Posts Tagged ‘microbiome’

Consumption of dietary fiber can prevent obesity, metabolic syndrome and adverse changes in the intestine by promoting growth of “good” bacteria in the colon, according to a study led by Georgia State University.

The researchers found enriching the diet of mice with the fermentable fiber inulin prevented metabolic syndrome that is induced by a high-fat diet, and they identified specifically how this occurs in the body. Metabolic syndrome is a cluster of conditions closely linked to obesity that includes increased blood pressure, high blood sugar, excess body fat around the waist and abnormal cholesterol or triglyceride levels. When these conditions occur together, they increase a person’s risk of heart disease, stroke and diabetes.

Obesity and metabolic syndrome are associated with alterations in gut microbiota, the microorganism population that lives in the intestine. Modern changes in dietary habits, particularly the consumption of processed foods lacking fiber, are believed to affect microbiota and contribute to the increase of chronic inflammatory disease, including metabolic syndrome. Studies have found a high-fat diet destroys gut microbiota, reduces the production of epithelial cells lining the intestine and causes gut bacteria to invade intestinal epithelial cells.

This study found the fermentable fiber inulin restored gut health and protected mice against metabolic syndrome induced by a high-fat diet by restoring gut microbiota levels, increasing the production of intestinal epithelial cells and restoring expression of the protein interleukin-22 (IL-22), which prevented gut microbiota from invading epithelial cells. The findings are published in the journal Cell Host & Microbe.

“We found that manipulating dietary fiber content, particularly by adding fermentable fiber, guards against metabolic syndrome,” said Dr. Andrew Gewirtz, professor in the Institute for Biomedical Sciences at Georgia State. “This study revealed the specific mechanism used to restore gut health and suppress obesity and metabolic syndrome is the induction of IL-22 expression. These results contribute to the understanding of the mechanisms that underlie diet-induced obesity and offer insight into how fermentable fibers might promote better health.”

For four weeks, the researchers fed mice either a grain-based rodent chow, a high-fat diet (high fat and low fiber content with 5 percent cellulose as a source of fiber) or a high-fat diet supplemented with fiber (either fermentable inulin fiber or insoluble cellulose fiber). The high-fat diet is linked to an increase in obesity and conditions associated with metabolic syndrome.

They discovered a diet supplemented with inulin reduced weight gain and noticeably reduced obesity induced by a high-fat diet, which was accompanied by a reduction in the size of fat cells. Dietary enrichment with inulin also markedly lowered cholesterol levels and largely prevented dysglycemia (abnormal blood sugar levels). The researchers found insoluble cellulose fiber only modestly reduced obesity and dysglycemia

Supplementing the high-fat diet with inulin restored gut microbiota. However, inulin didn’t restore the microbiota levels to those of mice fed a chow diet. A distinct difference in microbiota levels remained between mice fed a high-fat diet versus those fed a chow diet. Enrichment of high-fat diets with cellulose had a mild effect on microbiota levels.

In addition, the researchers found switching mice from a grain-based chow diet to a high-fat diet resulted in a loss of colon mass, which they believe contributes to low-grade inflammation and metabolic syndrome. When they switched mice back to a chow diet, the colon mass was fully restored.

https://www.technologynetworks.com/tn/news/fiber-rich-diet-fights-off-obesity-by-altering-microbiota-296642?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=60184554&_hsenc=p2ANqtz-9YDsGiTl44CBfQpgNtYgc43xBeVKpAbPZym9Lh_GzlHoEVts0rAwMhHHXIDam3Jit0D3aTqKGhCceUREgr6sZfLGMWpQ&_hsmi=60184554

Advertisements

By Ann Gibbons

Humans did not evolve alone. Tens of trillions of microbes have followed us on our journey from prehistoric ape, evolving with us along the way, according to a new study. But the work also finds that we’ve lost some of the ancient microbes that still inhabit our great ape cousins, which could explain some human diseases and even obesity and mental disorders.

Researchers have known for some time that humans and the other great apes harbor many types of bacteria, especially in their guts, a collection known as the microbiome. But where did these microbes come from: our ancient ancestors, or our environment? A study of fecal bacteria across all mammals suggested that the microbes are more likely to be inherited than acquired from the environment. But other studies have found that diet plays a major role in shaping the bacteria in our guts.

