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It's official. This month is 5 whole years being free of chronic sinusitis and off all antibiotics! Yes, that's correct - 5 whole years for all 4 family members, and our sinuses feel great!

Back in February 2013 - first I, and then the rest of my family, started using easy do-it-yourself sinusitis treatments containing the probiotic (beneficial bacteria) Lactobacillus sakei. Now we only treat with a L. sakei  product when occasionally needed - and it still works great. And it still feels miraculous.

After reading the original ground-breaking research on sinusitis done by Abreu et al (2012), it led to me trying L. sakei as a sinusitis treatment. Of course, there is an entire community of microbes (bacteria, fungi, viruses) that live in healthy sinuses - the sinus microbiome - but L. sakei seems to be a key one for sinus health. Since that original 2012 study, other studies have also found that in people with chronic sinusitis, the sinus microbial community is out of whack (dysbiosis). 

The one thing different this past year is that our sinus microbial community (sinus microbiome) seems better. If we need to treat (for example, after a virus that goes into sinusitis), then all four of us noticed that we need to use much less of a product than in the past. Incredibly little. So it seems that our sinus microbial community has definitely improved over time.

The post The One Probiotic That Treats Sinusitis (originally posted January 2015 and with many updates since then) contains information using my family's experiences (lots of self-experimentation!) and all the information that people have given me over the years. Thanks everyone! The post has a list of brands and products with L. sakei, treatment results, as well as information about some other promising probiotics (beneficial bacteria).

Thank you all who have contacted me  - whether publicly or privately. Please keep writing and tell me what has worked or hasn't worked for you as a sinusitis treatment. If you find another bacteria or microbe or product that works for you - please let me know. It all adds to the sinusitis treatment knowledge base. I will keep posting updates. 

(NOTE: I wrote our background story - Sinusitis Treatment Story back in December 2013, and there is also a  Sinusitis Treatment Summary page with the various treatment methods quickly discussed. One can also click on SINUSITIS under CATEGORIES to see more posts about what is going on in the world of sinusitis research.)

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 new study conducted at the University of Maryland has depressing results  for those of us concerned about the contagiousness of the flu (influenza) virus. According to the study, the flu virus is transmitted much easier than thought - don't need to cough or sneeze to spread it. Just breathing will do it.

The researchers found that those with the flu can shed infectious virus in exhaled "aerosol particles small enough to remain suspended in air". That means they can spread the flu virus just by exhaling little flu particles into the air when they breathe. So stay home if you can to avoid giving the flu to others.

Another very interesting finding was that those who had been vaccinated that year and the prior year for the flu actually had "increased shedding" of the flu virus in their exhaled breath - that is, they had increased influenza virus "aerosol generation". Yikes! The researchers said that this finding, along with recent other studies suggesting "reduced protection with annual vaccination" means we may have to rethink influenza vaccination recommendations and policies. From Science Daily:

Flu may be spread just by breathing

It is easier to spread the influenza virus (flu) than previously thought, according to a new University of Maryland-led study released today. People commonly believe that they can catch the flu by exposure to droplets from an infected person's coughs or sneezes or by touching contaminated surfaces. But, new information about flu transmission reveals that we may pass the flu to others just by breathingThe study "Infectious virus in exhaled breath of symptomatic seasonal influenza cases from a college community," published in the Proceedings of the National Academy of Sciences, provides new evidence for the potential importance of airborne transmission because of the large quantities of infectious virus researchers found in the exhaled breath from people suffering from flu.

"We found that flu cases contaminated the air around them with infectious virus just by breathing, without coughing or sneezing," explained Dr. Milton, M.D., MPH, professor of environmental health in the University of Maryland School of Public Health and lead researcher of this study. "People with flu generate infectious aerosols (tiny droplets that stay suspended in the air for a long time) even when they are not coughing, and especially during the first days of illness. So when someone is coming down with influenza, they should go home and not remain in the workplace and infect others."

Dr. Milton and his research team captured and characterized influenza virus in exhaled breath from 142 confirmed cases of people with influenza during natural breathing, prompted speech, spontaneous coughing, and sneezing, and assessed the infectivity of naturally occurring influenza aerosols. The participants provided 218 nasopharyngeal swabs and 218 30-minute samples of exhaled breath, spontaneous coughing, and sneezing on the first, second, and third days after the onset of symptoms.

