Arquivo da tag: Intestinos

Can the Bacteria in Your Gut Explain Your Mood? (New York Times)

Eighteen vials were rocking back and forth on a squeaky mechanical device the shape of a butcher scale, and Mark Lyte was beside himself with excitement. ‘‘We actually got some fresh yesterday — freshly frozen,’’ Lyte said to a lab technician. Each vial contained a tiny nugget of monkey feces that were collected at the Harlow primate lab near Madison, Wis., the day before and shipped to Lyte’s lab on the Texas Tech University Health Sciences Center campus in Abilene, Tex.

Lyte’s interest was not in the feces per se but in the hidden form of life they harbor. The digestive tube of a monkey, like that of all vertebrates, contains vast quantities of what biologists call gut microbiota. The genetic material of these trillions of microbes, as well as others living elsewhere in and on the body, is collectively known as the microbiome. Taken together, these bacteria can weigh as much as six pounds, and they make up a sort of organ whose functions have only begun to reveal themselves to science. Lyte has spent his career trying to prove that gut microbes communicate with the nervous system using some of the same neurochemicals that relay messages in the brain.

Inside a closet-size room at his lab that afternoon, Lyte hunched over to inspect the vials, whose samples had been spun down in a centrifuge to a radiant, golden broth. Lyte, 60, spoke fast and emphatically. ‘‘You wouldn’t believe what we’re extracting out of poop,’’ he told me. ‘‘We found that the guys here in the gut make neurochemicals. We didn’t know that. Now, if they make this stuff here, does it have an influence there? Guess what? We make the same stuff. Maybe all this communication has an influence on our behavior.’’

Since 2007, when scientists announced plans for a Human Microbiome Project to catalog the micro-organisms living in our body, the profound appreciation for the influence of such organisms has grown rapidly with each passing year. Bacteria in the gut produce vitamins and break down our food; their presence or absence has been linked to obesity, inflammatory bowel disease and the toxic side effects of prescription drugs. Biologists now believe that much of what makes us human depends on microbial activity. The two million unique bacterial genes found in each human microbiome can make the 23,000 genes in our cells seem paltry, almost negligible, by comparison. ‘‘It has enormous implications for the sense of self,’’ Tom Insel, the director of the National Institute of Mental Health, told me. ‘‘We are, at least from the standpoint of DNA, more microbial than human. That’s a phenomenal insight and one that we have to take seriously when we think about human development.’’

Given the extent to which bacteria are now understood to influence human physiology, it is hardly surprising that scientists have turned their attention to how bacteria might affect the brain. Micro-organisms in our gut secrete a profound number of chemicals, and researchers like Lyte have found that among those chemicals are the same substances used by our neurons to communicate and regulate mood, like dopamine, serotonin and gamma-aminobutyric acid (GABA). These, in turn, appear to play a function in intestinal disorders, which coincide with high levels of major depression and anxiety. Last year, for example, a group in Norway examined feces from 55 people and found certain bacteria were more likely to be associated with depressive patients.

At the time of my visit to Lyte’s lab, he was nearly six months into an experiment that he hoped would better establish how certain gut microbes influenced the brain, functioning, in effect, as psychiatric drugs. He was currently compiling a list of the psychoactive compounds found in the feces of infant monkeys. Once that was established, he planned to transfer the microbes found in one newborn monkey’s feces into another’s intestine, so that the recipient would end up with a completely new set of microbes — and, if all went as predicted, change their neurodevelopment. The experiment reflected an intriguing hypothesis. Anxiety, depression and several pediatric disorders, including autism and hyperactivity, have been linked with gastrointestinal abnormalities. Microbial transplants were not invasive brain surgery, and that was the point: Changing a patient’s bacteria might be difficult but it still seemed more straightforward than altering his genes.

When Lyte began his work on the link between microbes and the brain three decades ago, it was dismissed as a curiosity. By contrast, last September, the National Institute of Mental Health awarded four grants worth up to $1 million each to spur new research on the gut microbiome’s role in mental disorders, affirming the legitimacy of a field that had long struggled to attract serious scientific credibility. Lyte and one of his longtime colleagues, Christopher Coe, at the Harlow primate lab, received one of the four. ‘‘What Mark proposed going back almost 25 years now has come to fruition,’’ Coe told me. ‘‘Now what we’re struggling to do is to figure out the logic of it.’’ It seems plausible, if not yet proved, that we might one day use microbes to diagnose neurodevelopmental disorders, treat mental illnesses and perhaps even fix them in the brain.

In 2011, a team of researchers at University College Cork, in Ireland, and McMaster University, in Ontario, published a study in Proceedings of the National Academy of Science that has become one of the best-known experiments linking bacteria in the gut to the brain. Laboratory mice were dropped into tall, cylindrical columns of water in what is known as a forced-swim test, which measures over six minutes how long the mice swim before they realize that they can neither touch the bottom nor climb out, and instead collapse into a forlorn float. Researchers use the amount of time a mouse floats as a way to measure what they call ‘‘behavioral despair.’’ (Antidepressant drugs, like Zoloft and Prozac, were initially tested using this forced-swim test.)

For several weeks, the team, led by John Cryan, the neuroscientist who designed the study, fed a small group of healthy rodents a broth infused with Lactobacillus rhamnosus, a common bacterium that is found in humans and also used to ferment milk into probiotic yogurt. Lactobacilli are one of the dominant organisms babies ingest as they pass through the birth canal. Recent studies have shown that mice stressed during pregnancy pass on lowered levels of the bacterium to their pups. This type of bacteria is known to release immense quantities of GABA; as an inhibitory neurotransmitter, GABA calms nervous activity, which explains why the most common anti-anxiety drugs, like Valium and Xanax, work by targeting GABA receptors.

Cryan found that the mice that had been fed the bacteria-laden broth kept swimming longer and spent less time in a state of immobilized woe. ‘‘They behaved as if they were on Prozac,’’ he said. ‘‘They were more chilled out and more relaxed.’’ The results suggested that the bacteria were somehow altering the neural chemistry of mice.

