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Category: microbes

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This past week I came across two amazing and very different stories, but in both Lyme disease appears. So read with an open mind - because they may or may not work out. But I will say that living in the NY metro area, tick diseases are a big deal, and we all know people who have gotten diseases from ticks. Most get successfully treated with antibiotics, but then there are those people who are suffering years later. The first article is by Dr. Christie Wilcox (a freelance science writer and postdoctoral researcher). Do go read the whole article for her fascinating account of venoms. From Digg:

Poison As Medicine: How A Bee Sting Saved My Life

“I moved to California to die.” Ellie Lobel was 27 when she was bitten by a tick and contracted Lyme disease. And she was not yet 45 when she decided to give up fighting for survival. Caused by corkscrew-shaped bacteria called Borrelia burgdorferi, which enter the body through the bite of a tick, Lyme disease is diagnosed in around 300,000 people every year in the United States. It kills almost none of these people, and is by and large curable – if caught in time. If doctors correctly identify the cause of the illness early on, antibiotics can wipe out the bacteria quickly before they spread through the heart, joints and nervous system.

But back in the spring of 1996, Ellie didn’t know to look for the characteristic bull’s-eye rash when she was bitten – she thought it was just a weird spider bite. Then came three months with flu-like symptoms and horrible pains that moved around the body. Ellie was a fit, active woman with three kids, but her body did not know how to handle this new invader. She was incapacitated. “It was all I could do to get my head up off the pillow,” Ellie remembers.

As time wore on, Ellie went to doctor after doctor, each giving her a different diagnosis. Multiple sclerosis. Lupus. Rheumatoid arthritis. Fibromyalgia. None of them realised she was infected with Borrelia until more than a year after she contracted the disease – and by then, it was far too late. Lyme bacteria are exceptionally good at adapting, with some evidence that they may be capable of dodging both the immune system and the arsenal of antibiotics currently available. Borrelia are able to live all over the body, including the brain, leading to neurological symptoms. And even with antibiotic treatment, 10–20 per cent of patients don’t get better right away. There are testimonies of symptoms persisting – sometimes even resurfacing decades after the initial infection – though the exact cause of such post-treatment Lyme disease syndrome is a topic of debate among Lyme scientists.

I just kept doing this treatment and that treatment,” says Ellie. Her condition was constantly worsening....So she packed up everything and moved to California to die. And she almost did. Less than a week after moving, Ellie was attacked by a swarm of Africanised bees....Bees – and some other species in the order Hymenoptera, such as ants and wasps – are armed with a potent sting that many of us are all too aware of. This is their venom, and it’s a mixture of many compounds. Perhaps the most important is a tiny 26-amino-acid peptide called melittin, which constitutes more than half of the venom of honey bees and is found in a number of other bees and wasps. 

“I just went limp. I put my hands up and covered my face because I didn’t want them stinging me in the eyes… The next thing I know, the bees are gone.” When the bees finally dissipated, her caregiver tried to take her to the hospital, but Ellie refused to go... But Ellie didn’t die. Not that day, and not three to four months later...She believes the bees, and their venom, saved her life.

The idea that the same venom toxins that cause harm may also be used to heal is not new. Bee venom has been used as a treatment in East Asia since at least the second century BCE...Despite the wealth of history, the practical application of venoms in modern therapeutics has been minimal....Over the course of the 20th century, suggested venom treatments for a range of diseases have appeared in scientific and medical literature. Venoms have been shown to fight cancer, kill bacteria, and even serve as potent painkillers – though many have only gone as far as animal tests. 

The more we learn about the venoms that cause such awful damage, the more we realise, medically speaking, how useful they can be. Like the melittin in bee venom. Melittin does not only cause pain. In the right doses, it punches holes in cells’ protective membranes, causing the cells to explode. At low doses, melittin associates with the membranes, activating lipid-cutting enzymes that mimic the inflammation caused by heat. But at higher concentrations, and under the right conditions, melittin molecules group together into rings creating large pores in membranes, weakening a cell’s protective barrier and causing the entire cell to swell and pop like a balloon.Because of this, melittin is a potent antimicrobial, fighting off a variety of bacteria and fungi with ease. 

After the attack, Ellie watched the clock, waiting for anaphylaxis to set in, but it didn’t. Instead, three hours later, her body was racked with pains. A scientist by education before Lyme took its toll, Ellie thinks that these weren’t a part of an allergic response, but instead indicated a Jarisch–Herxheimer reaction – her body was being flooded with toxins from dying bacteria. The same kind of thing can happen when a person is cured from a bad case of syphilis. A theory is that certain bacterial species go down swinging, releasing nasty compounds that cause fever, rash and other symptoms. For three days, she was in pain. Then, she wasn’t.“I had been living in this… I call it a brown-out because it’s like you’re walking around in a half-coma all the time with the inflammation of your brain from the Lyme. My brain just came right out of that fog. I thought: I can actually think clearly for the first time in years.”

