evidence then at all about ulcers. It was only in the next two years,after other scientists had confirmed that there was indeed an association of the microbe with gastritis and ulcer disease,that I decided to see if I could make some contributions to understanding the nature of GCLO (which in 1989 was renamed Helicobacter pylori after genetic analysis revealed it to be in a separate genus from Campylobacter).Their relationship is a bit like that of lions (Panthera leo)and house cats (Felis catus):relatives for sure but far enough apart to be in different genera.My lab developed a blood test for the microbe and showed that if you carry it,your body has natural defenses against it. To their great credit,Marshall and his research partner,Robin Warren, conducted clinical studies that showed that eradicating H.pylori with antibiotics cured ulcers.Others confirmed and extended their observations.Marshall and Warren went on to win the 2005 Nobel Prize in Physiology or Medicine for this work Meanwhile,physicians everywhere commenced an all-out war against H pylori by prescribing antibiotics to anyone with gastric discomfort.Their mantra ultimately became"the only good H.pylori is a dead H.pylori."I too had been on this same bandwagon for almost a decade. But by the mid-1990s,I began to change my mind.Evidence was beginning to suggest that H.pylori is a member of our normal gut flora and plays a critical role in our health.It was only when I let go of the dogma proclaiming that"gastritis is bad"that I was able to re-evaluate the biology of H.pylori.Yes,H.pylori can be very harmful to some adults,but later we found that it may be very beneficial to many of our children.Eliminating it may be causing more harm than good.The details of my transition and the reasons for it are laid out in chapters 9,10,and 11. In 2000 I moved to New York University and set up a laboratory dedicated to studying how this ancient bacterium did its business in our stomach and what were the consequences to us.Over the following fourteen years,I have accumulated more and more evidence that the disappearance of this venerable microbe might be contributing to our current epidemics.And H.pylori led me to a broader study:the human microbiome itself. These days my lab is bustling We are currently working on more than twenty projects,looking at how antibiotics affect resident microbes and their hosts,in both mice and humans.In a typical animal experiment,we give mice antibiotics in their drinking water and compare them to mice that do not get the medication.We start very early in life,sometimes just before birth,and then we let the mice grow. studying how fat they become,how their livers are working,how immunity is developing in their gut,how their bones are growing and what happens to their hormones and to their brains. To us,the work is exciting,because in each of those areas we can see changes induced by early-life exposure to antibiotics.We have realized that early life is aevidence then at all about ulcers. It was only in the next two years, after other scientists had confirmed that there was indeed an association of the microbe with gastritis and ulcer disease, that I decided to see if I could make some contributions to understanding the nature of GCLO (which in 1989 was renamed Helicobacter pylori after genetic analysis revealed it to be in a separate genus from Campylobacter). Their relationship is a bit like that of lions (Panthera leo) and house cats (Felis catus): relatives for sure but far enough apart to be in different genera. My lab developed a blood test for the microbe and showed that if you carry it, your body has natural defenses against it. To their great credit, Marshall and his research partner, Robin Warren, conducted clinical studies that showed that eradicating H. pylori with antibiotics cured ulcers. Others confirmed and extended their observations. Marshall and Warren went on to win the 2005 Nobel Prize in Physiology or Medicine for this work. Meanwhile, physicians everywhere commenced an all-out war against H. pylori by prescribing antibiotics to anyone with gastric discomfort. Their mantra ultimately became “the only good H. pylori is a dead H. pylori.” I too had been on this same bandwagon for almost a decade. But by the mid-1990s, I began to change my mind. Evidence was beginning to suggest that H. pylori is a member of our normal gut flora and plays a critical role in our health. It was only when I let go of the dogma proclaiming that “gastritis is bad” that I was able to re-evaluate the biology of H. pylori. Yes, H. pylori can be very harmful to some adults, but later we found that it may be very beneficial to many of our children. Eliminating it may be causing more harm than good. The details of my transition and the reasons for it are laid out in chapters 9, 10, and 11. In 2000 I moved to New York University and set up a laboratory dedicated to studying how this ancient bacterium did its business in our stomach and what were the consequences to us. Over the following fourteen years, I have accumulated more and more evidence that the disappearance of this venerable microbe might be contributing to our current epidemics. And H. pylori led me to a broader study: the human microbiome itself. These days my lab is bustling. We are currently working on more than twenty projects, looking at how antibiotics affect resident microbes and their hosts, in both mice and humans. In a typical animal experiment, we give mice antibiotics in their drinking water and compare them to mice that do not get the medication. We start very early in life, sometimes just before birth, and then we let the mice grow, studying how fat they become, how their livers are working, how immunity is developing in their gut, how their bones are growing, and what happens to their hormones and to their brains. To us, the work is exciting, because in each of those areas we can see changes induced by early-life exposure to antibiotics. We have realized that early life is a 14