"Gluten, one of the most heavily consumed proteins on earth, is created when two molecules, glutenin and gliadin, come into contact and form a bond. When bakers knead dough, that bond creates an elastic membrane, which is what gives bread its chewy texture and permits pizza chefs to toss and twirl the dough into the air. Gluten also traps carbon dioxide, which, as it ferments, adds volume to the loaf. Humans have been eating wheat, and the gluten in it, for at least ten thousand years. For people with celiac disease—about one per cent of the population—the briefest exposure to gluten can trigger an immune reaction powerful enough to severely damage the brushlike surfaces of the small intestine. People with celiac have to be alert around food at all times, learning to spot hidden hazards in common products, such as hydrolyzed vegetable protein and malt vinegar. Eating in restaurants requires particular vigilance. Even reusing water in which wheat pasta has been cooked can be dangerous."
"But something strange is clearly going on. For reasons that remain largely unexplained, the incidence of celiac disease has increased more than fourfold in the past sixty years. Researchers initially attributed the growing number of cases to greater public awareness and better diagnoses. But neither can fully account for the leap since 1950. Murray and his colleagues at the Mayo Clinic discovered the increase almost by accident. Murray wanted to examine the long-term effects of undiagnosed celiac disease. To do that, he analyzed blood samples that had been taken from nine thousand Air Force recruits between 1948 and 1954. The researchers looked for antibodies to an enzyme called transglutaminase; they are a reliable marker for celiac disease. Murray assumed that one per cent of the soldiers would test positive, matching the current celiac rate. Instead, the team found the antibodies in the blood of just two-tenths of one per cent of the soldiers. Then they compared the results with samples taken recently from demographically similar groups of twenty- and seventy-year-old men. In both groups, the biochemical markers were present in about one per cent of the samples.
“That suggested that whatever has happened with celiac disease has happened since 1950,’’ Murray said. “The increase affected young and old people equally.” These results imply that the cause is environmental."
"Gluten anxiety has been building for years, but it didn’t become acute until 2011, when a group led by Peter Gibson, a professor of gastroenterology at Monash University and the director of the G.I. unit at the Alfred Hospital, in Melbourne, seemed to provide evidence that gluten was capable of causing illness even in people who did not have celiac disease. Gibson and his colleagues recruited thirty-four people with irritable-bowel syndrome, all of whom had complained of stomach ailments that largely disappeared when they stopped eating gluten. He put them all on a strictly monitored gluten-free diet, but, unbeknownst to the subjects, about half got muffins and bread with gluten. It was a double-blind study, so neither the doctors nor the patients knew which muffins and bread contained gluten. But most of those who ate the gluten reported that the pain returned; for most of the others it did not. The study was small but meticulous, and the results were compelling. Several similar studies are now under way, but dietary research is notoriously time-consuming and difficult.
Gibson published his findings in the American Journal of Gastroenterology, but, along with other experts, he urged restraint in interpreting data from such a small study. Nevertheless, millions of people with vague symptoms of gastric distress suddenly found something concrete for which to blame their troubles. The market boomed, but the essential mystery remained unsolved: Why was gluten suddenly so hazardous? Perhaps, researchers thought, farmers had increased the protein (and gluten) content of wheat so drastically that people could no longer digest it properly.
But there is more to wheat than gluten. Wheat also contains a combination of complex carbohydrates, and the Australian team wondered if these could be responsible for the problems. Gibson and his colleagues devised a different study: they recruited a group of thirty-seven volunteers who seemed unable to digest gluten properly. This time, the researchers attempted to rule out the carbohydrates and confirm gluten as the culprit. Gibson put all the volunteers on a diet that was gluten-free and also free of a group of carbohydrates that he and his colleagues called FODMAPs, an acronym for a series of words that few people will ever remember: fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. Not all carbohydrates are considered FODMAPs, but many types of foods contain them, including foods that are high in fructose, like honey, apples, mangoes, and watermelon; dairy products, like milk and ice cream; and fructans, such as garlic and onions.
Most people have no trouble digesting FODMAPs, but these carbohydrates are osmotic, which means that they pull water into the intestinal tract. That can cause abdominal pain, bloating, and diarrhea. When the carbohydrates enter the small intestine undigested, they move on to the colon, where bacteria begin to break them down. That process causes fermentation, and one product of fermentation is gas. In Gibson’s new study, when the subjects were placed on a diet free of both gluten and FODMAPs, their gastrointestinal symptoms abated. After two weeks, all of the participants reported that they felt better. Some subjects were then secretly given food that contained gluten; the symptoms did not recur. The study provided evidence that the 2011 study was wrong—or, at least, incomplete. The cause of the symptoms seemed to be FODMAPs, not gluten; no biological markers were found in the blood, feces, or urine to suggest that gluten caused any unusual metabolic response.
In fact, FODMAPs seem more likely than gluten to cause widespread intestinal distress, since bacteria regularly ferment carbohydrates but ferment protein less frequently. Although a FODMAP-free diet is complicated, it permits people to eliminate individual foods temporarily and then reintroduce them systematically to determine which, if any, are responsible for their stomach problems. FODMAPs are not as trendy as gluten and not as easy to understand. But, biologically, their role makes more sense, Murray says.