With a now-clear head, Ellie started wondering what had happened. So she did what anyone else would do: Google it. Disappointingly, her searches turned up very little. But she did find one small 1997 study by scientists at the Rocky Mountain Laboratories in Montana, who’d found that melittin killed Borrelia. Exposing cell cultures to purified melittin, they reported that the compound completely inhibited Borrelia growth. When they looked more closely, they saw that shortly after melittin was added, the bacteria were effectively paralysed, unable to move as their outer membranes were under attack. Soon after, those membranes began to fall apart, killing the bacteria.

Convinced by her experience and the limited research she found, Ellie decided to try apitherapy, the therapeutic use of materials derived from bees...She started on a regimen of ten stings a day, three days a week: Monday, Wednesday, Friday. Three years and several thousand stings later, Ellie seems to have recovered miraculously. Slowly, she has reduced the number of stings and their frequency – just three stings in the past eight months, she tells me (and one of those she tried in response to swelling from a broken bone, rather than Lyme-related symptoms). 

Since the 1997 study, no one had looked further into bee venom as a potential cure for Lyme disease, until Ellie. Ellie now runs a business selling bee-derived beauty products called BeeVinity, inspired after, she says, noticing how good her skin looked as she underwent apitherapy.....In addition, she sends some of the venom she purchases – which, due to the cost of the no-harm extraction method she uses, she says is “more expensive than gold” – to Eva Sapi, Associate Professor of Biology and Environmental Science at the University of New Haven, who studies Lyme disease.

Sapi’s research into the venom’s effects on Lyme bacteria is ongoing and as yet unpublished, though she told me the results from preliminary work done by one of her students look “very promising”. Borrelia bacteria can shift between different forms in the body, which is part of what makes them so hard to kill. Sapi has found that other antibiotics don’t actually kill the bacteria but just push them into another form that is more dormant. As soon as you stop the antibiotics, the Borrelia bounce back. Her lab is testing different bee venoms on all forms of the bacteria, and so far, the melittin venom seems effective...And they still don’t really know why the venom works for Ellie, not least because the exact cause of post-treatment Lyme disease symptoms remains unknown. “Is it effective for her because it’s killing Borrelia, or is it effective because it stimulates the immune system?” asks Sapi. It’s still a mystery.

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The researchers think that repeated courses of antibiotics destroy the gut bacteria resulting in gut bacteria imbalance. From Red Orbit:

Antibiotic overuse could up diabetes risk, study says

Repeated use of some antibiotics could increase a person’s risk of developing type 2 diabetes, according to research published online Tuesday in the European Journal of Endocrinology. In the study, scientists from the University of Pennsylvania found that men and women who had ever been prescribed with at least two courses of specific types of antibiotics were more likely to eventually be diagnosed with type 2 diabetes than those who had taken no more than one.

The antibiotics used in the research came from one of four categories, according to LiveScience: penicillins, cephalosporins, quinolones and macrolides. The authors reviewed a database of UK patients, looking at the number of antibiotic prescriptions given to over 200,000 diabetic patients at least one year before those individuals were diagnosed with the condition...They found that the more courses of antibiotics that were prescribed to a person, the greater the risk that he or she would go on to develop the disease.

Patients who had been prescribed between two and five courses of penicillin increased their risk of diabetes by 8 percent, according to the Daily Mail, and the risk increased by 23 percent for those receiving more than five courses of the frequently used antibiotic versus the one- or no-course group.

Those who were given between two and five courses of quinolones, which are used to treat respiratory and urinary tract infections, had an increased diabetes risk of 15 percent, and those receiving more than five courses saw that risk shoot up by 37 percent. 

Those who were given just one course of antibiotics showed no such increase in diabetes risk, the researchers reported. Nor was there any link found between exposure to anti-virals and anti-fungals and diabetes risk. The reason for the association between frequent antibiotic use and the risk of diabetes is not clear, but may be related to a gut bacteria imbalance, they wrote.“Gut bacteria have been suggested to influence the mechanisms behind obesity, insulin resistance and diabetes in both animal and human models. Previous studies have shown that antibiotics can alter the digestive ecosystem,” added lead author Dr. Ben Boursi.

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Discussions of the benefits of dietary fiber seem to be everywhere this week.

From Forbes: Eat Whole Grains For A Long Life, New Study Says

Eating lots of whole grains – especially those high in cereal fiber – may help people live longer, according to new research. The study out in BMC Medicine this week suggests that eating hefty amounts of cereal fibers can help reduce the risk of death from a number of causes, including cancer and diabetes, by almost 20%. Previous research has certainly linked whole grains to the reduction of certain chronic diseases and to reduced mortality, but this one is the largest of its kind to show a reduction in death from a number of different causes. So if you want to live longer, grab a bowl of cereal. The less refined, the better.

