Zoobiquity

  Farmers fattening chickens for meat have experimented with manipulating their weight through light exposure. In a study reported by the World Poultry newsletter, broiler hens “subjected to dim lighting were around 70g heavier than those in bright light.”

  And think about the Brookfield alligators. What changes for them in October and April isn’t their job. They aren’t suddenly being forced to stay awake or work a double shift. And it’s not temperature. The alligators are in a temperature-controlled enclosure. It’s light that makes them start and stop eating.

  Studies have shown that disrupting circadian rhythms by even one hour during the switch to daylight saving time may increase depression, traffic accidents, and heart attacks. These rhythms affect consumption and metabolism in animals—it is hard to imagine that they aren’t also playing a role in human appetites as well. Controlling environmental light with lamps, TVs, and computers gives us incredible flexibility and productivity. But it interrupts daily and yearly cycles that were billions of years in the making and are shared by countless creatures on our planet.†

  Global factors like circadian rhythms can influence an animal’s internal clock and govern when and how much it eats. But another set of even more intriguing and powerful processes are going on, out of sight, deep inside animals’ bodies. While silent and unseen, these internal drivers illuminate a mystery of variable weight gain: why the very same piece of food can be processed differently by two neighbors, two relatives, or even by the same animal at various times of the year.

  Some animal intestines perform an amazing trick. They expand and contract like accordions. This may not sound all that impressive, but its effect on weight can be profound. It allows the body to absorb varying quantities of calories from the same food, depending on the task at hand.

  The mechanism is simple: a ribbon of muscle running the length of the intestine allows it to contract and expand. When guts are clenched, they’re shorter, tighter, and smaller. When relaxed, they’re elongated.

  When intestines are in the longer, stretched-out mode, they expose more surface area to the food passing over them. This allows the cells to extract more nutrients and, therefore, energy. When the intestines shrink back to their shortened state, some of the food passes by essentially unused.

  The guts of some small songbirds increase by 25 percent during the weeks right before they migrate, when fattening quickly is crucial to power their journey. Similarly, the intestinal surface area of certain grebes and waders nearly doubles during premigration feeding. When they’ve fattened enough to fuel a long flight, the birds’ intestines shrink back down again.

  The ability to lengthen and shorten intestines has also been observed in fish, frogs, and mammals, including squirrels, voles, and mice. Jared Diamond, a UCLA physiologist and author, has studied python guts for clues to how these snakes can go months between meals. Like those of birds and small mammals, pythons’ intestines are dynamic, responsive organs, able to dramatically increase in size depending on what and when food is passing through.

  Animals may be doing “naturally” what we spend tens of thousands of dollars to accomplish with bariatric surgeries that cut out or bypass parts of the stomach or small intestine. In us, as in other animals, less “gut” means fewer calories and nutrition absorbed. For animals, it isn’t surgery but, rather, muscular action—triggered by certain foods, seasonal cues, and other unknown factors that expand and contract the gastrointestinal region.

  Could a similar accordion-like lengthening and shortening in human intestines underlie some unexplained weight gain in our species? Unfortunately, there’s little direct research on when and whether our guts pull off this same trick. But there are intriguing clues. Our intestines are also lined with smooth muscle. And we know from autopsies that human intestines are some 50 percent longer after death, when smooth muscle control is no longer exerted. Perhaps, during life, dynamic muscle activity allows the human intestine to vary its calorie-absorbing length in response to medications, hormones, and even stress—factors frequently pointed to when weight inexplicably increases even when a patient isn’t eating more. Many common drugs cause undesired weight gain through unclear mechanisms. It’s intriguing to consider whether the smooth muscle effects of these drugs contribute to a songbird-like intestinal stretch leading to greater calorie absorption and weight gain.

  But besides the astonishing physiology that makes our guts dynamic, animal intestines hold another key to the complex issue of weight. Within them is a universe invisible to the naked eye that scientists are just beginning to explore and understand.

  Deep inside every animal colon, ours included, thrives an entire cosmos of creatures more strange and wondrous than any dreamed up in a Hollywood special effects lab. There are whip-tailed bacteria and tripod-legged viruses, frilled fungi and microscopic worms. Trillions of these invisible creatures make our intestines their home—a dark, teeming world scientists call the microbiome. Our skin, mouths, teeth (and even areas once thought to be sterile, like the lungs) so swarm with invisible creatures that as few as one out of every ten cells in our bodies may actually be human. The rest are much smaller microbes. So profound is this colonization that some geneticists call adult humans “superorganisms,” meaning our cells plus those of all the creatures living within our bodies. Each of us is like a coral reef, an individual microhabitat harboring unique combinations of unseen wild inhabitants.‡

  In general, we should be grateful that these trillions of minuscule bugs and plants want to live in our guts. Many of them break down our food and prepare nutrients for our cells to absorb—processes human cells cannot do on their own. Microbiologists are only just starting to explore how human gene sequences interact with those of all our microbial residents. They’re finding that these colonies of aliens might not only influence how we digest and metabolize but even drive us to choose or crave certain foods.

