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There have been many posts on this blog about diet, fiber, microbes, and the association of diet with various diseases, such as cancer. A recent journal article by M. Song and A. Chan reviewed studies that looked at the link between diet, gut microbes (the gut microbiota or gut microbiome), and colorectal cancer (what we typically call colon cancer).

In summary, research from the last 20 years has found that diet and colorectal cancer (CRC) go hand in hand, and that diet determines the microbes (microbiota) living in the gut - that is, what you feed the microbes determines what microbes will live and thrive in the gut. Also, certain microbes in the gut are linked to inflammation and cancer formation, and others to its prevention. In other words, there is potential to prevent colorectal cancer with certain diets, and to increase the odds of colorectal cancer with other diets.

What are main dietary factors linked to colorectal cancer? Western diet (lots of processed foods, red and processed meat, low in fiber, refined grains), low levels of dietary fiber, low intake of omega-3 fatty acids from seafood (or fish oil), and obesity. The researchers point out that a Western diet is associated with gut dysbiosis (microbial imbalance), loss of gut barrier integrity, and increased levels of inflammation. What should one do? Basically think to yourself: "I need to feed the beneficial microbes in my gut, so I need to eat lots of fruits, vegetables, whole grains, and seafood (omega-3 fatty acids)" - this is what the researchers call a "prudent pattern diet". And try to maintain a normal weight. Some excerpts from Current Colorectal Cancer Reports:

Diet, Gut Microbiota, and Colorectal Cancer Prevention: a Review of Potential Mechanisms and Promising Targets for Future Research

AbstractDiet plays an important role in the development of colorectal cancer. Emerging data have implicated the gut microbiota in colorectal cancer. Diet is a major determinant for the gut microbial structure and function. Therefore, it has been hypothesized that alterations in gut microbes and their metabolites may contribute to the influence of diet on the development of colorectal cancer.We review several major dietary factors that have been linked to gut microbiota and colorectal cancer, including major dietary patterns, fiber, red meat and sulfur, and obesity

Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the fourth leading cause of cancer death in the world. Over the past few decades, numerous epidemiologic studies have identified a range of dietary factors that may potentially promote or prevent CRC. Likewise, increasing evidence has implicated the gut microbiota in CRC development. Biological plausibility is supported by habitation of numerous gut microbes in the large intestine and the functional importance of the gut microbiota in maintenance of the gut barrier integrity and immune homeostasis, the disruptions of which are among the most important mechanisms in colorectal carcinogenesis. Given the critical role of diet in the configurations of gut microbial communities and production of bacterial metabolites, it has been proposed that diet may influence CRC risk through modulation of the gut microbial composition and metabolism that in turn shape the immune response during tumor development.

Although gut bacterial abundance may respond rapidly to extreme changes in diet, predominant microbial community membership is primarily determined by long-term diet, and substantial inter-individual variation persists despite short-term dietary change. .... Thus, this review focuses on the dietary factors that have strong mechanistic support, including dietary pattern, fiber, red meat and sulfur, and omega-3 fatty acid. Given the close link between diet and obesity and the predominant role of obesity in CRC as well as the substantial data linking the gut microbiome to obesity, we also include obesity at the end of the review.

DIETARY PATTERNS: Convincing data indicate that a “Western dietary pattern,” characterized by high intake of red or processed meat, sweets, and refined grains, is associated with higher risk of colorectal neoplasia; in contrast, diets that are rich in fruits, vegetables, and whole grains (“prudent pattern diet”) are associated with lower risk of CRC. Western diets are associated with gut dysbiosis (microbial imbalance), loss of gut barrier integrity, increased levels of inflammatory proteins, and dysregulated immune signatures.

A potential role of the gut microbiota in mediating the dietary associations with CRC risk is suggested by the dramatic difference of the gut microbial structures between populations consuming different diets. Rural Africans, whose diet is high in fiber and low in fat, have a strikingly different gut microbial composition than urban Europeans or African Americans consuming a Western diet, which parallels the lower CRC rates in Africa than Western countries. For example, the African gut microbiota is characterized by a predominance of Prevotella genus that are involved in starch, hemicellulose, and xylan degradation, whereas the American microbiota is predominated by Bacteroides genus with a higher abundance of potentially pathogenic proteobacteria, such as Escherichia and Acinetobacter. .... Moreover, a crossover study indicates that switching African Americans to a high-fiber, low-fat diet for 2 weeks increases production of SCFAs, suppresses secondary bile acid synthesis, and reduces colonic mucosal inflammation and proliferation biomarkers of cancer risk.

Fiber: Numerous prospective studies have linked higher fiber intake to lower risk of CRC. The most recent expert report from the World Cancer Research Fund and the American Institute for Cancer Research in 2011 concludes that evidence that consumption of foods containing dietary fiber protects against CRC is convincing. Besides systemic benefits for insulin sensitivity and metabolic regulation, which have been implicated in colorectal carcinogenesis, fiber possesses gut-specific activities, such as diluting fecal content, decreasing transit time, and increasing stool weight, thereby minimizing exposure to intestinal carcinogens.

