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Author: Sima

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Interesting to think of bacteria and biofilms (bacterial communities resistant to treatment) involved in stress related heart attacks. From Science Daily:

Bacteria help explain why stress, fear trigger heart attacks

Scientists believe they have an explanation for the axiom that stress, emotional shock, or overexertion may trigger heart attacks in vulnerable people. Hormones released during these events appear to cause bacterial biofilms on arterial walls to disperse, allowing plaque deposits to rupture into the bloodstream, according to research published in published in mBio®, the online open-access journal of the American Society for Microbiology.

"Our hypothesis fitted with the observation that heart attack and stroke often occur following an event where elevated levels of catecholamine hormones are released into the blood and tissues, such as occurs during sudden emotional shock or stress, sudden exertion or over-exertion" said David Davies of Binghamton University, Binghamton, New York, an author on the study.

Davies and his colleagues isolated and cultured different species of bacteria from diseased carotid arteries that had been removed from patients with atherosclerosis. Their results showed multiple bacterial species living as biofilms in the walls of every atherosclerotic (plaque-covered) carotid artery tested.

In normal conditions, biofilms are adherent microbial communities that are resistant to antibiotic treatment and clearance by the immune system. However, upon receiving a molecular signal, biofilms undergo dispersion, releasing enzymes to digest the scaffolding that maintains the bacteria within the biofilm. These enzymes have the potential to digest the nearby tissues that prevent the arterial plaque deposit from rupturing into the bloodstream. According to Davies, this could provide a scientific explanation for the long-held belief that heart attacks can be triggered by a stress, a sudden shock, or overexertion.

To test this theory they added norepinephrine, at a level that would be found in the body following stress or exertion, to biofilms formed on the inner walls of silicone tubing."At least one species of bacteria -- Pseudomonas aeruginosa -- commonly associated with carotid arteries in our studies, was able to undergo a biofilm dispersion response when exposed to norepinephrine, a hormone responsible for the fight-or-flight response in humans," said Davies. Because the biofilms are closely bound to arterial plaques, the dispersal of a biofilm could cause the sudden release of the surrounding arterial plaque, triggering a heart attack.

To their knowledge, this is the first direct observation of biofilm bacteria within a carotid arterial plaque deposit, says Davies. This research suggests that bacteria should be considered to be part of the overall pathology of atherosclerosis and management of bacteria within an arterial plaque lesion may be as important as managing cholesterol.

Note the red biofilm bacterial colonies within the diseased arterial wall:

Bacteria stained with a fluorescent bacterial DNA probe show up as red biofilm microcolonies within the green tissues of a diseased carotid arterial wall.

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An interesting link. The thinking is that the number of moles (cutaneous nevi) are linked to higher levels of sex hormones. From Medical Xpress:

Moles linked to risk for breast cancer

Cutaneous nevi, commonly known as moles, may be a novel predictor of breast cancer, according to two studies published in this week's PLOS Medicine. Jiali Han and colleagues from Indiana University and Harvard University, United States, and Marina Kvaskoff and colleagues from INSERM, France, report that women with a greater number of nevi are more likely to develop breast cancer.

The researchers reached these conclusions by using data from two large prospective cohorts– the Nurses' Health Study in the United States, including 74,523 female nurses followed for 24 years, and the E3N Teachers' Study Cohort in France, including 89,902 women followed for 18 years. 

In the Nurses' Health Study, Han and colleagues asked study participants to report the number of nevi >3mm on their left arm at the initial assessment. They observed that women with 15 or more nevi were 35% more likely to be diagnosed with breast cancer than women who reported no nevi, corresponding to an absolute risk of developing breast cancer of 8.48% in women with no nevi and 11.4% for women with 15 or more nevi. In a subgroup of women, they observed that postmenopausal women with six or more nevi had higher blood levels of estrogen and testosterone than women with no nevi, and that the association between nevi and breast cancer risk disappeared after adjustment for hormone levels.

