Gut: The Inside Story of Our Body's Most Underrated Organ (Revised Edition)

by Giulia Enders

  Once inside the bird’s gut, the Salmonellae can multiply, and they are eventually excreted. Since chickens have only one hole for all export goods, the egg cannot avoid coming into contact with Salmonellae in the bird’s feces. The bacteria are then found only on the shells of eggs—they only get inside when the shell is cracked.

  But what about Salmonellae in chicken meat? How do they get there? That’s a rather unsavory story. Cheaply fed chickens are usually sent to large industrial slaughterhouses to meet their maker. Once they have been slaughtered and beheaded, they are dunked in huge tanks of water. Those tanks are like a wellness spa for Salmonella bacteria, complete with a colonic irrigation service for the chickens. In a slaughterhouse dispatching 200,000 birds a day, one batch of cheap-feed chickens is enough to give the gift of Salmonella to all the other birds in the bath. The chickens then end up in the freezers of discount supermarkets. If they are roasted or grilled at high-enough temperatures, the Salmonella germs are soon killed off and can no longer cause problems for anyone.

  Properly cooked meat is normally not the reason for most Salmonella infections. The problems begin when the frozen chicken is left to thaw in the kitchen sink or colander. Freezing and thawing does bacteria little harm. The huge library of bacteria in our laboratory includes germs, collected from patients, that easily survive temperatures of minus 112 degrees Fahrenheit (minus 80 degrees Celsius) and live merrily on when thawed. Heat is their nemesis. Even just ten minutes’ exposure to a temperature of 167 degrees Fahrenheit (75 degrees Celsius) is enough to see off all Salmonella bacteria. That’s why a carefully roasted chicken is not usually the culprit, but rather the lettuce leaves for the side salad, left to soak briefly in the same kitchen sink.

  We come into regular contact with the gut flora of the livestock we keep, but we only notice it when they happen to include unfamiliar, diarrhea-causing bacteria. The rest is routine, so to speak, and after all, we have to get our bacteria from somewhere. Sticking to organic country eggs from chickens fed with home-grown grain is usually a reliable way to avoid dangerous bacteria—unless the farmer himself eats cheap chicken from a discount supermarket.

  If our Sunday roast chicken is not roasted enough, we can end up eating not just chicken muscle cells but a few Salmonella cells, too. It takes between ten thousand and one million of these single-celled creatures to put us out of action. A million of these bacteria take up about one-fifth as much space as a grain of salt. So, how does an army of such tiny soldiers manage to move a colossus like us—with the volume of about 600,000,000 grains of salt—inexorably toward the toilet? It’s as if one hair of the American president’s head were to rule over the entire population of the United States.

  Salmonella bacteria double in number much more quickly than politicians’ hairs—that’s point one. As soon as the temperature rises above 50 degrees Fahrenheit (10 degrees Celsius), Salmonellae come out of hibernation and get busy breeding. They have delicate little arms that enable them to swim around until they find a place to attach to the gut. Once there, they invade our cells, which become infected and pump large quantities of fluid into the gut in an attempt to flush out the pathogen as quickly as possible.

  It can take a few hours to a few days from accidental ingestion to watery flush-out. A self-induced colonic irrigation like this usually works well, unless the victim is too young, too old, or too frail. Antibiotics would do more harm than good here. Despite this natural cure, it is better for the gut to flatly refuse entry to Salmonella, however rude that may seem. After a visit to the toilet or a retching session into a sick bag, you should not take them by the hand and show them what life is like in the outside world. They should be given the cold shoulder by washing with very hot water and soap to let them know: it’s not you, it’s me—I just can’t deal with your clinging personality.

  Salmonellae are the most common type of bad guys we take in with our food. They are not found exclusively in poultry products, but poultry products are one of Salmonellae’s favorite hang-outs. Salmonellae come in several varieties. When we receive stool samples from patients at our laboratory, we can test them by exposing them to different antibodies. When an antibody bonds with the Salmonellae, they clump together into blobs that are big enough to see with the naked eye.

  When that happens, we can say that the antibody to vomit-inducing Salmonella XY reacts strongly, so this must be vomit-inducing Salmonella XY. This is the same as the mechanism in our own body. Our immune system meets a couple of new Salmonellae and says, “Hmmm, I’m sure I must have a hat that fits them somewhere in my collection.” It then rummages around in its wardrobes to find the right hat, adjusts it a little to create the perfect fit, then commissions a hatter to make headgear for a million Salmonella germs. When all the Salmonella bacteria are wearing their new hats, they no longer look dangerous, but rather ridiculous. They are weighed down so much by the millinery that they are too heavy to swim around attacking anything. In this way, the test antibodies in the lab can be seen as a small selection of different hats. When the hat fits, the heavily sombreroed bacteria collapse into clumps and—depending on the hat—we can say which type of Salmonella was in the stool sample.

  For those who do not necessarily want to send their immune system searching for hats and who are no great fans of diarrhea and vomiting, there are a few simple rules to follow.

  Rule number one: Always use plastic chopping boards because they are easier to clean properly and provide fewer grooves and ridges for bacteria to hide in.