Until he joined his colleagues at Cork 10 years ago, Cryan thought about microbiology in terms of pathology: the neurological damage created by diseases like syphilis or H.I.V. ‘‘There are certain fields that just don’t seem to interact well,’’ he said. ‘‘Microbiology and neuroscience, as whole disciplines, don’t tend to have had much interaction, largely because the brain is somewhat protected.’’ He was referring to the fact that the brain is anatomically isolated, guarded by a blood-brain barrier that allows nutrients in but keeps out pathogens and inflammation, the immune system’s typical response to germs. Cryan’s study added to the growing evidence that signals from beneficial bacteria nonetheless find a way through the barrier. Somehow — though his 2011 paper could not pinpoint exactly how — micro-organisms in the gut tickle a sensory nerve ending in the fingerlike protrusion lining the intestine and carry that electrical impulse up the vagus nerve and into the deep-brain structures thought to be responsible for elemental emotions like anxiety. Soon after that, Cryan and a co-author, Ted Dinan, published a theory paper in Biological Psychiatry calling these potentially mind-altering microbes ‘‘psychobiotics.’’

It has long been known that much of our supply of neurochemicals — an estimated 50 percent of the dopamine, for example, and a vast majority of the serotonin — originate in the intestine, where these chemical signals regulate appetite, feelings of fullness and digestion. But only in recent years has mainstream psychiatric research given serious consideration to the role microbes might play in creating those chemicals. Lyte’s own interest in the question dates back to his time as a postdoctoral fellow at the University of Pittsburgh in 1985, when he found himself immersed in an emerging field with an unwieldy name: psychoneuroimmunology, or PNI, for short. The central theory, quite controversial at the time, suggested that stress worsened disease by suppressing our immune system.

By 1990, at a lab in Mankato, Minn., Lyte distilled the theory into three words, which he wrote on a chalkboard in his office: Stress->Immune->Disease. In the course of several experiments, he homed in on a paradox. When he dropped an intruder mouse in the cage of an animal that lived alone, the intruder ramped up its immune system — a boost, he suspected, intended to fight off germ-ridden bites or scratches. Surprisingly, though, this did not stop infections. It instead had the opposite effect: Stressed animals got sick. Lyte walked up to the board and scratched a line through the word ‘‘Immune.’’ Stress, he suspected, directly affected the bacterial bugs that caused infections.

To test how micro-organisms reacted to stress, he filled petri plates with a bovine-serum-based medium and laced the dishes with a strain of bacterium. In some, he dropped norepinephrine, a neurochemical that mammals produce when stressed. The next day, he snapped a Polaroid. The results were visible and obvious: The control plates were nearly barren, but those with the norepinephrine bloomed with bacteria that filigreed in frostlike patterns. Bacteria clearly responded to stress.

Then, to see if bacteria could induce stress, Lyte fed white mice a liquid solution of Campylobacter jejuni, a bacterium that can cause food poisoning in humans but generally doesn’t prompt an immune response in mice. To the trained eye, his treated mice were as healthy as the controls. But when he ran them through a plexiglass maze raised several feet above the lab floor, the bacteria-fed mice were less likely to venture out on the high, unprotected ledges of the maze. In human terms, they seemed anxious. Without the bacteria, they walked the narrow, elevated planks.

Credit: Illustration by Andrew Rae 

Each of these results was fascinating, but Lyte had a difficult time finding microbiology journals that would publish either. ‘‘It was so anathema to them,’’ he told me. When the mouse study finally appeared in the journal Physiology & Behavior in 1998, it garnered little attention. And yet as Stephen Collins, a gastroenterologist at McMaster University, told me, those first papers contained the seeds of an entire new field of research. ‘‘Mark showed, quite clearly, in elegant studies that are not often cited, that introducing a pathological bacterium into the gut will cause a change in behavior.’’

Lyte went on to show how stressful conditions for newborn cattle worsened deadly E. coli infections. In another experiment, he fed mice lean ground hamburger that appeared to improve memory and learning — a conceptual proof that by changing diet, he could change gut microbes and change behavior. After accumulating nearly a decade’s worth of evidence, in July 2008, he flew to Washington to present his research. He was a finalist for the National Institutes of Health’s Pioneer Award, a $2.5 million grant for so-called blue-sky biomedical research. Finally, it seemed, his time had come. When he got up to speak, Lyte described a dialogue between the bacterial organ and our central nervous system. At the two-minute mark, a prominent scientist in the audience did a spit take.

‘‘Dr. Lyte,’’ he later asked at a question-and-answer session, ‘‘if what you’re saying is right, then why is it when we give antibiotics to patients to kill bacteria, they are not running around crazy on the wards?’’

Lyte knew it was a dismissive question. And when he lost out on the grant, it confirmed to him that the scientific community was still unwilling to imagine that any part of our neural circuitry could be influenced by single-celled organisms. Lyte published his theory in Medical Hypotheses, a low-ranking journal that served as a forum for unconventional ideas. The response, predictably, was underwhelming. ‘‘I had people call me crazy,’’ he said.

But by 2011 — when he published a second theory paper in Bioessays, proposing that probiotic bacteria could be tailored to treat specific psychological diseases — the scientific community had become much more receptive to the idea. A Canadian team, led by Stephen Collins, had demonstrated that antibiotics could be linked to less cautious behavior in mice, and only a few months before Lyte, Sven Pettersson, a microbiologist at the Karolinska Institute in Stockholm, published a landmark paper in Proceedings of the National Academy of Science that showed that mice raised without microbes spent far more time running around outside than healthy mice in a control group; without the microbes, the mice showed less apparent anxiety and were more daring. In Ireland, Cryan published his forced-swim-test study on psychobiotics. There was now a groundswell of new research. In short order, an implausible idea had become a hypothesis in need of serious validation.

Late last year, Sarkis Mazmanian, a microbiologist at the California Institute of Technology, gave a presentation at the Society for Neuroscience, ‘‘Gut Microbes and the Brain: Paradigm Shift in Neuroscience.’’ Someone had inadvertently dropped a question mark from the end, so the speculation appeared to be a definitive statement of fact. But if anyone has a chance of delivering on that promise, it’s Mazmanian, whose research has moved beyond the basic neurochemicals to focus on a broader class of molecules called metabolites: small, equally druglike chemicals that are produced by micro-organisms. Using high-powered computational tools, he also hopes to move beyond the suggestive correlations that have typified psychobiotic research to date, and instead make decisive discoveries about the mechanisms by which microbes affect brain function.

Two years ago, Mazmanian published a study in the journal Cell with Elaine Hsiao, then a graduate student at his lab and now a neuroscientist at Caltech, that made a provocative link between a single molecule and behavior. Their research found that mice exhibiting abnormal communication and repetitive behaviors, like obsessively burying marbles, were mollified when they were given one of two strains of the bacterium Bacteroides fragilis.