In the E3N Study, including mostly teachers, Kvaskoff and colleagues asked study participants to report whether they had no, a few, many, or very many moles. They observed that women with "very many" nevi had a 13% higher breast cancer risk than women reporting no nevi, although the association was no longer significant after adjusting for known breast cancer risk factors, especially benign breast disease or family history of breast cancer, which were themselves associated with nevi number.

These studies do not suggest that nevi cause breast cancer, but raise the possibility that nevi are affected by levels of sex hormones, which may be involved in the development of breast cancer. The findings do suggest that the number of nevi could be used as a marker of breast cancer risk, but it is unclear whether or how this information would improve risk estimation based on established risk factors. The accuracy of the findings is limited by the use of self-reported data on nevus numbers. Moreover, these findings may not apply to non-white women given that these studies involved mostly white participants.

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From Medical Xpress:

Estimated risk of breast cancer increases as red meat intake increases

Higher red meat intake in early adulthood might be associated with an increased risk of breast cancer, and women who eat more legumes—such as peas, beans and lentils—poultry, nuts and fish might be at lower risk in later life, suggests a paper published BMJ today.

So far, studies have suggested no significant association between  intake and breast cancer. However, most have been based on diet during midlife and later, and many lines of evidence suggest that some exposures, potentially including dietary factors, may have greater effects on the development of breast cancer during early adulthood.

So a team of US researchers investigated the association between dietary protein sources in early adulthood and risk of breast cancer. They analysed data from 88,803 premenopausal women (aged 26 to 45) taking part in the Nurses' Health Study II who completed a questionnaire on diet in 1991. Adolescent food intake was also measured and included foods that were commonly eaten from 1960 to 1980, when these women would have been in high school. 

Medical records identified 2,830 cases of breast cancer during 20 years of follow-up.

This translated to an estimate that higher intake of red meat was associated with a 22% increased risk of breast cancer overall. Each additional serving per day of red meat was associated with a 13% increase in risk of breast cancer (12% in premenopausal and 8% in postmenopausal women).

In contrast, estimates showed a lower risk of breast cancer in postmenopausal women with higher consumption of poultry. Substituting one serving per day of poultry for one serving per day of red meat - in the statistical model - was associated with a 17% lower risk of breast cancer overall and a 24% lower risk of postmenopausal breast cancer.

Furthermore, substituting one serving per day of combined legumes, nuts, poultry, and fish for one serving per day of red meat was associated with a 14% lower risk of breast cancer overall and premenopausal breast cancer.

The authors conclude that higher red meat intake in early adulthood "may be a risk factor for breast cancer, and replacing red meat with a combination of legumes, poultry, nuts and fish may reduce the risk of breast cancer." 

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A big benefit to exercising - more microbial diversity, which means a healthier gut microbiome, which means better health. From Medscape:

Exercise Linked to More Diverse Intestinal Microbiome

Professional athletes are big winners when it comes to their gut microflora, suggesting a beneficial effect of exercise on gastrointestinal health, investigators report in an article published online June 9 in Gut.

DNA sequencing of fecal samples from players in an international rugby union team showed considerably greater diversity of gut bacteria than samples from people who are more sedentary.

Having a gut populated with myriad species of bacteria is thought by nutritionists and gastroenterologic researchers to be a sign of good health. Conversely, the guts of obese people have consistently been found to contain fewer species of bacteria, note Siobhan F. Clarke, PhD, from the Teagasc Food Research Centre, Moorepark, Fermoy. "Our findings show that a combination of exercise and diet impacts on gut microbial diversity. In particular, the enhanced diversity of the microbiota correlates with exercise and dietary protein consumption in the athlete group," the authors write.

The investigators used 16S ribosomal RNA amplicon sequencing to evaluate stool and blood samples from 40 male elite professional rugby players (mean age, 29 years) and 46 healthy age-matched control participants. 

Relative to control participants with a high BMI, athletes and control participants with a low BMI had improved metabolic markers. In addition, although athletes had significantly increased levels of creatine kinase, they also had overall lower levels of inflammatory markers than either of the control groups.