The analysis of the infectious virus recovered from these samples showed that a significant number of flu patients routinely shed infectious virus, not merely detectable RNA, into aerosol particles small enough to present a risk for airborne transmission. Surprisingly, 11 (48%) of the 23 fine aerosol samples acquired in the absence of coughing had detectable viral RNA and 8 of these 11 contained infectious virus, suggesting that coughing was not necessary for infectious aerosol generation in the fine aerosol droplets. In addition, the few sneezes observed were not associated with greater viral RNA copy numbers in either coarse or fine aerosols, suggesting that sneezing does not make an important contribution to influenza virus shedding in aerosols.

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). 

Shucks... A randomized controlled trial (the best kind of study) found that probiotics and xylitol did NOT help sore throat symptoms. Sore throats are medically known as pharyngitis. Xylitol is a birch sugar that causes local “bacterial interference” by inhibiting bacterial growth and the adherence of bacteria to the pharyngeal wall (the throat). The probiotics (beneficial bacteria) that they tested were strains of  Lactobacillus acidophilus, Bifidobacterium bifidum, and Bifidobacterium animalis. They also tested sorbitol chewing gum, which does not have any antiviral or antibacterial properties. Not one of these alone or combined had any effect on sore throat symptoms.

My take on this: perhaps other species of probiotics might help - maybe yes, maybe no. Just testing 3 strains of bacteria is too soon to rule out probiotics. This view is based on our (and others) experiences with chronic sinusitis - that it takes very specific bacteria species (especially Lactobacillus sakei) to treat sinusitis, and just taking some random strains may not help at all. From Science Daily:

New RCT shows no benefit from probiotics, xylitol chewing gum in alleviating sore throats

The use of probiotics and xylitol chewing gum to alleviate sore throat symptoms -- as an alternative to antibiotics -- appears to have no effect, according to a randomized controlled trial (RCT) published in CMAJ (Canadian Medical Association Journal).

Evidence exists that indicates probiotics and xylitol, a birch sugar that prevents bacterial growth, can help reduce recurrence of upper respiratory tract infections.

The study included 934 people in the UK during the four year study period (June 2010 to 2014), of whom 689 provided complete data for the trial. Using a symptom diary, participants reported the number of probiotic capsules and sticks of chewing gum used each day, as well as the severity of symptoms. They were study "compliant" if they had taken 75% of their allotted treatment.

Researchers found no significant effect of either probiotics or xylitol on sore throat (pharyngitis) symptoms. "There were no significant differences between groups for both the xylitol and the probiotic groups, which suggests that neither intervention helped in controlling acute symptoms," the authors write. [Original study.]

 Sore throat. Credit: Wikipedia

A new study provides evidence for what so many people complain about - that after being treated for Lyme disease with several weeks of antibiotics - they feel that they are not cured, but instead still suffer from Lyme disease. Lyme disease is caused by the bacterium Borrelia burgdorferi, which is transmitted to a person during a tick bite. However, many medical professionals deny that a person can still have Lyme disease after antibiotic treatment, and instead call the lingering symptoms post-treatment Lyme disease syndrome (PTLDS). It is thought that between 10 to 20% of persons treated with antibiotics for Lyme disease have symptoms of PTLDS.

Hah! The Tulane University researchers found that yes, the live bacteria (B. burgdorferi spirochetes) can still be there in different organs of the body even after 28 days of antibiotic treatment. They studied late Lyme disease in both treated (with antibiotics) and untreated rhesus macaques - primates in which Lyme disease has effects similar to humans. Other studies have also found that the Lyme disease bacteria can evade treatment (here and here). From Medical Xpress:

Lyme bacteria survive 28-day course of antibiotics months after infection

Bay Area Lyme Foundation, a leading sponsor of Lyme disease research in the US, today announced results of two papers published in the peer-reviewed journals PLOS ONE and American Journal of Pathology, that seem to support claims of lingering symptoms reported by many patients who have already received antibiotic treatment for the disease. Based on a single, extensive study of Lyme disease designed by Tulane University researchers, the study employed multiple methods to evaluate the presence of Borrelia burgdorferi spirochetes, the bacteria that cause Lyme disease, before and after antibiotic treatment in primates.