The study added to a working hypothesis in the field that microbes don’t just affect the permeability of the barrier around the brain but also influence the intestinal lining, which normally prevents certain bacteria from leaking out and others from getting in. When the intestinal barrier was compromised in his model, normally ‘‘beneficial’’ bacteria and the toxins they produce seeped into the bloodstream and raised the possibility they could slip past the blood-brain barrier. As one of his colleagues, Michael Fischbach, a microbiologist at the University of California, San Francisco, said: ‘‘The scientific community has a way of remaining skeptical until every last arrow has been drawn, until the entire picture is colored in. Other scientists drew the pencil outlines, and Sarkis is filling in a lot of the color.’’

Mazmanian knew the results offered only a provisional explanation for why restrictive diets and antibacterial treatments seemed to help some children with autism: Altering the microbial composition might be changing the permeability of the intestine. ‘‘The larger concept is, and this is pure speculation: Is a disease like autism really a disease of the brain or maybe a disease of the gut or some other aspect of physiology?’’ Mazmanian said. For any disease in which such a link could be proved, he saw a future in drugs derived from these small molecules found inside microbes. (A company he co-founded, Symbiotix Biotherapies, is developing a complex sugar called PSA, which is associated with Bacteroides fragilis, into treatments for intestinal disease and multiple sclerosis.) In his view, the prescriptive solutions probably involve more than increasing our exposure to environmental microbes in soil, dogs or even fermented foods; he believed there were wholesale failures in the way we shared our microbes and inoculated children with these bacteria. So far, though, the only conclusion he could draw was that disorders once thought to be conditions of the brain might be symptoms of microbial disruptions, and it was the careful defining of these disruptions that promised to be helpful in the coming decades.

The list of potential treatments incubating in labs around the world is startling. Several international groups have found that psychobiotics had subtle yet perceptible effects in healthy volunteers in a battery of brain-scanning and psychological tests. Another team in Arizona recently finished an open trial on fecal transplants in children with autism. (Simultaneously, at least two offshore clinics, in Australia and England, began offering fecal microbiota treatments to treat neurological disorders, like multiple sclerosis.) Mazmanian, however, cautions that this research is still in its infancy. ‘‘We’ve reached the stage where there’s a lot of, you know, ‘The microbiome is the cure for everything,’ ’’ he said. ‘‘I have a vested interest if it does. But I’d be shocked if it did.’’

Lyte issues the same caveat. ‘‘People are obviously desperate for solutions,’’ Lyte said when I visited him in Abilene. (He has since moved to Iowa State’s College of Veterinary Medicine.) ‘‘My main fear is the hype is running ahead of the science.’’ He knew that parents emailing him for answers meant they had exhausted every option offered by modern medicine. ‘‘It’s the Wild West out there,’’ he said. ‘‘You can go online and buy any amount of probiotics for any number of conditions now, and my paper is one of those cited. I never said go out and take probiotics.’’ He added, ‘‘We really need a lot more research done before we actually have people trying therapies out.’’

If the idea of psychobiotics had now, in some ways, eclipsed him, it was nevertheless a curious kind of affirmation, even redemption: an old-school microbiologist thrust into the midst of one of the most promising aspects of neuroscience. At the moment, he had a rough map in his head and a freezer full of monkey fecals that might translate, somehow, into telling differences between gregarious or shy monkeys later in life. I asked him if what amounted to a personality transplant still sounded a bit far-fetched. He seemed no closer to unlocking exactly what brain functions could be traced to the same organ that produced feces. ‘‘If you transfer the microbiota from one animal to another, you can transfer the behavior,’’ Lyte said. ‘‘What we’re trying to understand are the mechanisms by which the microbiota can influence the brain and development. If you believe that, are you now out on the precipice? The answer is yes. Do I think it’s the future? I think it’s a long way away.’’

Anúncios

The Surprising Link Between Gut Bacteria And Anxiety (Huff Post)

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Posted: 01/04/2015 10:05 am EST 

GUT BACTERIA

In recent years, neuroscientists have become increasingly interested in the idea that there may be a powerful link between the human brain and gut bacteria. And while a growing body of research has provided evidence of the brain-gut connection, most of these studies so far have been conducted on animals.

Now, promising new research from neurobiologists at Oxford University offers some preliminary evidence of a connection between gut bacteria and mental health in humans. The researchers found that supplements designed to boost healthy bacteria in the gastrointestinal tract (“prebiotics”) may have an anti-anxiety effect insofar as they alter the way that people process emotional information.

While probiotics consist of strains of good bacteria, prebiotics are carbohydrates that act as nourishment for those bacteria. With increasing evidence that gut bacteria may exert some influence on brain function and mental health, probiotics and prebiotics are being increasingly studied for the potential alleviation of anxiety and depression symptoms.

“Prebiotics are dietary fibers (short chains of sugar molecules) that good bacteria break down, and use to multiply,” the study’s lead author, Oxford psychiatrist and neurobiologist Dr. Philip Burnet, told The Huffington Post. “Prebiotics are ‘food’ for good bacteria already present in the gut. Taking prebiotics therefore increases the numbers of all species of good bacteria in the gut, which will theoretically have greater beneficial effects than [introducing] a single species.”

To test the efficacy of prebiotics in reducing anxiety, the researchers asked 45 healthy adults between the ages of 18 and 45 to take either a prebiotic or a placebo every day for three weeks. After the three weeks had passed, the researchers completed several computer tests assessing how they processed emotional information, such as positive and negatively-charged words.

The results of one of the tests revealed that subjects who had taken the prebiotic paid less attention to negative information and more attention to positive information, compared to the placebo group, suggesting that the prebiotic group had less anxiety when confronted with negative stimuli. This effect is similar to that which has been observed among individuals who have taken antidepressants or anti-anxiety medication.

The researchers also found that the subjects who took the prebiotics had lower levels of cortisol — a stress hormone which has been linked with anxiety and depression — in their saliva when they woke up in the morning.

While previous research has documented that altering gut bacteria has a similarly anxiety-reducing effect in mice, the new study is one of the first to examine this phenomenon in humans. As of now, research on humans is in its early stages. A study conducted last year at UCLA found that women who consumed probiotics through regularly eating yogurt exhibited altered brain function in both a resting state and when performing an emotion-recognition task.