Athletes were also found to have more diverse gut microbiota than controls, with organisms in approximately 22 different phyla, 68 families, and 113 genera. Participants with a low BMI were colonized by organisms in just 11 phyla, 33 families, and 65 genera, and participants with a high BMI had even fewer organisms in only 9 phyla, 33 families, and 61 genera.

The professional rugby players, as the investigators expected, had significantly higher levels of total energy intake than the control participants, with protein accounting for 22% of their total intake compared with 16% for control participants with a low BMI and 15% for control participants with a high BMI. When the authors looked for correlations between health parameters and diet with various microbes or microbial diversity, they found significant positive association between microbial diversity and protein intake, creatine kinase levels, and urea.

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It seems like the more microbe exposure in the first year of life, the better for the immune system. From Science Daily:

Newborns exposed to dirt, dander, germs may have lower allergy, asthma risk

Infants exposed to rodent and pet dander, roach allergens and a wide variety of household bacteria in the first year of life appear less likely to suffer from allergies, wheezing and asthma, according to results of a study conducted by scientists at the Johns Hopkins Children's Center and other institutions.

Previous research has shown that children who grow up on farms have lower allergy and asthma rates, a phenomenon attributed to their regular exposure to microorganisms present in farm soil. Other studies, however, have found increased asthma risk among inner-city dwellers exposed to high levels of roach and mouse allergens and pollutants. The new study confirms that children who live in such homes do have higher overall allergy and asthma rates but adds a surprising twist: Those who encounter such substances before their first birthdays seem to benefit rather than suffer from them. Importantly, the protective effects of both allergen and bacterial exposure were not seen if a child's first encounter with these substances occurred after age 1, the research found.

"What this tells us is that not only are many of our immune responses shaped in the first year of life, but also that certain bacteria and allergens play an important role in stimulating and training the immune system to behave a certain way."

The study was conducted among 467 inner-city newborns from Baltimore, Boston, New York and St. Louis whose health was tracked over three years.

Infants who grew up in homes with mouse and cat dander and cockroach droppings in the first year of life had lower rates of wheezing at age 3, compared with children not exposed to these allergens soon after birth. The protective effect, moreover, was additive.  In addition, infants in homes with a greater variety of bacteria were less likely to develop environmental allergies and wheezing at age 3.

When researchers studied the effects of cumulative exposure to both bacteria and mouse, cockroach and cat allergens, they noticed another striking difference. Children free of wheezing and allergies at age 3 had grown up with the highest levels of household allergens and were the most likely to live in houses with the richest array of bacterial species. Some 41 percent of allergy-free and wheeze-free children had grown up in such allergen and bacteria-rich homes. By contrast, only 8 percent of children who suffered from both allergy and wheezing had been exposed to these substances in their first year of life.

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Yesterday I read and reread a very interesting journal review paper from Sept. 2013 that discussed recent studies about probiotics and treatment of respiratory ailments, including sinusitis. Two of the authors are those from the Abreu et al sinusitis study from 2012 (that I've frequently mentioned and that guided our own Sinusitis Treatment) that found that Lactobacillus sakei protects against sinusitis and treats sinusitis. Some of the things this paper discussed are: microbial communities in the airways and sinuses vary between healthy and non-healthy individuals (and each area or niche seems to have distinct communities), that lactic acid bacteria (including Lactobacillus sakei) are generally considered the "good guys" in our sinus microbiomes (the communities of microbes living in our sinuses), and that treatments of the future could consist of "direct localized administration of microbial species" (for example, getting the bacteria directly into the sinuses through the nasal passages with a nasal spray, or dabbing fermented kimchi juice like I did). They also mentioned that maybe one could also get probiotics to the GI tract (e.g., by eating probiotics) and maybe this would have some benefits. So far it seems that administering something containing L.sakei directly (by nasal spray or dabbing kimchi juice - as I did) seems to work best for treating sinusistis.