To solve the mystery, Andrew Moeller turned to wild apes. As part of his doctoral dissertation, the evolutionary biologist, now a postdoc at the University of California, Berkeley, studied gut bacteria isolated from fecal samples from 47 chimpanzees from Tanzania, 24 bonobos from the Democratic Republic of the Congo, 24 gorillas from Cameroon, and 16 humans from Connecticut. In these samples, he and colleagues at the University of Texas (UT), Austin, compared the DNA sequences of a single rapidly evolving gene that is common in the gut bacteria in apes, including humans. They then sorted the different DNA gene sequences into family trees.

It turns out that most of our gut microbes have been evolving with us for a long time. Moeller found that two of three major families of gut bacteria in apes and humans trace their origins to a common ancestor more than 15 million years ago, not primarily to bugs picked up from their environment. But as the different species of apes diverged from this ancestor, their gut bacteria also split into new strains, and coevolved in parallel (a process known as cospeciation) to adapt to differences in the diets, habitats, and diseases in the gastrointestinal tracts of their hosts, the team reports today in Science. Today, these microbes are finely adapted to help train our immune systems, guide the development of our intestines, and even modulate our moods and behaviors.

“It’s surprising that our gut microbes, which we could get from many sources in the environment, have actually been coevolving inside us for such a long time,” says project leader Howard Ochman, an evolutionary biologist at UT Austin.

After the ape species diverged, some also lost distinct strains of bacteria that persisted in other primates, likely another sign of adaptation in the host, the team found.

In a final experiment, the researchers probed deeper into the human microbiome. They compared the same DNA sequence they had analyzed in all of the apes, but this time between the people from Connecticut and people from Malawi. They found that the bacterial strains from these Africans diverged from those of the Americans about 1.7 million years ago, which corresponds with the earliest exodus of human ancestors out of Africa. This suggests that gut bacteria can be used to trace early human and animal migrations, Moeller says. Interestingly, the Americans lacked some of the strains of bacteria found in Malawians—and in gorillas and chimps—which fits with the general reduction in gut microbiome diversity that has been observed in people in industrialized societies, perhaps because of changes in diet and the use of antibiotics.

The work “represents a significant step in understanding human microbiota coevolutionary history,” says Justin Sonnenburg of Stanford University in Palo Alto, California, who was not involved with the research. “It elegantly shows that gut microbes are passed vertically, between generations over millions of years.” Microbiologist Martin Blaser of New York University in New York City agrees: “The path of transmission was from mom apes to baby apes for hundreds of thousands of generations at least.”

But the extinction of some strains of bacteria that persist in other apes but not humans raises a red flag for our health. “What happens if a human mom takes antibiotic when she’s pregnant? What happens if she takes it at the moment of delivery?” Blaser asks.

“We are coming to understand how fundamental our gut microbes are for health,” Sonnenburg says. “These findings have huge implications for how we should pursue understanding what a truly healthy microbiome looks like.”

http://www.sciencemag.org/news/2016/07/microbes-our-guts-have-been-us-millions-years

Thanks to Kebmodee for bringing this to the It’s Interesting community.


Once scientists grew these Staphylococcus lugdunensis bacteria in a lab dish, they were able to isolate a compound that’s lethal to another strain commonly found in the nose that can make us sick — Staphylococcus aureus.

by Carolyn Beans

With antibiotic-resistant super bugs on the rise, researchers are on an urgent hunt for other bacteria that might yield chemicals we can harness as powerful drugs. Scientists once found most of these helpful bacteria in soil, but in recent decades this go-to search location hasn’t delivered.

Now, researchers at the University of Tübingen in Germany say that to find at least one promising candidate, we need look no further than our own noses.

The scientists report Wednesday in the journal Nature that a species of bacteria inside the human nose produces a substance capable of killing a range of bacteria, including the strain of drug-resistant Staphylococcus aureus known as MRSA.

The Tübingen team is delighted with their find. “It was totally unexpected,” says study author Andreas Peschel.

The scientists already knew that S. aureus lives in the noses of about 30 percent of humans, usually without causing harm — most people never know they are carriers of the bacterium. But if the body becomes compromised (whether by surgery, physical trauma, an underlying illness or suppressed immune system) the little cache of S. aureus in the nose can suddenly launch an attack against its human host. And if the strain of bacteria is MRSA, that infection can be lethal.

The scientists wondered how 70 percent of human noses are able to avoid harboring S. aureus. They guessed it might have something to do with neighboring bacteria.