Whole grains are grains in their most unadulterated form, still containing the endosperm, bran, and germ – most of the plant’s nutritional value lies in the bran and germ. When grains go through milling to become processed or refined, they’re typically stripped of the bran and germ parts, along with a number of B vitamins, fiber, and iron.

In the new study, the Harvard Medical School team tracked over 367,000 healthy people who were taking part in the NIH-AARP Diet and Health Study, for an average of 14 years. ..It turned out that people who ate more whole grains – 1.2 ounces of per day, on average – had a 17% reduced risk of death, compared to those who ate much less, around 0.13 ounces per day. And when it came to the cereal fiber itself, people who ate the most had a 19% reduced risk of death from any cause, compared to those who ate the least.

The researchers even broke it down by disease: People who ate the highest amounts of whole grains had a 48% reduced risk of death from diabetes, and an 11% reduced risk of dying from respiratory diseases. And people who ate the most cereal fiber had 15% and 34% reduced risk of death from cancer and diabetes, respectively. 

The study cannot of course determine causation, since it’s just observational...Still, a number of studies have pointed to a strong connection between whole grains and improved health and longevity in recent years. It may be the anti-inflammatory properties of fiber per se – and its effect of reducing c-reactive protein (CRP) and tumor necrosis factor – that are responsible for their health benefits. If you’re going to up your grain intake, make sure to choose whole ones, like steel cut oats, quinoa, or even whole grain bread, over refined ones like cereal flakes or white bread. 

From Scientific American: Fiber-Famished Gut Microbes Linked to Poor Health

Your gut is the site of constant turf wars. Hundreds of bacterial species—along with fungi, archaea and viruses—do battle daily, competing for resources. Some companies advocate for consuming more probiotics, live beneficial bacteria, to improve microbial communities in our gut, but more and more research supports the idea that the most powerful approach might be to better feed the good bacteria we already harbor. Their meal of choice? Fiber.  

Fiber has long been linked to better health, but new research shows how the gut microbiota might play a role in this pattern. One investigation discovered that adding more fiber to the diet can trigger a shift from a microbial profile linked to obesity to one correlated with a leaner physique. Another recent study shows that when microbes are starved of fiber, they can start to feed on the protective mucus lining of the gut, possibly triggering inflammation and disease.

"Diet is one of the most powerful tools we have for changing the microbiota," Justin Sonnenburg, a biologist at Stanford University, said earlier this month at a Keystone Symposia conference on the gut microbiome. "Dietary fiber and diversity of the microbiota complement each other for better health outcomes." In particular, beneficial microbes feast on fermentable fibers—which can come from various vegetables, whole grains and other foods—that resist digestion by human-made enzymes as they travel down the digestive tract. These fibers arrive in the large intestine relatively intact, ready to be devoured by our microbial multitudes. Microbes can extract the fiber's extra energy, nutrients, vitamins and other compounds for us. Short-chain fatty acids obtained from fiber are of particular interest, as they have been linked to improved immune function, decreased inflammation and protection against obesity.

Today's Western diet, however, is exceedingly fiber-poor by historical standards. It contains roughly 15 grams of fiber daily, Sonnenburg noted. For most of our early history as hunter-gatherers, we were likely eating close to 10 times that amount of fiber each day. "Imagine the effect that has on our microbiota over the course of our evolution," he said.

Not all helpful fiber, however, needs to come from the roots and roughage for which our ancestors foraged, new research suggests. Kelly Swanson, a professor of comparative nutrition at the University of Illinois at Urbana-Champaign, and his team found that simply adding a fiber-enriched snack bar to subjects' daily diets could swing microbial profiles in a matter of weeks... The findings were published in the January issue of the American Journal of Clinical Nutrition.

As gut microbes are starved of fermentable fiber, some do die off. Others, however, are able to switch to another food source in the gut: the mucus lining that helps keep the gut wall intact and free from infection. In a recent study presented at the Keystone meeting, Eric Martens of the University of Michigan Medical School, postdoctoral researcher Mahesh Desai and their colleagues found that this fuel switch had striking consequences in rodents. A group of mice fed a high-fiber diet had healthy gut lining, but for mice on a fiber-free diet, "the mucus layer becomes dramatically diminished," he explained at the meeting. This shift might sometimes have severe health consequences. Research by a Swedish team, published last year in the journal Gut, showed a link between bacteria penetrating the mucus layer and ulcerative colitis, a painful chronic bowel disease.

A third group of mice received high-fiber chow and fiber-free chow on alternating days—"like what we would do if we were being bad and eating McDonald's one day and eating our whole grains the next," Martens joked. Even the part-time high-fiber diet was not enough to keep guts healthy: these mice had a mucus layer about half the thickness of mice on the consistently high-fiber diet. If we can extend these results to humans, he said, it "tells us that even eating your whole fiber foods every other day is still not enough to protect you. You need to eat a high-fiber diet every day to keep a healthy gut." Along the same lines, Swanson's group found that the gut microbiomes of his adult subjects reverted back to initial profiles as soon as the high-fiber bars were discontinued.