They also discussed that lactic acid bacteria are found in healthy mucosal surfaces in the respiratory, GI, and vaginal tract. They then proposed that lactic acid bacteria (including L.sakei) act as pioneer, or keystone species, and that they act to shape mucosal ecosystems (the microbiomes), and permit other species to live there that share similar attributes, and so promote "mucosal homeostasis". It appears that having a healthy sinus microbiome protects against pathogenic species.

So yeah - the bottom line is that microbial supplementation of beneficial bacteria seems very promising in the treatment of respiratory ailments. And for long-term successful sinusitis treatment, one would need to improve the entire sinus microbial community (with a "mixed species supplement"), not just one bacteria species. (By the way, maybe that is also why using kimchi in our successful Sinusitis Treatment works - it is an entire microbial community with several lactic acid species, including the all important Lactobacillus sakei. (NOTE: See Sinusitis Treatment Summary page and The One Probiotic That Treats Sinusitis for some easy methods  using various probiotics to treat chronic sinusitis. These articles get updated frequently.) From Trends in Microbiology:

Probiotic strategies for treatment of respiratory diseases.

More recently, Abreu et al. profiled the sinus microbiome of CRS (chronic rhinosinusitis) patients and healthy controls at high resolution [2]. Microbial burden was not significantly different between healthy subject and CRS patient sinuses. Moreover, known bacterial pathogens such as H. influenza, P. aeruginosa, and S. aureus were detected in both healthy and CRS sinuses; however, the sinus microbiome of CRS patients exhibited characteristics of community collapse, in other words many microbial species associated with healthy individuals, in particular lactic acid bacteria, were significantly reduced in relative abundance in CRS patients. In this state of microbiome depletion, the species C. tuberculostearicum was significantly enriched. This indicates that composition of the microbiome is associated with disease status and appears to influence the activity of pathogens within these assemblages.

Although sinusitis patients in the Abreu study exhibited hallmark characteristics of community collapse, the comparator group – healthy individuals – represented an opportunity to mine microbiome data and identify those bacterial species specific to the sinus niche that putatively protect this site. The authors demonstrated that a relatively diverse group of phylogenetically distinct lactic acid bacteria were enriched in the healthy sinus microbiota [2]. As proof of principle that the sinonasal microbiome itself or indeed specific members of these consortia protect the mucosal surface from pathogenic effects, a series of murine studies were undertaken. These demonstrated that a replete, unperturbed sinus microbiome prevented C. tuberculostearicum pathogenesis. Moreover, even in the context of an antimicrobial-depleted microbiome, Lactobacillus sakei when co-instilled with C. tuberculostearicum into the nares of mice afforded complete mucosal protection against the pathogenic species. Although this is encouraging, it is unlikely that a single species can confer long-term protection in a system that is inherently multi-species and constantly exposed to the environment. Indeed, previous studies and ecological theory supports the hypothesis that multi-species consortia represent more robust assemblages, and tend to afford improved efficacy with respect to disease or infection outcomes [44,45]. This study therefore provides a basis for the identification of what may be termed a minimal microbial population (MMP) composed of multiple phylogenetically distinct lactic acid bacteria, including L. sakei. Such a mixed species assemblage would form the foundation of a rationally designed, sinus-specific bacterial supplement to combat established chronic diseases or, indeed, be used prophylactically to protect mucosal surfaces against acute infection.

Therefore, although site-specific diseases such as chronic sinusitis may well be confined to the sinus niche and be resolved simply by localized microbe-restoration approaches, it is also entirely plausible that an adjuvant oral microbe-supplementation strategy and dietary intervention (to sustain colonization by the introduced species) may increase efficacy and ultimately improve long-term patient outcomes. This two-pronged approach may be particularly efficacious for patients who have lost protective GI microbial species due to
administration of multiple courses of oral antimicrobials to manage their sinus disease.