So the researchers pitted 90 different human nasal bacteria in one-on-one battles with S. aureus in the lab. Indeed, one of these bacteria — Staphylococcus lugdunensis — prevented the dangerous pathogen from growing.

They then studied the arsenal of chemicals that S. lugdunensis produces until they found one that stops S. aureus in its tracks – a new antibiotic that they named lugdunin.

Follow-up work confirmed that lugdunin can treat S. aureus skin infections in mice, and limit the spread of S. aureus in a rat’s nose.

Lugdunin may already be keeping S. aureus out of our noses. In a group of 187 hospitalized people, the same scientists found S. aureus in the noses of just 5.9 percent of people who also harbored the lugdunin-producing bacteria, but 34.7 percent of those who didn’t.

Other recent studies have shown that bacteria living in humans carry genes that have the potential to make antibiotics. The Tübingen study takes those results a step further by showing that an antibiotic produced by a bacterium in the human nose can successfully treat an animal’s infection.

“This paper is a really nice follow-up,” says Dr. Nita Salzman, a pathologist at the Medical College of Wisconsin. “It’s a sort of proof of principle that the microbiome is a good source for novel antibiotics.”

The researchers have applied for a patent for lugdunin, but say that the prototype antibiotic is still many years away from being ready to treat humans.

The really important contribution of this study is not lugdunin itself, says microbiologist Kim Lewis of Northeastern University, but rather the new approach for finding antibiotic-producing bacteria within our own bodies.

“The reason we ran out of antibiotics in the first place is because most of them came from soil bacteria and they make up 1 percent of the total [bacterial] diversity,” Lewis says.

Scientists kept searching in soil, he says, because they already had some success there and know that soil bacteria are exceptionally good at producing antibiotics.

But now it’s time to look within us. And the team in Tübingen has only just begun their hunt.

“We have started a larger screening program and we’re sure there will be many additional antibiotics that can be discovered,” says Peschel.

http://www.npr.org/sections/health-shots/2016/07/27/487529338/nose-y-bacteria-could-yield-a-new-way-to-fight-infection

by Tim Spector

Everyone who has ever been camping or walking in the wild with friends can’t have failed to notice how insects seem to prefer some people’s flesh to others. Some unlucky souls are totally covered in itchy red blotches and others are miraculously spared. Sometimes only some family members are affected.

My mother has never been bitten by a mosquito (though fleas like her) while my brother and I are often the targets.

Previous observations have shown a higher mosquito preference for larger people (who produce more CO2), beer drinkers and pregnant women, and although diet was often suspected as a factor, nothing in what we eat (even garlic) stood up to scrutiny.

The authors of a new study in PLOS One claim to have found the answer. They studied the differences in attraction of skin odours to mosquitoes, specifically Aedes aegypti, in a group of brave volunteers drawn from a group of female identical and non-identical twins – part of the large national TwinsUK cohort that I set up 21 years ago. The reason for using both kinds of twin was to separate the effects of nature and nurture (or genes and environment). In humans this is the only way to get a good estimate of the contribution of genetics to the differences between people.

Our valiant twins put their hands into a specially constructed plexiglass sealed dome where the odours either attract or repel 20 female mosquitoes without being allowed to bite. Each subject was given an attractiveness score compared to the other hand at the other end of the dome. Sure enough the identical twins, who share all their genes, had consistently more similar scores compared to fraternal twins – showing a clear genetic component. This comparison estimated that 67% of the differences between people (called heritability) was down to their genes.

Repel With Smell

Why might this be? Many years ago in another twin study we showed that underarm body odour as perceived by human sniffers had a genetic basis – with huge variability in how strong smells were perceived. This showed that we have gene variations controlling both the odours we perceive and the chemical odours we produce. In this way we are similar to mosquitoes because they also have big differences in which odours and chemicals attract and repel them.

Different mosquitoes prefer different parts of our bodies to others. The species Aedes Gambiae prefers the odours of our hands and feet to other bits like groins and armpits. Some animals use their body odour to keep insects away and companies have been trying to unravel what the best chemicals are.

The twin study authors realised that the chemicals could come from glands in our skin or from the billions of microbes on the surface. They discounted the bacteria as a cause as the dogma is that bacteria can’t be influenced genetically. It turns out they were wrong.

