Could this be true? Probiotics for seasonal allergies? A study by Univ. of Florida researchers reported that taking a combination probiotic of Lactobacillus gasseri, Bifidobacterium bifidum, and Bifidobacterium longum (sold as Kyo-Dophilus) for 8 weeks during spring allergy season resulted in an improvement in seasonal allergy symptoms. It must be noted that the people participating had mild seasonal allergies, not severe allergies. While they reported overall allergy symptom improvement, there was no significant improvement with eye symptoms. Too bad, because for those suffering from itchy eyes, it is a symptom that causes anguish during allergy season.
All participants had their stool (fecal) samples tested (with modern genetic sequencing) and it was found that the group taking the probiotic supplements had a beneficial shift in their overall microorganisms in the gut - with some bacteria such as Escherichia coli decreasing and the very beneficial and anti-inflammatory bacteria Faecalibacterium prausnitzii increasing. (See posts here and here on F. prausnitzii.) What was really good about the study was that it was a "double-blind, randomized clinical trial", meaning that people were randomly assigned to the probiotic treatment or placebo group, and no one knew who was getting a placebo or the probiotic until the end of the study. The researchers say that why the probiotics improved allergy symptoms is s till not clear, but they have some theories. From Science Daily:
As we head into allergy season, you may feel less likely to grab a hanky and sneeze. That's because new University of Florida research shows a probiotic combination might help reduce hay fever symptoms, if it's taken during allergy season. Many published studies have shown a probiotic's ability to regulate the body's immune response to allergies, but not all of the probiotics show a benefit, UF researchers say. Scientists already know that the probiotic combination of lactobacilli and bifidobacteria, sold as Kyo-Dophilus in stores, helps maintain digestive health and parts of the immune system. They suspect that probiotics might work by increasing the human body's percentage of regulatory T-cells, which in turn might increase tolerance to hay fever symptoms.
UF researchers wanted to know if the components in this combination probiotic would help alleviate allergy symptoms. To do that, they enrolled 173 healthy adults who said they suffered seasonal allergies and randomly split them into two groups: Some took the combination probiotic; others took a placebo. Each week during the eight-week experiment, participants responded to an online survey to convey their discomfort level. Scientists also analyzed DNA from participants' stool samples to determine how their bacteria changed, because probiotics aim to deliver good bacteria to the human's intestinal system.
Participants who took the probiotic reported improvements in quality of life, compared to those taking the placebo, the study showed. For example, participants suffered fewer allergy-related nose symptoms, which meant that they were less troubled during daily activities. Researchers note that this study did not includesevere allergy sufferers. But the combination of probiotics showed clinical benefit for those with more mild seasonal allergies, Langkamp-Henken said. [Original study.]
People assume that taking probiotics results in the beneficial probiotic bacteria colonizing and living in the gut (or sinuses when using L. sakei). It is common to hear the phrase "take probiotics to repopulate the gut" or "improve the gut microbes". The human gut microbiota (human gut microbiome) refers to all the microbes that reside inside the gut (hundreds of species). Probiotics are live bacteria, that when taken or administered, result in a health benefit. But what does the evidence say?
First, it is important to realize that currently supplements and foods contain only a small variety of probiotic species, with some Lactobacillus and Bifidobacterium species among the most common. But they are not the most common bacteria found in the gut. And very important bacteria such as Faecalibacterium prausnitzii (a reduction of which is associated with a number of diseases) are not available at all in supplements. One problem is the F. prausnitzii are "oxygen sensitive" and they die within minutes upon exposure to air, a big problem when trying to produce supplements.
The evidence from the last 4 years of L. sakei use for sinusitis treatment is that for some reason, the L. sakei is not sticking around and colonizing in the sinuses. My family's experiences and the experience of other people contacting me is that every time a person becomes sick with a cold or sore throat, it once again results in sinusitis, and then another treatment with a L. sakei product is needed to treat the sinusitis. And of course this has been a surprise and a big disappointment.