Moreover, soluble fiber can be fermented by bacteria in the lumen of the colon into SCFAs [short-chain fatty acids], including butyrate, acetate,and propionate. Higher fiber intake has been shown to enrich butyrate-producing bacteria in the gut, such as Clostridium, Anaerostipes, Eubacterium, and Roseburia species, and increase production of SCFAs. SCFAs have been suggested as the key metabolites linking the gut microbes to various health conditions, especially CRC

Red Meat and Sulfur: There is convincing evidence that red and processed meats are associated with increased risk of CRC. Recently, the Int. Agency for Research on Cancer has classified processed meat as a carcinogen to humans. Mechanisms underlying the pro-cancer effects of red or processed meats include heme iron, N-nitroso compounds, or heterocyclic amines, and hydrogen sulfide production. Hydrogen sulfide has been implicated in inflammatory disorders associated with risk of CRC, such as ulcerative colitis, and directly with CRC.

Omega-3 Fatty Acid: Marine omega-3 polyunsaturated fatty acid, including eicosapentaenoic acid, docosahexaenoic acid, and docosapentaenoic acid, possesses potent anti-inflammatory activity and may protect against CRC. Fish oil, a rich source of omega-3 fatty acid, is the most popular natural product used by US adults. Substantial data support the beneficial effect of omega-3 fatty acid on CRC prevention and treatment.

Dietary fat composition is a major driver of the gut microbial community structure. Compared to other types of fat, omega-3 fatty acid have been associated with higher intestinal microbiota diversity and omega-3 fatty acid-rich diet ameliorates the gut dysbiosis induced by omega-6 polyunsaturated fatty acid or antibiotics.

Obesity: Since the 1970–1980s, the prevalence of obesity has markedly increased worldwide. The obesity epidemic is believed to be largely driven by global westernization characterized by overconsumption of easily accessible and energy-dense food and a sedentary lifestyle. Obesity is an established risk factor for CRC and several other cancers. Possible mechanisms include increased insulin levels and bioavailability of insulin-like growth factor 1, altered secretion of adipokines and inflammatory cytokines, and changes in sex hormone levels.

A recent study tested a variety of probiotic (beneficial) Lactobacillus and Bifidobacteria species of bacteria as a treatment for chronic sinusitis. Unfortunately, it found that the microbes tested had NO effect on chronic sinusitis symptoms. It was a nice study conducted in Sweden, with 21 people with chronic sinusitis (but without nasal polyps) randomly assigned to receive a nasal spray (that they used 2 x daily for 14 days) containing either a mixture of 13 bacteria or a "sham" nasal spray. No one knew who received what, and then after a few weeks they did a crossover - meaning who got what was switched for another 2 weeks.

But...the main finding is that after 14 days of using the nasal sprays, there was no improvement in either group, no improvement in symptoms, no effect on the sinus "microbial flora", and no effect on inflammation. In fact, 2 individuals wound up taking antibiotics while testing the bacteria nasal spray. In other words, a big fat zero.

The bacteria tested were what the researchers called a honeybee lactic acid (LAB) microbiome, with both Lactobacillus and Bifidobacteria species: Lactobacillus apinorumL. melliferL. mellis, L. kimbladiiL. melliventrisL. helsingborgensisL. kullabergensisL. kunkeei, L. apisBifidobacterium asteroidesB. coryneforme, Bifidobacterium Bin7N, and Bifidobacterium Hma3N. These species are not typically found in probiotic supplements.

Why did they choose those strains of bacteria? Because "in vitro" testing (meaning in a test tube or culture dish) suggested that they would be effective against the pathogenic bacteria frequently found in chronic sinusitis (that they were antimicrobial). But real world testing in actual humans in this study showed that those specific Lactobacillus and Bifidobacteria microbes had no effect on sinusitis symptoms. Their premise was good - that the sinus microbiome was "disturbed" or out of whack (dysbiosis) in chronic sinusitis, but unfortunately they chose the wrong bacteria to test as a treatment.

The SNOT-22 questionnaire that asked questions of sinusitis sufferers at several points in the study to see if there was improvement in sinusitis symptoms, is one typically given to those with chronic sinusitis. [By the way, when reviewing the questionnaire, I realized it left out some major sinusitis symptoms such as "gagging on phlegm", "waking up with sore throat", "teeth hurt", "headache" - all of which are frequently mentioned by many contacting me, and which I remember well from pre-L. sakei days. In other words - it is incomplete, yet it is the questionnaire typically used to assess quality of life and symptoms for those with chronic sinusitis.]

