Friday, May 31, 2013

1078. Manly Sweat Makes Other Men More Cooperative

By Paul Gabrielsen, Science Now, May 31, 2013

Take a whiff, men. A chemical component of other guys' sweat makes men more cooperative and generous, new research says. The study is the first to show that this pheromone, called androstadienone, influences other men's behavior and reinforces the developing finding that humans are susceptible and responsive to these chemical signals.
Pheromones are everywhere in the animal world. Bugs in particular give off these chemicals to sound an alarm, identify a food source, or attract a mate. And smitten animals may indeed have "chemistry" together—pheromone signals are a subconscious part of their communication.
Scientists didn't know if humans played that game as well. But in the last 30 years, they've identified both male and female putative pheromones that are linked to mood and reproductive cycles. Some fragrancemakers have even incorporated them into their products, hoping to add an extra emotional punch to colognes and perfumes. Real-life pheromones don't smell so nice, however: The specialized glands that produce these chemical compounds are located near the armpit, where they mix with sweat. Previous investigations focused on the chemicals as sexual attractants—studying a male pheromone's effect on female mood and behavior, for example.
Turns out that women aren't the only ones susceptible to the power of male pheromones. Evolutionary biologist Markus Rantala of the University of Turku in Finland crafted an experiment in which 40 men in their mid-20s played a computer game in which two players decided how to share €10. One player offers a possible split, and the other decides whether to accept or reject it. Each participant took a turn making or deciding on offers.
Then they took a hefty whiff of either yeast (a control) or androstadienone, a suspected male pheromone present in sweat (which was also mixed with yeast to mask any perceptible odor), and played the game again.
The 20 men who sniffed the pheromone offered, on average, half a euro more than the control group (about €5), and accepted offers around half a euro lower (about €3), the researchers report this week in PLOS ONE. Rantala and colleague Paavo Huoviala monitored the men's hormone levels throughout the experiment and found, to their surprise, that men with higher testosterone levels were the most generous players after sniffing the pheromone. "I didn't know that this pheromone could interact with testosterone at all," Rantala says.
The researchers speculate that their finding may hearken back to a time when cooperation between males conferred a survival advantage. "[A]pparently such behaviour is considered attractive by the opposite sex," they write.
Rantala doesn't think that it's too far-fetched to see this pheromone used as an advertising gimmick. "They could spray a pheromone in a car, for example," he says. "People will feel happier in the car and will probably buy more readily."
Don't expect your teammates to be more generous in your next pick-up basketball game, though. Rantala used high concentrations of the pheromone in his experiments, anthropologist Jan Havlíček of Charles University in Prague, who was not involved in the research, writes in an e-mail to ScienceNOW. "We don't know whether we would be able to observe a similar effect with [the] use of more realistic concentrations." The power of pheromones depends on context as well, he adds. "It would be interesting to see whether production of androstadienone is affected by the outcome of an actual competition," he writes, "such as a sports match."

Thursday, May 30, 2013

1077. U.S. Women on the Rise as Family Breadwinner

By Catherine Rampell, The New York Times, May 30, 2013

Women are not only more likely to be the primary caregivers in a family. Increasingly, they are primary breadwinners, too.

Four in 10 American households with children under age 18 now include a mother who is either the sole or primary earner for her family, according to a Pew Research Center analysis of Census and polling data released Wednesday. This share, the highest on record, has quadrupled since 1960.
The shift reflects evolving family dynamics.
For one, it has become more acceptable and expected for married women to join the work force. It is also more common for single women to raise children on their own. Most of the mothers who are chief breadwinners for their families — nearly two-thirds — are single parents.
The recession may have played a role in pushing women into primary earning roles, as men are disproportionately employed in industries like construction and manufacturing that bore the brunt of the layoffs during the downturn. Women, though, have benefited from a smaller share of the job gains during the recovery; the public sector, which employs a large number of women, is still laying off workers.

Women’s attitudes toward working have also changed. In 2007, before the recession officially began, 20 percent of mothers told Pew that their ideal situation would be to work full time rather than part time or not at all. The share had risen to 32 percent by the end of 2012.
The public is still divided about whether it is a good thing for mothers to work. About half of Americans say that children are better off if their mother is at home and doesn’t have a job. Just 8 percent say the same about a father. Even so, most Americans acknowledge that the increasing number of working women makes it easier for families “to earn enough to live comfortably.”
Demographically and socioeconomically, single mothers and married mothers differ, according to the Census Bureau’s 2011 American Community Survey. The median family income for single mothers — who are more likely to be younger, black or Hispanic, and less educated — is $23,000. The median household income for married women who earn more than their husbands — more often white, slightly older and college educated — is $80,000. When the wife is the primary breadwinner, the total family income is generally higher.
Such marriages are still relatively rare, even if their share is growing. Of all married couples, 24 percent include a wife who earns more, versus 6 percent in 1960. (The percentages are similar for married couples who have children.)

The implications for the stability of marriages is unclear. In surveys, Americans usually indicate that they accept marriages where the wife is the greater earner. Just 28 percent of Americans surveyed by Pew agreed that it is “generally better for a marriage if the husband earns more than his wife.”
But the data on actual marriage and divorce rates suggests slightly different attitudes.
A recent working paper by economists at the University of Chicago Booth School of Business and the National University of Singapore found that, in looking at the distribution of married couples by income of husband versus wife, there is a sharp drop-off in the number of couples in which the wife earns more than half of the household income. This suggests that the random woman and random man are much less likely to pair off if her income exceeds his, the paper says.
The economists also found that wives with a better education and stronger earning potential than their husbands are less likely to work. In other words, women are more likely to stay out of the work force if there is a big risk that they will make more than their husbands.
Perhaps even more tellingly, couples in which the wife earns more report less satisfaction with their marriage and higher rates of divorce. When the wife brings in more money, couples often revert to more stereotypical sex roles; in such cases, wives typically take on a larger share of household work and child care.
“Our analysis of the time use data suggests that gender identity considerations may lead a woman who seems threatening to her husband because she earns more than he does to engage in a larger share of home production activities, particularly household chores,” the authors write.
Of course, these patterns may change as the job market evolves. College degrees, for example, are becoming increasingly important to both finding and keeping a job. And women are more likely than men to get college degrees.
As of 2011, there were more married-couple families with children in which the wife was more educated than the husband, according to Pew. In roughly 23 percent of married couples with children, the women had more education; in 17 percent of the couples, the men had higher education. The remaining 61 percent of two-parent families involve spouses with about equal levels of education.

Norms are also changing: Newlyweds seem to show more openness to having the wife earn more than her husband than do longer-married couples. In about 30 percent of newly married couples in 2011, the wife earned more, versus just 24 percent of all married couples.
Americans are becoming more accepting of single mothers as well. In a survey conducted April 25-28, Pew found that 64 percent of Americans said the growing number of children born to unmarried mothers is a “big problem,” down from 71 percent in 2007. Republicans are more likely than Democrats or independents to be concerned about the trend.
Today’s single mothers are much more likely to have never been married than in the past, Pew found. In 1960, the share of never-married single mothers was just 4 percent; as of 2011, it had risen to 44 percent. Never-married mothers tend to make less money than their divorced or widowed counterparts, and are more likely to be a member of a racial or ethnic minority.

Monday, May 27, 2013

1076. Breeding the Nutrition Out of Our Food

By Jo Robinson, The New York Times, May 25, 2013

WE like the idea that food can be the answer to our ills, that if we eat nutritious foods we won’t need medicine or supplements. We have valued this notion for a long, long time. The Greek physician Hippocrates proclaimed nearly 2,500 years ago: “Let food be thy medicine and medicine be thy food.” Today, medical experts concur. If we heap our plates with fresh fruits and vegetables, they tell us, we will come closer to optimum health.