The same appears to be true for probiotics (whether added to a food or in a supplement) that are taken for other reasons, including intestinal health. Study after study, and a review article, finds that the beneficial bacteria do not colonize in the gut even if there are health benefits from the probiotics. That is, there may be definite health benefits from the bacteria, but within days of stopping the probiotic (whether in a food or a supplement) it is no longer found in the gut. Researchers know this because they can see what bacteria are in the gut by analyzing (using modern genetic sequencing tests) what is in the fecal matter (the stool).
However, the one exception to all of the above is a fecal microbiota transplant (FMT) - which is transfer of fecal matter from one person to another. There the transplanted microbes of the donor do colonize the recipient's gut, referred to as "engraftment of microbes". Some researchers found that viruses in the fecal matter helped with the engraftment. So it looks like more than just some bacterial strains are involved. Another thing to remember is that study after study finds that dietary changes result in microbial changes in the gut, and these changes can occur very quickly.
What scientists know is that probiotics in healthy individuals are associated with a number of benefits. Meta-analyses of randomized, controlled trials show that probiotics help prevent upper respiratory tract infections, urinary tract infections, allergy, and cardiovascular disease risk in adults. But between the input and the output, what happens? A common assumption is that probiotics work by influencing the gut microbe community, leading to an increase in the diversity of bacterial species in the gut ecosystem and measurable excretion in the stool.
But this theory doesn’t seem to be true, according to a recently published systematic review by Kristensen and colleagues in Genome Medicine. Authors of the review analyzed seven studies and found no evidence that probiotics have the ability to change fecal microbiota composition. So even though individuals in the different studies were ingesting live bacterial species, the bacteria didn’t stick around to increase the diversity of the gut fecal microbiota.
“Do probiotics alter the fecal composition of healthy adults? The answer seems to be no,” says Dr. Mary Ellen Sanders, Executive Science Officer for the International Scientific Association for Probiotics and Prebiotics (ISAPP)....Dr. Dan Merenstein, Research Division Director and Associate Professor of Family Medicine at Georgetown University Medical Center in Washington, DC (USA), agrees. “Initially when probiotics were studied, some people expected to see permanent colonization. We now realize that is unlikely to occur,” he says. “This study shows that the probiotics tested to date do not result in overarching bacterial community structure changes in healthy subjects. But clinical effects are clearly demonstrated for probiotics, and likely some are mediated by microbiome changes.”
At issue, then, is not what probiotics do for healthy individuals, but exactly how they work: the so-called ‘mechanism’. Sanders, who described some alternative mechanisms in her BMC Medicine commentary about the Kristensen review, points out a logical error in news stories worldwide that covered the article: the assumption that if probiotics fail to change the microbiota composition, they fail to have any health effects. Sanders emphasizes that probiotics might work in many possible ways. “Probiotics may act through changing the function of the resident microbes, not their composition. They may interact with host immune cells,” she says. “They may inhibit opportunistic pathogens that are not dominant members of the microbiota. They may promote microbiota stability… .”
A new study found differences in gut microbes between active women (they exercised at least the recommended amount) and those that are sedentary. When the gut bacteria were analyzed with modern tests (genetic sequencing) the active women had more of the health promoting beneficial bacteria such as Faecalibacterium prausnitzii,Roseburia hominis, and Akkermansia muciniphila than the sedentary women. The sedentary women also had some bacterial species not seen in the active women. The researchers said that exercise "modifies the composition of gut microbiota" (the gut microbes) in a way beneficial for health.
And what is the recommended minimal amount of exercise? The World Health Organization recommends at least 3 days of exercise per week for 30 minutes at a moderate intensity. Note that exercise can mean doing exercises, but it can also include walking briskly, intense housework (scrubbing, vacuuming with lots of bending, etc.), gardening (digging, raking, etc), or shoveling snow, etc. In this study the group of active women had at least 3 hours of physical exercise per week. Note that asedentary lifestyle is associated with a high incidence of chronic diseases such as cardiovascular disease, cancer and diabetes, while physical exercise or activity has metabolic and immune health benefits (prevents disease).
