Zoobiquity (24 page)

When Richard Jackson calls obesity a “disease of the environment,” the setting he’s taking issue with is the one we’ve built with human ingenuity. The food we’ve tinkered with. The marketing that encourages us to consume it. The activity-lessening conveniences that have allowed us to become more sedentary than ever before. Living with abundant food and ready access to it will cause obesity no matter what species you belong to.

But a zoobiquitous perspective reveals other environmental factors, ones we can’t even see and rarely think about that may be playing an unacknowledged role in obesity. It turns out that there are cosmic and microscopic drivers of appetite and metabolism—forces more complicated and unexpected than portion size, calorie count, and exercise levels.
And they make the story of animals’ weight gain much, much more interesting.

Every autumn, around the second week of October, the two male alligators at Brookfield Zoo abruptly stop eating. For nearly six months, Gaston and Tiboy refuse all food. Come early April, when they start bellowing and trying to charge their keepers, their nutritionist, Jennifer Watts, knows they’re ready to resume their diet of rats and rabbits, until October, when they’ll go off their feed again.

There’s a reason the alligators’ feeding schedule is like clockwork: clockwork.

As we all know, yearly life on our planet goes predictably from season to season. The amount of sunlight every day increases and decreases with perfect regularity, depending on the time of year and latitude.

Daily life, too, follows a regular schedule that is simultaneously grand and utterly familiar.
Every day, as it has for billions of days, light follows dark in our planet’s steady circadian rhythm. For more than three billion years, Earth’s living creatures, starting with earliest single-celled organisms, have evolved in concert with this simple fact. Circadian rhythms, together with the diurnal rhythms of Earth’s yearly trek around the sun, influence hunger, appetite, ingestion, and even digestion.

When I started medical school thirty years ago, I’d have been laughed out of seminar for suggesting that diurnal and circadian rhythms had anything to do with food choice and nutrition, much less obesity. These forces were like tidbits in the
Old Farmer’s Almanac
—intriguingly consistent and predictable, observed in both plants and animals, but folksy and inscrutable enough to make them uncomfortably hard to use in any standard scientific sense.

During the past decade, that has changed. Molecular biologists have identified the underlying basis of circadian rhythms: the actual “clocks” that track time throughout our bodies. We’d been sensing their inaudible “ticking,” but suddenly we could see how many and varied and yet how consistent they are.

The cells of all human beings, from those on our scalps to those deep in our hearts, contain oscillators built by what are called clock genes. Oscillators influence everything from how fast you burn your calories to when you want to eat them. Oscillators aren’t just found in animals’
cells. Primitive and species-spanning, they vibrate away in the cells of plants, bacteria, fungi, and yeast as well. Even cyanobacteria, some of the oldest single-celled organisms on Earth, display circadian rhythms organized by their oscillators.

So-called higher creatures—those with brains—have evolved a “mission control” apparatus that coordinates the messages from all these countless oscillator “droids” in the far-off cells. It’s called the suprachiasmatic nucleus, or SCN. In humans, it’s a pinecone-shaped collection of cells about the size of a sesame seed that sits at the point where the optic nerves intersect in the hypothalamus. The external signals the body takes in, called zeitgebers, exert a powerful effect on all of our physical functions. Temperature, eating, sleep, and even socializing influence our bodies’ clocks. But by far the most influential of the zeitgebers is light. When light comes through the eyes, it hits the SCN, which then syncs up the external time signals with the internal oscillators throughout the body.

New research suggests that when, and how much, light beams through your eyes and hits your SCN may play a quiet and unrecognized role in determining your dress or pants size.
Several studies have linked shift work to obesity in humans. One assumption has been that the weight gain can be attributed to a lack of sleep. But studies coming out of the animal world suggest that the culprit may not be the hours of missed sleep but the breaking up of light-dark cycles.
A rodent study published in the
Proceedings of the National Academy of Sciences
showed that mice housed with constant light—whether bright or dim—had higher body mass indexes (BMIs) and blood sugar levels than mice housed with standard cycles of dark and light.

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.
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In fact, veterinarians have long recognized the power of the microbiome over an animal’s metabolic function.
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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. Although 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.