This health directive needs to be revised. If we want to get maximum health benefits from fruits and vegetables, we must choose the right varieties. Studies published within the past 15 years show that much of our produce is relatively low in phytonutrients, which are the compounds with the potential to reduce the risk of four of our modern scourges: cancer, cardiovascular disease, diabetes and dementia. The loss of these beneficial nutrients did not begin 50 or 100 years ago, as many assume. Unwittingly, we have been stripping phytonutrients from our diet since we stopped foraging for wild plants some 10,000 years ago and became farmers.
These insights have been made possible by new technology that has allowed researchers to compare the phytonutrient content of wild plants with the produce in our supermarkets. The results are startling.
Wild dandelions, once a springtime treat for Native Americans, have seven times more phytonutrients than spinach, which we consider a “superfood.” A purple potato native to Peru has 28 times more cancer-fighting anthocyanins than common russet potatoes. One species of apple has a staggering 100 times more phytonutrients than the Golden Delicious displayed in our supermarkets.
Were the people who foraged for these wild foods healthier than we are today? They did not live nearly as long as we do, but growing evidence suggests that they were much less likely to die from degenerative diseases, even the minority who lived 70 years and more. The primary cause of death for most adults, according to anthropologists, was injury and infections.
Each fruit and vegetable in our stores has a unique history of nutrient loss, I’ve discovered, but there are two common themes. Throughout the ages, our farming ancestors have chosen the least bitter plants to grow in their gardens. It is now known that many of the most beneficial phytonutrients have a bitter, sour or astringent taste. Second, early farmers favored plants that were relatively low in fiber and high in sugar, starch and oil. These energy-dense plants were pleasurable to eat and provided the calories needed to fuel a strenuous lifestyle. The more palatable our fruits and vegetables became, however, the less advantageous they were for our health.
The sweet corn that we serve at summer dinners illustrates both of these trends. The wild ancestor of our present-day corn is a grassy plant called teosinte. It is hard to see the family resemblance. Teosinte is a bushy plant with short spikes of grain instead of ears, and each spike has only 5 to 12 kernels. The kernels are encased in shells so dense you’d need a hammer to crack them open. Once you extract the kernels, you wonder why you bothered. The dry tidbit of food is a lot of starch and little sugar. Teosinte has 10 times more protein than the corn we eat today, but it was not soft or sweet enough to tempt our ancestors.
Over several thousand years, teosinte underwent several spontaneous mutations. Nature’s rewriting of the genome freed the kernels of their cases and turned a spike of grain into a cob with kernels of many colors. Our ancestors decided that this transformed corn was tasty enough to plant in their gardens. By the 1400s, corn was central to the diet of people living throughout Mexico and the Americas.
When European colonists first arrived in North America, they came upon what they called “Indian corn.” John Winthrop Jr., governor of the colony of Connecticut in the mid-1600s, observed that American Indians grew “corne with great variety of colours,” citing “red, yellow, blew, olive colour, and greenish, and some very black and some of intermediate degrees.” A few centuries later, we would learn that black, red and blue corn is rich in anthocyanins. Anthocyanins have the potential to fight cancer, calm inflammation, lower cholesterol and blood pressure, protect the aging brain, and reduce the risk of obesity, diabetes and cardiovascular disease.
EUROPEAN settlers were content with this colorful corn until the summer of 1779 when they found something more delectable — a yellow variety with sweeter and more tender kernels. This unusual variety came to light that year after George Washington ordered a scorched-earth campaign against Iroquois tribes. While the militia was destroying the food caches of the Iroquois and burning their crops, soldiers came across a field of extra-sweet yellow corn. According to one account, a lieutenant named Richard Bagnal took home some seeds to share with others. Our old-fashioned sweet corn is a direct descendant of these spoils of war.
Up until this time, nature had been the primary change agent in remaking corn. Farmers began to play a more active role in the 19th century. In 1836, Noyes Darling, a onetime mayor of New Haven, and a gentleman farmer, was the first to use scientific methods to breed a new variety of corn. His goal was to create a sweet, all-white variety that was “fit for boiling” by mid-July.

He succeeded, noting with pride that he had rid sweet corn of “the disadvantage of being yellow.”The disadvantage of being yellow, we now know, had been an advantage to human health. Corn with deep yellow kernels, including the yellow corn available in our grocery stores, has nearly 60 times more beta-carotene than white corn, valuable because it turns to Vitamin A in the body, which helps vision and the immune system.
SUPERSWEET corn, which now outsells all other kinds of corn, was born in a cloud of radiation. Beginning in the 1920s, geneticists exposed corn seeds to radiation to learn more about the normal arrangement of plant genes. They mutated the seeds by exposing them to X-rays, toxic compounds, cobalt radiation and then, in the 1940s, to blasts of atomic radiation. All the kernels were stored in a seed bank and made available for research.
In 1959, a geneticist named John Laughnan was studying a handful of mutant kernels and popped a few into his mouth. (The corn was no longer radioactive.) He was startled by their intense sweetness. Lab tests showed that they were up to 10 times sweeter than ordinary sweet corn. A blast of radiation had turned the corn into a sugar factory!
Mr. Laughnan was not a plant breeder, but he realized at once that this mutant corn would revolutionize the sweet corn industry. He became an entrepreneur overnight and spent years developing commercial varieties of supersweet corn. His first hybrids began to be sold in 1961. This appears to be the first genetically modified food to enter the United States food supply, an event that has received scant attention.
Within one generation, the new extra sugary varieties eclipsed old-fashioned sweet corn in the marketplace. Build a sweeter fruit or vegetable — by any means — and we will come. Today, most of the fresh corn in our supermarkets is extra-sweet, and all of it can be traced back to the radiation experiments. The kernels are either white, pale yellow, or a combination of the two. The sweetest varieties approach 40 percent sugar, bringing new meaning to the words “candy corn.” Only a handful of farmers in the United States specialize in multicolored Indian corn, and it is generally sold for seasonal decorations, not food.
We’ve reduced the nutrients and increased the sugar and starch content of hundreds of other fruits and vegetables. How can we begin to recoup the losses?
Here are some suggestions to get you started. Select corn with deep yellow kernels. To recapture the lost anthocyanins and beta-carotene, cook with blue, red or purple cornmeal, which is available in some supermarkets and on the Internet. Make a stack of blue cornmeal pancakes for Sunday breakfast and top with maple syrup.
In the lettuce section, look for arugula. Arugula, also called salad rocket, is very similar to its wild ancestor. Some varieties were domesticated as recently as the 1970s, thousands of years after most fruits and vegetables had come under our sway. The greens are rich in cancer-fighting compounds called glucosinolates and higher in antioxidant activity than many green lettuces.
Scallions, or green onions, are jewels of nutrition hiding in plain sight. They resemble wild onions and are just as good for you. Remarkably, they have more than five times more phytonutrients than many common onions do. The green portions of scallions are more nutritious than the white bulbs, so use the entire plant. Herbs are wild plants incognito. We’ve long valued them for their intense flavors and aroma, which is why they’ve not been given a flavor makeover. Because we’ve left them well enough alone, their phytonutrient content has remained intact.
Experiment with using large quantities of mild-tasting fresh herbs. Add one cup of mixed chopped Italian parsley and basil to a pound of ground grass-fed beef or poultry to make “herb-burgers.” Herbs bring back missing phytonutrients and a touch of wild flavor as well.
The United States Department of Agriculture exerts far more effort developing disease-resistant fruits and vegetables than creating new varieties to enhance the disease resistance of consumers. In fact, I’ve interviewed U.S.D.A. plant breeders who have spent a decade or more developing a new variety of pear or carrot without once measuring its nutritional content.
We can’t increase the health benefits of our produce if we don’t know which nutrients it contains. Ultimately, we need more than an admonition to eat a greater quantity of fruits and vegetables: we need more fruits and vegetables that have the nutrients we require for optimum health.
Jo Robinson is the author of the forthcoming book “Eating on the Wild Side: The Missing Link to Optimum Health.”