“That first paper, in 2011, blew our minds,” Murray told me. “Essentially, it said that people are intolerant of gluten, and it was based on a well-designed, double-blind study. When people were challenged with gluten, by eating the muffins, they got sick. We just couldn’t figure it out. But then came the second study. By then, it was almost too late to put the genie back in the bottle. You have millions of people out there completely convinced that they feel better when they don’t eat gluten—and they don’t want to hear anything different.”"
First, a first piece of research establishes an increase in celiac disease since the 50ies:
"But something strange is clearly going on. For reasons that remain largely unexplained, the incidence of celiac disease has increased more than fourfold in the past sixty years. Researchers initially attributed the growing number of cases to greater public awareness and better diagnoses. But neither can fully account for the leap since 1950. Murray and his colleagues at the Mayo Clinic discovered the increase almost by accident. Murray wanted to examine the long-term effects of undiagnosed celiac disease. To do that, he analyzed blood samples that had been taken from nine thousand Air Force recruits between 1948 and 1954. The researchers looked for antibodies to an enzyme called transglutaminase; they are a reliable marker for celiac disease. Murray assumed that one per cent of the soldiers would test positive, matching the current celiac rate. Instead, the team found the antibodies in the blood of just two-tenths of one per cent of the soldiers. Then they compared the results with samples taken recently from demographically similar groups of twenty- and seventy-year-old men. In both groups, the biochemical markers were present in about one per cent of the samples.
“That suggested that whatever has happened with celiac disease has happened since 1950,’’ Murray said. “The increase affected young and old people equally.” These results imply that the cause is environmental."
But this has to be contrasted with the much larger fraction of the population claiming that they are gluten intolerant. An there, it seems that research has played an unfortunate role...:
"Gluten anxiety has been building for years, but it didn’t become acute until 2011, when a group led by Peter Gibson, a professor of gastroenterology at Monash University and the director of the G.I. unit at the Alfred Hospital, in Melbourne, seemed to provide evidence that gluten was capable of causing illness even in people who did not have celiac disease. Gibson and his colleagues recruited thirty-four people with irritable-bowel syndrome, all of whom had complained of stomach ailments that largely disappeared when they stopped eating gluten. He put them all on a strictly monitored gluten-free diet, but, unbeknownst to the subjects, about half got muffins and bread with gluten. It was a double-blind study, so neither the doctors nor the patients knew which muffins and bread contained gluten. But most of those who ate the gluten reported that the pain returned; for most of the others it did not. The study was small but meticulous, and the results were compelling. Several similar studies are now under way, but dietary research is notoriously time-consuming and difficult.
Gibson published his findings in the American Journal of Gastroenterology, but, along with other experts, he urged restraint in interpreting data from such a small study. Nevertheless, millions of people with vague symptoms of gastric distress suddenly found something concrete for which to blame their troubles. The market boomed, but the essential mystery remained unsolved: Why was gluten suddenly so hazardous? Perhaps, researchers thought, farmers had increased the protein (and gluten) content of wheat so drastically that people could no longer digest it properly.
But there is more to wheat than gluten. Wheat also contains a combination of complex carbohydrates, and the Australian team wondered if these could be responsible for the problems. Gibson and his colleagues devised a different study: they recruited a group of thirty-seven volunteers who seemed unable to digest gluten properly. This time, the researchers attempted to rule out the carbohydrates and confirm gluten as the culprit. Gibson put all the volunteers on a diet that was gluten-free and also free of a group of carbohydrates that he and his colleagues called FODMAPs, an acronym for a series of words that few people will ever remember: fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. Not all carbohydrates are considered FODMAPs, but many types of foods contain them, including foods that are high in fructose, like honey, apples, mangoes, and watermelon; dairy products, like milk and ice cream; and fructans, such as garlic and onions.
Most people have no trouble digesting FODMAPs, but these carbohydrates are osmotic, which means that they pull water into the intestinal tract. That can cause abdominal pain, bloating, and diarrhea. When the carbohydrates enter the small intestine undigested, they move on to the colon, where bacteria begin to break them down. That process causes fermentation, and one product of fermentation is gas. In Gibson’s new study, when the subjects were placed on a diet free of both gluten and FODMAPs, their gastrointestinal symptoms abated. After two weeks, all of the participants reported that they felt better. Some subjects were then secretly given food that contained gluten; the symptoms did not recur. The study provided evidence that the 2011 study was wrong—or, at least, incomplete. The cause of the symptoms seemed to be FODMAPs, not gluten; no biological markers were found in the blood, feces, or urine to suggest that gluten caused any unusual metabolic response.
In fact, FODMAPs seem more likely than gluten to cause widespread intestinal distress, since bacteria regularly ferment carbohydrates but ferment protein less frequently. Although a FODMAP-free diet is complicated, it permits people to eliminate individual foods temporarily and then reintroduce them systematically to determine which, if any, are responsible for their stomach problems. FODMAPs are not as trendy as gluten and not as easy to understand. But, biologically, their role makes more sense, Murray says.
“That first paper, in 2011, blew our minds,” Murray told me. “Essentially, it said that people are intolerant of gluten, and it was based on a well-designed, double-blind study. When people were challenged with gluten, by eating the muffins, they got sick. We just couldn’t figure it out. But then came the second study. By then, it was almost too late to put the genie back in the bottle. You have millions of people out there completely convinced that they feel better when they don’t eat gluten—and they don’t want to hear anything different.”"