  It turns out that within our microbiomes there are two dominant groups of bacteria: the Firmicutes and the Bacteroidetes. In the early 2000s, geneticists at Washington University in St. Louis, were looking at how these bacteria break down food we can’t digest on our own. And the geneticists made an interesting discovery.

  Obese humans had a higher proportion of Firmicutes in their intestines. Lean humans had more Bacteroidetes. As the obese humans lost weight over the course of a year, the microflora in their guts started looking more like those of lean individuals—with Bacteroidetes outnumbering Firmicutes.

  When the researchers looked at mice, they found the same thing. Obese mice had more intestinal Firmicutes. Interestingly, these fat mice produced feces that had fewer calories left in them than the feces of lean mice—suggesting that the obese mice were somehow absorbing more energy from the same amount of mouse chow. This led the researchers to suspect that the Firmicutes are superefficient at mining calories from food passing through the digestive tract. As a December 2006 Nature article about the study put it, “The bacteria in obese mice seemed to assist their host in extracting extra calories from ingested food that could then be used as energy.”

  What this means is that a booming Firmicute colony might help harvest, say, one hundred calories from one person’s apple. That person’s friend may have a dominant Bacteroidetes population that would extract only seventy calories from the same apple. This could be one factor in why your co-worker can eat twice as much as everyone else but never seems to gain a pound.

  If our personal “house blends” of gut bacteria influence the amount of energy we extract from food, then diet and exercise may not be the only factors driving weight gain and loss. The effects of the microbiome challenge the once-unassailable calories-in, calories-out paradigm.§

  In fact, veterinarians have long recognized the power of the microbiome over an animal’s metabolic function.‖ In ruminants and other so-called gut fermenters, such as horses, turtles, and even some apes, nutrition and digestion simply cannot function without the proper balance of microorganisms. Al
though I learned almost nothing about the power of gut flora during medical school, Brookfield Zoo nutritionist Jennifer Watts related to me a core principle emphasized to her during her nutrition training: “Feed the gut bugs first, then the animal.” She does it by making sure animals are fed a healthy balance of browse (fresh leafy greens) and silage (partly fermented vegetation). Could it be that eating vegetables is good for us not only for the fiber they provide but because they nourish colonies of beneficial microflora in our intestines? Perhaps we’re in effect feeding our gut bugs every time we eat a salad.

  The power of the microbiome is well known to another group of veterinarians, the ones who oversee the care of animals we make fat on purpose: livestock. Nowadays, it’s common for factory farming operations to administer antibiotics to food animals from fifteen-hundred-pound steers to one-ounce baby chicks. The effect of those antibiotics on the living colonies of gut bugs in the animals’ intestines may hold a profound clue to the human obesity epidemic.

  I’d long known that antibiotics are used in farming to stop the spread of certain diseases, especially under cramped and stressful living conditions. But antibiotics don’t kill just the bugs that make animals sick. They also decimate beneficial gut flora. And these drugs are routinely administered even when infection is not a concern. The reason may surprise you. Simply by giving antibiotics, farmers can fatten their animals using less feed. The scientific jury is still out on exactly why these antibiotics promote fattening, but a plausible hypothesis is that by changing the animals’ gut microflora, antibiotics create an intestine dominated by colonies of microbes that are calorie-extraction experts. This may be why antibiotics act to fatten not just cattle, with their multistomached digestive systems, but also pigs and chickens, whose GI tracts are more similar to ours.

  This is a really key point: antibiotic use can change the weight of farm animals. It’s possible that something similar occurs in other animals—namely, us. Anything that alters gut flora, including but not limited to antibiotics, has implications not only for body weight but for other elements of our metabolism, such as glucose intolerance, insulin resistance, and abnormal cholesterol. And don’t forget the trillions of creatures making up our microbiomes are constantly interacting in complex ways with one another. They have oscillators that respond to circadian rhythms. The dynamic population of that tiny, contained universe exerts more influence over metabolism than physicians have ever suspected.

  When the Firmicutes/Bacteroidetes study appeared in Nature, it sparked an interest in other obesity risk factors that are less obviously under our control than diet and exercise. Blogs were soon buzzing about a different study showing that having a fat friend increases a person’s chance of becoming overweight himself. The Harvard medical sociologist Nicholas Christakis and U.C. San Diego scientist James Fowler were describing a “contagion” of social habits and practices. Your fat friend’s bad food choices and exercising habits could influence your own willpower and attitude toward food. Christakis and Fowler were quick to explain that the finding was not literal but symbolic. You couldn’t catch the “fat flu” from an ill-aimed sneeze in the waiting room of a lap band clinic. Rather, what was “infectious” was other people’s attitudes toward eating.

  But when I studied the animal literature, I learned that infectious obesity may not be solely metaphorical. According to some experts, it is altogether literal and real. Nikhil Dhurandhar, a nutrition and food scientist at Wayne State University, in Detroit, explains: “It has been proven that animals became obese when infected with certain viruses.” He calls it “infectobesity.” Dhurandhar reports that seven viruses and a prion have been linked with obesity in animals as varied as chickens, horses, lions, and rats. That’s right: infectious weight gain, spread or facilitated by microscopic pathogens.

