of genetics or because of the mix of microbes already there. Most of the colonization probably happens in the first few years, which explains why the microflora fingerprints of adult twins, who shared an intimate environment (and a mother) in childhood, more closely resemble each other than they do those of their spouses, with whom they became intimate later in life.

No one yet knows whether an individual’s microflora community tends to remain stable for a lifetime, but it is known that certain environmental changes, like taking antibiotics, can alter it at least temporarily. Stop the antibiotics, and the microflora seems to bounce back — but it might not bounce back to exactly what it was before the antibiotics.

In 2004, a group of microbiologists at Stanford University led by David Relman conducted the first census of the gut microflora. It took them a year to do an analysis of just three healthy subjects, by which time they had counted 395 species of bacteria. They stopped counting before the census was complete; Relman has said the real count might be anywhere from 500 species to a few thousand.

About a year ago, Relman joined with other scientists, including Jeffrey Gordon, to begin to sequence all the genes of the human gut microflora. In early June, they published their results in Science: some 78 million base pairs in all. But even this huge number barely scratches the surface; the total number of base pairs in the gut microflora might be 100 times that. Because there are so many trillions of microbes in the gut, the vast majority of the genes that a person carries around are more microbial than human. “Humans are superorganisms,” the scientists wrote, “whose metabolism represents an amalgamation of microbial and human attributes.” They call this amalgamation — human genes plus microbial genes — the metagenome.

Gordon first began studying the connection between the microflora and obesity when he saw what happened to mice without any microbes at all. These germ-free mice, reared in sterile isolators in Gordon’s lab, had 60 percent less fat than ordinary mice. Although they ate voraciously, usually about 30 percent more food than the others, they stayed lean. Without gut microbes, they were unable to extract calories from some of the types of food they ate, which passed through their bodies without being either used or converted to fat.

When Gordon’s postdoctoral researcher Fredrik Bäckhed transplanted gut microbes from normal mice into the germ-free mice, the germ-free mice started metabolizing their food better, extracting calories efficiently and laying down fat to store for later use. Within two weeks, they were just as fat as ordinary mice. Bäckhed and Gordon found at least one mechanism that helps explain this observation. As they reported in the Proceedings of the National Academy of Sciences in 2004, some common gut bacteria, including B. theta, suppress the protein FIAF, which ordinarily prevents the body from storing fat. By suppressing FIAF, B. theta allows fat deposition to increase. A different gut microbe, M. smithii, was later found to interact with B. theta in a way that extracts additional calories from polysaccharides in the diet, further increasing the amount of fat available to be deposited after the mouse eats a meal. Mice whose guts were colonized with both B. theta and M. smithii — as usually happens in humans in the real world — were found to have about 13 percent more body fat than mice colonized by just one or the other.

Gordon likes to explain his hypothesis of what gut microbes do by talking about Cheerios. The cereal box says that a one-cup serving contains 110 calories. But it may be that not everyone will extract 110 calories from a cup of Cheerios. Some may extract more, some less, depending on the particular combination of microbes in their guts. “A diet has a certain amount of absolute energy,” he said. “But the amount that can be extracted from that diet may vary between individuals — not in a huge way, but if the energy balance is affected by just a few calories a day, over time that can make a big difference in body weight.”

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Viruses, Fat, and Obesity

My research indicates that there are dozens of viruses stored in the fatty tissue of everyone, particularly in the gut. There are at least nine different variations of altered cells caused by each virus, along with a dozen or more other components that are side effects of virus construction and replication.

These altered cells are difficult to eliminate in the abdomen and certain viruses like the one below cause them to proliferate. Once the viruses are eliminated by frequencies, many burn off immediately, fat redistributes normally in the body, and diet and exercise appear to burn off fat normally.

Scientists Say Common Virus Could Cause Obesity
Medical News Today - Featured Article
21 Aug 2007 - 3:00 PDT

Scientists at the 234th national meeting of the American Chemical Society in Boston, Massachusetts this week presented the results of a study that suggests a common virus could be partly responsible for the obesity epidemic that is sweeping across America and other nations. They hope their findings will develop antiviral medication to treat "viral obesity".

According to the National Institutes of Health (NIH), some 97 million adult Americans are obese. Obesity increases risk of many illnesses, including type 2 diabetes, heart disease, stroke, and osteoarthritis.

So far scientists have shown that genetic predisposition increases risk of obesity, as do other contributory factors including over-eating, eating foods high in fat, lack of physical exercise, genetics, and some medications.

In this latest study, researchers used lab experiments to show that infection with a common virus that causes respiratory and eye infections in humans, called human adenovirus-36 (Ad-36) turns adult stem cells retrieved from fat tissue into fat cells. But stem cells that were not exposed to Ad-36 did not turn into fat cells.

The scientists have also discovered that a specific gene in the virus causes the transformation from stem cells into fat cells.

Presenting the results of the study was Dr Magdalena Pasarica, obesity researcher at the Pennington Biomedical Research Center, part of Louisiana State University:

"We're not saying that a virus is the only cause of obesity, but this study provides stronger evidence that some obesity cases may involve viral infections."

Pasarica explained that:

"Not all infected people will develop obesity. We would ultimately like to identify the underlying factors that predispose some obese people to develop this virus and eventually find a way to treat it."

Pasarica and colleagues took adult stem cells from the fatty tissue of a range of patients who had undergone liposuction. They exposed half of the stem cells to Ad-36, but not the other half.

After a week, most of the virus infected stem cells had transformed into fat cells, but the ones that were not infected had not changed.

Pasarica was involved in an earlier study led by Dr Nikhil Dhurandhar, now associate professor at Pennington Biomedical Research Center. The study showed that Ad-36 caused fat accumulation in animals infected with the virus. The research team then carried out an epidemiological study that showed 30 per cent of obese people were infected with Ad-36, compared with only 11 per cent of lean people.

It was not until this latest study that they were able to show how the virus actually increases fat in humans, according to the researchers.

The research team has also identified a gene in the Ad-36 virus, called E4Orfl, that seems to play a key role in switching on the fat accumulation process in infected animals. The gene could be a target for a range of human therapies, including vaccines and anti-virals, to treat obesity, said Pasarica.

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Health, Hope, Joy & Healing :
May you Prosper, even as your Soul Prospers  3John 2
 
Jennifer Ruby
 
Email advice is not a substitute for medical treatment.
 
http://www.rubysemporium.com
http://groups.yahoo.com/group/SymphonicHealth
http://groups.yahoo.com/group/Therapeutic-Laser_Therapy
http://www.lazrpulsr.com
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Fri Oct 19, 2007 4:31 pm

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Hi! I cleared on these test vials of the following bacterias and this gene - With me they were autoimmune, and even with V's Rainbow LED Litebox, took me an...
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