But...reading the full study, the research also showed that the active group ate more fruits and vegetables - which we know has an effect on the gut microbiome and feeds beneficial bacteria. Although the diets of the 2 groups of women were similar in total carbohydrates, protein and fat content eaten, the active women ate more fruits, vegetables, and fiber, and the sedentary group ate more processed meat. So it looks like both exercise and a good amount of fruits and vegetables may be important for nurturing beneficial bacteria. By the way, the 3 species of beneficial bacteria mentioned currently are not found in any probiotic supplements on the market. (Earlier posts on the beneficial F. prausnitzii and Akkermansia muciniphila). From PLoS ONE:
Physical exercise is a tool to prevent and treat some of the chronic diseases affecting the world’s population. A mechanism through which exercise could exert beneficial effects in the body is by provoking alterations to the gut microbiota, an environmental factor that in recent years has been associated with numerous chronic diseases. Here we show that physical exercise performed by women to at least the degree recommended by the World Health Organization can modify the composition of gut microbiota. Using high-throughput sequencing of the 16s rRNA gene, eleven genera were found to be significantly different between active and sedentary women. Quantitative PCR analysis revealed higher abundance of health-promoting bacterial species in active women, including Faecalibacterium prausnitzii, Roseburia hominis and Akkermansia muciniphila. Moreover, body fat percentage, muscular mass and physical activity significantly correlated with several bacterial populations. In summary, we provide the first demonstration of interdependence between some bacterial genera and sedentary behavior parameters, and show that not only does the dose and type of exercise influence the composition of gut microbiota, but also the breaking of sedentary behavior.
Sedentary lifestyle is associated with a high incidence of chronic diseases such as cardiovascular disease, cancer and diabetes. Physical exercise is a powerful preventative and treatment intervention that is known to be effective in generating metabolic and immune health benefits. The gut microbiota is essential for processing dietary components and has a major role in shaping the immune system.... Dysbiosis or imbalance in gut microbiota has been associated with many diseases, among which are ulcerative colitis, Crohn's disease, colon cancer, metabolic syndrome, type I and type II diabetes, cardiovascular disease, allergy, asthma, eczema and autism.....Several studies in experimental models have addressed the relationship between gut microbiota composition and physical exercise....Collectively, these findings indicate that modulation of the microbiota by exercise depends not only on the physiological state of the individual, but also on the diet.
A total of 15 phyla were detected, in order of presence: Bacteroidetes (54%), Firmicutes (44%), Proteobacteria (0.96%), Tenericutes (0.39%), Verrucomicrobia (0.11%), Euryarchaeota (0.08%), Actinobacteria (0.07%), Lentisphaerae (0.06%), Cyanobacteria (0.050%), Spirochaetes (0.04%), Fusobacteria (0.014%), Elusimicrobia (0.009%), Synergistetes (0.007%), kTM7 (0.003%), and Acidobacteria (0.0001%). Acidobacteria (2 subjects), Elusimicrobia (2 subjects) and Spirochaetes (2 subjects) phyla were detected only in sedentary subjects.... At the genus level, there were significant differences in eleven genera: Bifidobacterium, Barnesiellaceae, Odoribacter, Paraprevotella, Turicibacter, Clostridiales, Coprococcus, Ruminococcus, and two unknown genera of Ruminococcaceae family. Given the importance of some bacterial species in health, the presence of Bifidobacterium longum, Faecalibacterium prausnitzii, Roseburia hominis, Akkermansia muciniphila was measured by qPCR. Analyses revealed a more significant abundance of F. prautznnii, R. hominis and A. muciniphila in active than in sedentary women.
Among all the genera studied, the abundance of eleven of them was significantly different between the active and sedentary group, with Paraprevotella and an unclassified genus of the Desulfovibrionaceae family specifically associated with sedentarism parameters, while the remaining genera where largely associated with diet parameters.....Nonetheless, as exercise and diet often go hand in hand, an active lifestyle is frequently associated with a high consumption of fruits and vegetables, whereas sedentarism is associated with the consumption of high-calorie and fatty foods. Indeed, exercise interventions in human populations have resulted in an improvement in diet habits. Although the diets were similar in our study regarding total carbohydrates, protein and fat content, significant differences were observed for fiber (higher in the active group) and processed meat (higher in the sedentary group).