Although it is impossible to define the precise strains or species that will be used in future microbial supplementation strategies to treat chronic inflammatory diseases, there is a convergence of evidence indicating that healthy mucosal surfaces in the respiratory, GI, and vaginal tract are colonized by lactic acid bacteria. We would venture that members of this group act as pioneer, keystone species that, through their multitude of functions (including bacteriocin production, competitive colonization, lactate and fatty acid production), can shape mucosal ecosystems, thereby permitting co-colonization by phylogenetically distinct
species that share functionally similar attributes. Together, these subcommunities promote mucosal homeostasis and represent the most promising species for future microbe-supplementation strategies.

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It is now more than 69 weeks since I first successfully started using kimchi to treat the chronic sinusitis that had plagued me (and my family) for so many years. I originally reported on the Sinusitis Treatment on Dec. 6, 2013 (the method is described there) and followed up on Feb. 21, 2014.

Based on the sinus microbiome research of N. Abreu et al (from Sept. 2012 in Sci.Transl.Med.) that discussed Lactobacillus sakei as a sinusitis treatment, I had looked for a natural source of L.sakei and found it in kimchi. Since dabbing the kimchi juice in our nostrils as needed, all 4 of us are still free of chronic sinusitis and off all antibiotics at close to a year and a half (I'm optimistic). So how is year two shaping up?

Well, it is different and even better than year one. Much of the first year seemed to be about needing to build up our beneficial bacteria sinus community (sinus microbiome) through kimchi treatments, eating fermented foods (such as kimchi, kefir, yogurt), whole grains, vegetables, and fruits. And of course not having to take antibiotics helped our sinus microbial community.

But now in year two we notice that we absolutely don't need or want frequent kimchi treatments - even when sick. Daily kimchi treatments, even during acute sinusitis (after a cold), actually seems to be too much and makes us feel worse (for ex., the throat becomes so dry, almost like a sore throat). But one treatment every 2 or 3 days while sick is good. In fact, this year we have done so few treatments, that even when ill, each time the sick person stopped doing kimchi treatments before he/she was fully recovered, and any sinusitis symptoms kept improving on their own until full recovery! Amazing!

To us, this is a sign that all of us have much improved sinus microbiomes from a year ago. And interestingly, we are getting fewer colds/viruses than ever.  Our guiding principle this year is: "Less is more." In other words, at this point only do a kimchi sinus treatment when absolutely needed, and then only do it sparingly. Looking back, we think we should have adopted the "less is more" last year after the first 6 months of kimchi treatments.

The other thing we've done is cut back on daily saline nasal irrigation, especially when ill and doing kimchi treatments. We've started thinking that the saline irrigation also flushes out beneficial bacteria.

The conclusion is: YES, a person's microbiome can improve, even after years or decades of chronic sinusitis. It is truly amazing and wonderful to not struggle with it, and to feel normal.

(UPDATE: See Sinusitis Treatment Summary page and The Best Probiotic For Sinus Infections for more information, more products one can use, and more L. sakei treatment information. We are using the high quality refrigerated product Lacto Sinus these days.)

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SUMMARY OF TREATMENT METHOD USING KIMCHI

The following is a quick summary of the method we use (see Sinusitis Treatment Summary page).We use live (fermented and not pasteurized) vegan (no seafood added) kimchi. Choosing vegan (no seafood added) kimchi is a personal preference. Lactobacillus sakei is found in meat, seafood, and some vegetables.

Treatment Method: 1) Wash hands, and then use a clean teaspoon to put a little juice from the kimchi jar into a small clean bowl. 2) Dip finger in the kimchi juice and dab it or smear it along the insides of one nostril (about 1/2" into the nostril). 3) Dip finger in kimchi juice again and repeat in other nostril. 4) Do this several times. If I needed to blow my nose at this point I would, and afterwards I would put more kimchi juice up each nostril (again repeating the procedure) and then not blow my nose for at least an hour (or more). 5) Afterwards, any unused kimchi in the little bowl was thrown out and not replaced in the main kimchi jar. (Note: Put the main kimchi jar back in the refrigerator. Also, once opened, take kimchi juice from it for no more than 6 days.)