The researchers end the journal article by stating "Further studies are warranted to explore whether other tentative probiotic assemblages [other bacterial species] can confer positive health effects to patients suffering from inflammatory conditions of the upper airways." Huh... If only they had asked...  I've been writing about Lactobacillus sakei as an excellent treatment for chronic sinusitis since 2013 (based on results of Abreu et al study), and I've been getting positive feedback from others about L. sakei since early 2014. For those who find that L. sakei works as a sinusitis treatment, the results seem miraculous - typically with major improvement within a few days. (Please note: Perhaps other microbes may also work as a sinusitis treatment.) Excerpts from Laryngoscope Investigative Otolaryngology:

Clinical efficacy of a topical lactic acid bacterial microbiome in chronic rhinosinusitis: A randomized controlled trial

A locally disturbed commensal microbiome might be an etiological factor in chronic rhinosinusitis (CRS) in general and in CRS without nasal polyps (CRSsNP) in particular. Lactic acid bacteria (LAB) have been suggested to restore commensal microbiomes. A honeybee LAB microbiome consisting of various lactobacilli and bifidobacteria have been found potent against CRS pathogens in vitro. Recently, we examined effects of single nasal administrations of this microbiome in healthy subjects and found it inert. In this study, we examined effects of repeated such administrations in patients with CRSsNP.

The study was of a randomized, double‐blinded, crossover, and sham‐controlled design. Twenty patients received 2 weeks' treatment administered using a nasal spray‐device. The subjects were monitored with regard to symptoms (SNOT‐22 questionnaire, i.e., the primary efficacy variable), changes to their microbiome, and inflammatory products (IL‐6, IL‐8, TNF‐, IL‐8,a, and MPO) in nasal lavage fluids.

ResultsNeither symptom scores, microbiological explorations, nor levels of inflammatory products in nasal lavage fluids were affected by LAB (c.f. sham). Conclusion: Two weeks' nasal administration of a honeybee LAB microbiome to patients with CRSsNP is well tolerated but affects neither symptom severity nor the microbiological flora/local inflammatory activity.

 In this study, involving patients with well‐defined CRSsNP, we demonstrate that repeated nasal administration of a LAB microbiota composed of several species of lactobacilli and bifidobacteria over 2 weeks neither affects symptoms as assessed by SNOT‐22 questionnaire nor the bacterial composition or the inflammatory activity in the nasal cavity. The observations are of relevance to the evaluation of topical LAB treatment in the management of upper respiratory tract conditions such as CRS.

Just read a small study that compared the microbes in the sinus microbiome between 12 healthy people with no sinusitis (controls) and 14 with chronic sinusitis, their neurotransmitter levels (serotonin, dopamine, and GABA), and also looked at depression scores in the 2 groups. Well, of course they found some microbial differences between healthy people and those with chronic rhinosinusitis (CRS), but they also found that those with the most severe chronic sinusitis tended to have the most depressive symptoms, and lower amounts of the neurotransmitters studied, but they did not find significant differences overall.

I found their summary and conclusions problematic, since they discussed that "possibly" the sinus microbes influence brain neurotransmitters. And they pointed out that as certain disease associated microbes increased (especially Moraxella), the neurotransmitter concentrations tended to decrease in those with sinusitis. But since there were no significant group differences, they did not prove their hypotheses, and conclusions can not be made. So saying there is "the potential for downstream effects of the sinonasal microbiota on neural signaling and, subsequently, brain function and behavior" is misleading and overreaching. The researchers also said it was "difficult to discern disease associations from natural variation." Hah!

It should be obvious that the worse the chronic sinusitis, the more depressive symptoms, because having chronic sinusitis is DEPRESSING. One suffers with it. Some people have told me how chronic sinusitis has destroyed their life - whether their health, financially, with relationships, etc. Of course they will have higher depressive scores! And when a Lactobacillus sakei product or other probiotic successfully treats sinusitis (usually very quickly), then the mood is one of elation as symptoms go away (finally health!).

All one can say (based on studies) is: the sinus microbiomes in healthy people (normal sinus microbial community) are somewhat different from those with chronic sinusitis (out-of-whack microbial community or dysbiosis). And one would expect that those with less severe/milder sinusitis have a "better" community of sinus microbes - that is, more microbes that are associated with health, and fewer of those associated with sickness, than sicker people. Which is what this study suggested. Excerpts from the International Forum of Allergy & Rhinology:

The sinonasal microbiota, neural signaling, and depression in chronic rhinosinusitis

The complex relationships between the human microbiota, the immune system, and the brain play important roles in both health and disease, and have been of increasing interest in the study of chronic inflammatory mucosal conditions. We hypothesized that the sinonasal microbiota may act as a modifier of interkingdom neural signaling and, subsequently, mental health, in the upper respiratory inflammatory condition chronic rhinosinusitis (CRS). In this study we investigated associations between the sinonasal microbiota; local concentrations of the neurotransmitters serotonin, dopamine, and γ-aminobutyric acid (GABA); and depression severity in a cohort of 14 CRS patients and 12 healthy controls.

Several commonly “health-associated” sinonasal bacterial taxa were positively associated with higher neurotransmitter concentrations and negatively associated with depression severity. In contrast, several taxa commonly associated with an imbalanced sinonasal microbiota negatively associated with neurotransmitters and positively with depression severity. Few significant differences were identified when comparing between control and CRS subject groups, including neurotransmitter concentrations, depression scores, or sinonasal microbiota composition or abundance. Conclusion: The findings obtained lend support to the potential for downstream effects of the sinonasal microbiota on neural signaling and, subsequently, brain function and behavior.