Your Own Personal Microbes

We all have very different and unique microbial species in our mouths, guts and on our skin. We share only a small fraction of our microbial species with each other – but still have a unique microbial signature fingerprint. Until recently it was thought this variety was random or due to where we lived. But recent studies, again using UK twins, have shown the importance of genes in influencing which type of gut bacteria flourish inside us – and the same is likely to be true for our skin.

Our 100 trillion microbes outnumber our own human cells ten to one and it turns out we don’t pick them – they pick us – based on our genetic makeup. This means that, just like mosquitoes, certain microbes prefer to coexist with us and other find us rather unpleasant and settle elsewhere.

Our microbes produce many of our vitamins and chemicals in our blood, and far from being the bad guys, their diversity contributes to our health. They are also probably responsible for most of our smells and odours. Even regular hand washing can’t remove these bacteria.

The special smell many of us have between our toes comes from a bacteria called Brevibacteria linens. This is identical to the bacterial species that gives Limburger cheese its distinctive smell.

To demonstrate that bacterial species are the same wherever they grow a team of microbiologists at UCLA performed an unusual experiment. They have started making and eating cheese from human skin – and reportedly this gourmet belly-button food tastes just fine.

So, the next time you get bitten by a mosquito on the ankle – don’t blame bad luck or your cheap repellent – think of the amazing evolutionary match-making processes that hooked up your special mix of genes to a particular community of microbes that feed off your skin and produce a chemical that only certain species of mosquito find irresistible.

http://theconversation.com/chemical-attraction-why-mosquitos-zone-in-on-some-people-but-not-others-40705

Why do some people remain healthy into their 80s and beyond, while others age faster and suffer serious diseases decades earlier? New research led by UCLA life scientists may produce a new way to answer that question—and an approach that could help delay declines in health.

Specifically, the study suggests that analyzing intestinal bacteria could be a promising way to predict health outcomes as we age.

The researchers discovered changes within intestinal microbes that precede and predict the death of fruit flies. The findings were published in the open-source journal Cell Reports.

“Age-onset decline is very tightly linked to changes within the community of gut microbes,” said David Walker, a UCLA professor of integrative biology and physiology, and senior author of the research. “With age, the number of bacterial cells increase substantially and the composition of bacterial groups changes.”

The study used fruit flies in part because although their typical life span is just eight weeks, some live to the age equivalent of humans’ 80s and 90s, while others age and die much younger. In addition, scientists have identified all of the fruit fly’s genes and know how to switch individual ones on and off.

In a previous study, the UCLA researchers discovered that five or six days before flies died, their intestinal tracts became more permeable and started leaking.

In the latest research, which analyzed more than 10,000 female flies, the scientists found that they were able to detect bacterial changes in the intestine before the leaking began. As part of the study, some fruit flies were given antibiotics that significantly reduce bacterial levels in the intestine; the study found that the antibiotics prevented the age-related increase in bacteria levels and improved intestinal function during aging.

The biologists also showed that reducing bacterial levels in old flies can significantly prolong their life span.

“When we prevented the changes in the intestinal microbiota that were linked to the flies’ imminent death by feeding them antibiotics, we dramatically extended their lives and improved their health,” Walker said. (Microbiota are the bacteria and other microorganisms that are abundant in humans, other mammals, fruit flies and many other animals.)

Flies with leaky intestines that were given antibiotics lived an average of 20 days after the leaking began—a substantial part of the animal’s life span. On average, flies with leaky intestines that did not receive antibiotics died within a week.

The intestine acts as a barrier to protect our organs and tissue from environmental damage.

“The health of the intestine—in particular the maintenance of the barrier protecting the rest of the body from the contents of the gut—is very important and might break down with aging,” said Rebecca Clark, the study’s lead author. Clark was a UCLA postdoctoral scholar when the research was conducted and is now a lecturer at England’s Durham University.

The biologists collaborated with William Ja, an assistant professor at Florida’s Scripps Research Institute, and Ryuichi Yamada, a postdoctoral research associate in Ja’s laboratory, to produce an additional group of flies that were completely germ-free, with no intestinal microbes. Those flies showed a very dramatic delay in intestinal damage, and they lived for about 80 days, approximately one-and-a-half times as long as the animal’s typical life span.

Scientists have recently begun to connect a wide variety of diseases, including diabetes and Parkinson’s, among many others, to changes in the microbiota, but they do not yet know exactly what healthy microbiota look like.