My rationale was that I was inhaling the bacteria this way and that it would travel up the nasal passages on their own to my sinuses. I did this regimen once or twice a day initially until I started feeling better, then started doing it less frequently, and eventually only as needed.

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I spent time this past week searching the medical literature (US National Library of Medicine - Medline/PubMed) for the latest in sinusitis research. I wish I could tell you that amazing research has been happening recently, especially with the sinus microbiome (which could mean treating sinusitis with microbes), but I was disappointed. Really disappointed.

I did four searches: one for "sinusitis" (looked at 600+ studies dating back to summer 2013), then "chronic sinusitis" (going back to fall 2012), then "sinusitis, probiotics", and finally "sinusitis, microbiome". The "sinusitis, probiotics" search turned up 10 studies dating back to 2002. The "sinusitis, microbiome" search turned up a grand total of 13 studies, with the oldest dating back to 2004. Of course the sinus microbiome research by Abreu et al from September 2012  discussing Lactobacillus sakei and which I based my personal (and successful) kimchi sinusitis treatment was on the list (see my Dec. 5 post for a discussion of their research). But none of the other studies looked at Lactobacillus sakei (which is in kimchi).

Some of the findings among the many chronic sinusitis studies: microbial diversity is lower in antibiotic treated chronic sinusitis sufferers (than in healthy controls) and the microbial communities more uneven (meaning some microbes dominated over others), and greater Staphylococcus aureus populations among those with chronic sinusitis. After antibiotic treatment patients typically became colonized by microbes that are less susceptible to the prescribed antibiotics. One study found that Staphylococcus epidermidis (SE) may have some effectiveness against Staphylococcus aureus (SA) in the sinusitis microbiome in mice. Lactobacillus rhamnosus was not found to be effective against sinusitis. A number of studies reported biofilms in the sinuses which are highly resistant to medicines. Some studies found that smoking or exposure to second-hand smoke is linked to chronic sinusitis. (June 2016 UPDATE: I should have said that Lactobacillus rhamnosus (R0011 strain) was not effective against sinusitis when taken orally (a tablet) twice a day for 4 weeks in the study. There have been no further studies since then looking at L. rhamnosus for sinusitis treatment. It is unknown whether spraying or smearing/dabbing L. rhamnosus directly into the nostrils would have a positive effect)

Everyone agreed that state of the art genetic analyses found many more microbial species than older methods (the least effective was the traditional culture method). Several studies suggested that perhaps chronic sinusitis is due to immunological defects and one suggested that it was due to "immune hyperresponsiveness" to organisms in the sinuses. Surprisingly, some studies reported that there are more microbes or microbial species in chronic sinusitis patients than in control patients and that Staphylococcus aureus may be dominant (NOTE: These results may be due to not having been done with state of the art genetic analyses which would have picked up more microbial diversity. Another issue is where in the respiratory tract the samples were taken from, because it seems that the different areas have different microbial communities).

There was frequent mention that chronic sinusitis affects millions of people each year in the US, that little is known about its exact cause, and that there is controversy over appropriate treatment. Originally doctors thought that healthy sinuses were sterile, and it has taken a while to realize that is untrue. It is clear that researchers are only now trying to discover what microbial communities live in healthy individuals compared to those with chronic sinusitis.

But it appeared to me that the majority of the studies from the last 2 years indicated that treatment of chronic sinusitis is still: first try antibiotics, then antibiotics plus inhaled corticosteroids and perhaps nasal saline irrigation, then followed by endoscopic sinus surgery (or sometimes balloon dilation), then perhaps steroid drip implants (steroid-eluting sinus implants), and then there may be revision surgeries.

So I'm sticking with my easy-to-do, inexpensive, and fantastically successful kimchi (Lactobacillus sakei) sinusitis treatment. Of course! (see my Dec. 6, 2013 and Feb. 21, 2014 posts or click on the Sinusitis Treatment link for further information).