  Rule number two: Always wash anything that comes into contact with raw meat or eggshells thoroughly with hot water—chopping boards, hands, cutlery, kitchen sponges, and colanders, for example.

  Rule number three: Whenever possible make sure that meat and egg-based foods are cooked through. Of course, that doesn’t mean you have to interrupt your romantic dinner to stick the tiramisu in the microwave. If you are planning a dish of that sort, make sure you always use good-quality, fresh eggs and always store them at a temperature of less than 50 degrees Fahrenheit (10 degrees Celsius).

  Rule number four: Think beyond the kitchen. Anyone who has had to rush to the toilet after feeding their pet iguana and then themselves (without washing their hands properly) will remember my words: Salmonella bacteria are part of the normal gut flora of reptiles.

  Helicobacter pylori—Humanity’s First Pet

  THOR HEYERDAHL WAS a phlegmatic man with strongly held views. He observed ocean currents and winds. He was interested in ancient fishhooks and clothing made of tree bark. All this convinced him that the Polynesian islands were first colonized by seafarers from South America and Southeast Asia. He theorized that they could have used currents to help them reach the islands on rafts. At the time, no one thought it possible that a simple raft could survive a five-thousand-mile journey (eight thousand kilometers) across the Pacific. Heyerdahl was not a man to waste time trying to convince doubters with theoretical arguments. He went to South America, built a primitive raft out of balsawood logs, grabbed a couple of coconuts and cans of pineapple, and set out for Polynesia. After four months, he could safely say, “Yes, it is possible!”

  Thirty years later, another scientist set off on an equally exciting expedition. But his journey did not take him across oceans; it took him to a small laboratory with neon strip lighting on the ceiling. There, Barry Marshall picked up a petri dish of liquid, placed it to his lips, and bravely swallowed its contents. His colleague observed him with interest as he did so. After a few days, Barry Marshall developed a stomach inflammation and could proudly say, “Yes, it is possible!”

  Another thirty years went by before scientists in Berlin and Ireland made a connection between the research of these two very different pioneers. Marshall’s stomach bug was destined to provide information about the first colonization of Polynesia. This time no one sailed an ocean and no one drank a lab culture. Researchers asked a few desert-dwelling Aboriginals in Australia and highland tribesmen from New Guinea for a s
ample of their stomach contents.

  It is a story about disproving prevailing paradigms, dedication to research, a tiny creature with a propeller, and a big, hungry cat.

  The bacterium Helicobacter pylori lives in the stomachs of at least half of humankind. This insight is relatively new and was initially ridiculed. Why should an organism live in such an inhospitable environment? A cave full of acid and enzymes bent on breaking it down? It takes more than that to discourage Helicobacter pylori. This bacterium has developed two strategies that enable it to cope excellently with that harsh environment.

  Firstly, the products of its metabolism are so alkaline that they can neutralize any acid in its immediate vicinity. Secondly, it burrows beneath the mucus membrane that protects the stomach from digesting itself with its acidic juices. This membrane usually has a gelatinous consistency, but H. pylori is able to liquefy it so that it can swim more easily through the mucoid lining. It has long threads of proteins it uses as flagella to whizz around.

  Marshall and Warren believed H. pylori caused stomach inflammations (gastritis) and gastric ulcers. The prevailing scientific opinion at the time was that those stomach problems were psychosomatic in origin (as a result of stress, for example) or caused when the stomach secreted too much acid. Marshall and Warren had to both counter the preconception that nothing could survive in the acid environment of the stomach and prove that a tiny bacterium could cause diseases that were not traditional bacterial infections. Until that time, it was believed that bacteria could only infect wounds, and cause fevers and colds.

  After the otherwise healthy Marshall deliberately swallowed H. pylori bacteria and gave himself gastritis, which cleared up after a course of antibiotics, it took another ten years before the scientific world accepted his discovery. Today, it is standard practice to test patients with stomach complaints for the presence of these bacteria. The patient is given a fluid to drink and if H. pylori bacteria are present in the stomach, they break down the ingredients of the fluid and a marked, odorless gas can be identified in the breath of the patient using a special machine. Drink, wait, breathe. A relatively simple test.

  What the two scientists did not realize is that they had not only discovered a cause of illness, they had also discovered one of humankind’s oldest pets. H. pylori bacteria have been living inside human beings for more than fifty thousand years, and they have evolved in tandem with us. When our ancestors began to migrate around the world, H. pylori went along for the ride and founded new populations, just like those human pioneers. Today, three African, two Asian, and one European type of this bacterium have been identified. The farther the population groups spread from each other in both space and time, the greater the difference between their stomach bacteria.

  The slave trade transported the African types to America. In northern India, the Buddhist and Muslim populations have different strains in their stomachs. Families in industrialized nations often have their own family strain of H. pylori, while people living in societies with more contact between individuals, for example, in parts of Africa, have communal H. pylori strains.

