WHY? Because even though milk may seem soothing at first, it makes your body secrete gastrin — a hormone that encourages the release of MORE ACID!

Smarter remedy. Cabbage juice! This homegrown cure turns out to be real because it’s incredibly rich in the natural compounds glutamine and gefarnate. These substances are so good at rebuilding your stomach lining, one of them is now the basis of an antiulcer drug!

Sourced & published by Henry Sapiecha

Gut Bacteria Affect Multiple Sclerosis

Science (July 20, 2010) — Biologists at the California Institute of Technology (Caltech) have demonstrated a connection between multiple sclerosis (MS) — an autoimmune disorder that affects the brain and spinal cord — and gut bacteria.

The work — led by Sarkis K. Mazmanian, an assistant professor of biology at Caltech, and postdoctoral scholar Yun Kyung Lee — appears online the week of July 19-23 in the Proceedings of the National Academy of Sciences.

Multiple sclerosis results from the progressive deterioration of the protective fatty myelin sheath surrounding nerve cells. The loss of myelin hinders nerve cells from communicating with one another, leading to a host of neurological symptoms including loss of sensation, muscle spasms and weakness, fatigue, and pain. Multiple sclerosis is estimated to affect about half a million people in the United States alone, with rates of diagnosis rapidly increasing. There is currently no cure for MS.

Although the cause of MS is unknown, microorganisms seem to play some sort of role. “In the literature from clinical studies, there are papers showing that microbes affect MS,” Mazmanian says. “For example, the disease gets worse after viral infections, and bacterial infections cause an increase in MS symptoms.”

On the other hand, he concedes, “it seems counterintuitive that a microbe would be involved in a disease of the central nervous system, because these are sterile tissues.”

And yet, as Mazmanian found when he began examining the multiple sclerosis literature, the suggestion of a link between bacteria and the disease is more than anecdotal. Notably, back in 1993, Caltech biochemist Leroy Hood — who was then at the University of Washington — published a paper describing a genetically engineered strain of mouse that developed a lab-induced form of multiple sclerosis known as experimental autoimmune encephalomyelitis, or EAE.

When Hood’s animals were housed at Caltech, they developed the disease. But, oddly, when the mice were shipped to a cleaner biotech facility — where their resident gut bacterial populations were reduced — they didn’t get sick. The question was, why? At the time, Mazmanian says, “the authors speculated that some environmental component was modulating MS in these animals.” Just what that environmental component was, however, remained a mystery for almost two decades.

But Mazmanian — whose laboratory examines the relationships between gut microbes, both harmful and helpful, and the immune systems of their mammalian hosts — had a hunch that intestinal bacteria were the key. “As we gained an appreciation for how profoundly the gut microbiota can affect the immune system, we decided to ask if symbiotic bacteria are the missing variable in these mice with MS,” he says.

To find out, Mazmanian and his colleagues tried to induce MS in animals that were completely devoid of the microbes that normally inhabit the digestive system. “Lo and behold, these sterile animals did not get sick,” he says.

Then the researchers decided to see what would happen if bacteria were reintroduced to the germ-free mice. But not just any bacteria. They inoculated mice with one specific organism, an unculturable bug from a group known as segmented filamentous bacteria. In prior studies, these bacteria had been shown to lead to intestinal inflammation and, more intriguingly, to induce in the gut the appearance of a particular immune-system cell known as Th17. Th17 cells are a type of T helper cell — cells that help activate and direct other immune system cells. Furthermore, Th17 cells induce the inflammatory cascade that leads to multiple sclerosis in animals.

“The question was, if this organism is inducing Th17 cells in the gut, will it be able to do so in the brain and central nervous system?” Mazmanian says. “Furthermore, with that one organism, can we restore to sterile animals the entire inflammatory response normally seen in animals with hundreds of species of gut bacteria?”

The answer? Yes on all counts. Giving the formerly germ-free mice a dose of one species of segmented filamentous bacteria induced Th17 not only in the gut but in the central nervous system and brain — and caused the formerly healthy mice to become ill with MS-like symptoms.

“It definitely shows that gut microbes have a strong role in MS, because the genetics of the animals were the same. In fact, everything was the same except for the presence of those otherwise benign bacteria, which are clearly playing a role in shaping the immune system,” Mazmanian says. “This study shows for the first time that specific intestinal bacteria have a significant role in affecting the nervous system during MS — and they do so from the gut, an anatomical location very, very far from the brain.”

Mazmanian and his colleagues don’t, however, suggest that gut bacteria are the direct cause of multiple sclerosis, which is known to be genetically linked. Rather, the bacteria may be helping to shape the immune system’s inflammatory response, thus creating conditions that could allow the disease to develop. Indeed, multiple sclerosis also has a strong environmental component; identical twins, who possess the same genome and share all of their genes, only have a 25 percent chance of sharing the disease. “We would like to suggest that gut bacteria may be the missing environmental component,” he says.