1075. Masters of War by Bob Dylan: On the Occasion of Memorial Day in the United States

Masters of War by Bob Dylan

Come you masters of war
You that build all the guns
You that build the death planes
You that build the big bombs
You that hide behind walls
You that hide behind desks
I just want you to know
I can see through your masks

You that never done nothin'
But build to destroy
You play with my world
Like it's your little toy
You put a gun in my hand
And you hide from my eyes
And you turn and run farther
When the fast bullets fly

Like Judas of old
You lie and deceive
A world war can be won
You want me to believe
But I see through your eyes
And I see through your brain
Like I see through the water
That runs down my drain

You fasten the triggers
For the others to fire
Then you set back and watch
When the death count gets higher
You hide in your mansion
As young people’s blood
Flows out of their bodies
And is buried in the mud

You've thrown the worst fear
That can ever be hurled
Fear to bring children
Into the world
For threatening my baby
Unborn and unnamed
You ain't worth the blood
That runs in your veins

How much do I know
To talk out of turn
You might say that I'm young
You might say I’m unlearned
But there's one thing I know
Though I'm younger than you
Even Jesus would never
Forgive what you do

Let me ask you one question
Is your money that good
Will it buy you forgiveness
Do you think that it could
I think you will find
When your death takes its toll
All the money you made
Will never buy back your soul

And I hope that you die
And your death'll come soon
I will follow your casket
In the pale afternoon
And I'll watch while you’re lowered
Down to your deathbed
And I'll stand o'er your grave
Till I'm sure that you're dead

Friday, May 24, 2013

1074. Cockroaches Evolve to Avoid Glucose Used in Traps

By Rachel Nuwer, Science Now, May 23, 2013
Cockroaches have evolved to avoid glucose-laden food used in traps
Roach motels sit at the back of many a kitchen cupboard, bedroom closet, or bathroom cabinet. Yet, to the bane of human residents, only a few years after the traps were introduced in the 1980s, they lost their allure for an increasing number of German cockroaches. Researchers soon realized that some roaches had developed an aversion to glucose—the sugary bait disguising the poison—and that the insects were passing that trait on to their young. Now, scientists have figured out how this behavior evolved. Roaches, like other insects, detect taste through special receptors that line hairlike appendages on their mouthparts. The receptors differentiate between sweet and bitter flavors, which signal to the roach whether to eat or avoid the food, respectively. The researchers performed experiments on more than 1000 German cockroaches from the field and about 250 raised in the lab. The normal roaches happily lapped up both glucose and fructose, but the glucose-averse roaches ate only the fructose and spat out the glucose, the team reports online today in Science. Electrophysiological recordings indicated that glucose triggered sweet receptors in the normal roaches but bitter receptors in the other roaches. The change in behavior may save the insects' lives, but it does have its disadvantages: Glucose-averse roaches grow and reproduce more slowly than those with less finicky tastes. 

1073. Whales Freed from Fishing Gear May Still Die a Slow Death

By Paul Gabrielsen, Science Now, May 23, 2013
Whale caught in fishing net 
On Christmas Day 2010, an aerial team of wildlife spotters saw a whale in distress off the eastern coast of Florida. Her head, mouth, and fins were tangled in 132 meters of commercial fishing rope. Marine veterinarians and biologists untangled the whale, diving into the water and cutting the lines that had wrapped around her upper jaw and cut into her flesh. But the damage had been done. Weeks later, the giant mammal was found floating at the surface, the victim of a shark attack. The incident, according to a new study, shows that whales' fight against fishing gear can kill them long after they've been freed from it.
Researchers already know that heavy-duty commercial fishing lines and lobster and crab traps, connected to the surface by long ropes, pose a formidable threat to whales in the North Atlantic, by inflicting deep wounds and sapping their energy reserves. Accidental entrapment is the leading cause of death for Atlantic whales in records going back to 1970. The National Marine Fisheries Service reported 25 sightings of entangled whales in 2010. Five did not survive the encounter. Many of the surviving whales were described as thin and weak.
The whale spotted on Christmas, a 2-year-old female right whale cataloged as Eg 3911 (Eg for the species' scientific name, Eubalaena glacialis), tangled with a fishing trap line sometime between February and December 2010. By the time researchers rescued her on 15 January 2011, she was 20% thinner than other right whales her age. The team suspects she wasn't able to dive deep enough to reach the plankton and crustaceans she'd normally feed on.
Once liberated, Eg 3911 began swimming faster and diving deeper, but she had no way to bulk back up. Right whales normally feed in cool northern waters during the summer, and Florida's winter waters offered no food sources. "You're tired, you're hungry, you're really skinny, and there's nothing for you to eat," says Julie van der Hoop, a marine mammal biologist at the Woods Hole Oceanographic Institution in Massachusetts and lead author of a new paper documenting the incident. Eg 3911 was found dead in the water on 1 February, sporting lethal shark attack wounds. Van der Hoop suspects that the whale was lethargically bobbing at the surface when she was bitten.
Following Eg 3911's death, van der Hoop and colleagues wondered how much the gear taxed the emaciated whale's energy reserves. Scientists lowered some of the very fishing gear removed from Eg 3911 into the water behind a moving skiff to estimate how much drag the lines and buoys generated, and how much energy the whale would have to expend to compensate. They estimated that Eg 3911 was burning up to twice as much energy while entangled. Their results appear online this week in Marine Mammal Science.
The team doesn't know how long Eg 3911 was entangled—it could have been only weeks, or closer to a year. Whales can live with the tight, cutting, restricting lines for 6 months to a year before succumbing to injury, infection, or starvation, van der Hoop says. "That is a really long time to be subject to this type of injury."
Long-term consequences may linger long after entrapment, even when whales return to health. Marine mammal biologist Scott Kraus of the New England Aquarium in Boston, who was not involved in the study, says that he plans to use these results to reexamine the life history of whales postentanglement. "We've tended to think that entangled animals either get free or die," he says. "The sublethal effects of entanglement have not been considered."
Kraus says that he's learned a sobering lesson from Eg 3911's story—whales are not home free once they're loosed from entangling lines. "The impact of humanity on these creatures does not end when they go out of sight."