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Another article stating that the future is feces in treating a number of diseases. From Pacific Standard:

Medicine’s Dirty Secret: Fecal Transplants Are the Next Big Thing in Health Care

POO IS A DECIDEDLY IMPERFECT delivery vehicle for a medical therapy. It’s messy. It stinks. It’s inconsistent, not to mention a regulatory nightmare. But it can be incredibly potent. A classic study of nine healthy British volunteers found that bacteria accounted for more than half of the mass of their fecal solids. That astonishing concentration of microorganisms, both living and dead, makes sense when you consider that the microbial colonists inhabiting our gastrointestinal tract outnumber our own cells roughly three to one, on recent estimates.

In the ideal conditions of the human gut, a thriving ecosystem of 1,000 or more bacterial species that rivals the complexity of a rainforest has co-evolved with us. This microscopic jungle is constantly adapting in response to our diet, antibiotic use and other environmental influences. As the science has progressed, researchers are now comparing the entire collection of microbial inhabitants of the human gut, our microbiome, to a “hidden metabolic organ.” Scientists have linked disruptions to this organ, a condition known as dysbiosis, to everything from inflammatory bowel disease and high blood pressure to diabetes and obesity.

Viewed in this light, a fecal microbiota transplant is nothing more than an attempt to reseed an intestinal tract, often after antibiotics have killed off the native flora that might have kept invasive species at bay. No other medical therapy can claim such a high cure rate for the infection widely known as C. diff.

Some doctors have likened the recoveries of desperately ill patients to those seen with anti-HIV protease inhibitors in the mid-1990s. After the Mayo Clinic in Scottsdale, Arizona, performed its first fecal microbiota transplant in 2011, a patient who had been bed-ridden for weeks left the hospital 24 hours later. And in 2013, researchers in the Netherlands halted a landmark C. diff. clinical trial early for ethical reasons when they saw that the overall cure rate of 94 percent with donor feces had far outpaced the 31 percent cured with the antibiotic vancomycin.

Yet few other interventions elicit such disgust, revulsion, and ridicule. Chronicling a potential advance by a team of Canadian scientists, one newspaper account warned readers: “Hold your nose and don’t spit out your coffee.” In 2013, the founder of a patient advocacy blog called The Power of Poop wrote an open letter to 13 gastroenterology associations detailing the story of a Kentucky man who contracted an acute case of C. diff. Despite his family’s pleas, his doctor dismissed the idea of a fecal transplant as “quackery.” The man died the next day.

Although most providers haven’t published their overall success rates, their self-reported results are surprisingly similar, and consistent with what published reports there are. Khoruts says he has achieved a success rate of about 90 percent after one infusion, 99 percent after two. “In medicine, it’s pretty startling to have therapy that’s that effective for the most refractory patients with that condition,” he says. Colleen Kelly, a gastroenterologist with the Women’s Medicine Collaborative in Providence, Rhode Island, has performed the procedure on 130 patients with recurrent C. diff., with a success rate of about 95 percent. Most of the transplants have taken after just one attempt.

For a relatively simple bacterial infection, Petrof says, the potential remedy may be fairly straightforward. “With recurrent C. diff. what you’ve done is you’ve basically torched the forest,” she says. Nearly everything has been killed off by the antibiotics, leaving very low bacterial diversity. “So the C. diff. can just take root and grow.” Adding back almost any other flora—the equivalent of planting seedlings in the dirt—could help the ecosystem keep interloping pathogens at bay.

For more complicated conditions, though, a simple fecal transplant may not be enough, at least with donors from the Western world. One hypothesis suggests that people in lower-income countries might harbor more diverse bacterial populations in their guts than those who have grown up in a more sterile, antibiotic-rich environment. And in fact, a 2012 study found that residents of Venezuela’s Amazonas state and rural Malawi had markedly more diverse gut microbiomes than people living in three U.S. metropolitan areas. Scientists have already raised the idea that a rise in allergies and autoimmunity in industrialized nations may derive from a kind of collective defect of reduced microbial diversity.