Interesting idea - that perhaps our community of gut microbes being out of whack (dysbiosis) leads to hypertension. This study was done in both humans and mice - with an analysis of bacteria in both hypertensive individuals and pre-hypertensives, and also healthy individuals (the controls). Then the microbes from 2 hypertensive individuals were transplanted into mice (fecal microbiota transplants). And lo and behold - the mice became hypertensive with an alteration of their gut microbes. This is amazing!
The study showed that transplanting microbes from hypertensives to non-hypertensivescaused an elevation in blood pressure in the formerly healthy group. This shows the direct influence of gut microbes on blood pressure. The bacteria found in both the pre-hypertensives and hypertensives (especially an overgrowth of Prevotella and Klebsiella bacteria) are those linked to inflammation. And what kind of diet is linked to that bacteria? A high fat diet. Yes, the Western diet with lots of fat and highly processed foods.
The researchers talked about other research also showing Prevotella being associated not only with hypertension, but also other diseases (e.g., periodontal diseases and rheumatoid arthritis). On the other hand, Faecalibacterium, Oscillibacter, Roseburia, Bifidobacterium, Coprococcus, and Butyrivibrio, which were "enriched" in healthy controls, were lower in pre-hypertensive and hypertensive persons. In the past I have posted about a "special" bacteria that is even called a "keystone" gut bacteria - Faecalibacterium prausnitzii - that is linked to health and is low or absent in the gut in a number of diseases ((here and here). It is not available in a supplement at this time (because it dies within a few minutes upon exposure to oxygen), but diet influences it. A high animal meat, high animal fat, high sugar, highly processed foods, and low fiber diet (the typical Western diet) lowersF. prausnitzii numbers, while a high-fiber, low meat diet increasesF. prausnitzii numbers.
What you can do: Feed the beneficial gut microbes by increasing the amount of fruits, vegetables, whole grains, seeds, nuts that you eat. And cut back on the greasy, high fat processed and fast foods.
The following excerpt is misleading - for example, it ignores the first part of the actual study which looked at the gut bacteria of pre-hypertensives, hypertensive, and healthy people. Then gut bacteria from hypertensive people were transplanted into healthy mice, and gut bacteria from healthy people were transplanted into hypertensive mice. Also, it wasn't rats, but mice used in the study. It goes to show why it's important to look at original studies - not just believe articles out there blindly. [See original study.] From Science Daily: Unhealthy gut microbes a cause of hypertension, researchers find
Researchers have found that the microorganisms residing in the intestines (microbiota) play a role in the development of high blood pressure in rats mice....Scientists studied two sets of rats mice, one group with high blood pressure ("hypertensive") and one with normal blood pressure ("normal").... All animals were then given antibiotics for 10 days to reduce their natural microbiota. After the course of antibiotics, the researchers transplanted hypertensive microbiota to normal blood pressure rats mice and normal microbiota to the hypertensive group.
The researchers found that the group treated with hypertensive microbiota developed elevated blood pressure. A more surprising result is that the rats mice treated with normal microbiota did not have a significant drop in blood pressure, although readings did decrease slightly. This finding is "further evidence for the continued study of the microbiota in the development of hypertension in humans and supports a potential role for probiotics as treatment for hypertension," wrote the researchers. "Studies showing that supplementing the diet with probiotics (beneficial microorganisms found in the gut) can have modest effects on blood pressure, especially in hypertensive models."
NOTE that the actual study said in its CONCLUSIONS: "Taken together, we have described clearly the disordered profiles of gut microbiota and microbial products in human patients with pre-hypertension and hypertension, established the relationship between gut dysbiosis and hypertension, and provided important evidence for the novel role of gut microbiota dysbiosis as a key factor for blood pressure changes. Our findings point towards a new strategy aimed at preventing the development of hypertension and reducing cardiovascular risks through restoring the homeostasis of gut microbiota, by improving diet and lifestyle or early intervening with drugs or probiotics."
Exciting new research about what is going on in the gut microbiome (the community of microbes) of people with Crohn's disease - a debilitating intestinal bowel disease (IBD) which causes severe abdominal pain, diarrhea, weight loss, and fatigue. A number of earlier studies focused on gut bacteria and found dysbiosis (microbial community out of whack) in those with Crohn's disease.