Thursday, May 23, 2013

1072. Cuba Lifts Ban on Energy-Hogging Appliances

By Ann-Marie Garcia, The Associated Press, May 21, 2013
A basic Cuban kitchen
Cuba has authorized individual imports of appliances such as air conditioners, refrigerators and microwave ovens, lifting a ban imposed in 2005 amid a wave of energy shortages and blackouts.
Islanders can now bring up to two such appliances per person into the country for noncommercial purposes, according to a law enacted with its publication Monday in the Official Gazette.
The list of approved items includes air conditioners with a capacity of less than 1 ton, ovens that consume less than 1,500 watts and microwaves under 2,000 watts.
The change could strain even further the already-overstuffed cargo holds of flights from places like Miami, Ecuador and Panama to Havana. Cuba-bound travelers who routinely check bulky bundles and multiple plasma-screen TVs will now start thinking about things like air conditioners, chest freezers, microwaves and ovens.
Even accounting for import taxes, it will often be cheaper to bring those items in from abroad than to pay for them in state-run hard-currency stores where the markup is said to be around triple as a rule of thumb.
In one shop in Old Havana on Friday, for example, a Hamilton Beach sandwich maker that lists for $29.99 on the company's website was on sale for the equivalent of $94.40.
"Prices for those products in Cuba are very high. Nobody has enough to buy something like that," said Maria Rosas, a 42-year-old office worker who added that she makes about $12.50 a month. "I see things like a blender, a sandwich maker or one of those steam irons, and I'd like to have them, but I can't afford to."
Rosas' salary is low even for Cuba, where government wages average around $20 a month. The socialist system greatly subsidizes a number of basic staples and housing, however, along with distributing ration cards that cover part of islanders' nutritional needs and offering free health care and education.
Cubans often make do by running something on the side, be it a legitimate small business opened up under President Raul Castro's recent economic reform program, or by offering black-market services or goods pilfered from state enterprises.
Others gain access to hard currency through tourism-sector jobs or by working for foreign companies, and just about everyone has a relative in Florida or elsewhere who's a potential source of remittances.
The new rules on importing appliances would seem to benefit most the few-but-increasing number of Cubans who are traveling abroad, said Roberto Fortin, a 45-year-old independent worker.
Some predicted that as is already happening with television sets, computers and other high-ticket items, those travelers will often bring in the maximum allowed, and sell at a hefty profit while still undercutting the state-run stores.
"What the government is not going to be able to avoid with this measure is that people who travel won't just buy for their personal use, but also to resell it later," said Gregorio Santos, a 72-year-old retiree. "They might lower the prices in stores, but I don't think so because the people who make those decisions don't have the slightest idea about business."
Personal importation of energy-sucking appliances was restricted eight years ago during an energy crisis that prompted then-President Fidel Castro to launch the so-called Energy Revolution seeking to lower consumption.
Castro went on state TV to promote more efficient rice steamers and pressure cookers, government workers fanned out across the island replacing incandescent light bulbs in homes and the country's creaky electrical grid got an update.
Blackouts are much rarer today, thanks in part to a steady flow of oil on preferential terms from close ally Venezuela.
In 2011, Cuba resumed local sales of domestic appliances in response to demand and to support private small businesses that have been launched under Cuba's economic reforms.
Authorities have continued to stress the importance of conservation to keep Cuba's power grid from being overtaxed.

Tuesday, May 21, 2013

1071. Germs R Us: A Biological View of the Self

By Michael Pollen, The New York Times, May 15, 2013
Ten trillion microbes live in a human body; all but a tiny percentage may be keeping us healthy
I can tell you the exact date that I began to think of myself in the first-person plural — as a superorganism, that is, rather than a plain old individual human being. It happened on March 7. That’s when I opened my e-mail to find a huge, processor-choking file of charts and raw data from a laboratory located at the BioFrontiers Institute at the University of Colorado, Boulder. As part of a new citizen-science initiative called the American Gut project, the lab sequenced my microbiome — that is, the genes not of “me,” exactly, but of the several hundred microbial species with whom I share this body. These bacteria, which number around 100 trillion, are living (and dying) right now on the surface of my skin, on my tongue and deep in the coils of my intestines, where the largest contingent of them will be found, a pound or two of microbes together forming a vast, largely uncharted interior wilderness that scientists are just beginning to map.

I clicked open a file called Taxa Tables, and a colorful bar chart popped up on my screen. Each bar represented a sample taken (with a swab) from my skin, mouth and feces. For purposes of comparison, these were juxtaposed with bars representing the microbiomes of about 100 “average” Americans previously sequenced.

Here were the names of the hundreds of bacterial species that call me home. In sheer numbers, these microbes and their genes dwarf us. It turns out that we are only 10 percent human: for every human cell that is intrinsic to our body, there are about 10 resident microbes — including commensals (generally harmless freeloaders) and mutualists (favor traders) and, in only a tiny number of cases, pathogens. To the extent that we are bearers of genetic information, more than 99 percent of it is microbial. And it appears increasingly likely that this “second genome,” as it is sometimes called, exerts an influence on our health as great and possibly even greater than the genes we inherit from our parents. But while your inherited genes are more or less fixed, it may be possible to reshape, even cultivate, your second genome.
Justin Sonnenburg, a microbiologist at Stanford, suggests that we would do well to begin regarding the human body as “an elaborate vessel optimized for the growth and spread of our microbial inhabitants.” This humbling new way of thinking about the self has large implications for human and microbial health, which turn out to be inextricably linked. Disorders in our internal ecosystem — a loss of diversity, say, or a proliferation of the “wrong” kind of microbes — may predispose us to obesity and a whole range of chronic diseases, as well as some infections. “Fecal transplants,” which involve installing a healthy person’s microbiota into a sick person’s gut, have been shown to effectively treat an antibiotic-resistant intestinal pathogen named C. difficile, which kills 14,000 Americans each year. (Researchers use the word “microbiota” to refer to all the microbes in a community and “microbiome” to refer to their collective genes.) We’ve known for a few years that obese mice transplanted with the intestinal community of lean mice lose weight and vice versa. (We don’t know why.) A similar experiment was performed recently on humans by researchers in the Netherlands: when the contents of a lean donor’s microbiota were transferred to the guts of male patients with metabolic syndrome, the researchers found striking improvements in the recipients’ sensitivity to insulin, an important marker for metabolic health. Somehow, the gut microbes were influencing the patients’ metabolisms.
Our resident microbes also appear to play a critical role in training and modulating our immune system, helping it to accurately distinguish between friend and foe and not go nuts on, well, nuts and all sorts of other potential allergens. Some researchers believe that the alarming increase in autoimmune diseases in the West may owe to a disruption in the ancient relationship between our bodies and their “old friends” — the microbial symbionts with whom we coevolved.
These claims sound extravagant, and in fact many microbiome researchers are careful not to make the mistake that scientists working on the human genome did a decade or so ago, when they promised they were on the trail of cures to many diseases. We’re still waiting. Yet whether any cures emerge from the exploration of the second genome, the implications of what has already been learned — for our sense of self, for our definition of health and for our attitude toward bacteria in general — are difficult to overstate. Human health should now “be thought of as a collective property of the human-associated microbiota,” as one group of researchers recently concluded in a landmark review article on microbial ecology — that is, as a function of the community, not the individual.
Such a paradigm shift comes not a moment too soon, because as a civilization, we’ve just spent the better part of a century doing our unwitting best to wreck the human-associated microbiota with a multifronted war on bacteria and a diet notably detrimental to its well-being. Researchers now speak of an impoverished “Westernized microbiome” and ask whether the time has come to embark on a project of “restoration ecology” — not in the rain forest or on the prairie but right here at home, in the human gut.
In March I traveled to Boulder to see the Illumina HiSeq 2000 sequencing machine that had shed its powerful light on my own microbiome and to meet the scientists and computer programmers who were making sense of my data. The lab is headed by Rob Knight, a rangy, crew-cut 36-year-old biologist who first came to the United States from his native New Zealand to study invasive species, a serious problem in his home country. Knight earned his Ph.D. in ecology and evolutionary biology from Princeton when he was 24 and then drifted from the study of visible species and communities to invisible ones. Along the way he discovered he had a knack for computational biology. Knight is regarded as a brilliant analyst of sequencing data, skilled at finding patterns in the flood of information produced by the machines that “batch sequence” all the DNA in a sample and then tease out the unique genetic signatures of each microbe. This talent explains why so many of the scientists exploring the microbiome today send their samples to be sequenced and analyzed by his lab; it is also why you will find Knight’s name on most of the important papers in the field.
Over the course of two days in Boulder, I enjoyed several meals with Knight and his colleagues, postdocs and graduate students, though I must say I was a little taken aback by the table talk. I don’t think I’ve ever heard so much discussion of human feces at dinner, but then one thing these scientists are up to is a radical revaluation of the contents of the human colon. I learned about Knight’s 16-month-old daughter, who has had most of the diapers to which she has contributed sampled and sequenced. Knight said at dinner that he sampled himself every day; his wife, Amanda Birmingham, who joined us one night, told me that she was happy to be down to once a week. “Of course I keep a couple of swabs in my bag at all times,” she said, rolling her eyes, “because you never know.”

