It isn’t the job of a bac­terium to make you sick or kill you.  Like all other organ­isms, bac­te­ria just want to sur­vive and pass their genes onto the next generation.

The bac­te­r­ial species that destroys its host wouldn’t last too long.  It would be like a fam­ily that tried to keep warm by set­ting fire to the rug.  Sure, Mom, Dad and the kids could warm their hands for a few min­utes, but before long their house would be a pile of ashes.

If infec­tious bac­te­ria kill the patient, they have no place to live.

That’s why, of the mil­lions of bac­te­ria liv­ing in our diges­tive tract, only the occa­sional few are poten­tial agents of dan­ger­ous infec­tion.  The other 99.99% have evolved over the mil­len­nia to live in har­mony with us.  And we’ve evolved to live in har­mony with them.  In fact, we often derive ben­e­fit from the organ­isms liv­ing inside us.

Sci­en­tists con­tinue to dis­cover new aspects of the mutu­ally sym­bi­otic rela­tion­ship of human and bacterium.

Here’s a new exam­ple of our deep­en­ing wis­dom about the ben­e­fi­cial role of our inter­nal flora, reported in the June 2012 issue of Sci­en­tific Amer­i­can.

About 25 years ago, sci­en­tists dis­cov­ered that pep­tic ulcers were caused by the pres­ence of a par­tic­u­lar species of bac­te­ria – Heli­cobac­ter pylori.  In most cases, once a patient took antibi­otics to wipe out their inter­nal colonies of H. pylori, the ulcers went away.

Antibi­otics became a rou­tine treat­ment for ulcers.  As result, ulcers are a much less com­mon cause of distress.

But lately we’ve learned that there’s more to the story. 

Before the antibi­otic era, col­o­niza­tion of the stom­ach with H. pylori was extremely wide­spread.  Yet only a small frac­tion of peo­ple har­bor­ing the bac­te­ria ever got pep­tic ulcers.   Recently, sci­en­tists have begun to explore the poten­tial upside in our rela­tion­ship with H. pylori.

The first ben­e­fit of H. pylori to be dis­cov­ered is its role in reg­u­lat­ing stom­ach acid.   If the stom­ach churns out too much acid, it isn’t good for you – you get heart­burn and acid reflux.  But it isn’t good for the bac­te­ria either.  To pro­tect itself, H. pylori emits a sig­nal­ing mol­e­cule that turns off stom­ach acid pro­duc­tion when it’s too high.  That’s good for the human host, too.

But there’s more.  Researchers have now dis­cov­ered that H. pylori plays a role in appetite regulation.

Before you eat, your blood­stream has high lev­els of the hunger-signaling hor­mone ghre­lin.  In peo­ple with H. pylori in their stom­ach, ghre­lin lev­els dimin­ish after eat­ing, sig­nal­ing satiety.

But if you’re lack­ing H. pylori, your ghre­lin lev­els remain ele­vated.  You don’t know that you’re full and you keep eating.

Mar­tin Blaser, one of the sci­en­tists lead­ing the research, spec­u­lates that peo­ple with­out H. pylori, such as chil­dren given antibi­otics to treat ear infec­tions, are the most likely to gain weight.

Along with our seden­tary lifestyle, super-sized por­tions of soft drinks and fries, and hormone-laced meat, we might soon be adding antibi­otic use to the list of cul­prits con­tribut­ing to the obe­sity epidemic.

There’s much more we need to know.  But for now, we’re learn­ing that only a few bac­te­ria are pathogens.  It’s not us ver­sus them.  There’s a del­i­cate sym­bio­sis that’s evolved between our hor­monal sig­nal­ing sys­tems and the organ­isms that live inside.

______________________________________

Deepen Your Body of Knowledge

Gut bac­te­ria and fibromyalgia