“Time and time again, we hear from patients that they never felt depressed or anxious until they started experiencing problems with their gut,” Dr. Kirsten Tillisch, the study’s lead author, said in a statement. “Our study shows that the gut–brain connection is a two-way street.”

So are we moving towards a future in which mental illness may be able to be treated (or at least managed) using targeted probiotic cocktails? Burnet says it’s possible, although they’re unlikely to replace conventional treatment.

“I think pre/probiotics will only be used as ‘adjuncts’ to conventional treatments, and never as mono-therapies,” Burnet tells HuffPost. “It is likely that these compounds will help to manage mental illness… they may also be used when there are metabolic and/or nutritional complications in mental illness, which may be caused by long-term use of current drugs.”

The findings were published in the journal Psychopharmacology.

Gut bacteria from a worm can degrade plastic (Science Daily)

Date: December 3, 2014

Source: American Chemical Society

Summary: Plastic is well-known for sticking around in the environment for years without breaking down, contributing significantly to litter and landfills. But scientists have now discovered that bacteria from the guts of a worm known to munch on food packaging can degrade polyethylene, the most common plastic.The finding could lead to new ways to help get rid of the otherwise persistent waste, the scientists say.

Some bacteria from the guts of waxworms could help us eliminate plastic trash. Credit: ACS

Plastic is well-known for sticking around in the environment for years without breaking down, contributing significantly to litter and landfills. But scientists have now discovered that bacteria from the guts of a worm known to munch on food packaging can degrade polyethylene, the most common plastic. Reported in the ACS journal Environmental Science & Technology, the finding could lead to new ways to help get rid of the otherwise persistent waste, the scientists say.

Jun Yang and colleagues point out that the global plastics industry churns out about 140 million tons of polyethylene every year. Much of it goes into the bags, bottles and boxes that many of us use regularly — and then throw out. Scientists have been trying to figure out for years how to make this plastic trash go away. Some of the most recent studies have tried siccing bacteria on plastic to degrade it, but these required first exposing the plastic to light or heat. Yang’s team wanted to find bacteria that could degrade polyethylene in one step.

The researchers turned to a plastic-eating moth larva, known as a waxworm. They found that at least two strains of the waxworm’s gut microbes could degrade polyethylene without a pretreatment step. They say the results point toward a new, more direct way to biodegrade plastic.

The authors acknowledge funding from the National Natural Science Foundation of China, the National Basic Research Program of China and the Shenzhen Key Laboratory of Bioenergy.

Journal Reference:

  1. Jun Yang, Yu Yang, Wei-Min Wu, Jiao Zhao, Lei Jiang. Evidence of Polyethylene Biodegradation by Bacterial Strains from the Guts of Plastic-Eating WaxwormsEnvironmental Science & Technology, 2014; 48 (23): 13776 DOI: 10.1021/es504038a

How the bacteria in our gut affect our cravings for food (Conversation)

November 6 2014, 10.00pm EST

Vincent Ho

Gut bacteria can manufacture special proteins that are very similar to hunger-regulating hormones. Lighthunter/Shutterstock

We’ve long known that that the gut is responsible for digesting food and expelling the waste. More recently, we realised the gut has many more important functions and acts a type of mini-brain, affecting our mood and appetite. Now, new research suggests it might also play a role in our cravings for certain types of food.

How does the mini-brain work?

The gut mini-brain produces a wide range of hormones and contains many of the same neurotransmitters as the brain. The gut also contains neurons that are located in the walls of the gut in a distributed network known as the enteric nervous system. In fact, there are more of these neurons in the gut than in the entire spinal cord.

The enteric nervous system communicates to the brain via the brain-gut axis and signals flow in both directions. The brain-gut axis is thought to be involved in many regular functions and systems within the healthy body, including the regulation of eating.

Let’s consider what happens to the brain-gut axis when we eat a meal. When food arrives in the stomach, certain gut hormones are secreted. These activate signalling pathways from the gut to the brainstem and the hypothalamus to stop food consumption. Such hormones include the appetite-suppressing hormones peptide YY and cholecystokinin.

Gut hormones can bind and activate receptor targets in the brain directly but there is strong evidence that the vagus nerve plays a major role in brain-gut signalling. The vagus nerve acts as a major highway in the brain-gut axis, connecting the over 100 million neurons in the enteric nervous system to the medulla (located at the base of the brain).

Research has shown that vagus nerve blockade can lead to marked weight loss, while vagus nerve stimulation is known to trigger excessive eating in rats.

This brings us to the topic of food cravings. Scientists have largely debunked the myth that food cravings are our bodies’ way of letting us know that we need a specific type of nutrient. Instead, an emerging body of research suggests that our food cravings may actually be significantly shaped by the bacteria that we have inside our gut. In order to explore this further we will cover the role of gut microbes.

Gut microbiota

As many as 90% of our cells are bacterial. In fact, bacterial genes outnumber human genes by a factor of 100 to one.

The gut is an immensely complex microbial ecosystem with many different species of bacteria, some of which can live in an oxygen-free environment. An average person has approximately 1.5 kilograms of gut bacteria. The term “gut microbiota” is used to describe the bacterial collective.

We each have around 1.5kg of bacteria in our guts. Christopher PooleyCC BY

Gut microbiota send signals to the brain via the brain-gut axis and can have dramatic effects on animal behaviour and health.

In one study, for example, mice that were genetically predisposed to obesity remained lean when they were raised in a sterile environment without gut microbiota. These germ-free mice were, however, transformed into obese mice when fed a faecal pellet that came from an obese mouse raised conventionally.

The role of gut microbiota in food cravings

There is growing evidence to support the role of gut microbiota in influencing why we crave certain foods.

We know that mice that are bred in germ-free environments prefer more sweets and have greater number of sweet taste receptors in their gut compared to normal mice. Research has also found that persons who are “chocolate desiring” have microbial breakdown products in their urine that are different from those of “chocolate indifferent individuals” despite eating identical diets.

Many gut bacteria can manufacture special proteins (called peptides) that are very similar to hormones such as peptide YY and ghrelin that regulate hunger. Humans and other animals have produced antibodies against these peptides. This raises the distinct possibility that microbes might be able to directly influence human eating behaviour through their peptides that mimic hunger-regulating hormones or indirectly through antibodies that can interfere with appetite regulation.

Practical implications

There are substantial challenges to overcome before we can apply this knowledge about gut microbiota in a practical sense.