A result of the family’s extensive self-study has been a series of papers examining family microbial dynamics. The data helped demonstrate that the microbial communities of couples sharing a house are similar, suggesting the importance of the environment in shaping an individual’s microbiome. Knight also found that the presence of a family dog tended to blend everyone’s skin communities, probably via licking and petting. One paper, titled “Moving Pictures of the Human Microbiome,” tracked the day-to-day shifts in the microbial composition of each body site. Knight produced animations showing how each community — gut, skin and mouth — hosted a fundamentally different cast of microbial characters that varied within a fairly narrow range over time.

Knight’s daily sampling of his daughter’s diapers (along with those of a colleague’s child) also traced the remarkable process by which a baby’s gut community, which in utero is sterile and more or less a blank slate, is colonized. This process begins shortly after birth, when a distinctive infant community of microbes assembles in the gut. Then, with the introduction of solid food and then weaning, the types of microbes gradually shift until, by age 3, the baby’s gut comes to resemble an adult community much like that of its parents.
The study of babies and their specialized diet has yielded key insights into how the colonization of the gut unfolds and why it matters so much to our health. One of the earliest clues to the complexity of the microbiome came from an unexpected corner: the effort to solve a mystery about milk. For years, nutrition scientists were confounded by the presence in human breast milk of certain complex carbohydrates, called oligosaccharides, which the human infant lacks the enzymes necessary to digest. Evolutionary theory argues that every component of mother’s milk should have some value to the developing baby or natural selection would have long ago discarded it as a waste of the mother’s precious resources.
It turns out the oligosaccharides are there to nourish not the baby but one particular gut bacterium called Bifidobacterium infantis, which is uniquely well-suited to break down and make use of the specific oligosaccharides present in mother’s milk. When all goes well, the bifidobacteria proliferate and dominate, helping to keep the infant healthy by crowding out less savory microbial characters before they can become established and, perhaps most important, by nurturing the integrity of the epithelium — the lining of the intestines, which plays a critical role in protecting us from infection and inflammation.
“Mother’s milk, being the only mammalian food shaped by natural selection, is the Rosetta stone for all food,” says Bruce German, a food scientist at the University of California, Davis, who researches milk. “And what it’s telling us is that when natural selection creates a food, it is concerned not just with feeding the child but the child’s gut bugs too.”
Where do these all-important bifidobacteria come from and what does it mean if, like me, you were never breast-fed? Mother’s milk is not, as once was thought, sterile: it is both a “prebiotic” — a food for microbes — and a “probiotic,” a population of beneficial microbes introduced into the body. Some of them may find their way from the mother’s colon to her milk ducts and from there into the baby’s gut with its first feeding. Because designers of infant formula did not, at least until recently, take account of these findings, including neither prebiotic oligosaccharides or probiotic bacteria in their formula, the guts of bottle-fed babies are not optimally colonized.
Most of the microbes that make up a baby’s gut community are acquired during birth — a microbially rich and messy process that exposes the baby to a whole suite of maternal microbes. Babies born by Caesarean, however, a comparatively sterile procedure, do not acquire their mother’s vaginal and intestinal microbes at birth. Their initial gut communities more closely resemble that of their mother’s (and father’s) skin, which is less than ideal and may account for higher rates of allergy, asthma and autoimmune problems in C-section babies: not having been seeded with the optimal assortment of microbes at birth, their immune systems may fail to develop properly.
At dinner, Knight told me that he was sufficiently concerned about such an eventuality that, when his daughter was born by emergency C-section, he and his wife took matters into their own hands: using a sterile cotton swab, they inoculated the newborn infant’s skin with the mother’s vaginal secretions to insure a proper colonization. A formal trial of such a procedure is under way in Puerto Rico.

While I was in Boulder, I sat down with Catherine A. Lozupone, a microbiologist who had just left Knight’s lab to set up her own at the University of Colorado, Denver, and who spent some time looking at my microbiome and comparing it with others, including her own. Lozupone was the lead author on an important 2012 paper in Nature, “Diversity, Stability and Resilience of the Human Gut Microbiota,” which sought to approach the gut community as an ecologist might, trying to determine the “normal” state of the ecosystem and then examining the various factors that disturb it over time. How does diet affect it? Antibiotics? Pathogens? What about cultural traditions? So far, the best way to begin answering such questions may be by comparing the gut communities of various far-flung populations, and researchers have been busy collecting samples around the world and shipping them to sequencing centers for analysis. The American Gut project, which hopes to eventually sequence the communities of tens of thousands of Americans, represents the most ambitious such effort to date; it will help researchers uncover patterns of correlation between people’s lifestyle, diet, health status and the makeup of their microbial community.
It is still early days in this research, as Lozupone (and everyone else I interviewed) underscored; scientists can’t even yet say with confidence exactly what a “healthy” microbiome should look like. But some broad, intriguing patterns are emerging. More diversity is probably better than less, because a diverse ecosystem is generally more resilient — and diversity in the Western gut is significantly lower than in other, less-industrialized populations. The gut microbiota of people in the West looks very different from that of a variety of other geographically dispersed peoples. So, for example, the gut community of rural people in West Africa more closely resembles that of Amerindians in Venezuela than it does an American’s or a European’s.
These rural populations not only harbor a greater diversity of microbes but also a different cast of lead characters. American and European guts contain relatively high levels of bacteroides and firmicutes and low levels of the prevotella that dominate the guts of rural Africans and Amerindians. (It is not clear whether high or low levels of any of these is good or bad.) Why are the microbes different? It could be the diet, which in both rural populations features a considerable amount of whole grains (which prevotella appear to like), plant fiber and very little meat. (Many firmicutes like amino acids, so they proliferate when the diet contains lots of protein; bacteroides metabolize carbohydrates.) As for the lower biodiversity in the West, this could be a result of our profligate use of antibiotics (in health care as well as the food system), our diet of processed food (which has generally been cleansed of all bacteria, the good and the bad), environmental toxins and generally less “microbial pressure” — i.e., exposure to bacteria — in everyday life. All of this may help explain why, though these rural populations tend to have greater exposures to infectious diseases and lower life expectancies than those in the West, they also have lower rates of chronic disorders like allergies, asthma, Type 2 diabetes and cardiovascular disease.
“Rural people spend a lot more time outside and have much more contact with plants and with soil,” Lozupone says. Another researcher, who has gathered samples in Malawi, told me, “In some of these cultures, children are raised communally, passed from one set of hands to another, so they’re routinely exposed to a greater diversity of microbes.” The nuclear family may not be conducive to the health of the microbiome.
As it happens, Lozupone and I had something in common, microbially speaking: we share unusually high levels of prevotella for Americans. Our gut communities look more like those of rural Africans or Amerindians than like those of our neighbors. Lozupone suspects that the reasons for this might have to do with a plant-based diet; we each eat lots of whole grains and vegetables and relatively little meat. (Though neither of us is a vegetarian.) Like me, she was proud of her prevotella, regarding it as a sign of a healthy non-Western diet, at least until she began doing research on the microbiota of H.I.V. patients. It seems that they, too, have lots of prevotella. Further confusing the story, a recent study linking certain gut microbes common in meat eaters to high levels of a blood marker for heart disease suggested that prevotella was one such microbe. Early days, indeed.
Two other features of my microbiome attracted the attention of the researchers who examined it. First, the overall biodiversity of my gut community was significantly higher than that of the typical Westerner, which I decided to take as a compliment, though the extravagantly diverse community of microbes on my skin raised some eyebrows. “Where have your hands been, man?” Jeff Leach of the American Gut project asked after looking over my results. My skin harbors bacteria associated with plants, soil and a somewhat alarming variety of animal guts. I put this down to gardening, composting (I keep worms too) and also the fact that I was fermenting kimchi and making raw-milk cheese, “live-culture” foods teeming with microbes.
Compared to a rain forest or a prairie, the interior ecosystem is not well understood, but the core principles of ecology — which along with powerful new sequencing machines have opened this invisible frontier to science — are beginning to yield some preliminary answers and a great many more intriguing hypotheses. Your microbial community seems to stabilize by age 3, by which time most of the various niches in the gut ecosystem are occupied. That doesn’t mean it can’t change after that; it can, but not as readily. A change of diet or a course of antibiotics, for example, may bring shifts in the relative population of the various resident species, helping some kinds of bacteria to thrive and others to languish. Can new species be introduced? Yes, but probably only when a niche is opened after a significant disturbance, like an antibiotic storm. Just like any other mature ecosystem, the one in our gut tends to resist invasion by newcomers.
You acquire most of the initial microbes in your gut community from your parents, but others are picked up from the environment. “The world is covered in a fine patina of feces,” as the Stanford microbiologist Stanley Falkow tells students. The new sequencing tools have confirmed his hunch: Did you know that house dust can contain significant amounts of fecal particles? Or that, whenever a toilet is flushed, some of its contents are aerosolized? Knight’s lab has sequenced the bacteria on toothbrushes. This news came during breakfast, so I didn’t ask for details, but got them anyway: “You want to keep your toothbrush a minimum of six feet away from a toilet,” one of Knight’s colleagues told me.