SOME OTHER EXCERPTS: Depression scores were also not significantly different between controls and CRS patients. .... The serotonin levels in CRS patients compared with control subjects tended to be lower, but not significantly so. Although median values for dopamine, GABA, and serotonin were generally lower in CRS patients than controls, all 3 neurotransmitters had a greater range among those with CRS, and no differences were significant. ... For both CRS and control individuals, bacterial communities were generally dominated by OTUs of the genera Corynebacterium and Staphylococcus.

Correlation analyses identified associations between members of the genera Staphylococcus, Finegoldia, Propionibacterium, Peptoniphilus, and Anaerococcus, as well as bacterial community diversity overall. Members of these genera have been previously identified as representative of more “health-associated” sinonasal bacterial community types, whereas their depletion has been associated with lower bacterial community diversity, increased bacterial load, increased rates of asthma, and elevated markers of inflammation. Similarly, members of the genera Burkholderia and Propionibacterium have been identified as 2 potential “gatekeepers” that help maintain bacterial community stability in the sinonasal tract. In the present study, several of these same bacterial taxa were significantly positively correlated with neurotransmitter levels and negatively with depression severity, whereas several other OTUs (including members of Streptococcus, Rothia, Enterobacteriaceae, Corynebacterium, and Moraxella) showed the opposite pattern (negatively associated with neurotransmitter levels and positively with depression severity). 

Two studies (one in mice and one in humans) from researchers at the University of Illinois found that no matter what your diet - exercise changes the gut bacteria in a beneficial way. And when you go back to a sedentary lifestyle, your gut microbes change again and beneficial microbes such as short chain fatty acids (SCFAs), especially butyrates, decline. The effect was more pronounced in lean sedentary adults (as compared to obese sedentary adults).

Beneficial microbes that increased with exercise in humans were species of Faecalibacterium, Roseburia, Lachnospira, Lachnospiraceae, and Clostridiales. Faecalibacterium prausnitzii has been discussed in earlier posts as a beneficial keystone species in the gut (here, here, and here). What kind of exercises did they do? They did three supervised 30 to 60 minute moderate to vigorous intensity aerobic/endurance exercise sessions per week for 6 weeks, and they could use a cycle ergometer (stationary bicycle) or treadmill each session.

Besides beneficial microbial changes, 6 weeks of exercising resulted in improved body composition (total lean body mass, decreased body fat, increased bone mineral density), and an improvement in cardiorespiratory fitness. These changes reversed in everyone when they went back to 6 weeks of a sedentary lifestyle. Bottom line: get out and move, move, move. Your gut microbes and your body will thank you. From Science Daily:

Exercise changes gut microbial composition independent of diet, team reports

Two studies -- one in mice and the other in human subjects -- offer the first definitive evidence that exercise alone can change the composition of microbes in the gut. The studies were designed to isolate exercise-induced changes from other factors -- such as diet or antibiotic use -- that might alter the intestinal microbiota.

In the first study, scientists transplanted fecal material from exercised and sedentary mice into the colons of sedentary germ-free mice, which had been raised in a sterile facility and had no microbiota of their own. In the second study, the team tracked changes in the composition of gut microbiota in human participants as they transitioned from a sedentary lifestyle to a more active one -- and back again.

Recipients of the exercised mouse microbiota also had a higher proportion of microbes that produce butyrate, a short-chain fatty acid that promotes healthy intestinal cells, reduces inflammation and generates energy for the host. They also appeared to be more resistant to experimental ulcerative colitis, an inflammatory bowel disease.

In the human study, the team recruited 18 lean and 14 obese sedentary adults, sampled their gut microbiomes, and started them on an exercise program during which they performed supervised cardiovascular exercise for 30-60 minutes three times a week for six weeks. The researchers sampled participants' gut microbiomes again at the end of the exercise program and after another six weeks of sedentary behavior. Participants maintained their usual diets throughout the course of the study. Fecal concentrations of SCFAs, in particular butyrate, went up in the human gut as a result of exercise. These levels declined again after the participants reverted to a sedentary lifestyle.

The most dramatic increases were seen in lean participants, who had significantly lower levels of SCFA-producing microbes in their guts to begin with. Obese participants saw only modest increases in the proportion of SCFA-producing microbes. The ratios of different microbes in the gut also differed between lean and obese participants at every stage of the study, the researchers said. "The bottom line is that there are clear differences in how the microbiome of somebody who is obese versus somebody who is lean responds to exercise," Woods said. " [Original study in humans.]

Another study has shown health benefits from eating a diet rich in whole grains, as compared to one with lots of refined grains (think bagels, muffins, white bread). Fifty overweight Danish adults were randomly assigned to either a group where all grains eaten were whole grains or a group where all grain products were of refined grains. They did this for 8 weeks, then ate their usual diet for a few weeks (the "washout period"), and then were assigned to the other dietary group for 8 weeks.