“We cannot find people who’ve never been on antibiotics,” Khoruts says of his donors. For complex autoimmune diseases such as ulcerative colitis, fecal transplants may offer only a partial solution. And with some data suggesting that susceptibility may be linked in part to past antibiotic exposure, perhaps no Western donor can provide the microbes needed to fully reseed the gut.

What then? Khoruts says it may be necessary to seek out ancestral microbial communities—the ones all humans hosted before the advent of the antibiotic era—within people in Africa or the Amazon. “It’s just a disappearing resource,” he says.

By the beginning of April 2014, nearly 30 fecal transplant clinical trials were underway around the world. Roughly half were aimed at C. diff., including two testing the therapy in combination with vancomycin, and another multi-center trial evaluating the effectiveness of fresh versus frozen donor poo.

As the therapy becomes more widely established, via something akin to a “poop pill” or “crapsule,” perhaps the infectious pool of C. diff. patients may start to dwindle. More clinicians, then, might feel emboldened to explore how our bowel flora may affect not only the gastrointestinal system but also the immune and neurological systems. At least a dozen trials are now investigating whether fecal transplants can help treat some form of inflammatory bowel disease, be it Crohn’s disease or ulcerative colitis. Another is looking into Type 2 diabetes, and one is even using lean donors to test fecal transplants on patients with metabolic syndrome. Researchers say it won’t be along before they’re joined by studies investigating whether the therapy might aid diseases like multiple sclerosis and autism.

For those who want to know more, another article form The Pacific Standard:

6 Ways to Transplant Fecal Matter, at Home or at the Hospital

And the following two groups:  The Fecal Transplant Foundation

The Power of Poop

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Two studies that look at the role of diet, weight, and obesity in breast cancer. From Science News:

Fighting cancer with dietary changes 

Calorie restriction during treatment for breast cancer changes cellular programming in a way that lowers the chance of metastases in mice. Breast cancer patients are often treated with hormonal therapy to block tumor growth, and steroids to counteract the side effects of chemotherapy. However, both treatments can cause a patient to have altered metabolism which can lead to weight gain. In fact, women gain an average of 10 pounds in their first year of treatment. Recent studies have shown that too much weight makes standard treatments for breast cancer less effective, and those who gain weight during treatment have worse cancer outcomes.

From Medical Daily:

Breast Cancer Patients Suffering From Obesity Face Higher Death Risk Than Healthy-Weight Women

Obesity increases the risk of another cancer, which adds to the long list of life-threatening health hazards that accompany obesity. A new study reveals more evidence that obesity is a risk factor for cancer prognosis and its development, which will be presented at the annual meeting of the American Society of Clinical Oncology (ASCO) in Chicago on May 30.

Researchers found that out of the 80,000 women in the study who had early stage breast cancer, obesity increased the risk of death by 34 percent for women who were pre-menopausal and were susceptible to higher levels of the hormone estrogen.

"No matter how we look at it, obesity is slated to replace tobacco as the leading modifiable risk for cancer," Dr. Clifford Hudis, ASCO president and chief of Memorial Sloan Kettering Cancer Center's Breast Cancer Medicine Service in New York, announced at a news conference.

Fat tissue produces an excess amount of estrogen, and those with increased levels have been associated with the risk of breast cancer. Obese women unquestionably have more fat tissue, which is why their estrogen levels are naturally higher. This leads to a more rapid growth of estrogen-responsive breast tumors. Obese patients also have increased level of insulin and insulin-like growth factor-1, which has been known to promote the development of tumor tissue.

They did find, as they had expected, there was no link between obesity and breast cancer death risk among women who were postmenopausal and either had an estrogen receptor positive or estrogen receptor negative breast cancer. This meant the tumors did not rely on estrogen to grow at a time in a woman’s life when her estrogen levels are fairly low.

Obesity has been linked to an increased risk of many other common cancers as well, which include colon, pancreas, esophagus, kidney, thyroid, gallbladder, and endometrium. Endometrial cancer is found within the lining of the uterus, and those who are obese increase risk by up to 40 percent.