Some scientists in the field borrow the term “ecosystem services” from ecology to catalog all the things that the microbial community does for us as its host or habitat, and the services rendered are remarkably varied and impressive. “Invasion resistance” is one. Our resident microbes work to keep pathogens from gaining a toehold by occupying potential niches or otherwise rendering the environment inhospitable to foreigners. The robustness of an individual’s gut community might explain why some people fall victim to food poisoning while others can blithely eat the same meal with no ill effects.
Our gut bacteria also play a role in the manufacture of substances like neurotransmitters (including serotonin); enzymes and vitamins (notably Bs and K) and other essential nutrients (including important amino acid and short-chain fatty acids); and a suite of other signaling molecules that talk to, and influence, the immune and the metabolic systems. Some of these compounds may play a role in regulating our stress levels and even temperament: when gut microbes from easygoing, adventurous mice are transplanted into the guts of anxious and timid mice, they become more adventurous. The expression “thinking with your gut” may contain a larger kernel of truth than we thought.
The gut microbes are looking after their own interests, chief among them getting enough to eat and regulating the passage of food through their environment. The bacteria themselves appear to help manage these functions by producing signaling chemicals that regulate our appetite, satiety and digestion. Much of what we’re learning about the microbiome’s role in human metabolism has come from studying “gnotobiotic mice” — mice raised in labs like Jeffrey I. Gordon’s at Washington University, in St. Louis, to be microbially sterile, or germ-free. Recently, Gordon’s lab transplanted the gut microbes of Malawian children with kwashiorkor — an acute form of malnutrition — into germ-free mice. The lab found those mice with kwashiorkor who were fed the children’s typical diet could not readily metabolize nutrients, indicating that it may take more than calories to remedy malnutrition. Repairing a patient’s disordered metabolism may require reshaping the community of species in his or her gut.
Keeping the immune system productively engaged with microbes — exposed to lots of them in our bodies, our diet and our environment — is another important ecosystem service and one that might turn out to be critical to our health. “We used to think the immune system had this fairly straightforward job,” Michael Fischbach, a biochemist at the University of California, San Francisco, says. “All bacteria were clearly ‘nonself’ so simply had to be recognized and dealt with. But the job of the immune system now appears to be far more nuanced and complex. It has to learn to consider our mutualists” — e.g., resident bacteria — “as self too. In the future we won’t even call it the immune system, but the microbial interaction system.” The absence of constructive engagement between microbes and immune system (particularly during certain windows of development) could be behind the increase in autoimmune conditions in the West.
So why haven’t we evolved our own systems to perform these most critical functions of life? Why have we outsourced all this work to a bunch of microbes? One theory is that, because microbes evolve so much faster than we do (in some cases a new generation every 20 minutes), they can respond to changes in the environment — to threats as well as opportunities — with much greater speed and agility than “we” can. Exquisitely reactive and adaptive, bacteria can swap genes and pieces of DNA among themselves. This versatility is especially handy when a new toxin or food source appears in the environment. The microbiota can swiftly come up with precisely the right gene needed to fight it — or eat it. In one recent study, researchers found that a common gut microbe in Japanese people has acquired a gene from a marine bacterium that allows the Japanese to digest seaweed, something the rest of us can’t do as well.
This plasticity serves to extend our comparatively rigid genome, giving us access to a tremendous bag of biochemical tricks we did not need to evolve ourselves. “The bacteria in your gut are continually reading the environment and responding,” says Joel Kimmons, a nutrition scientist and epidemiologist at the Centers for Disease Control and Prevention in Atlanta. “They’re a microbial mirror of the changing world. And because they can evolve so quickly, they help our bodies respond to changes in our environment.”
A handful of microbiologists have begun sounding the alarm about our civilization’s unwitting destruction of the human microbiome and its consequences. Important microbial species may have already gone extinct, before we have had a chance to learn who they are or what they do. What we think of as an interior wilderness may in fact be nothing of the kind, having long ago been reshaped by unconscious human actions. Taking the ecological metaphor further, the “Westernized microbiome” most of us now carry around is in fact an artifact of civilization, no more a wilderness today than, say, the New Jersey Meadowlands.
To obtain a clearer sense of what has been lost, María Gloria Dominguez-Bello, a Venezuelan-born microbiologist at New York University, has been traveling to remote corners of the Amazon to collect samples from hunter-gatherers who have had little previous contact with Westerners or Western medicine. “We want to see how the human microbiota looks before antibiotics, before processed food, before modern birth,” she told me. “These samples are really gold.”