For their part, Th17 cells are needed for the immune system to properly combat infection. Problems only arise when the cells are activated in the absence of infection — just as disease can arise, Mazmanian and others suspect, when the species composition of gut bacteria become imbalanced, say, by changes in diet, because of improved hygiene (which kills off the beneficial bacteria as well as the dangerous ones), or because of stress or antibiotic use. One impact of the dysregulation of normal gut bacterial populations — a phenomenon dubbed “dysbiosis” — may be the rising rate of multiple sclerosis seen in recent years in more hygienic societies.

“As we live cleaner, we’re not just changing our exposure to infectious agents, but we’re changing our relationship with the entire microbial world, both around and inside us, and we may be altering the balance between pro- and anti-inflammatory bacteria,” leading to diseases like MS, Mazmanian says. “Perhaps treatments for diseases such as multiple sclerosis may someday include probiotic bacteria that can restore normal immune function in the gut… and the brain.”

The work was supported by funding from the California Institute of Technology, the Weston Havens Foundation, and the Edward Mallinckrodt, Jr. Foundation.

Sourced & published by Henry Sapiecha

Remedy Disease and Enhance Health

Science (June 28, 2010) — We are what we eat, but who are “we”? New, high-powered genomic analytical techniques have established that as many as 1,000 different single-celled species coexist in relative harmony in every healthy human gut.

“For each human cell in your body there are 10 microbial cells, most of them living in the gut and helping us digest things we can’t digest on our own,” said Justin Sonnenburg, PhD, assistant professor of microbiology and immunology at the Stanford University School of Medicine. “In turn, what you eat is proving to be one of the major determinants of the components of your ‘inner self’ — that community of bacteria living in your intestine.”

Each individual’s microbial ecosystem is different in its relative composition, with potential implications for our health. Disorders such as inflammatory bowel disease, colorectal cancer and even obesity have been linked to skewed intestinal microbe distributions.

Scientists hope that someday they will be able to manipulate microbial populations in the gut as a way of remedying disease and enhancing health. One step toward this goal would be taking “genomic censuses” to categorize and count the interacting components of each individual’s bacterial community and characterize how they respond to interventions, such as changes in diet. That’s no small task, because the aggregate gene count of the micro-organisms dwelling in a typical human gut outnumbers our own by a hundredfold — millions of them, versus the 20,000 human genes that have been identified.

In an animal study to be published June 25 in Cell, Sonnenburg and his colleagues showed that zeroing in on just a small set of bacterial genes, while ignoring the vast majority, allowed them to predict how bugs would respond to a diet change. The results highlight the potential of the burgeoning new field of prebiotics, which (in contrast to probiotics — the seeding of food with healthful bacterial organisms) involves adding substances to the diet in an effort to shift the mix of bugs in our gut in a healthy direction.

In conducting the study, the researchers used a vastly simplified model of the internal mammalian microbial ecosystem to prove that they could predict, by looking at a mere handful of microbial genes, how a shift in diet can alter the microbial composition of the gut. Sonnenburg’s team introduced two distinct species of bacteria, both known to abound in the human digestive tract, into mice that had been raised in a sterile environment and so lack the normally resident microbes — also known as “germ-free” mice. Then they fed the mice a diet rich in a particular complex carbohydrate that one bacterial species seemed genetically better equipped to digest, based on the presence of a small set of genes in its genome. As predicted, that bacterial species became predominant in the mice’s intestines.

These results set the stage for scaling up germ-free mice into living laboratories into which scientists can introduce, one by one, steadily increasing numbers of bacteria found in the human intestine, eventually enabling a sophisticated understanding of the astonishingly complex microbial superorganism that dwells inside each of us.

The complex carbohydrate the Stanford researchers added to the mice’s diet was inulin, which is found in certain bulbous plants — onions, garlic, Jerusalem artichokes — and has gained wide use as a prebiotic supplement (for instance, in yogurt or in powdered form) by people who believe it encourages the proliferation of healthful “good” bacteria. We humans can’t digest inulin on our own, but some bacteria are equipped with genes that encode enzymes capable of sawing through the chemical links joining this substance’s constituent sugar molecules.

“Think of these enzymes as a unique set of utensils that allow them to eat this food we can’t cut,” said Sonnenburg. The byproducts of bacterial metabolism are often valuable nutrients for humans — a win-win situation.

Previous genomic analyses had determined that only one of the two bacterial species the investigators introduced to the germ-free mice featured, among its 5,000 or so genes, a roughly 10-gene assemblage that permits the breakdown of inulin.