They found that eating the diet rich in whole grains resulted in: consuming fewer calories (the whole grains made them feel fuller), losing weight, and a decrease in chronic low-grade inflammation (by measuring blood inflammation markers). The whole grain rye seemed to be especially beneficial. But interestingly, the researchers found that the whole grain diet did not significantly change the gut microbe composition. But they did find that 4 strains of Faecalibacterium prausntzii and one of Prevotella copri increased in abundance after whole grain and decreased after refined grain consumption. F.prausnitzii is a desirable and beneficial keystone species in the gut (here and here).

Other studies show that eating a diet rich in whole grains (rather than refined grains) is associated with a decreased risk of several diseases, including type 2 diabetes and cardiovascular diseases. Bottom line: choose whole grains whenever possible. From Science Daily:

Several reasons why whole grains are healthy

When overweight adults exchange refined grain products -- such as white bread and pasta -- with whole grain varieties, they eat less, they lose weight and the amount of inflammation in their bodies decreases. These are some of the findings of a large Danish study headed by the National Food Institute, Technical University of Denmark. 

The study included 50 adults at risk of developing cardiovascular disease or type 2 diabetes. Blood tests showed that the participants had less inflammation in their bodies when eating whole grains. In particular, it appeared that rye had a beneficial effect on the blood's content of inflammatory markers. Inflammation is the natural response of the body to an infection, but some people have slightly elevated levels of inflammation (so-called low-grade inflammation) even though there is no infection. This is particularly the case in overweight people. In overweight people, an increased level of 'unnecessary' (subclinical) inflammation may lead to increased risk of developing type 2 diabetes.

The study also shows that participants eat less when whole grain products are on the menu -- presumably because whole grain consumption causes satiety. While eating the whole grain diet, participants have generally lost weight. The researchers used DNA sequencing to analyze stool samples from the participants in order to examine whether the different diet types affected the participants' gut bacteria composition. Overall, the analysis did not shown major effects of the dietary grain products on the composition of the gut bacteria. [Original study.]

A while ago I posted the results of studies showing differences in infant  microbiomes (community of microbes) depending on whether the babies were delivered vaginally or by C-section, and also that "vaginal seeding" may eliminate some of these differences. [C-section babies also have a higher incidence of some health issues, such as allergies, asthma, etc.] Well....that research generated a lot of controversy both for and against, and resulted in many women requesting that "vaginal seeding" be done to their babies after they were delivered by C-section. Even the noted microbiome researcher Rob Knight publicly admitted that the procedure was done to his baby after his partner received a C-section.

Vaginal seeding is the process of swabbing the bodies of C-section babies (including the mouth and nose) with a gauze pad containing the vaginal fluids from their mothers in the minutes after birth - so that the baby is exposed to the same maternal microbes as a baby born vaginally (because mothers transmit microbes to the baby as it moves through the birth canal). Initial research showed this made the microbiomes of the C-section babies look a lot like vaginally born babies, especially their skin and oral microbiomes, but whether these differences persist after a few months is unclear.

Now the American College of Obstetrics and Gynecology (ACOG) has come out with a position paper that vaginal seeding should not be done to babies, except as part of an official clinical trial. Their main opposition to the procedure is fear of transmitting pathogenic bacteria or viruses (e.g. group B streptococci, and STDs). The main reasons in support of doing the  vaginal seeding procedure is the body of research finding differences among C-section and vaginally delivered babies (allergies, asthma, etc.), and the concern that at least some of this may be due to lack of  exposure to maternal vaginal microbes during delivery. Instead, ACOG suggests breastfeeding the baby to transmit maternal microbes to the baby to "seed the gut". And if "a patient insists on performing the procedure herself, ACOG recommends ob-gyns have a documented discussion of the potential risks".

As can be expected, there is an outcry and rejection by some (many?) of the ACOG position paper. At least the ACOG paper acknowledges that every woman can make her own decision regarding this issue, even though they may not support it. And absolutely everyone agrees that more research is needed. From Ars Technica:

Doctors warn new parents: Step away from the vaginal fluid swabs

To slather, or not to slather—that is the question that has been roiling doctors, scientists, and new parents recently. And a new ruling by a doctor’s group stands to muck up the debate further. Amid the birth of microbiome research, some scientists have advocated for smearing bacteria-laden vaginal secretions on any newborns who missed out—namely those born via Caesarian section. Scientists keenly hypothesize that such a gooey glaze can “seed” a more-or-less sterile infant with life-long microbial companions. These wee chums may help train an infant's immune system and dodge issues like allergies and asthma later in life. Several studies have indeed found correlations between C-section deliveries and higher risks of those conditions.

In the latest turn to the controversy, the American College of Obstetricians and Gynecologists’ (ACOG) Committee on Obstetric Practice issued a November opinion firmly wiping up the slimy idea. In its opinion, the committee said it: “…does not recommend or encourage vaginal seeding outside of the context of an institutional review board-approved research protocol, and it is recommended that vaginal seeding otherwise not be performed until adequate data regarding the safety and benefit of the process become available.”