Preliminary results indicate that a pristine microbiome — of people who have had little or no contact with Westerners — features much greater biodiversity, including a number of species never before sequenced, and, as mentioned, much higher levels of prevotella than is typically found in the Western gut. Dominguez-Bello says these vibrant, diverse and antibiotic-naïve microbiomes may play a role in Amerindians’ markedly lower rates of allergies, asthma, atopic disease and chronic conditions like Type 2 diabetes and cardiovascular disease.
One bacterium commonly found in the non-Western microbiome but nearly extinct in ours is a corkscrew-shaped inhabitant of the stomach by the name of Helicobacter pylori. Dominguez-Bello’s husband, Martin Blaser, a physician and microbiologist at N.Y.U., has been studying H. pylori since the mid-1980s and is convinced that it is an endangered species, the extinction of which we may someday rue. According to the “missing microbiota hypothesis,” we depend on microbes like H. pylori to regulate various metabolic and immune functions, and their disappearance is disordering those systems. The loss is cumulative: “Each generation is passing on fewer of these microbes,” Blaser told me, with the result that the Western microbiome is being progressively impoverished.
He calls H. pylori the “poster child” for the missing microbes and says medicine has actually been trying to exterminate it since 1983, when Australian scientists proposed that the microbe was responsible for peptic ulcers; it has since been implicated in stomach cancer as well. But H. pylori is a most complicated character, the entire spectrum of microbial good and evil rolled into one bug. Scientists learned that H. pylori also plays a role in regulating acid in the stomach. Presumably it does this to render its preferred habitat inhospitable to competitors, but the effect on its host can be salutary. People without H. pylori may not get peptic ulcers, but they frequently do suffer from acid reflux. Untreated, this can lead to Barrett’s esophagus and, eventually, a certain type of esophageal cancer, rates of which have soared in the West as H. pylori has gone missing.
When after a recent bout of acid reflux, my doctor ordered an endoscopy, I discovered that, like most Americans today, my stomach has no H. pylori. My gastroenterologist was pleased, but after talking to Blaser, the news seemed more equivocal, because H. pylori also does us a lot of good. The microbe engages with the immune system, quieting the inflammatory response in ways that serve its own interests — to be left in peace — as well as our own. This calming effect on the immune system may explain why populations that still harbor H. pylori are less prone to allergy and asthma. Blaser’s lab has also found evidence that H. pylori plays an important role in human metabolism by regulating levels of the appetite hormone ghrelin. “When the stomach is empty, it produces a lot of ghrelin, the chemical signal to the brain to eat,” Blaser says. “Then, when it has had enough, the stomach shuts down ghrelin production, and the host feels satiated.” He says the disappearance of H. pylori may be contributing to obesity by muting these signals.
But what about the diseases H. pylori is blamed for? Blaser says these tend to occur only late in life, and he makes the rather breathtaking suggestion that this microbe’s evolutionary role might be to help shuffle us off life’s stage once our childbearing years have passed. So important does Blaser regard this strange, paradoxical symbiont that he has proposed not one but two unconventional therapeutic interventions: inoculate children with H. pylori to give them the benefit of its services early in life, and then exterminate it with antibiotics at age 40, when it is liable to begin causing trouble.
These days Blaser is most concerned about the damage that antibiotics, even in tiny doses, are doing to the microbiome — and particularly to our immune system and weight. “Farmers have been performing a great experiment for more than 60 years,” Blaser says, “by giving subtherapeutic doses of antibiotics to their animals to make them gain weight.” Scientists aren’t sure exactly why this practice works, but the drugs may favor bacteria that are more efficient at harvesting energy from the diet. “Are we doing the same thing to our kids?” he asks. Children in the West receive, on average, between 10 and 20 courses of antibiotics before they turn 18. And those prescribed drugs aren’t the only antimicrobials finding their way to the microbiota; scientists have found antibiotic residues in meat, milk and surface water as well. Blaser is also concerned about the use of antimicrobial compounds in our diet and everyday lives — everything from chlorine washes for lettuce to hand sanitizers. “We’re using these chemicals precisely because they’re antimicrobial,” Blaser says. “And of course they do us some good. But we need to ask, what are they doing to our microbiota?” No one is questioning the value of antibiotics to civilization — they have helped us to conquer a great many infectious diseases and increased our life expectancy. But, as in any war, the war on bacteria appears to have had some unintended consequences.
One of the more striking results from the sequencing of my microbiome was the impact of a single course of antibiotics on my gut community. My dentist had put me on a course of Amoxicillin as a precaution before oral surgery. (Without prophylactic antibiotics, of course, surgery would be considerably more dangerous.) Within a week, my impressively non-Western “alpha diversity” — a measure of the microbial diversity in my gut — had plummeted and come to look very much like the American average. My (possibly) healthy levels of prevotella had also disappeared, to be replaced by a spike in bacteroides (much more common in the West) and an alarming bloom of proteobacteria, a phylum that includes a great many weedy and pathogenic characters, including E. coli and salmonella. What had appeared to be a pretty healthy, diversified gut was now raising expressions of concern among the microbiologists who looked at my data.
“Your E. coli bloom is creepy,” Ruth Ley, a Cornell University microbiologist who studies the microbiome’s role in obesity, told me. “If we put that sample in germ-free mice, I bet they’d get inflamed.” Great. Just when I was beginning to think of myself as a promising donor for a fecal transplant, now I had a gut that would make mice sick. I was relieved to learn that my gut community would eventually bounce back to something resembling its former state. Yet one recent study found that when subjects were given a second course of antibiotics, the recovery of their interior ecosystem was less complete than after the first.
Few of the scientists I interviewed had much doubt that the Western diet was altering our gut microbiome in troubling ways. Some, like Blaser, are concerned about the antimicrobials we’re ingesting with our meals; others with the sterility of processed food. Most agreed that the lack of fiber in the Western diet was deleterious to the microbiome, and still others voiced concerns about the additives in processed foods, few of which have ever been studied for their specific effects on the microbiota. According to a recent article in Nature by the Stanford microbiologist Justin Sonnenburg, “Consumption of hyperhygienic, mass-produced, highly processed and calorie-dense foods is testing how rapidly the microbiota of individuals in industrialized countries can adapt.” As our microbiome evolves to cope with the Western diet, Sonnenburg says he worries that various genes are becoming harder to find as the microbiome’s inherent biodiversity declines along with our everyday exposure to bacteria.

Catherine Lozupone in Boulder and Andrew Gewirtz, an immunologist at Georgia State University, directed my attention to the emulsifiers commonly used in many processed foods — ingredients with names like lecithin, Datem, CMC and polysorbate 80. Gewirtz’s lab has done studies in mice indicating that some of these detergentlike compounds may damage the mucosa — the protective lining of the gut wall — potentially leading to leakage and inflammation.
A growing number of medical researchers are coming around to the idea that the common denominator of many, if not most, of the chronic diseases from which we suffer today may be inflammation — a heightened and persistent immune response by the body to a real or perceived threat. Various markers for inflammation are common in people with metabolic syndrome, the complex of abnormalities that predisposes people to illnesses like cardiovascular disease, obesity, Type 2 diabetes and perhaps cancer. While health organizations differ on the exact definition of metabolic syndrome, a 2009 report from the Centers for Disease Control and Prevention found that 34 percent of American adults are afflicted with the condition. But is inflammation yet another symptom of metabolic syndrome, or is it perhaps the cause of it? And if it is the cause, what is its origin?
One theory is that the problem begins in the gut, with a disorder of the microbiota, specifically of the all-important epithelium that lines our digestive tract. This internal skin — the surface area of which is large enough to cover a tennis court — mediates our relationship to the world outside our bodies; more than 50 tons of food pass through it in a lifetime. The microbiota play a critical role in maintaining the health of the epithelium: some bacteria, like the bifidobacteria and Lactobacillus plantarum (common in fermented vegetables), seem to directly enhance its function. These and other gut bacteria also contribute to its welfare by feeding it. Unlike most tissues, which take their nourishment from the bloodstream, epithelial cells in the colon obtain much of theirs from the short-chain fatty acids that gut bacteria produce as a byproduct of their fermentation of plant fiber in the large intestine.
But if the epithelial barrier isn’t properly nourished, it can become more permeable, allowing it to be breached. Bacteria, endotoxins — which are the toxic byproducts of certain bacteria — and proteins can slip into the blood stream, thereby causing the body’s immune system to mount a response. This resulting low-grade inflammation, which affects the entire body, may lead over time to metabolic syndrome and a number of the chronic diseases that have been linked to it.
Evidence in support of this theory is beginning to accumulate, some of the most intriguing coming from the lab of Patrice Cani at the Université Catholique de Louvain in Brussels. When Cani fed a high-fat, “junk food” diet to mice, the community of microbes in their guts changed much as it does in humans on a fast-food diet. But Cani also found the junk-food diet made the animals’ gut barriers notably more permeable, allowing endotoxins to leak into the bloodstream. This produced a low-grade inflammation that eventually led to metabolic syndrome. Cani concludes that, at least in mice, “gut bacteria can initiate the inflammatory processes associated with obesity and insulin resistance” by increasing gut permeability.
These and other experiments suggest that inflammation in the gut may be the cause of metabolic syndrome, not its result, and that changes in the microbial community and lining of the gut wall may produce this inflammation. If Cani is correct — and there is now some evidence indicating that the same mechanism is at work in humans — then medical science may be on the trail of a Grand Unified Theory of Chronic Disease, at the very heart of which we will find the gut microbiome.
My first reaction to learning all this was to want to do something about it immediately, something to nurture the health of my microbiome. But most of the scientists I interviewed were reluctant to make practical recommendations; it’s too soon, they told me, we don’t know enough yet. Some of this hesitance reflects an understandable abundance of caution. The microbiome researchers don’t want to make the mistake of overpromising, as the genome researchers did. They are also concerned about feeding a gigantic bloom of prebiotic and probiotic quackery and rightly so: probiotics are already being hyped as the new panacea, even though it isn’t at all clear what these supposedly beneficial bacteria do for us or how they do what they do. There is some research suggesting that some probiotics may be effective in a number of ways: modulating the immune system; reducing allergic response; shortening the length and severity of colds in children; relieving diarrhea and irritable bowel symptoms; and improving the function of the epithelium. The problem is that, because the probiotic marketplace is largely unregulated, it’s impossible to know what, if anything, you’re getting when you buy a “probiotic” product. One study tested 14 commercial probiotics and found that only one contained the exact species stated on the label.
But some of the scientists’ reluctance to make recommendations surely flows from the institutional bias of science and medicine: that the future of microbiome management should remain firmly in the hands of science and medicine. Down this path — which holds real promise — lie improved probiotics and prebiotics, fecal transplants (with better names) and related therapies. Jeffrey Gordon, one of those scientists who peers far over the horizon, looks forward to a time when disorders of the microbiome will be treated with “synbiotics” — suites of targeted, next-generation probiotic microbes administered along with the appropriate prebiotic nutrients to nourish them. The fecal transplant will give way to something far more targeted: a purified and cultured assemblage of a dozen or so microbial species that, along with new therapeutic foods, will be introduced to the gut community to repair “lesions” — important missing species or functions. Yet, assuming it all works as advertised, such an approach will also allow Big Pharma and Big Food to stake out and colonize the human microbiome for profit.