  One out of four North Americans is a carrier for H. pylori. Not everyone who carries it in their stomach is doomed to develop stomach problems, but most people who do have stomach problems have H. pylori to thank for their woes. This is because some H. pylori bacteria are more dangerous than others. Two factors are known to be responsible for the more virulent version. One is called CagA. CagA enables the bacteria to inject certain substances into our cells like a tiny syringe. The second factor is called VacA. VacA needles the cells of the stomach continuously, causing them damage that is eventually fatal to the cell. There is a much higher probability of developing stomach problems if the H. pylori microbes in the stomach possess the injecting-syringe or cell-damaging gene. If those genes are not present, H. pylori is much less harmful as it swims around in the stomach.

  Although they share many similarities, each H. pylori bacterium is as unique as the person carrying it. These bacteria adapt to their host and change as she changes. Scientists can make use of this fact to trace who infected whom with the germ. Big cats have their own feline Helicobacter. Its name is Helicobacter acinonychis. The fact that it bears such a resemblance to human Helicobacter raises the question: who was eating whom in prehistoric times? Was it a case of man eating tiger or tiger eating man?

  Genetic analysis shows that the genes that were deactivated in the feline version of the bacterium were mainly those that would otherwise enable it to latch on to the cells of the human stomach—but the reverse was not the case. When devouring a prehistoric person, a large cat must also have devoured that person’s stomach bacteria. These bacteria are not killed by even the sharpest of tiger teeth, so Helicobacter colonized the stomach of the predator and its descendants. A tiny bit of redress, at least.

  But is H. pylori good or bad?

  H. pylori Is Bad

  BY INFILTRATING OUR stomach’s mucus membrane and swimming around in it, H. pylori weakens this protective barrier. As a result, the aggressive acids in our stomach digest not only our food, but a little bit of our own stomach, as well. If the bacteria also possess the injection-syringe or cell-damaging gene, our stomach cells have little hope. About one-fifth of people who harbor this bacterium develop tiny lesions in their stomach wall. Two-thirds of stomach ulcers and almost all ulcers in the small intestine are caused by an H. pylori infection. If the microbes can be wiped out with antibiotics, the patient’s stomach problems disappear. A new product could soon provide an alternative to antibiotics: sulforaphane, which is contained in broccoli and similar vegetables. This substance is able to block the enzyme that H. pylori uses to neutralize gastric acid. Those who would like to try it as an alternative to antibiotics should make sure they use very high-quality broccoli and consult their doctor after two weeks to test whether their H. pylori population has really disappeared.

  Constant irritation is never a good thing. We are all familiar with itchy insect bites. At some point we can no longer resist scratching them to make the itching stop, even though we know we will end up with a bleeding wound. Something similar happens with the cells of the stomach. A chronic inflammation means the cells are permanently irritated until they finally give up the ghost and break down. In older people, this can also be a cause of appetite loss.

  The stomach has a battery of stem cells, which constantly replace lost cells. If these replacement manufacturers are overworked, they may begin to make mistakes. Cancer cells are the result. Statistically, this does not look too serious: around 1 percent of H. pylori carriers develop stomach cancer. But if you bear in mind that half of humanity harbor these bacteria in their stomach, 1 percent turns out to be a pretty big number. The probability of developing stomach cancer without the presence of H. pylori is about forty times less than with it.

  In 2005, Marshall and Warren received a Nobel Prize for their discovery of the connection between Helicobacter pylori and gastritis, stomach ulcers, and cancer. The journey from bacteria cocktail in Perth to celebratory cocktail in Stockholm took twenty years.

  It took even longer for the connection between Helicobacter pylori and Parkinson’s disease to be realized. Although doctors had known since the 1960s that patients with Parkinson’s have an increased incidence of stomach problems, they did not know the nature of the connection between sore stomachs and trembling hands. It took a study of different population groups on the Pacific island of Guam to shed light on the subject.

  In some parts of the island, there was an astonishingly high incidence of Parkinson’s-like symptoms among the population. Those affected suffered from trembling hands, facial paralysis, and motor problems. Researchers realized that the symptoms were most common in areas where people’s diets included cycad seeds. These seeds contain neurotoxins—substances that damage the nerves. H. pylori can produce an almost identical substance. When laboratory mice were fed with an extract of the bacteria, without being infected with the living bac
terium itself, they displayed symptoms very similar to those of the cycad-eating Guamanians. Once again, not every H. pylori bacterium produces this substance, but for those people who harbor the ones that do, it is not good news.

  In summary, it can be said that H. pylori can manipulate our protective barriers, irritate and destroy our cells, and manufacture toxins and damage our entire body by doing so. So, how has our vulnerable body been able to survive many millennia of infection with this bad bacterium? Why have these bacteria been so widely tolerated by our immune system for so long?

  H. pylori Is Good

  A LARGE-SCALE STUDY of H. pylori and its effects reached the following conclusion. The bacterium, especially that much-feared strain with the injection-syringe gene, can also interact with the body in beneficial ways. After more than twelve years of observing over ten thousand subjects, it was concluded that carriers of this type of H. pylori do have an increased risk of stomach cancer, but their risk of dying of lung cancer or a stroke was much lower. In fact, it was only half that of other subjects in the study.