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My last post A Special Gut Microbe was on the very essential and beneficial microbe Faecalibacterium prausnitzii. It is one of the most abundant  bacteria in the gut of healthy individuals, but low or depleted levels are associated with inflammation and found in a number of diseases, including intestinal bowel diseases such as Crohn's disease. It is a butyrate producing bacteria (beneficial).

F. prausnitzii is viewed as so essential that it has been called a "keystone species" in the gut. A question I've been asked is: how can one increase the numbers of this bacteria in the gut and where can one buy some to take as a probiotic? (Probiotics are live bacteria that are beneficial to health when consumed.)

The typical bacteria added to yogurts or sold as supplements are able to survive when exposed to air (oxygen). However, F. prausnitzii are "oxygen sensitive" and they die within minutes upon exposure to air. Researchers view this beneficial bacteria as a "probiotic of the future" and currently there is research going on to figure out ways it can be easily stored and be exposed to air a few hours and not die. Currently there is NO way to take a probiotic F. prausnitzii supplement. So what else can one do?

After reviewing the scientific literature, it seems that the current ways to get F. prausnitzii into the gut or increase its numbers are: fecal microbiota transplant or FMT (currently only done with desperately ill individuals), drastically restricting calories for one week by obese individuals increases beneficial bacteria, and making changes to the diet. For example, a high animal meat, high animal fat, high sugar, highly processed foods, and low fiber diet (the typical westernized diet) lowers F. prausnitzii numbers, while a high-fiber, low meat diet increases F. prausnitzii numbers.

Repeat: the number one thing a person can do to increase numbers of F. prausnitzii is to increase fiber in the diet. By the way, increasing dietary fiber increases butyrate, and butyrate is involved with colon health, is anti-inflammatory, and anti-cancer . See, it's all related.

High fiber is: whole grains, vegetables, fruits, nuts, seeds, and legumes. Eat a varied plant-based diet, which means lots of plant based foods. It seems that Michael Pollan's emphasis on "Eat real foods. Mostly plants. Not too much." is just right. And variety seems important - with different types of fiber feeding different bacteria.

While F. prausnitzii may be an important beneficial bacteria in the gut, it is not the only beneficial one. So a food labeled "with added fiber" may not be the right fiber for bacteria, This is even true for enteral formula supplementation, for example, one formula containing fiber used pea fiber and this did not feed the F. prausnitzii.

In the first paragraph I mentioned that research has consistently shown F. prausnitzii depletion in adults sick with IBDs such as Crohn's disease. So it was interesting to find that one recent study found that even people sick with Crohn's disease showed significant improvement and remission (92% remission at 2 years) on a semi-vegetarian diet, namely a lacto-ovo-vegetarian diet (daily 32.4 g of dietary fiber in 2000 calories). [High Amount of Dietary Fiber Not Harmful But Favorable for Crohn Disease ]This is totally opposite from the current prevailing medical view which currently encourages people with IBD to "rest the intestine" with a fiber-restricted diet.

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In the past year I keep coming across one special gut microbe: Faecalibacterium prausnitzii. This bacteria is considered beneficial and is one of the most prevalent intestinal bacterial species in healthy adults. The reduction of this bacteria in the gut (as measured by analyzing bacteria in fecal samples) is seen in several diseases, including Intestinal Bowel Disease (IBD). This bacteria has also been found to be anti-inflammatory. In other words, you really, really want a healthy population in your gut.

But now the question is: how does the bacteria get there? And how can you increase it if you have a low population in your gut? It certainly isn't found in any probiotic supplement that I know of.  Part of the answer seems to be eating foods with fiber, lots of it, to feed the good microbes. Eat fruits, vegetables, whole grains, seeds, legumes, and nuts.

The following lengthy article discusses the importance of keystone species (F. prausnitzii is one). From Scientific American:

Among Trillions of Microbes in the Gut, a Few Are Special

In the mid-2000s Harry Sokol, a gastroenterologist at Saint Antoine Hospital in Paris, was surprised by what he found when he ran some laboratory tests on tissue samples from his patients with Crohn's disease, a chronic inflammatory disorder of the gut.. But when Sokol did a comparative DNA analysis of diseased sections of intestine surgically removed from the patients, he observed a relative depletion of just one common bacterium, Faecalibacterium prausnitzii. Rather than “bad” microbes prompting disease, he wondered, could a single “good” microbe prevent disease?

Sokol transferred the bacterium to mice and found it protected them against experimentally induced intestinal inflammation. And when he subsequently mixed F. prausnitzii with human immune cells in a test tube, he noted a strong anti-inflammatory response. Sokol seemed to have identified a powerfully anti-inflammatory member of the human microbiota.