First, there is the challenge of collecting the gut microbes. Traditionally this is collected from stools but gut microbiota is known to vary between different regions of the gut, such as the small intestine and colon. Obtaining bacterial tissue through endoscopy or another invasive collection technique in addition to stool samples may lead to more accurate representation of the gut microbiome.

Second, the type of sequencing that is currently used for gut microbiota screening is expensive and time-consuming. Advances will need to be made before this technology is in routine use.

Probably the greatest challenge in gut microbiota research is the establishment of a strong correlation between gut microbiota patterns and human disease. The science of gut microbiota is in its infancy and there needs to be much more research mapping out disease relationships.

Probiotics contain live microorganisms. Quanthem/Shutterstock

But there is reason to be hopeful. There is now strong interest in utilising both prebiotics and probiotics to alter our gut micro biome. Prebiotics are non-digestible carbohydrates that trigger the growth of beneficial gut bacteria, while probiotics are beneficial live microorganisms contained in foods and supplements.

Faecal transplantation is also now an accepted treatment for those patients that have a severe form of gut bacterial infection called Clostridium difficile, which has been unresponsive to antibiotics.

The use of such targeted strategies is likely to become increasingly common as we better understand how gut microbiota influence our bodily functions, including food cravings.

Certain gut bacteria may induce metabolic changes following exposure to artificial sweeteners (Science Daily)

Date: September 17, 2014

Source: Weizmann Institute of Science

Summary: Artificial sweeteners have long been promoted as diet and health aids. But breaking research shows that these products may be leading to the very diseases they were said to help prevent: scientists have discovered that, after exposure to artificial sweeteners, our gut bacteria may be triggering harmful metabolic changes.


This image depicts gut microbiota. Credit: Weizmann Institute of Science

Artificial sweeteners — promoted as aids to weight loss and diabetes prevention — could actually hasten the development of glucose intolerance and metabolic disease, and they do so in a surprising way: by changing the composition and function of the gut microbiota — the substantial population of bacteria residing in our intestines. These findings, the results of experiments in mice and humans, were published September 17 in Nature. Dr. Eran Elinav of the Weizmann Institute of Science’s Department of Immunology, who led this research together with Prof. Eran Segal of the Department of Computer Science and Applied Mathematics, says that the widespread use of artificial sweeteners in drinks and food, among other things, may be contributing to the obesity and diabetes epidemic that is sweeping much of the world.

For years, researchers have been puzzling over the fact that non-caloric artificial sweeteners do not seem to assist in weight loss, with some studies suggesting that they may even have an opposite effect. Graduate student Jotham Suez in Dr. Elinav’s lab, who led the study, collaborated with lab member Gili Zilberman-Shapira and graduate students Tal Korem and David Zeevi in Prof. Segal’s lab to discover that artificial sweeteners, even though they do not contain sugar, nonetheless have a direct effect on the body’s ability to utilize glucose. Glucose intolerance — generally thought to occur when the body cannot cope with large amounts of sugar in the diet — is the first step on the path to metabolic syndrome and adult-onset diabetes.

The scientists gave mice water laced with the three most commonly used artificial sweeteners, in amounts equivalent to those permitted by the U.S. Food and Drug Administration (FDA). These mice developed glucose intolerance, as compared to mice that drank water, or even sugar water. Repeating the experiment with different types of mice and different doses of the artificial sweeteners produced the same results — these substances were somehow inducing glucose intolerance.

Next, the researchers investigated a hypothesis that the gut microbiota are involved in this phenomenon. They thought the bacteria might do this by reacting to new substances like artificial sweeteners, which the body itself may not recognize as “food.” Indeed, artificial sweeteners are not absorbed in the gastrointestinal tract, but in passing through they encounter trillions of the bacteria in the gut microbiota.

The researchers treated mice with antibiotics to eradicate many of their gut bacteria; this resulted in a full reversal of the artificial sweeteners’ effects on glucose metabolism. Next, they transferred the microbiota from mice that consumed artificial sweeteners to “germ-free,” or sterile, mice — resulting in a complete transmission of the glucose intolerance into the recipient mice. This, in itself, was conclusive proof that changes to the gut bacteria are directly responsible for the harmful effects to their host’s metabolism. The group even found that incubating the microbiota outside the body, together with artificial sweeteners, was sufficient to induce glucose intolerance in the sterile mice. A detailed characterization of the microbiota in these mice revealed profound changes to their bacterial populations, including new microbial functions that are known to infer a propensity to obesity, diabetes, and complications of these problems in both mice and humans.

Does the human microbiome function in the same way? Dr. Elinav and Prof. Segal had a means to test this as well. As a first step, they looked at data collected from their Personalized Nutrition Project (www.personalnutrition.org), the largest human trial to date to look at the connection between nutrition and microbiota. Here, they uncovered a significant association between self-reported consumption of artificial sweeteners, personal configurations of gut bacteria, and the propensity for glucose intolerance. They next conducted a controlled experiment, asking a group of volunteers who did not generally eat or drink artificially sweetened foods to consume them for a week, and then undergo tests of their glucose levels and gut microbiota compositions.

The findings showed that many — but not all — of the volunteers had begun to develop glucose intolerance after just one week of artificial sweetener consumption. The composition of their gut microbiota explained the difference: the researchers discovered two different populations of human gut bacteria — one that induced glucose intolerance when exposed to the sweeteners, and one that had no effect either way. Dr. Elinav believes that certain bacteria in the guts of those who developed glucose intolerance reacted to the chemical sweeteners by secreting substances that then provoked an inflammatory response similar to sugar overdose, promoting changes in the body’s ability to utilize sugar.

Prof. Segal states, “The results of our experiments highlight the importance of personalized medicine and nutrition to our overall health. We believe that an integrated analysis of individualized ‘big data’ from our genome, microbiome, and dietary habits could transform our ability to understand how foods and nutritional supplements affect a person’s health and risk of disease.”

According to Dr. Elinav, “Our relationship with our own individual mix of gut bacteria is a huge factor in determining how the food we eat affects us. Especially intriguing is the link between use of artificial sweeteners — through the bacteria in our guts — to a tendency to develop the very disorders they were designed to prevent; this calls for reassessment of today’s massive, unsupervised consumption of these substances.”