The few studies we do have on infant microbiomes provide no clear answers on the significance of an early “seeding” for health. A 2016 review looking at the patterns of microbial communities in the guts of infants in their first year found that C-section babies did show differences in the first three months. However, those differences disappeared by six months. Similarly, a small study of 18 babies also published last year found that vaginal seeding could eliminate microbial differences between vaginally and C-section delivered babies. But the study only looked at the infants' microbiomes in that first month, and the health effects—if any—are unknown.

The most concerning thing about vaginal seeding, the committee argues, is the potential for transmitting pathogens, such as herpes simplex virus, human papilloma virus (HPV), group B streptococci, and Neisseria gonorrhea. .... If a woman insists on the seeding, the committee recommended she be thoroughly tested and informed of the risks—as well as discouraged.

The following is a nice article about a recently published study finding a link between some bacteria commonly found in the mouth and inflammatory bowel diseases (IBD). The researchers found that some strains of oral bacteria are also found in the gut of people with inflammatory bowel diseases.

They theorize that these bacteria make it down to the gut when saliva is swallowed - and for susceptible people this may trigger inflammatory disease. They did a number of experiments to determine that the antibiotic-resistant, inflammation causing species of Klebsiella pneumoniae and Klebsiella aeromobilis could be triggering IBD. These bacteria are able to replace normal colon microbes after antibiotic therapy.

However, it must be noted that other studies also find other microbial differences among those with IBD and healthy people - e.g. low or absent levels of Faecalibacterium prausnitzii, and even fungal and viral differences. From Harvard Magazine:

Gut Health May Begin in the Mouth

Chronic gastrointestinal problems may begin with what is in a patient’s mouth. In a study published Thursday in Science, an international team of researchers—including one from Harvard—reported on strains of oral bacteria that, when swallowed in the 1.5 liters of saliva that people ingest every day, can lodge in the gut and trigger inflammatory bowel conditions like Crohn’s disease and ulcerative colitis.

“For some time now, we’ve noticed that when we look at the microbiome of patients with inflammatory bowel disease, or IBD, we’ve found microbes there that normally reside in the oral cavity,” says study co-author Ramnik Xavier, chief of gastroenterology at Massachusetts General Hospital (MGH)....

Simultaneously, “There’s always been this other search, asking, ‘Are there pathobionts?’”—in other words, microbes that live innocuously in one part of the body but can turn pathogenic when moved to another. “For some time we have been looking for pathobiont organisms for Crohn’s and colitis.”

The researchers believe they have found them: two strains of Klebsiella bacteria, microbes commonly found in the mouth. ....the researchers pinpointed a strain of Klebsiella pneumoniae as the trigger for the immune response. A subsequent experiment using samples from two ulcerative colitis patients turned up another inflammation-causing strain, of Klebsiella aeromobilis

Checking databases of thousands of IBD patients at MGH and the Hospital of the University of Pennsylvania, Xavier and others found that people with inflammatory bowel conditions had significantly more Klebsiella bacteria in their gut microbiome than healthy patients did. Most likely, he explains, oral bacteria, including Klebsiella, traffics through everyone’s gut in the saliva we swallow. Usually it passes through harmlessly; but in people with a genetic susceptibility to IBD that alters the gut microbiome, the Klebsiella has a chance to take hold in the intestine and proliferate, inducing an immune response that causes the disease. 

And there is another twist: Klebsiella bacteria are often extremely resistant to multiple antibiotics. That explains, Xavier says, “why antibiotics have limited value in treating patients with Crohn’s disease and ulcerative colitis....  “Because we also showed in a 2014 paper that patients who took antibiotics—and this has been seen in the old clinical data accumulated before the microbiome was even examined in IBD—that patients who took antibiotics early in the disease had more complicated outcomes.” 

Klebsiella  pneumoniae Credit: Wikipedia

A number of recent studies have suggested that as people age, the community of gut microbes (gut microbiota or gut microbiome) becomes less diverse than in younger people. And note that greater gut microbial diversity is generally viewed as healthy and good. However, now a study done in China finds a different result. The study examined the gut microbes of more than 1000 very healthy people, from ages 3 to over 100, and found that the gut microbial communities were very similar among very healthy people in their mid 30s to over 100 years in age.

Whether this is cause or effect is unknown. But the researchers speculate that the similarities in the gut microbiota among people from their 30s to 100+ is a consequence of an active healthy lifestyle and diet. And it suggests that somehow changing an elderly person's gut microbial community (if it's not "normal") to that of a 30-year-old might help promote health. From Science Daily:

'Ridiculously healthy' elderly have the same gut microbiome as healthy 30-year-olds

In one of the largest microbiota studies conducted in humans, researchers at Western University, Lawson Health Research Institute and Tianyi Health Science Institute in Zhenjiang, Jiangsu, China have shown a potential link between healthy aging and a healthy gut.