Each of us harbors a teeming ecosystem of microbes that outnumbers the total number of cells in the human body by a factor of 10 to one and whose collective genome is at least 150 times larger than our own... The microbiome varies dramatically from one individual to the next and can change quickly over time in a single individual. The great majority of the microbes live in the gut, particularly the large intestine, which serves as an anaerobic digestion chamber. 

Independent researchers around the world have identified a select group of microbes that seem important for gut health and a balanced immune system. They belong to several clustered branches of the clostridial group. Dubbed “clostridial clusters,” these microbes are distantly related to Clostridium difficile, a scourge of hospitals and an all too frequent cause of death by diarrhea. But where C. difficile prompts endless inflammation, bleeding and potentially catastrophic loss of fluids, the clostridial clusters do just the opposite—they keep the gut barrier tight and healthy, and they soothe the immune system. Scientists are now exploring whether these microbes can be used to treat a bevy of the autoimmune, allergic and inflammatory disorders that have increased in recent decades, including Crohn's and maybe even obesity.

F. prausnitzii was one of the first clostridial microbes to be identified. In Sokol's patients those with higher counts of F. prausnitzii consistently fared best six months after surgery. After he published his initial findings in 2008, scientists in India and Japan also found F. prausnitzii to be depleted in patients with inflammatory bowel disease... This suggested that whereas different genetic vulnerabilities might underlie the disorder, the path to disease was similar: a loss of anti-inflammatory microbes from the gut. And although Sokol suspects that other good bacteria besides F. prausnitzii exist, this similarity hinted at a potential one-size-fits-all remedy for Crohn's and possibly other inflammatory disorders: restoration of peacekeeping microbes.

One of the questions central to microbiome research is why people in modern society, who are relatively free of infectious diseases, a major cause of inflammation, are so prone to inflammatory, autoimmune and allergic diseases. Many now suspect that society-wide shifts in our microbial communities have contributed to our seemingly hyperreactive immune systems. Drivers of these changes might include antibiotics; sanitary practices that are aimed at limiting infectious disease but that also hinder the transmission of symbiotic microbes; and, of course, our high-sugar, high-fat modern diet. Our microbes eat what we eat, after all. Moreover, our particular surroundings may seed us with unique microbes, “localizing” our microbiota.

A number of studies have found a small but significant correlation between the early-life use of antibiotics and the later development of inflammatory disorders, including asthma, inflammatory bowel disease and, more recently, colorectal cancer and childhood obesity. One explanation for this association might be that sickly people take more antibiotics. Antibiotics are not the cause, in other words, but the result of preexisting ill health. Honda's studies suggest another explanation: antibiotics may deplete the very bacteria that favorably calibrate the immune system, leaving it prone to overreaction. 

A number of studies over the years have linked having fewer sanitary amenities in childhood with a lower risk of inflammatory bowel disease in adulthood. And a 2014 study from Aarhus University in Denmark found that among northern Europeans, growing up on a farm with livestock—another microbially enriched environment—halved the risk of being stricken with inflammatory bowel disease in adulthood.

These patterns suggest that perhaps by seeding the gut microbiota early in life or by direct modification of the immune system the environment can affect our risk of inflammatory bowel disease despite the genes we carry. And they raise the question of what proactive steps those of us who do not live on farms can take to increase our chances of harboring a healthy mix of microbes.

One of the more surprising discoveries in recent years is how much the gut microbiota of people living in North America differs from those of people living in rural conditions in Africa and South America. The microbial mix in North America is geared to digesting protein, simple sugars and fats, whereas the mix in rural African and Amazonian environments is far more diverse and geared to fermenting plant fiber. Some think that our hunter-gatherer ancestors harbored even greater microbial diversity in their guts.

What troubles Sonnenburg about this shift is that the bacteria that seem most anti-inflammatory—including the clostridial clusters—often specialize in fermenting soluble fiber...Some hunter-gatherers consumed up to 10 times as much soluble fiber as modern populations, and their bodies likely were flooded with far more fermentation by-products. Our fiber-poor modern diet may have weakened that signal, producing a state of “simmering hyperreactivity,” Sonnenburg says, and predisposing us to the “plagues” of civilization. He calls this problem “starving our microbial self.” We may not be adequately feeding some of the most important members of our microbiota.

Mouse experiments support the idea. Diets high in certain fats and sugars deplete anti-inflammatory bacteria, thin the mucous layer and foster systemic inflammation. ...In rodents, adding fermentable fiber to a diet otherwise high in fat keeps the “good” microbes happy, the mucous layer healthy and the gut barrier intact, and it prevents systemic inflammation. Taken together, these studies suggest that it is not only what is in your food that matters for your health but also what is missing.