“One of the big questions in the biology of aging relates to the large variation in how we age and how long we live,” said Walker, who added that scientific interest in intestinal microbes has exploded in the last five years.

When a fruit fly’s intestine begins to leak, its immune response increases substantially and chronically throughout its body. Chronic immune activation is linked with age-related diseases in people as well, Walker said.

Walker said that the study could lead to realistic ways for scientists to intervene in the aging process and delay the onset of Parkinson’s disease, Alzheimer’s disease, cancer, stroke, cardiovascular disease, diabetes and other diseases of aging—although such progress could take many years, he said.

Have you ever been on the subway and seen something that you did not quite recognize, something mysteriously unidentifiable?

Well, there is a good chance scientists do not know what it is either.

Researchers at Weill Cornell Medical College released a study on Thursday that mapped DNA found in New York’s subway system — a crowded, largely subterranean behemoth that carries 5.5 million riders on an average weekday, and is filled with hundreds of species of bacteria (mostly harmless), the occasional spot of bubonic plague, and a universe of enigmas. Almost half of the DNA found on the system’s surfaces did not match any known organism and just 0.2 percent matched the human genome.

“People don’t look at a subway pole and think, ‘It’s teeming with life,’ ” said Dr. Christopher E. Mason, a geneticist at Weill Cornell Medical College and the lead author of the study. “After this study, they may. But I want them to think of it the same way you’d look at a rain forest, and be almost in awe and wonder, effectively, that there are all these species present — and that you’ve been healthy all along.”

Dr. Mason said the inspiration for the study struck about four years ago when he was dropping off his daughter at day care. He watched her explore her new surroundings by happily popping objects into her mouth. As is the custom among tiny children, friendships were made on the floor, by passing back and forth toys that made their way from one mouth to the next.

“I couldn’t help thinking, ‘How much is being transferred, and on which kinds of things?’ ” Dr. Mason said. So he considered a place where adults can get a little too close to each other, the subway.

Thus was the project, called PathoMap, born. Over the past 17 months, a team mainly composed of medical students, graduate students and volunteers fanned out across the city, using nylon swabs to collect DNA, in triplicate, from surfaces that included wooden benches, stairway handrails, seats, doors, poles and turnstiles.

In addition to the wealth of mystery DNA — which was not unexpected given that only a few thousand of the world’s genomes have been fully mapped — the study’s other findings reflected New York’s famed diversity, both human and microbial.

The Bronx was found to be the most diverse borough in terms of microbial species. Brooklyn claimed second place, followed by Manhattan, Queens and Staten Island, where researchers took samples on the Staten Island Railway.

On the human front, Dr. Mason said that, in some cases, the DNA that was found in some subway stations tended to match the neighborhood’s demographic profile. An area with a high concentration of Hispanic residents near Chinatown in Manhattan, for example, yielded a large amount of Hispanic and Asian genes.

In an area of Brooklyn to the south of Prospect Park that roughly encompassed the Kensington and Windsor Terrace neighborhoods, the DNA gathered frequently read as British, Tuscan, and Finnish, three groups not generally associated with the borough. Dr. Mason had an explanation for the finding: Scientists have not yet compiled a reliable database of Irish genes, so the many people of Irish descent who live in the area could be the source of DNA known to be shared with other European groups. The study produced some less appetizing news. Live, antibiotic-resistant bacteria were discovered in 27 percent of the collected samples, though among all the bacteria, only 12 percent could be associated with disease. Researchers also found three samples associated with bubonic plague and two with DNA fragments of anthrax, though they noted that none of those samples showed evidence of being alive, and that neither disease had been diagnosed in New York for some time. The presence of anthrax, Dr. Mason said, “is consistent with the many documented cases of anthrax in livestock in New York State and the East Coast broadly.”

The purpose of the study was not simply to satisfy scientific curiosity, the authors said. By cataloging species now, researchers can compare them against samples taken in the future to determine whether certain diseases, or even substances used as bioterrorism weapons, had spread.

City and transit officials did not sound grateful for the examination.

“As the study clearly indicates, microbes were found at levels that pose absolutely no danger to human life and health,” Kevin Ortiz, a spokesman for the Metropolitan Transportation Authority, said in an email. And the city’s health department called the study “deeply flawed” and misleading.

Dr. Mason responded by saying he and his team had simply presented their complete results.