With the establishment of the China-Canada Institute, the researchers studied the gut bacteria in a cohort of more than 1,000 Chinese individuals in a variety of age-ranges from 3 to over 100 years-old who were self-selected to be extremely healthy with no known health issues and no family history of disease. The results showed a direct correlation between health and the microbes in the intestine. ....The study, published this month in the journal mSphere, showed that the overall microbiota composition of the healthy elderly group was similar to that of people decades younger, and that the gut microbiota differed little between individuals from the ages of 30 to over 100.

"The main conclusion is that if you are ridiculously healthy and 90 years old, your gut microbiota is not that different from a healthy 30 year old in the same population," said Greg Gloor, the principal investigator on the study and also a professor at Western's Schulich School of Medicine & Dentistry and Scientist at Lawson Health Research Institute. Whether this is cause or effect is unknown, but the study authors point out that it is the diversity of the gut microbiota that remained the same through their study group.

"This demonstrates that maintaining diversity of your gut as you age is a biomarker of healthy aging, just like low-cholesterol is a biomarker of a healthy circulatory system," Gloor said. The researchers suggest that resetting an elderly microbiota to that of a 30-year-old might help promote health. "By studying healthy people, we hope to know what we are striving for when people get sick," said Reid. [Original study.]

Centenarian in Bama County, China. Credit: National Geographic.

Finally - research is being done on ear microbiomes (the community of microbes that live in the ears) and how they differ in people with ear infections and those without ear infections. A recently presented ear microbiome study (at the annual American Academy of Otolaryngology meeting) makes perfect sense, and ties in perfectly with sinus microbiome research. Specifically, that there are microbial communities or microbiomes in the ears, and if the microbial communities go out of whack (dysbiosis) it can cause symptoms (ear infection).

This research reminds me of a wonderful anecdote about ear infections and how they could possibly be treated - an ear wax transplant. From a 2012 article in ENT Today: Restoring Microbial Balance Key to Keeping Sinuses Healthy

Andrew Goldberg, MD, never tires of telling people about how he was outsmarted by a patient while working as a second-year otolaryngology resident at the University of Pittsburgh. Now the director of rhinology and sinus surgery at the University of California San Francisco Medical Center, Dr. Goldberg recalled how he assisted in the examination of a patient with a history of chronic otiti sexterna [ear infection] in one ear. Despite repeated trips to doctors for antibiotics, vinegar washes and drops, the patient’s ear trouble always came back.

Not this time. The doctors assumed that their treatments had finally done the trick, only to be told by the patient that he had likely cured himself by taking earwax from his good ear and sticking it in his bad ear. “I had no idea what that meant. I’m sure that we assumed, at the time, that what he was telling us was nonsense, that he was a little nutty,” Dr. Goldberg said. “We never thought anything more about it.”

The home remedy, however, now seems prescient in light of accumulating research suggesting that microbiomes, or distinct bacterial communities that coexist with us throughout our bodies, may play key roles in maintaining human health. When he began conducting his own microbiome research about five years ago, Dr. Goldberg realized that his former patient may have taken an intact, healthy microbiome and used it to re-inoculate the disrupted bacterial community in his bad ear.

Description of the recently presented study - unfortunately no details were given about specific microbes. From Health Day News at Medline Plus: 'Microbiomes' May Hold Key to Kids' Ear Infections

Recurrent ear infections are the bane of many children -- and the parents who have to deal with their care. Now, research suggests that naturally occurring, "helpful" bacterial colonies in the ear -- called "microbiomes" by scientists -- may help decide a person's vulnerability to these infections. "The children and adults with normal middle ears differed significantly in terms of middle ear microbiomes," concluded a team of Japanese researchers led by Dr. Shujiro Minami of the National Institute of Sensory Organs in Tokyo.

These bacterial ear infections -- called otitis media -- typically start in the middle ear, and 5 out of 6 kids will develop at least one ear infection by the time they turn 3. In the new study, Minami and colleagues wanted to see what role the ear's microbiome might play in these outbreaks. To do so, they took swab samples of the middle ears of 155 children and adults who were having ear surgery due to recurrent ear infections (88 cases) or some other condition.

Among patients with a history of ear infections, the researchers found significant differences in the makeup of microbial communities for people with active ("wet") or inactive ("dry") inflammation. In fact, people whose ear infection was dormant "had similar middle ear microbiomes as the normal [no ear infection] middle ears group," the researchers said. On the other hand, the researchers found that people with an active ear infection had bacterial communities that differed widely from those of people not suffering such outbreaks.

An opinion piece in a journal raises the question of whether having some parasites in the gut is beneficial. We tend to think of parasites as harmful (and yes, some parasite species cause tremendous human suffering and death), but some others seem to exist harmlessly in humans. I'm posting this article because the authors raise the question of whether with progress (sanitation, antibiotics, a Western diet, etc.) we have also lost something beneficial to humans - one-celled organisms (protozoa) that are parasites. They are found in people living in undeveloped countries, but people in developed countries have usually few or none.