The data show that living B. burgdorferi spirochetes were found in ticks that fed upon the primates and in multiple organs after treatment with 28 days of oral doxycycline. The results also indicated that the immune response to the bacteria varied widely in both treated and untreated subjects. "It is apparent from these data that B. burgdorferi bacteria, which have had time to adapt to their host, have the ability to escape immune recognition, tolerate the antibiotic doxycycline and invade vital organs such as the brain and heart," said lead author Monica Embers, PhD, assistant professor of microbiology and immunology at Tulane University School of Medicine.

"In this study, we were able to observe the existence of microscopic disease and low numbers of bacteria, which would be difficult to 'see' in humans but could possibly be the cause of the variable and nonspecific symptoms that are characteristic of post-treatment Lyme disease syndrome. Although current antibiotic regimens may cure most patients who are treated early, if the infection is allowed to progress, the 28-day treatment may be insufficient, based on these findings," Embers said.

The findings also demonstrated: All subjects treated with antibiotics were found to have some level of infection 7 - 12 months post treatment. Despite testing negative by antibody tests for Lyme disease, two of 10 subjects were still infected with Lyme bacteria in heart and bladder. Lyme bacteria which persist are still viable.

To better elucidate previous animal studies demonstrating that some B. burgdorferi bacteria survive antibiotics, the study explored Lyme disease infection in rhesus macaque primates treated with antibiotics and a control group who were also infected but not treated. 

In the study, ticks carrying B. burgdorferi spirochetes fed on ten primates. Four months post infection, half of the primates (five) received the antibiotic doxycycline orally for 28 days at a proportional dose to that used in human treatment...... The results show: Few subjects displayed a rash. Although all subjects were infected, only one of the 10 displayed a rash with central clearing, the classical "bulls-eye" rash. ... Organs may be infected even if antibody tests are negative...... Intact spirochetes were found in three of five treated and four of five untreated subjects based on xenodiagnosis results 12 months after the tick bite.

Immune responses to B. burgdorferi varied greatly posttreatment .... This is significant because it demonstrates that subjects infected with the same strain of B. burgdorferi may have different immune responses to the same antigen. And, because humans, like primates, are genetically diverse, it underscores that testing antibody responses may be inherently unreliable as a singular diagnostic modality for Lyme disease.

Widespread and variable microscopic disease was observed in all infected subjects, despite antibiotic treatment. Compared to uninfected subjects of the same age, infected subjects in this study (treated and untreated) demonstrated inflammation in and around the heart, in skeletal muscles, joints, and the protective sheath that covers the brain, and near peripheral nerves. Rare, but intact B. burgdorferi spirochetes were found in the tissues of both the treated and untreated subjects. In two subjects treated with doxycycline, multiple Lyme bacteria were observed in the brain tissue [Original study.]

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.]

A large study by researchers at the State University of NY, of 65,869 postmenopausal women found that those who have a history  of gum or periodontal disease also have an overall higher risk of cancer. The women with a history of periodontal disease also had an increased risk for several specific cancers: breast, esophageal, gallbladder, lung and melanoma cancers. This cancer and gum disease association occurred in both nonsmokers and smokers.

How is periodontal disease "promoting" cancer? How it occurs is still unclear, but one theory suggests the gum disease bacteria are in the saliva, which is swallowed, and so the bacteria get into the gut, esophagus, or lungs. Or bacteria from diseased gum tissues get into "systemic circulation" and so get to distant sites in the body.  One of the researchers pointed out that "Certain periodontal bacteria have been shown to promote inflammation even in tiny amounts, and these bacteria have been isolated from many organ systems and some cancers including esophageal cancers."

From Medscape: Gum Disease and Increased Link to Many Cancers

Brushing, flossing, and regular dental checkups appear to do much more than maintain a healthy smile. Now, a large prospective cohort study shows that postmenopausal women with a history of periodontal disease, including those who have never smoked, are at significantly increased overall risk for cancer as well as site-specific cancers, including lung, breast, esophageal, gallbladder, and melanoma skin cancers.

The study authors note that these results add to the growing body of evidence from smaller studies and studies in men that link periodontal disease to total cancer risk. The Centers for Disease Control and Prevention (CDC) estimate that 47% of adults 30 years of age and older in the United States have some form of periodontal disease, ranging from mild to severe. At age 65 years and older, however, 70% of adults have moderate to severe periodontal disease, according to the CDC.