This new research also looked at fungal species and found that there is an "abundance" of 2species of bacteria (Serratia marcescens and Escherichia coli) and one fungal species (Candida tropicalis)and that these interact in the gut in persons with Crohn's disease. In persons with Crohn's disease the abundance of potentially pathogenic bacteria is increased (Escherichia coli, Serratia marcescens, and Ruminococcus gnavus), while beneficial bacteria (such as Faecalibacterium prausnitzii) are decreased. From Science Daily:
A Case Western Reserve University School of Medicine-led team of international researchers has for the first time identified a fungus as a key factor in the development of Crohn's disease. The researchers also linked a new bacterium to the previous bacteria associated with Crohn's. The groundbreaking findings, published on September 20th in mBio, could lead to potential new treatments and ultimately, cures for the debilitating inflammatory bowel disease, which causes severe abdominal pain, diarrhea, weight loss, and fatigue. "We already know that bacteria, in addition to genetic and dietary factors, play a major role in causing Crohn's disease," said the study's senior and corresponding author, Mahmoud A Ghannoum, PhD.
Both bacteria and fungi are microorganisms -- infinitesimal forms of life that can only be seen with a microscope. Fungi are eukaryotes: organism whose cells contain a nucleus; they are closer to humans than bacteria, which are prokaryotes: single-celled forms of life with no nucleus. Collectively, the fungal community that inhabits the human body is known as the mycobiome, while the bacteria are called the bacteriome. (Fungi and bacteria are present throughout the body; previously Ghannoum had found that people harbor between nine and 23 fungal species in their mouths.)
The researchers assessed the mycobiome and bacteriome of patients with Crohn's disease and their Crohn's-free first degree relatives in nine families in northern France and Belgium, and in Crohn's-free individuals from four families living in the same geographic area....The researchers found strong fungal-bacterial interactions in those with Crohn's disease: two bacteria (Escherichia coli and Serratia marcescens) and one fungus (Candida tropicalis) moved in lock step. The presence of all three in the sick family members was significantly higher compared to their healthy relatives, suggesting that the bacteria and fungus interact in the intestines. Additionally, test-tube research by the Ghannoum-led team found that the three work together (with the E. coli cells fusing to the fungal cells and S. marcescens forming a bridge connecting the microbes) to produce a biofilm -- a thin, slimy layer of microorganisms found in the body that adheres to, among other sites, a portion of the intestines -- which can prompt inflammation that results in the symptoms of Crohn's disease.
This is first time any fungus has been linked to Crohn's in humans; previously it was only found in mice with the disease. The study is also the first to include S. marcescens in the Crohn's-linked bacteriome. Additionally, the researchers found that the presence of beneficial bacteria was significantly lower in the Crohn's patients, corroborating previous research findings.
Important new research was published in January 2016 about a fecal microbiota transplant (FMT) or "poop transplant". The research compared only one patient's gut microbes (thus a case study) to her fecal transplant donor's gut microbes, but it is important for looking at how gut microbes change long-term after a fecal microbiota transplant (poop transplant) and the actual length of time that it takes for the recipient's gut microbial community to become like the donor's gut microbiome. The patient was quickly "cured" of a serious recurrent Clostridium difficile infection after one fecal micriobiota transplant (FMT) from her sister, but there were ongoing long-term changes in the patient's gut microbes for 4.5 years, at which point the microbes (bacteria and viruses) were like the donor's (at the phylum, class, and order levels), and with similar bacterial diversity. At this point the researchers said that "full engraftment" of microbes had occurred.
Until 7 months post-FMT, the patient's microbial communities varied over time and showed little overall similarity to the donor, indicating "ongoing gut microbiota adaption" during the first seven months.But right after the transplant, the changes were enough for the patient to be immediately "cured" of her recurrent Clostridium difficile infection. The long-term results also suggested that phages (viruses) may play an important role in gut health. From Cold Spring Harbor Molecular Case Studies:
Fecal microbiota transplantation (FMT) is an effective treatment for recurrent Clostridium difficile infections (RCDIs). However, long-term effects on the patients’ gut microbiota and the role of viruses remain to be elucidated. Here, we characterized bacterial and viral microbiota in the feces of a cured RCDI patient at various time points until 4.5 yr post-FMT compared with the stool donor. Feces were subjected to DNA sequencing to characterize bacteria and double-stranded DNA (dsDNA) viruses including phages.