Which leads to the question - is the loss of these parasites one of the reasons for the major increase in autoimmune disorders and such diseases as Crohn's disease and colitis? The answers to these questions are unknown at this time, so studies are needed. The authors point out that after millions of years of coevolution, the protists could be providing some beneficial effects to their human hosts - and that they may be part of a normal, healthy gut microbial community (microbiome).

As we know, studies show that in developed Western countries (as compared to undeveloped countries) there is lower microbial diversity in the gut - in other words, with industrialization comes lower bacterial diversity. But... higher microbial diversity is considered beneficial. Normally the human gut has hundreds of microbial species (bacteria, viruses, fungi) living in it and interacting. Some diseases or conditions result in alterations in these microbes, and even "microbial communities being out of whack" (dysbiosis).  The authors of the paper give examples of how the presence of certain non-pathogenic protozoan species in the gut is linked to higher gut microbial diversity and with the presence of bacteria that are anti-inflammatory and beneficial.

KEEP IN MIND: Gut protozoa are one-celled organisms (called protists) that live in the gut as parasites. Numerous protozoa can inhabit the gastrointestinal tract of humans.  According to a Tulane Univ. site "The majority of these protozoa are non-pathogenic commensals, or only result in mild disease", but some of these organisms can cause severe disease under certain conditions. [NOTE: commensal = characterized by a relationship in which one species is benefited while the other is unaffected]. In the following excerpts, a helminth refers to a parasitic worm, such as a fluke, tapeworm, or nematode.

Excerpts from Trends in Parasitology:  Gut Protozoa: Friends or Foes of the Human Gut Microbiota?

The importance of the gut microbiota for human health has sparked a strong interest in the study of the factors that shape its composition and diversity.... We argue that protozoa, like helminths, represent an important factor to take into account when studying the gut microbiome, and that their presence – especially considering their long coevolutionary history with humans – may be beneficial. From this perspective, we examine the relationship between the protozoa and their hosts, as well as their relevance for public health.

The human gut microbiota spans the tree of life and includes bacteria, viruses, and eukaryotes such as fungi, helminths, and protozoa. ...The observation that the gut bacterial microbiome is less diverse in populations from industrialized countries, compared to nonindustrialized countries, has been mostly explained by differences in dietary fiber intake, food sterilization, and the use of antibiotics. Here, we propose that the decreased prevalence of helminths and gut protozoa in industrialized countries is partly responsible for this loss of bacterial diversity.

We argue, based on the knowledge of helminths, that some intestinal protozoa might have beneficial effects on their host through their influence on the gut bacterial microbiome. The role of protozoa in shaping the gut microbiome of healthy individuals remains, however, largely unrecognized. The mechanisms through which protozoa influence the gut bacteria – and the consequences for human health of their absence in developed countries – are poorly understood and call for further attention. 

 The question is therefore whether gut eukaryotes are simply parasites that are detrimental to human health or whether, on the contrary, they could provide, after millions of years of coevolution, some beneficial effects to their hosts. Historically, protozoa and helminths have been considered parasites and assumed to have a detrimental effect on the host organism. Indeed, foodborne and waterborne parasitic diseases are important worldwide, resulting in considerable morbidity and mortality. However, while the focus remains on pathogens that have been investigated from a parasitological point of view, the eukaryotic residents of the gut are often commensal (i.e., benefiting from interacting with the host without affecting it) or even beneficial.

For example, even though some helminths can cause severe illness, infections are often asymptomatic, probably reflecting a long coevolutionary history (since at least 500 million years) and tolerance of these parasites by humans. Similarly, although the best-known protozoan microorganisms found in the human gut are pathogens (i.e., Cryptosporidium spp., Giardia intestinalis, Entamoeba histolytica), it is important to remember that many protozoa, in particular Blastocystis spp., can be found with high prevalence in healthy populations, and are common (and likely ancient) members of healthy microbiomes. Indeed, although protozoan cysts are not as resistant to decay as helminth eggs, they can be found in coprolites, confirming that protozoa, like helminths, were part of our ancestral gut community. 

Interestingly, recent findings also showed that the presence of commensal protozoa (Entamoeba spp. other than Entamoeba histolytica) was strongly associated with increased diversity and various shifts in composition of the gut bacterial microbiota in rural nonindustrialized populations. Higher diversity has also been found in subjects carrying Blastocystis spp., one of the few protozoa to be present at appreciable frequency in industrialized populations. These results suggest similarities between helminths and protozoa in their effect on the gut bacterial microbiome, and raise the possibility of a potentially beneficial effect of (some) protozoa on human health.

Here, we argue that some intestinal protozoan inhabitants could play an important, yet largely unrecognized, role in shaping the gut bacterial microbiota and in maintaining the host–microbe equilibrium, and they should be considered as ‘friends’ of the human gut.

Entamoeba coli - a non-pathogenic species that frequently lives as a commensal parasite in the human gastrointestinal tract. Credit: Wikipedia.