Journal Reference:

  1. Jotham Suez, Tal Korem, David Zeevi, Gili Zilberman-Schapira, Christoph A. Thaiss, Ori Maza, David Israeli, Niv Zmora, Shlomit Gilad, Adina Weinberger, Yael Kuperman, Alon Harmelin, Ilana Kolodkin-Gal, Hagit Shapiro, Zamir Halpern, Eran Segal, Eran Elinav. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature, 2014; DOI: 10.1038/nature13793

Gut bacteria that protect against food allergies identified (Science Daily)

Date: August 25, 2014

Source: University of Chicago Medical Center

Summary: The presence of Clostridia, a common class of gut bacteria, protects against food allergies, a new study in mice finds. The discovery points toward probiotic therapies for this so-far untreatable condition. Food allergies affect 15 million Americans, including one in 13 children, who live with this potentially life-threatening disease that currently has no cure, researchers note.

Artist’s rendering of bacteria (stock illustration). Credit: © zuki70 / Fotolia

The presence of Clostridia, a common class of gut bacteria, protects against food allergies, a new study in mice finds. By inducing immune responses that prevent food allergens from entering the bloodstream, Clostridia minimize allergen exposure and prevent sensitization — a key step in the development of food allergies. The discovery points toward probiotic therapies for this so-far untreatable condition, report scientists from the University of Chicago, Aug 25 in the Proceedings of the National Academy of Sciences.

Although the causes of food allergy — a sometimes deadly immune response to certain foods — are unknown, studies have hinted that modern hygienic or dietary practices may play a role by disturbing the body’s natural bacterial composition. In recent years, food allergy rates among children have risen sharply — increasing approximately 50 percent between 1997 and 2011 — and studies have shown a correlation to antibiotic and antimicrobial use.

“Environmental stimuli such as antibiotic overuse, high fat diets, caesarean birth, removal of common pathogens and even formula feeding have affected the microbiota with which we’ve co-evolved,” said study senior author Cathryn Nagler, PhD, Bunning Food Allergy Professor at the University of Chicago. “Our results suggest this could contribute to the increasing susceptibility to food allergies.”

To test how gut bacteria affect food allergies, Nagler and her team investigated the response to food allergens in mice. They exposed germ-free mice (born and raised in sterile conditions to have no resident microorganisms) and mice treated with antibiotics as newborns (which significantly reduces gut bacteria) to peanut allergens. Both groups of mice displayed a strong immunological response, producing significantly higher levels of antibodies against peanut allergens than mice with normal gut bacteria.

This sensitization to food allergens could be reversed, however, by reintroducing a mix of Clostridia bacteria back into the mice. Reintroduction of another major group of intestinal bacteria, Bacteroides, failed to alleviate sensitization, indicating that Clostridia have a unique, protective role against food allergens.

Closing the door

To identify this protective mechanism, Nagler and her team studied cellular and molecular immune responses to bacteria in the gut. Genetic analysis revealed that Clostridia caused innate immune cells to produce high levels of interleukin-22 (IL-22), a signaling molecule known to decrease the permeability of the intestinal lining.

Antibiotic-treated mice were either given IL-22 or were colonized with Clostridia. When exposed to peanut allergens, mice in both conditions showed reduced allergen levels in their blood, compared to controls. Allergen levels significantly increased, however, after the mice were given antibodies that neutralized IL-22, indicating that Clostridia-induced IL-22 prevents allergens from entering the bloodstream.

“We’ve identified a bacterial population that protects against food allergen sensitization,” Nagler said. “The first step in getting sensitized to a food allergen is for it to get into your blood and be presented to your immune system. The presence of these bacteria regulates that process.” She cautions, however, that these findings likely apply at a population level, and that the cause-and-effect relationship in individuals requires further study.

While complex and largely undetermined factors such as genetics greatly affect whether individuals develop food allergies and how they manifest, the identification of a bacteria-induced barrier-protective response represents a new paradigm for preventing sensitization to food. Clostridia bacteria are common in humans and represent a clear target for potential therapeutics that prevent or treat food allergies. Nagler and her team are working to develop and test compositions that could be used for probiotic therapy and have filed a provisional patent.

“It’s exciting because we know what the bacteria are; we have a way to intervene,” Nagler said. “There are of course no guarantees, but this is absolutely testable as a therapeutic against a disease for which there’s nothing. As a mom, I can imagine how frightening it must be to worry every time your child takes a bite of food.”

“Food allergies affect 15 million Americans, including one in 13 children, who live with this potentially life-threatening disease that currently has no cure,” said Mary Jane Marchisotto, senior vice president of research at Food Allergy Research & Education. “We have been pleased to support the research that has been conducted by Dr. Nagler and her colleagues at the University of Chicago.”


Journal Reference:

  1. A. T. Stefka, T. Feehley, P. Tripathi, J. Qiu, K. McCoy, S. K. Mazmanian, M. Y. Tjota, G.-Y. Seo, S. Cao, B. R. Theriault, D. A. Antonopoulos, L. Zhou, E. B. Chang, Y.-X. Fu, C. R. Nagler. Commensal bacteria protect against food allergen sensitization. Proceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1412008111

Our Microbiome May Be Looking Out for Itself (New York Times)

A highly magnified view of Enterococcus faecalis, a bacterium that lives in the human gut. Microbes may affect our cravings, new research suggests.CreditCenters for Disease Control and Prevention

Your body is home to about 100 trillion bacteria and other microbes, collectively known as your microbiome. Naturalists first became aware of our invisible lodgers in the 1600s, but it wasn’t until the past few years that we’ve become really familiar with them.

This recent research has given the microbiome a cuddly kind of fame. We’ve come to appreciate how beneficial our microbes are — breaking down our food, fighting off infections and nurturing our immune system. It’s a lovely, invisible garden we should be tending for our own well-being.

But in the journal Bioessays, a team of scientists has raised a creepier possibility. Perhaps our menagerie of germs is also influencing our behavior in order to advance its own evolutionary success — giving us cravings for certain foods, for example.

Maybe the microbiome is our puppet master.

“One of the ways we started thinking about this was in a crime-novel perspective,” said Carlo C. Maley, an evolutionary biologist at the University of California, San Francisco, and a co-author of the new paper. “What are the means, motives and opportunity for the microbes to manipulate us? They have all three.”

The idea that a simple organism could control a complex animal may sound like science fiction. In fact, there are many well-documented examples of parasites controlling their hosts.

Some species of fungi, for example, infiltrate the brains of ants and coax them to climb plants and clamp onto the underside of leaves. The fungi then sprout out of the ants and send spores showering onto uninfected ants below.