The patient's microbial communities varied over time and showed little overall similarity to the donor until 7 mo post-FMT, indicating ongoing gut microbiota adaption in this time period. After 4.5 yr, the patient's bacteria attained donor-like compositions at phylum, class, and order levels with similar bacterial diversity. Differences in the bacterial communities between donor and patient after 4.5 yr were seen at lower taxonomic levels.
C. difficile remained undetectable throughout the entire time span. This demonstrated sustainable donor feces engraftment and verified long-term therapeutic success of FMT on the molecular level. Full engraftment apparently required longer than previously acknowledged, suggesting the implementation of year-long patient follow-up periods into clinical practice. The identified dsDNA viruses were mainly Caudovirales phages. Unexpectedly, sequences related to giant algae–infecting Chlorella viruses were also detected. Our findings indicate that intestinal viruses may be implicated in the establishment of gut microbiota.
FMT has shown impressive success rates of ∼90% against RCDIs and no severe adverse effects (Gough et al. 2011; Cammarota et al. 2014; O'Horo et al. 2014).... FMT led to increased donor-like intestinal bacterial diversities within 2 wk (van Nood et al. 2013).....Because viruses, especially phages, are the most abundant intestinal entities with the ability to influence microbial communities (Barr et al. 2013; Virgin 2014), they may well be relevant to C. difficile infection and the microbial changes following FMT.
Briefly, the female patient was 51 years old when admitted to the University Hospital of Zurich with her sixth episode of RCDI, suffering from severe diarrhea and weight loss.....Following FMT, the patient reported changes in bowel movements and intermittent obstipation, both of which ceased within 10 wk. Ever since, the patient has remained free of symptoms for almost 5 yr now..
The analysis of viral dsDNA sequences reported earlier revealed the presence of 22 viruses throughout samples D0, P1, P2, and P3 . In each sample, eight to 11 different viruses were identified, mainly belonging to the Caudovirales order (tailed dsDNA phages) that contains the viral families Myo-, Podo-, and Siphoviridae. Most viruses, 14 of 22, were identified uniquely in either sample. Three phages, the Erwinia phage vB_EamP-L1 (Podoviridae) and the two Bacteroides phages B124-14 and B40-8 (Siphoviridae), were consistently detected in all four samples and each contained phages of all three Caudovirales groups.
The bacterial composition of the donor was relatively stable and comparable at the time of FMT and 4.5 yr later (Fig. 1B), which is in accordance with the known temporal stability of adult intestinal microbiota (Zoetendal et al. 1998)....The patient's fecal microbiota underwent extensive compositional fluctuations and were dominated by Firmicutes up to 7 mo post-FMT, suggesting ongoing adaptation processes of donor microbiota in the patient's intestine that may also reflect changes in nutrition over the observation period. This is in accordance with our and other groups’ recent findings that showed high degrees of bacterial variation in RCDI patients up to 7 mo post-FMT (Broecker et al. 2013; Weingarden et al. 2015).
However, 4.5 yr post-FMT, the patient's bacteria have attained a donor-like composition at the phylum level, indicating full and stable engraftment of the donor's microbiota.....Of note, four of the five most prominent genera identified in both donor samples as well as the patient sample after 4.5 yr, Alistipes, Bacteroides, Dialister, and Faecalibacterium (Fig. 1D), are known constituents of healthy fecal microbiota (Claesson et al. 2011; Joossens et al. 2011). This further indicated that FMT led to healthy and sustainable microbiota in the patient.
One notable species detected in these three samples is Faecalibacterium prausnitzii (Fig. 1D). This species was also detected in the patient samples 6–7 mo post-FMT with abundances of <0.1% (data not shown). Faecalibacterium prausnitzii is recognized as one of the most important species of healthy individuals and normally constitutes >5% of the gut microbiota (Miquel et al. 2013).