The human studies are even more intriguing... Scientists at Catholic University of Louvain in Belgium recently showed that adding inulin, a fermentable fiber, to the diet of obese women increased counts of F. prausnitzii and other clostridial bacteria and reduced that dangerous systemic inflammation...Those without the bacteria did not benefit, which suggests that once species disappear from the “microbial organ,” the associated functions might also vanish. These individuals might not require ecosystem engineering so much as an ecosystem restoration.

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The researchers were interested in lifestyle factors that are associated with lower rates of allergies.  Prior research has shown that such lifestyle factors are : living on a farm, introducing fish into the child’s diet at an early age, having pets early in life, parental cleaning of the child’s pacifier by sucking it, crowded living conditions, early daycare attendance, and having siblings. This study found that in households washing dishes by hand, rather than in a dishwasher, there are lower rates of allergies and eczema in children. In addition, the study found that consuming fermented or farm-bought food could decrease the likelihood of allergies further. It is thought that early exposure to microbes stimulates the immune system in beneficial ways. Dishwashers leave fewer bacteria behind on dishes than hand washing dishes. Living in a household that hand-washes means family members are eating off of plates and cutlery that have more bacteria, and therefore they are getting more microbial exposure. There could also be more bacteria in the air when dishes are hand washed or even some other lifestyle factor that these households have in common.From NPR:

Kids, Allergies And A Possible Downside To Squeaky Clean Dishes

Could using a dishwashing machine increase the chances your child will develop allergies? That's what some provocative new research suggests — but don't tear out your machine just yet.The study involved 1,029 Swedish children (ages 7 or 8) and found that those whose parents said they mostly wash the family's dishes by hand were significantly less likely to develop eczema, and somewhat less likely to develop allergic asthma and hay fever.

The findings are the latest to support the "hygiene hypothesis," a still-evolving proposition that's been gaining momentum in recent years. The hypothesis basically suggests that people in developed countries are growing up way too clean because of a variety of trends, including the use of hand sanitizers and detergents, and spending too little time around animals.As a result, children don't tend to be exposed to as many bacteria and other microorganisms, and maybe that deprives their immune system of the chance to be trained to recognize microbial friend from foe.That may make the immune system more likely to misfire and overreact in a way that leads to allergies, eczema and asthma, Hesselmar says.

"The hypothesis was that these different dishwashing methods ... are not equally good in reducing bacteria from eating utensils and so on," Hesselmar says. "So we thought that perhaps hand dishwashing was less effective, so that you are exposed to more bacteria" in a way that's helpful.

In a study released Monday in the online version of the journal Pediatrics, the researchers report what they found: In families who said they mostly wash dishes by hand, significantly fewer children had eczema, and somewhat fewer had either asthma or hay fever, compared to kids from families who let machines wash their dishes.

Still, there are other possible explanations, Hesselmar and Mahr both caution. Though the researchers took economic status into account in the study, it could be that people who don't have dishwashers are alike in some other way that reduces their tendency to get allergies. Interestingly, for example, certain other lifestyle characteristics — eating fermented foods regularly, and tending to buy some foods straight from the farm — seemed to strengthen the "protective" effect in families without dishwashers.

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Healthy women were followed during their pregnancies and postpartum, and it was found that vaginal microbial communities change over the course of pregnancy, and then really change postpartum. They also found differences in the predominant Lactobacillus bacteria species between the women. In this study it was found that Lactobacillus bacteria were most dominant during pregnancy, especially L. gaserii, L. crispatus, L. iners, and L. jensenii, and there were ethnic differences in the species. And they found that the vaginal microbiome changes postpartum, with bacteria becoming more diverse and the numbers of Lactobacillus dropping. The message here is that what are "normal and healthy" microbial communities can vary between women (in this study which Lactobacillus species were "healthy and normal" varied among women). Remember: dysbiosis means that the normal microbial community is "out of whack". And sequenced the microbiomes means state of the art genetic analysis of the microbial communities From American Microbiome Institute:

The vaginal microbiome changes during and after pregnancy

The vaginal microbiome is critically important to a healthy pregnancy, and studies have shown that vaginal dysbiosis during pregnancy can lead to infection and preterm birth.  In order to help understand what the microbiome looks like throughout and just after pregnancy, researchers from England performed longitudinal studies on 42 pregnant women.  They published their results last week in Nature Scientific Reports.

The scientists sequenced the microbiomes of the 42 women throughout their pregnancies, and then for the 6 weeks afterwards for some of the women.  They discovered, in agreement with other literature on the subject, that the vaginal microbiome becomes dominated by Lactobacilli species during pregnancy.  The Lactobacilli are thought to prevent pathogens from colonizing the vagina because they produce lactic acid which decreases the overall pH of the vagina, and they secrete antibacterial toxins.  These Lactobacilli are also important as they are normally the first to colonize the new infants' guts after they pass through the birth canal. 