When I asked Gordon about do-it-yourself microbiome management, he said he looked forward to a day “when people can cultivate this wonderful garden that is so influential in our health and well-being” — but that day awaits a lot more science. So he declined to offer any gardening tips or dietary advice. “We have to manage expectations,” he said.
Alas, I am impatient. So I gave up asking scientists for recommendations and began asking them instead how, in light of what they’ve learned about the microbiome, they have changed their own diets and lifestyles. Most of them have made changes. They were slower to take, or give their children, antibiotics. (I should emphasize that in no way is this an argument for the rejection of antibiotics when they are medically called for.) Some spoke of relaxing the sanitary regime in their homes, encouraging their children to play outside in the dirt and with animals — deliberately increasing their exposure to the great patina. Many researchers told me they had eliminated or cut back on processed foods, either because of its lack of fiber or out of concern about additives. In general they seemed to place less faith in probiotics (which few of them used) than in prebiotics — foods likely to encourage the growth of “good bacteria” already present. Several, including Justin Sonnenburg, said they had added fermented foods to their diet: yogurt, kimchi, sauerkraut. These foods can contain large numbers of probiotic bacteria, like L. plantarum and bifidobacteria, and while most probiotic bacteria don’t appear to take up permanent residence in the gut, there is evidence that they might leave their mark on the community, sometimes by changing the gene expression of the permanent residents — in effect turning on or off metabolic pathways within the cell — and sometimes by stimulating or calming the immune response.
What about increasing our exposure to bacteria? “There’s a case for dirtying up your diet,” Sonnenburg told me. Yet advising people not to thoroughly wash their produce is probably unwise in a world of pesticide residues. “I view it as a cost-benefit analysis,” Sonnenburg wrote in an e-mail. “Increased exposure to environmental microbes likely decreases chance of many Western diseases, but increases pathogen exposure. Certainly the costs go up as scary antibiotic-resistant bacteria become more prevalent.” So wash your hands in situations when pathogens or toxic chemicals are likely present, but maybe not after petting your dog. “In terms of food, I think eating fermented foods is the answer — as opposed to not washing food, unless it is from your garden,” he said.
With his wife, Erica, also a microbiologist, Sonnenburg tends a colony of gnotobiotic mice at Stanford, examining (among other things) the effects of the Western diet on their microbiota. (Removing fiber drives down diversity, but the effect is reversible.) He’s an amateur baker, and when I visited his lab, we talked about the benefits of baking with whole grains.
“Fiber is not a single nutrient,” Sonnenburg said, which is why fiber supplements are no magic bullet. “There are hundreds of different polysaccharides” — complex carbohydrates, including fiber — “in plants, and different microbes like to chomp on different ones.” To boost fiber, the food industry added lots of a polysaccharide called inulin to hundreds of products, but that’s just one kind (often derived from the chicory-plant root) and so may only favor a limited number of microbes. I was hearing instead an argument for a variety of whole grains and a diverse diet of plants and vegetables as well as fruits. “The safest way to increase your microbial biodiversity is to eat a variety of polysaccharides,” he said.

His comment chimed with something a gastroenterologist at the University of Pittsburgh told me. “The big problem with the Western diet,” Stephen O’Keefe said, “is that it doesn’t feed the gut, only the upper G I. All the food has been processed to be readily absorbed, leaving nothing for the lower G I. But it turns out that one of the keys to health is fermentation in the large intestine.” And the key to feeding the fermentation in the large intestine is giving it lots of plants with their various types of fiber, including resistant starch (found in bananas, oats, beans); soluble fiber (in onions and other root vegetables, nuts); and insoluble fiber (in whole grains, especially bran, and avocados).
With our diet of swiftly absorbed sugars and fats, we’re eating for one and depriving the trillion of the food they like best: complex carbohydrates and fermentable plant fibers. The byproduct of fermentation is the short-chain fatty acids that nourish the gut barrier and help prevent inflammation. And there are studies suggesting that simply adding plants to a fast-food diet will mitigate its inflammatory effect.
The outlines of a diet for the new superorganism were coming clear, and it didn’t require the ministrations of the food scientists at Nestlé or General Mills to design it. Big Food and Big Pharma probably do have a role to play, as will Jeffrey Gordon’s next-generation synbiotics, in repairing the microbiota of people who can’t or don’t care to simply change their diets. This is going to be big business. Yet the components of a microbiota-friendly diet are already on the supermarket shelves and in farmers’ markets.
Viewed from this perspective, the foods in the markets appear in a new light, and I began to see how you might begin to shop and cook with the microbiome in mind, the better to feed the fermentation in our guts. The less a food is processed, the more of it that gets safely through the gastrointestinal tract and into the eager clutches of the microbiota. Al dente pasta, for example, feeds the bugs better than soft pasta does; steel-cut oats better than rolled; raw or lightly cooked vegetables offer the bugs more to chomp on than overcooked, etc. This is at once a very old and a very new way of thinking about food: it suggests that all calories are not created equal and that the structure of a food and how it is prepared may matter as much as its nutrient composition.
It is a striking idea that one of the keys to good health may turn out to involve managing our internal fermentation. Having recently learned to manage several external fermentations — of bread and kimchi and beer — I know a little about the vagaries of that process. You depend on the microbes, and you do your best to align their interests with yours, mainly by feeding them the kinds of things they like to eat — good “substrate.” But absolute control of the process is too much to hope for. It’s a lot more like gardening than governing.
The successful gardener has always known you don’t need to master the science of the soil, which is yet another hotbed of microbial fermentation, in order to nourish and nurture it. You just need to know what it likes to eat — basically, organic matter — and how, in a general way, to align your interests with the interests of the microbes and the plants. The gardener also discovers that, when pathogens or pests appear, chemical interventions “work,” that is, solve the immediate problem, but at a cost to the long-term health of the soil and the whole garden. The drive for absolute control leads to unanticipated forms of disorder.
This, it seems to me, is pretty much where we stand today with respect to our microbiomes — our teeming, quasi-wilderness. We don’t know a lot, but we probably know enough to begin taking better care of it. We have a pretty good idea of what it likes to eat, and what strong chemicals do to it. We know all we need to know, in other words, to begin, with modesty, to tend the unruly garden within.