The fact that the patient's clinical symptoms, which included severe diarrhea in the absence of antibiotic treatment against C. difficile (Broecker et al. 2013), resolved promptly after FMT suggests that gut microbiota were able to exert normal metabolic functions even before full engraftment. This may be explained by the fact that the patient's bacterial diversity even during the highly variable time period up to 7 mo post-FMT was already in the range of the healthy donor. In agreement with the absence of symptoms until today, C. difficile bacteria were undetectable in the samples of the patient, similar to the donor who tested negative for C. difficile before FMT.....The finding that the patient's fecal microbiota attained a highly donor-like composition after 4.5 yr suggests that long-term follow-up should be implemented into clinical practice.
The analysis of viral dsDNA sequences from a previous study revealed the presence of Caudovirales phages in all investigated samples of the donor and the patient. Caudovirales have been shown before to be the dominant viruses in the human intestine, followed by ssDNA phages of the Microviridae family that we were unable to detect with the metagenomic sequencing approach (Lepage et al. 2008; Norman et al. 2015). Three phages were identified in all of the analyzed samples of the donor and the patient.
How much fiber is there in the different foods we eat? And how much should we eat? Recent posts (Where Do I Get That Beneficial Gut Bacteria? and A Special Gut Microbe) stressed the importance of eating dietary fiber for various health benefits and to feed the beneficial bacteria (such as Faecalibacterium prausnitzii) in our gut. But how much should we be eating daily? Are there different types of fiber and does it matter?
Currently the average American adult eats about 12 to 18 grams of dietary fiber daily. But the latest advice (from both National Academy of Sciences and Academy of Nutrition and Dietetics) is to eat over 20 grams of dietary fiber daily to about 35 grams daily, depending on weight. So a person eating a 2000 calorie daily diet should have about 25 grams of fiber daily.Their recommendation for children is that intake should equal age in years plus 5 g/day (e.g., a 4 year old should consume 9 g/day). Good fiber foods are: fruits, vegetables, whole grains, legumes (beans), nuts, and seeds.But people eating a typical westernized diet are instead eating a high fat, high meat, highly processed food diet which neglects plant-based foods. Go look at the ingredient labels of favorite American foods and see that many don't have fiber or are low in dietary fiber (e.g., hot dogs, salami, candy, cookies, potato chips).
Dietary fiber or roughage is the indigestible portion of food derived from plants. There are two types of fiber: soluble and insoluble, and both should be eaten for good health because they benefit health in a number of ways. Insoluble fiber doesn't dissolve in water and passes through the intestines (it provides bulking), while soluble fiber dissolves in water, and becomes a gel. Plant foods contain both types of fiber in varying degrees, depending on the plant's characteristics. For example, plums and prunes have a thick skin covering a juicy pulp. The skin is a source of insoluble fiber, whereas soluble fiber is in the pulp. One can also take fiber supplements, but actual real foods have many more benefits to them, and also provide a variety of fiber sources. Eating a variety of whole plant-based foods is beneficial in many ways, including feeding the variety of bacteria species in your gut. Remember that different bacteria need different foods, and so eating a variety of foods is best.
To increase your daily dietary fiber intake, first take a look at the amount of fiber in different foods. And then eat lots of fruits, vegetables, whole grains, legumes (beans), seeds, and nuts. The following tables give approximate fiber amounts in some high fiber foods (NOTE: different sources give slightly different numbers):
Fresh & Dried Fruit
Apples with skin
1.5 oz box
Grains, Beans (Legumes), Nuts, Seeds
Black beans, cooked
Bread, whole wheat
Brown rice, dry
Garbanzo beans, cooked
Kidney beans, cooked
Lentils, red cooked
Lima beans, cooked
Oats, rolled dry
Quinoa (seeds) dry
Pasta, whole wheat
Bok choy, cooked
Brussels sprouts, cooked
Collard greens, cooked
Pop corn, air-popped
Potato, baked w/ skin
Summer squash, cooked
Sweet potato, cooked
Swiss chard, cooked
Winter squash, cooked
The tables were from http://commonsensehealth.com/high-fiber-foods-list-for-a-high-fiber-diet/
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. Now the 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. So 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. By high fiber is meant: 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. Association between Faecalibacterium prausnitzii and dietary fibre in colonic fermentation in healthy human subjects
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.
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. This lengthy article also discusses the importance of keystone species (F. prausnitzii is one).From Scientific American:
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 andAmazonian 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.