  On the hottest days between mid-May and late August, alongside one of the many ponds around State College, Pennsylvania, chances are good you’ll spy a tall, thin biologist creeping through the cattails in khaki shorts and a battered cap. He’ll be crouched, moving in barely perceptible super slo-mo. Suddenly, with an expert forehand swing, he’ll swipe a wood-handled net through a stand of reeds or bulrushes. (The move, he explains, is similar to a lacrosse catch or a tennis stroke, which is why he likes to hire grad students who’ve played these sports before.) Nipping the mesh shut with his free hand, he’ll peek inside to see if he captured his quarry: Libellula pulchella, the twelve-spotted skimmer dragonfly.

  James Marden is an entomologist and professor of biology at Penn State University. For more than two decades at ponds in central Pennsylvania he has studied the flight mechanics of dragonfly wings. He told me that these insects are among the fittest animals on Earth, extraordinarily lean and muscular. Over 300 million years, dragonflies have evolved so perfectly to the acrobatic demands of hovering, bobbing, and looping the loop that Marden calls them “world-class, elite animal athletes.”

  Usually dragonflies are pugnacious and extremely territorial, always up for a skirmish with another male. When two meet, they zoom at each other in belligerent, balletic aerial combat that ends with the loser being chased off. Some males, however, loiter on the outskirts of the action. Instead of spoiling for fights and flying straight into brawls, they “glide”—easing their way past challengers without coming to blows, as if to say, “I’m just passing through. No problem. Pay no attention to me. I was just leaving.”

  In the early 2000s, intrigued by this behavior, and whether it might have something to do with muscle performance, Marden collected some of these slower, evasive dragonflies. And when he got them back to his lab, he discovered something shocking. Although on the outside the dragonflies looked perfectly normal—lean and combat ready—Marden’s examination showed that they were actually very, very sick. But their disease was peculiar for these “jet fighters of the insect world.” They were all medically obese.

  Fat was collecting in their body tissues instead of converting into energy to fuel their extraordinary wing muscles. Their blood sugara concentrations were double that of healthy dragonflies, putting them in an insulin resistant–like state—similar to what’s seen in human patients with type 2 diabetes. They were slow, weak, sluggish, and unable to fight for females or defend territory.

  That a wild dragonfly could develop a form of metabolic syndromeb has the potential to revise thinking about human weight gain and maybe even the obesity epidemic itself. When Marden looked inside the dragonflies’ guts, he found something that surprised him. Freckling their intestines were large white parasites. Some of them were so big—up to one-fiftieth of an inch—that Marden could see them without a microscope. Magnified, they looked mild-mannered enough: like plump little grains of rice.

  What the parasites caused in the dragonflies, however, was anything but mild. They were gregarines, protozoans from the family that causes malaria and cryptosporidiosis in humans. In the dragonflies they triggered an inflammatory response that interfered with the insects’ ability to metabolize fat. That’s why it was collecting in their body tissues, particularly around their muscles. Their fat deposits were reducing their muscle performance, causing the dragonflies to relinquish territory and abandon mating opportunities.

  By measuring the way the dragonflies’ muscles exchanged oxygen and carbon dioxide, Marden and his graduate student Rudolf Schilder could see that the infection was directly causing these changes. He told me it wasn’t just that the dragonflies were weakened by the presence of the parasites, making them duller and slower. Rather, “specific components of their metabolism had changed.”

  The gregarine infections also caused chronic activation of a signaling molecule involved in immune and stress responses, called p38 MAP kinase. In humans, the same molecule is implicated in insulin resistance that can lead to type 2 diabetes.

  Intriguingly, the parasites were noninvasive, meaning they didn’t chew into or visibly damage the gut walls. Their inflammatory effect seemed to be triggered by substances they secr
eted and excreted. Eerily, the blood sugars of uninfected dragonflies became abnormal after they simply drank water containing trace amounts of the gregarines’ excretions or secretions.

  At first, the possibility that obesity has an infectious component seemed ludicrous to me. Having been steeped in the simple diet-and-exercise, calories-in, calories-out approach, and knowing that reducing intake and increasing activity does result in at least temporary weight loss, I thought that infectobesity seemed unexpected and, frankly, even unlikely.

  But although I had never heard about it, the search for infectious pathogens that promote weight gain has been under way since at least 1965, when a microbiologist at the State University of New York, Syracuse, explored how a certain worm caused mice and hamsters to become obese. He suggested that the worms might be “leaking” a hormone into the bloodstreams of the rodents, causing them to eat more in order to satisfy the chemistry of the parasite.

  And, indeed, infections of many kinds influence appetite. Tapeworms make you hungry. Certain viruses put you off your feed. In fact, appetite is one of the first things doctors ask patients about when we’re taking a medical history, because it’s one of the most sensitive markers of infection. These facts made me consider more seriously the real possibility that microbial invaders might manipulate what, how, and when we eat.