The researchers used a standard laboratory technique to precisely assess changes in each of the two species’ relative abundance before and after dietary inulin supplementation. “Within one or two weeks, there was a significant change in the composition of the mice’s gut communities,” said Erica Sonnenburg, PhD, senior research scientist in Justin Sonnenburg’s lab and first author of the study. As predicted, the ratio of inulin-digesting to non-digesting species shifted in favor of the former in the inulin-fed mice.

Both Erica and Justin Sonnenburg (they’re married) warned that it will be a while before the results in this simple experimental system — two competing bacterial species — can be extrapolated to the nearly-1,000-species jungle that is the real, human gut-dwelling microbial community. But the Sonnenburg lab has already embarked on increasing the complexity of their experimental system by increasing the number of human-associated bacteria into germ-free mice that have been “humanized” so that their intestines contain a microbial community similar to that of the human gut.

“We’ve now got germ-free mice to which we’ve introduced batches of bacteria representative of an entire human gut community in all its complexity,” said Erica Sonnenburg. “We’re looking to see if the bugs that we think should do better actually do better in this more competitive environment.”

The study was funded in part by the National Institutes of Health. Other Stanford co-authors were Steven Higginbottom and Payal Joglekar of the Department of Microbiology and Immunology.

Sourced & published by Henry Sapiecha

TRUE / FALSE

1. Only men get bowel cancer.
2. Only people with a family history of bowel cancer need be concerned.
3. There’s nothing you can do to prevent getting bowel cancer.
4. If you feel healthy and don’t have any symptoms then you don’t need to be tested

If you answered FALSE to ALL of these then congratulations!  You’re doing well!

If you answered TRUE to any of these then you need to brush up on your bowel facts!

Read on for more information on each of these statements.

1. Only men get bowel cancer.

Although there is a higher incidence in men, women DO get bowel cancer.  In fact, 1 in 14 women will be diagnosed with bowel cancer before the age of 85. This compares to 1 in 10 for men.

In Queensland in 2006 (the latest statistics available), 2741 people were diagnosed with bowel cancer, 1491 of these were male and 1250 of these were female (Cancer Council Queensland, 2008).

1. Only people with a family history of bowel cancer need be concerned.

Only around 5% of bowel cancers are attributed to a family history. Age and lifestyle choices are the main contributing factors. However, if you do have a family history of bowel cancer, it is important that you speak with your GP.

1. There’s nothing you can do to prevent getting bowel cancer.

While you can never completely eliminate your risk of getting bowel cancer, there are a number of steps you can take to reduce the risk.  It is estimated that up to 75% of bowel cancers could be prevented through leading a healthy lifestyle.  Things like maintaining a healthy body weight, eating well, being active, limiting your alcohol intake and not smoking all contribute to reducing your risk of bowel cancer.

1. If you feel healthy and don’t have any symptoms then you don’t need to be tested.

Bowel cancer often doesn’t show any symptoms until it is further advanced.  ‘Screening’ is about testing people with no symptoms who ‘feel healthy’ to find early signs of disease before it causes harm.  Bowel cancer is actually one of the most treatable cancers if detected early and can be prevented with regular screening.

The Australian Government is currently inviting men and women turning 50, 55 or 65 between 2008 and 2010 to participate in bowel cancer screening. Invitations, which include a simple screening test known as a Faecal Occult Blood Test (FOBT), are being sent directly to people in the mail. People who receive a kit are encouraged to participate.

If you are not yet eligible for the Program and if you have any concerns, speak to your GP about your options.

For more information about bowel cancer or bowel cancer screening phone your local Queensland Bowel Cancer Screening Program team on 1300 766 927 or visit www.health.qld.gov.au/bowelcancer.

Received and published by Henry Sapiecha 17th May 2010

Juicier than the latest celeb gossip and more crisp than HDTV, apples may do a lot more than be the perfect fruit. The type of fibre in apples, called pectin, lowers your colon cancer risk by bumping up colon-protective compounds and clamping down on cancer-causing ones. In the lab, apple pectin increased levels of butyrate, a fatty acid that manages to do this colon-health double duty. That’s fabulous, since colon cancer is the third most common type of cancer for both men and women.

Unlike chocolate cake or entire buckets of wings, apples are one case where you really want to eat the whole thing. In other words, don’t peel it first. If you pitch the skin, you’re ditching compounds called triterpenoids (we’re not going to test you on that), which have strong potential against colon cancer and against breast and liver cancers, too. More reasons to go whole: The peels also contain quercetin, a compound that may bolster your immune system (it may even help stave off the flu when you’re under stress), and that can help defend your body against cardiovascular disease and even Alzheimer’s.

Of course, apples aren’t the only thing you should do to keep your colon cancer risk down. You also need regular screenings. Do an annual Hemoccult test after age 40 (available at pharmacies and not as gross as you think) and colonoscopy screening every 10 years, starting at age 50.

Sourced and published by Henry Sapiecha 7th Oct 2009