How parasites control their hosts remains mysterious. But it looks as if they release molecules that directly or indirectly can influence their brains.

Our microbiome has the biochemical potential to do the same thing. In our guts, bacteria make some of the same chemicals that our neurons use to communicate with one another, such as dopamine and serotonin. And the microbes can deliver these neurological molecules to the dense web of nerve endings that line the gastrointestinal tract.

A number of recent studies have shown that gut bacteria can use these signals to alter the biochemistry of the brain. Compared with ordinary mice, those raised free of germs behave differently in a number of ways. They are more anxious, for example, and have impaired memory.

Adding certain species of bacteria to a normal mouse’s microbiome can reveal other ways in which they can influence behavior. Some bacteria lower stress levels in the mouse. When scientists sever the nerve relaying signals from the gut to the brain, this stress-reducing effect disappears.

Some experiments suggest that bacteria also can influence the way their hosts eat. Germ-free mice develop more receptors for sweet flavors in their intestines, for example. They also prefer to drink sweeter drinks than normal mice do.

Scientists have also found that bacteria can alter levels of hormones that govern appetite in mice.

Dr. Maley and his colleagues argue that our eating habits create a strong motive for microbes to manipulate us. “From the microbe’s perspective, what we eat is a matter of life and death,” Dr. Maley said.

Different species of microbes thrive on different kinds of food. If they can prompt us to eat more of the food they depend on, they can multiply.

Microbial manipulations might fill in some of the puzzling holes in our understandings about food cravings, Dr. Maley said. Scientists have tried to explain food cravings as the body’s way to build up a supply of nutrients after deprivation, or as addictions, much like those for drugs like tobacco and cocaine.

But both explanations fall short. Take chocolate: Many people crave it fiercely, but it isn’t an essential nutrient. And chocolate doesn’t drive people to increase their dose to get the same high. “You don’t need more chocolate at every sitting to enjoy it,” Dr. Maley said.

Perhaps, he suggests, the certain kinds of bacteria that thrive on chocolate are coaxing us to feed them.

John F. Cryan, a neuroscientist at University College Cork in Ireland who was not involved in the new study, suggested that microbes might also manipulate us in ways that benefited both them and us. “It’s probably not a simple parasitic scenario,” he said.

Research by Dr. Cryan and others suggests that a healthy microbiome helps mammals develop socially. Germ-free mice, for example, tend to avoid contact with other mice.

That social bonding is good for the mammals. But it may also be good for the bacteria.

“When mammals are in social groups, they’re more likely to pass on microbes from one to the other,” Dr. Cryan said.

“I think it’s a very interesting and compelling idea,” said Rob Knight, a microbiologist at the University of Colorado, who was also not involved in the new study.

If microbes do in fact manipulate us, Dr. Knight said, we might be able to manipulate them for our own benefit — for example, by eating yogurt laced with bacteria that would make us crave healthy foods.

“It would obviously be of tremendous practical importance,” Dr. Knight said. But he warned that research on the microbiome’s effects on behavior was “still in its early stages.”

The most important thing to do now, Dr. Knight and other scientists said, was to run experiments to see if microbes really are manipulating us.

Mark Lyte, a microbiologist at the Texas Tech University Health Sciences Center who pioneered this line of research in the 1990s, is now conducting some of those experiments. He’s investigating whether particular species of bacteria can change the preferences mice have for certain foods.

“This is not a for-sure thing,” Dr. Lyte said. “It needs scientific, hard-core demonstration.”

Altering the Community of Gut Bacteria Promotes Health and Increases Lifespan (Science Daily)

Jan. 16, 2014 — Scientists at the Buck Institute for Research on Aging have promoted health and increased lifespan in Drosophila by altering the symbiotic, or commensal, relationship between bacteria and the absorptive cells lining the intestine. The research, appearing in the January 16, 2014 edition of Cell, provides a model for studying many of the dysfunctions that are characteristic of the aging gut and gives credence to the growing supposition that having the right balance of gut bacteria may be key to enjoying a long healthy life.

Even though recent research in humans has linked the composition of gut flora with diet and health in the elderly and the list of age-related diseases associated with changes in gut bacteria include cancer, diabetes, and inflammatory bowel disease, lead author and Buck faculty Heinrich Jasper, PhD, says there is no systematic understanding of how we go from having a young, healthy gut to one that is old and decrepit. “Our study explores age-related changes in the gut that include increased oxidative stress, inflammation, impaired efficiency of the immune response, and the over-proliferation of stem cells,” said Jasper. “It puts these changes into a hierarchical, causal relationship and highlights the points where we can intervene to rescue the negative results of microbial imbalance.”

Jasper says the bacterial load in fly intestines increases dramatically with age, resulting in an inflammatory condition. The imbalance is driven by chronic activation of the stress response gene FOXO (something that happens with age), which suppresses the activity of a class of molecules (PGRP-SCs, homologues of PGLYRPs in humans) that regulate the immune response to bacteria. PGRP-SC suppression deregulates signaling molecules (Rel/NFkB) that are important to mount an effective immune response to gut bacteria. The resulting immune imbalance allows bacterial numbers to expand, triggering an inflammatory response that includes the production of free radicals. Free radicals, in turn, cause over-proliferation of stem cells in the gut, resulting in epithelial dysplasia, a pre-cancerous state.

Jasper said the most exciting result of their study occurred when his group increased the expression of PGRP-SC in epithelial cells of the gut, which restored the microbial balance and limited stem cell proliferation. This enhancement of PGRP-SC function, which could be mimicked by drugs, was sufficient to increase lifespan of flies. “If we can understand how aging affects our commensal population — first in the fly and then in humans — — our data suggest that we should be able to impact health span and life span quite strongly, because it is the management of the commensal population that is critical to the health of the organism.”

Journal Reference:

  1. Linlin Guo, Jason Karpac, Susan L. Tran, Heinrich Jasper.PGRP-SC2 Promotes Gut Immune Homeostasis to Limit Commensal Dysbiosis and Extend LifespanCell, 2014; 156 (1-2): 109 DOI: 10.1016/j.cell.2013.12.018

Digest This: Cure for Cancer May Live in Our Intestines (Science Daily)

July 31, 2013 — Treating a cancerous tumor is like watering a houseplant with a fire hose — too much water kills the plant, just as too much chemotherapy and radiation kills the patient before it kills the tumor.