“For us to not report the fragments of anthrax and plague in the context of a full analysis would have been irresponsible,” he said. “Our findings indicate a normal, healthy microbiome, and we welcome others to review the publicly available data and run the same analysis.”

http://www.nytimes.com/2015/02/06/nyregion/among-the-new-york-city-subways-millions-of-riders-a-study-finds-many-mystery-microbes.html?hp&action=click&pgtype=Homepage&module=mini-moth&region=top-stories-below&WT.nav=top-stories-below

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

BY Erika Engelhaupt

A new nonprofit called OpenBiome is hoping to do for fecal transplants what blood banks have done for transfusions. It’s a kind of Brown Cross.

And it’s an idea whose time has come. Recent trials testing transplants of fecal microbes from the healthy to the sick have been so promising that people are attempting dangerous do-it-yourself fecal transplants by enema, for lack of access to authorized medical procedures.

Graduate students Carolyn Edelstein and Mark B. Smith got the idea for OpenBiome after a friend had trouble getting a fecal transplant to treat an infection with Clostridium difficile. The bacterium causes dangerous, even fatal, diarrhea and in an increasing number of cases is resistant to antibiotics.

People tend to get C. difficile infections after antibiotics or chemotherapy has knocked out helpful bacteria, allowing what is normally a background player to take over. Transplants of fecal bacteria from healthy donors can help reset the microbiome, the mix of bacteria in the body, and crowd out C. difficile. A 2011 review of 317 patients treated for C. difficile found that fecal transplants cleared up infections in 92 percent of patients. And more recent research showed that taking a round of pills containing bacteria isolated from fecal matter (without the feces itself) resolved C. difficile infections in all of 32 patients treated.

There’s also interest in transplanting healthy fecal microbiomes into people with inflammatory bowel disease or even obesity. In one recent test, mice implanted with fecal microbes from thin humans stayed thin, while mice given bacteria from obese people gained weight.

But the transplants are hard to get. As Edelstein and Smith’s friend learned, the U.S. Food and Drug Administration requires lots of paperwork for the experimental therapy, and donor feces has to be screened for a host of potential pathogens.

That’s where OpenBiome steps in. The nonprofit offers hospitals fecal samples for $250 that have been prescreened to ensure they are free of pathogens and parasites. Since October, they’ve sent more than 100 samples to a dozen hospitals and clinics, according to an interview with Smith in the Chronicle of Higher Education. Edelstein, who’s studying public affairs at Princeton, and Smith, who’s studying microbiology at MIT, recruited friends and donors and negotiated permissions with the FDA to set up the organization, which houses its samples at MIT. OpenBiome is also offering to collaborate with researchers for long-term follow-up on patients’ microbiomes.

Because FDA considers feces to be a drug in the context of transplants, OpenBiome is providing stool only for treatment of C. difficile. People hoping to shift their microbiomes for other purposes are still out of luck. Until more testing and approval comes through, that leaves open the risk that some people may resort to home transplants.

Let me be very clear about this: Whipping up an enema of your friend’s stool is a terrible idea.There are excellent reasons why people normally avoid poop: It can carry pathogens and parasites that cause serious disease. Even a donor who appears perfectly healthy might be carrying around bacteria or viruses that his or her immune system or particular microbiome mix is able to deal with. Your mileage may vary.

Your genetics, your immune system, your diet and environment — all these things create the ecology of your insides, making it hard to predict what your outcome might be. What’s more, you may need to make other medically supervised changes along with the transplant. Research on microbiome links to obesity, for instance, suggests that a new “skinny” microbiome has to be accompanied by a switch to a diet lower in fat and calories, or else the new microbes will just be outcompeted.

These dangers and complicating factors are why a supply of prescreened stool is so important. The procedures need to be done under medical supervision, and when done right the results look really promising. The recently tested pill approach avoids some of the yuck factor of fecal transplants, but most transplants are done via an enema, colonoscopy or nose tube to the gut.

If you get transplant material from OpenBiome, you’ll have to submit to one of the usual transplant methods rather than a pill, but you can rest assured you’re getting high-quality stuff. Not only are the samples screened, the donors are among the best and brightest: a few young researchers and scientists from Harvard and MIT.

https://www.sciencenews.org/blog/gory-details/introducing-first-bank-feces?mc_cid=325756381e&mc_eid=9da0429978

Thanks to Jody Troupe for bringing this to the attention of the It’s Interesting community.