The researchers also learned that the microbiome shifts away from Lactobacilli and towards a more diverse microbiome in the period immediately following birth.  The new bacteria that colonize are often associated with vaginosis, and these can lead to inflammation and infection of the birth canal in some women.  The scientists suspect this shift occurs because there is a sudden drop in estrogen production upon removal of the placenta.  The increase in circulating estrogen is thought to be important for Lactobacilli colonization, so it makes sense that the rapid decrease in estrogen decreases Lactobacilli abundance.

Finally, this study showed that there were geographic and ethnic variations to the pregnant microbiome.  While each microbiome was associated with a healthy pregnancy, there were important differences, especially on the species level.  For example, Asian and Caucasian women’s pregnant microbiomes were dominated by Lactobacillus gasseri, while this species was absent in black women’s pregnant microbiomes.

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Something new and complex to think about. We humans  have genes (about 20, 000), and then the microbes (bacteria, viruses, fungi) within us have genes (between 2 million and 20 million) . And now it looks like some of their genes have slipped into our genes (horizontal gene transfer). An example: the genes that determine blood types (A, B, O) . Whew....Another totally new thing to think about in our evolutionary history. From Time:

You may be your germs: Microbe genes slipped into human DNA, study says

Evolutionary diagrams usually connect humans and monkeys with common primate ancestors, but now, scientists say there's a missing link that deserves a spot on that family tree -- our bacteria, fungi, and viruses. Though most of our genes come from primate ancestors, many of them slipped into our DNA from microbes living in our bodies, says British researcher Alastair Crisp. It's called horizontal gene transfer. Scientists have known of examples of this for a long time: Bacteria slip genes to each other, and it helps them evolve. 

Some researchers have disputed that microbes have swapped genes with the cells of complex animals, such as humans. But a new study at the University of Cambridge indicates it has probably happened a lot. Humans may have as many as hundreds of so-called foreign genes they picked up from microbes.

"Surprisingly, far from being a rare occurrence, it appears that (horizontal gene transfer) has contributed to the evolution of many, perhaps all, animals and that the process is ongoing, meaning that we may need to re-evaluate how we think about evolution," Crisp said.

That may not surprise microbiologists.We humans and other complex animals are full of microbes, gajillions of them. People have so many that microbe cells living in our bodies outnumber our own vastly. A body has about 10 trillion human cells, says microbiologist Rob Knight. The microbe cells living inside of us number around 100 trillion. That's a ratio of 10 to one. The biggest collection is in our gut.

They're mostly helpful, and we we'd have a hard time living without them. Their genetic material dwarfs ours. The human genome adds up to 20,000 genes. The collective genomes of the many varieties of microbes in our bodies adds up to between 2 million and 20 million, Knight says.

In recent decades, scientists laid down genomes -- a detailed description of gene sequences -- for all kinds of species, including humans. The Cambridge researchers compared the genomes of various species of fruit flies, worms and primates, including humans.

They calculated similarities and differences between the genes across those species to look for ones that stuck out as not being part of a smooth evolutionary lineage, but instead probably popped in at some point. They found 128 formerly unidentified "foreign" genes in humans and confirmed 17 that had previously been reported. Most of them play a role in digestion. But the scientists also found that the gene that determines blood types -- A, B and O -- is "foreign." Some "foreign" genes that transferred in from microbes help our bodies' immune systems defend against microbial infections like bacteria and fungi.

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Are there differences between male and female gut microbiomes? (NOTE: gut microbiome is the community of microbes living in the gut.) I always thought YES, based on that there seem to be so many biological differences between males and females. But according to this blog entry from uBiome (a microbiome sequencing service which has analyzed thousands of gut microbiomes - the microbes living in the gut ) there aren't. They only looked at gut microbiomes (by analyzing fecal samples), and not at other body sites in this comparison. Other past studies have found  that other body sites have bacteria differences. Even the comments after the post were interesting. From the uBiome Blog:

A Surprising Comparison of Male vs. Female Microbiomes

I must admit, I was curious. So I went over to the desk of our brilliant Lead Data Scientist, Dr. Siavosh Rezvan-Behbahani, to find out. Could you look at all of uBiome’s gut samples, I asked, and see what the difference in microbiome composition is between men and women? And the corollary, is it possible to predict from microbiomial data whether the person giving the sample was male or female? With human DNA, of course you can determine gender based on the chromosome signature XX vs. XY. But does the microbiome have a gender signature too?

Siavosh dove in. He spent many hours analyzing, plotting numbers, running different machine learning classifier algorithms. He looked at healthy male and female samples in part of our dataset, all the way down to genus level. And here’s what he found, which blew my mind.

It turns out that in our dataset, there is no statistically significant difference between male microbiomes and female microbiomes. And, given a random sample, we would not be able to determine if it came from a man or a woman.