The study involved almost 66,000 postmenopausal women in the United States, who were enrolled in the ongoing Women's Health Initiative Observational Study (WHI-OS). During a mean follow-up of 8.32 years, the team identified 7149 cancers and found that periodontal disease history was associated with a 14% increased total cancer risk. When analyses were limited to 34,097 never-smokers, there was also an increased risk for overall cancer.

An association between periodontal disease and site-specific cancers was observed in breast, lung, esophageal, gallbladder, and melanoma skin cancers. There was a borderline association with stomach cancer, the study authors report, and periodontal disease was not associated with cancers of the pancreas; liver; lower digestive tract organs; or lip, oral cavity, and pharynx combined. Similarly, there was no association with genitourinary and lymphoid and hematopoietic malignancies.

For the study, the investigators looked at periodontal disease information in 65,869 women aged 54 to 86 years at 40 US centers. Mean age was 68 years. Most women were non-Hispanic whites with some college education. All participants answered the question "Has a dentist or dental hygienist ever told you that you had periodontal or gum disease? (No/Yes)" between 1999 and 2003 on the annual Year-5 WHI-OS follow-up questionnaire. Cancer outcomes were documented through September 2013 with a maximum 15-year follow-up period.

 Women who reported a history of periodontal disease were also more likely to report a history of smoking, secondhand smoke exposure, alcohol use, hormone therapy (estrogen plus progestin), and a cancer diagnosis, the study authors report. At the same time, no significant differences were observed in body mass index, physical activity levels, or history of diabetes between women with periodontal disease and those without. [Original study.]

A recent study found that significantly increasing  dietary fiber intake after a diagnosis of colorectal cancer was associated with a lower death rate - from both colorectal cancer and overall mortality (from any cause). The 1575 men and women (all healthcare professionals) in the study had received a nonmetastatic colorectal cancer diagnosis (it had not spread beyond the colon), and the follow-up was about 8 years. These results were from food, not supplements.

How much did extra dietary fiber lower the death rate? For each additional 5  grams of fiber added to their daily diet (after diagnosis) was associated with a 18% lower colorectal cancer death rate, and a 14% lower death rate from any cause. In this study, whole grains, especially in cereals, were found to be the most beneficial. Current dietary guidelines recommend a fiber intake of 25 to 38 grams per day, but most Americans eat far lessDietary fiber is found in plant foods, such as beans, whole grains, nuts, seeds,  vegetables, and fruits. Plant fiber feeds the millions of gut microbes, especially beneficial microbes (here, here, and here) - something that was not really discussed in the study.

The researchers pointed out that a high fiber diet (especially from whole grains and cereals) is linked to a lower risk of getting colorectal (colon) cancer in the first place.  Also, that "higher intake of fiber, especially cereal fiber", has been linked to improved insulin sensitivity, reduced inflammation, type 2 diabetes, cardiovascular disease, and total mortality. Other studies have found that  vitamin D supplementation, exercise, and eating fish all increase survival from colorectal cancer. From From Medical Xpress:

Fiber-rich diet boosts survival from colon cancer

A diet rich in fiber may lessen the chances of dying from colon cancer, a new study suggests. Among people treated for non-metastatic colon cancer, every 5 grams of fiber added to their diet reduced their odds of dying by nearly 25 percent, said lead researcher Dr. Andrew Chan. He is an associate professor in the department of medicine at Harvard Medical School.

"What you eat after you've been diagnosed may make a difference," Chan said. "There is a possibility that increasing your intake of fiber may actually lower the rate of dying from colon cancer and maybe even other causes." Chan cautioned, however, that the study does not prove that the additional fiber caused people to live longer, only that the two were associated.

Fiber has been linked to better insulin control and less inflammation, which may account for better survival, he suggested. In addition, a high-fiber diet may protect people from developing colon cancer in the first place. The greatest benefit was attributed to fiber from cereals and whole grains, according to the report. Vegetable fiber was linked to an overall reduction in death, but not specifically in death from colon cancer, and fiber from fruit was not linked to a reduction in death from any cause. 

For the study, Chan and his colleagues collected data on 1,575 men and women who took part in the Nurses' Health Study and Health Professionals Follow-up Study, and who had been treated for colon or rectal cancer that had not spread beyond the colon. Specifically, the study looked at total fiber consumption in the six months to four years after the participants' cancer diagnosis. The researchers also looked at deaths from colon cancer and any other cause. In an eight-year period, 773 participants died, including 174 from colorectal cancer. [Original study.]