The discovery of Robo1 protein in the intestinal stem cells (depicted in yellow) leads to tolerance of higher doses of chemoradiation for cancer patients. (Credit: Dr. Wei-Jie Zhou)

However, if the patient’s gastrointestinal tract remains healthy and functioning, the patient’s chances of survival increase exponentially, said Jian-Guo Geng, associate professor at the University of Michigan School of Dentistry. Recently, Geng’s lab discovered a biological mechanism that preserves the gastrointestinal tracts in mice who were delivered lethal doses of chemotherapy.

The findings, which will appear in the journal Nature, could revolutionize cancer therapy, Geng said.

“It’s our belief that this could eventually cure later-staged metastasized cancer. People will not die from cancer, if our prediction is true,” said Geng, who emphasized that the findings had not yet been proven in humans. “All tumors from different tissues and organs can be killed by high doses of chemotherapy and radiation, but the current challenge for treating the later-staged metastasized cancer is that you actually kill the patient before you kill the tumor.

“Now you have a way to make a patient tolerate to lethal doses of chemotherapy and radiotherapy. In this way, the later-staged, metastasized cancer can be eradicated by increased doses of chemotherapy and radiation.”

Geng’s lab found that when certain proteins bind with a specific molecule on intestinal stem cells, it revs intestinal stem cells into overdrive for intestinal regeneration and repair. Stem cells naturally heal damaged organs and tissues, but so-called “normal” amounts of stem cells in the intestine simply cannot keep up with the wreckage left behind by the lethal doses of chemotherapy and radiation required to successfully treat late-stage tumors.

However, the phalanx of extra stem cells protect the intestine and gastrointestinal tract, which means the patient can ingest nutrients, the body can perform other critical functions and the bacterial toxins in the intestine are prevented from entering the blood circulation, Geng said.

These factors could give the patient just enough of an extra edge to survive the stronger doses of chemotherapy and radiation, until the tumor or tumors are eradicated.

In the study, 50-to-75 percent of the mice treated with the molecule survived otherwise lethal doses of chemotherapy. All of the mice that did not receive the molecule died, Geng said.

“If you can keep the gut going, you can keep the patient going longer,” Geng said. “Now we have found a way to protect the intestine. The next step is to aim for a 100-percent survival rate in mice who are injected with the molecules and receive lethal doses of chemotherapy and radiation.”

Geng’s lab has worked with these molecules, called R-spondin1 and Slit2, for more than a decade. These molecules repair tissue in combination with intestinal stem cells residing in the adult intestine.

Journal Reference:

  1. Wei-Jie Zhou, Zhen H. Geng, Jason R. Spence & Jian-Guo Geng. Induction of intestinal stem cells by R-spondin 1 and Slit2 augments chemoradioprotectionNature, 2013 DOI: 10.1038/nature12416

What do chimps and humans have in common? Gut bacteria (MSNBC)

It’s nearly identical, and suggests patterns evolved before the two split and went own ways

Chimpanzees at Gombe Stream National Park in Tanzania have a lot in common with humans. And they both like to eat, apparently. Photo: Ian Gilby

By Stephanie Pappas

updated 11/13/2012 3:30:35 PM ET

 

Humans share about 99 percent of our genomes with chimpanzees. Now, research finds we share something else: gut bacteria.

The bacterial colonies that populate the chimpanzee intestinal tract are mirror images of those found in the human gut, researchers report Tuesday in the journal Nature Communications. The findings suggest gut bacteria patterns evolved before chimps and humans split and went their evolutionarily separate ways.

Human gut bacteria are crucial to health, with infants relying on healthy microbe populations to influence the developing immune system. Problems with microbe populations may also contribute to obesity and inflammatory bowel diseases.

Three intestinal ecosystems

In 2011, researchers learned that everyone’s gut bacteria fall into one of three different types, almost analogous to blood types. In each type, certain bacteria dominate. These types weren’t linked to any personal characteristics such as geographic area, age or gender. Researchers dubbed these distinct bacterial ecosystems “enterotypes.” (“Entero” means gut or intestine.)

“No one really knows why these three enterotypes exist,” said study researcher Andrew Moeller, a doctoral student at Yale University.

Along with his adviser Howard Ochman and their colleagues, Moeller wants to understand how these enterotypes arose. They could be distinctly human, he told LiveScience, which would suggest they arose relatively recently, perhaps in response to the development of agriculture. Or they could be ancient, shared among our closest primate relatives.

The researchers analyzed gut bacteria samples from 35 chimpanzees from Gombe Stream National Park in Tanzania. The chimpanzees were all in the subspecies Pan troglodytes schweinfurthii, the eastern chimpanzee, which arose about the same time as Homo sapiens.

Shared bacteria

The researchers found that, just like humans, chimps’ guts harbor one of three distinct types of bacterial colonies. Even more intriguingly, these enterotypes matched humans’ precisely. In type 1, for example, both humans and chimps show a predominance of Bacteroides,Faecalibacterium and Parabacteroides.

There were some differences. For example, in humans and chimps, enterotype 2 is marked by an overabundance of bacteria called Lachnospiraceae. In humans, the bacteria Prevotellae is also prevalent in type 2. In chimps, Prevotellae appears in significant numbers in all three enterotypes, perhaps because it is associated with a high-carbohydrate diet.

Other differences could help explain certain human health issues. By comparing human and chimpanzee gut bacteria, the researchers found many of the bacteria present only in humans are linked to diseases such as inflammatory bowel diseases, conditions that cause pain, diarrhea and vomiting.

Seven of the chimps in the study were tested repeatedly over eight years, and their gut microbes were found to change from type to type over that time period. No one has ever tested humans for changes over a period longer than two weeks, Moeller said, but the results suggest our enterotypes may shift over time, too.

Our shared history

The similarities between chimp and human colonies suggest enterotypes predate our species, which in turn suggests that none of the three ecosystems are better than the others, Moeller said.

“Before we found this in chimpanzees, there was a possibility that enterotypes were a product of modernization, which could mean they have some negative effects on health,” he said. “I don’t think there’s any reason to think one enterotype is going to have an effect on health that’s going to be better” than the others.

Moeller and his colleagues are now examining gorilla fecal samples to find out where they stand as slightly more distant primate relatives to humans.

“The next step is to try to find out the processes and mechanisms responsible for producing these three community states,” Moeller said, “which is kind of a lofty goal, but I think more sampling will actually reveal why these communities exist.”