This result is fascinating to me, because it suggests that maybe men and women aren’t that different in some ways. We all have two eyes, and belly buttons, and similar proportions of bacteria swimming around inside our intestines.

(Of course there’s the standard disclaimer that this is just what we observe in our gut dataset, and may not be representative of the entire human population. It’s also possible that there is a difference but it’s much more subtle than we expect. In any case, this result is encouraging me to think up other questions to ask!)

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This interesting study raises the possibility that eating certain foods or probiotics  (beneficial bacteria) may prevent diabetes. Note that Akkermansia is a bacteria with one species Akkermansia muciniphila . In Wikipedia:"Researchers have discovered that Akkermansia muciniphila may be able to be used to combat obesity and type 2 diabetes...The bacterium is naturally present in the human digestive tract at 3-5%, but has been seen to fall with obesity." Regarding Prevotella, in Wikipedia: "Studies also indicate that long-term diet is strongly associated with the gut microbiome composition—those who eat plenty of protein and animal fats typical of Western diet have predominantly Bacteroides bacteria, while for those who consume more carbohydrates, especially fiber, the Prevotella species dominate." From Science Daily:

Gut bacteria may contribute to diabetes in black males

African American men at elevated risk for developing type 2 diabetes may have fewer beneficial and more harmful intestinal bacteria, according to new research.

"The 'signature' of the gut microbiota -- the relative abundance of various bacteria and other microbes in the digestive system -- could be another useful tool in assessing a person's risk for developing diabetes," said Ciubotaru. Ciubotaru and her colleagues, including principal investigator Dr. Elena Barengolts,... found that a specific microbiota is associated with stable, normal blood glucose levels, while a different profile is associated with glucose levels that indicate pre-diabetes.

"The study provides additional reasons for physicians to recommend foods, such as prebiotics, which improve the growth and activity of helpful gut bacteria," said Barengolts. The gut microbiota helps digest food; fights infections; and plays an important role in keeping the immune system healthy. It is greatly influenced by genetics, diet and other environmental factors. Previous research has implicated an unhealthy or unbalanced microbiota as a contributing factor to metabolic disorders, including obesity and diabetes. The species that make up an individual's gut microbiota, as well as their abundance, can be identified by stool sample analysis.

The researchers determined the gut microbiotas of 116 African-American male veterans, age 45 to 75, participating in the D Vitamin Intervention in VA, or DIVA study. The aim of the DIVA study, which has 173 total participants and is funded by the Department of Veterans Affairs, is to determine if vitamin D supplementation can prevent diabetes in men with risk factors for developing the disease.

Participants were divided into four groups based on changes in their blood sugar levels as determined at the start and end of the one-year study. The groups included men whose glucose levels remained normal (non-pre-diabetic); those with stable levels indicative of pre-diabetes; those whose levels indicated a worsening of glucose control; and those whose levels improved. All the men provided stool samples for analysis of their gut microbiota.

Men whose blood sugar levels stayed normal over the year had more gut bacteria that are considered beneficial for metabolic health, whereas those who stayed pre-diabetic had fewer beneficial bacteria and more harmful bacteria. In addition, the group whose levels improved had more abundant Akkermansia--healthy bacteria--than the group that maintained normal blood sugar control throughout the year.

The study suggests that differences in the gut microbiota already exist in pre-diabetes, Barengolts said. Although the study found connections between composition of the gut microbiota and blood sugar control, Barengolts said further research is needed to confirm these findings and evaluate whether certain intestinal bacteria cause type 2 diabetes. However, based on other research her group has conducted and studies in animals, she speculated that the foods we eat affect our diabetes risk through our gut microbiota. If the mix of organisms in the intestinal tract is indeed responsible for the development of type 2 diabetes, she said, it may be possible to lower one's risk by changing the gut bacteria.

More details about that same study. From Medpage Today:

Prediabetes Patients Have Fewer Gut Bugs

They were put into one of four groups: those with a stable glucose tolerance, those with stable impaired fasting glucose or stable impaired glucose tolerance, those with worsened glucose tolerance, and those with improved glucose tolerance. There were significant differences in bacterial composition between the first and second groups (P=0.03) at the phylum level. Bacteroidetes was higher and Firmicutes was lower with worse glycemic control in the second group. 

Proteobacteria decreased over the period in groups 2 and 4 compared with group 1 (P=0.04 for both). At the family and genus levels, in group 2 versus group 1 there was less Prevotella, and a higher Bacteroides/Prevotella ratio in the second group at 5.6 to 2.7 (P=0.05). There was also less Enterobacteriaceae (P=0.03), and more Ruminococcae (P=0.01) and Veillonellaceae (P=0.02).

"We speculate that lower abundance of Prevotella may be associated with worsening glycemia, and, conversely, higher abundance of Akkermansia might be associated with improving glycemia, thus corroborating suggestions from previous studies," the researchers said.