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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.]

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

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

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

Several reasons why whole grains are healthy

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Gut Health May Begin in the Mouth

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

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

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

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

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

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

Klebsiella  pneumoniae Credit: Wikipedia

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

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

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

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

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

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

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

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

OK, this study was done in mice, but it's the kind of study results that everyone hopes (and thinks) is also true for humans. So drink a nice cuppa black tea and think about how you're increasing bacteria in the gut associated with weight loss.

Black tea (as well as green tea) has polyphenols that stimulate the growth of gut bacterium and the formation of short-chain fatty acids. By the way, the mice were given decaffeinated tea extracts, so theoretically both decaf and caffeinated tea should have benefits. The big question though is - will drinking black tea daily actually result in weight loss? From Medical Xpress:

Black tea may help with weight loss, too

UCLA researchers have demonstrated for the first time that black tea may promote weight loss and other health benefits by changing bacteria in the gut. In a study of mice, the scientists showed that black tea alters energy metabolism in the liver by changing gut metabolites. The research is published in the European Journal of Nutrition. The study found that both black and green tea changed the ratio of intestinal bacteria in the animals: The percentage of bacteria associated with obesity decreased, while bacteria associated with lean body mass increased.

Previous studies indicated that chemicals in green tea called polyphenols are absorbed and alter the energy metabolism in the liver. The new findings show that black tea polyphenols, which are too large to be absorbed in the small intestine, stimulate the growth of gut bacterium and the formation of short-chain fatty acids, a type of bacterial metabolites that has been shown to alter the energy metabolism in the liver.

The researchers also collected samples from the mice's large intestines (to measure bacteria content) and liver tissues (to measure fat deposits). In the mice that consumed either type of tea extract, there was less of the type of bacteria associated with obesity and more of the bacteria associated with lean body mass. However, only the mice that consumed black tea extract had an increase in a type of bacteria called Pseudobutyrivibrio, which could help explain the difference between how black tea and green tea change energy metabolism.

The new study also concluded that both green tea and black tea have different effects on liver metabolism. According to Henning, the molecules in green tea are smaller and can more readily be absorbed into the body and reach the liver directly, while black tea molecules are larger and stay in the intestine rather than being absorbed. When black tea molecules stay in the intestinal tract, they enhance the growth of beneficial bacteria and the formation of microbial metabolites involved in the regulation of energy metabolism. [Original study.]

Another article was published this month raising the issue of whether Alzheimer's disease is caused by a microbe - which can explain why all the medicines and experimental drugs aimed at treating the "tangles" or amyloid plaques in the brain are not working as a treatment (because that's the wrong approach). The microbe theory of Alzheimer's disease has been around for decades, but only recently is it starting to be taken seriously. Some of the microbes found in patients with Alzheimer's disease (from analyses of both normal brains and Alzheimer patient brains after death): fungi, Borrelia burgdorferi (Lyme disease), herpes simplex virus Type 1 (HSV1), and Chlamydia pneumoniae.

The general hypotheses seem to be that Alzheimer’s disease is caused by infection, but it isn't linked to any one pathogenic microbe.  Instead, the evidence seems to support that "following infection, certain pathogens gain access to brain, where immune responses result in the accumulation of amyloid-β, leading to plaque formation". So the microbes act as "triggers" for Alzheimer's disease - the microbes get into the brain, and immune responses somehow eventually result in the amyloid plaques and Alzheimer's disease. From The Scientist:

Do Microbes Trigger Alzheimer’s Disease?

In late 2011, Drexel University dermatology professor Herbert Allen was astounded to read a new research paper documenting the presence of long, corkscrew-shape bacteria called spirochetes in postmortem brains of patients with Alzheimer’s disease. Combing data from published reports, the International Alzheimer Research Center’s Judith Miklossy and colleagues had found evidence of spirochetes in 451 of 495 Alzheimer’s brains. In 25 percent of cases, researchers had identified the spirochete as Borrelia burgdorferi, a causative agent of Lyme disease. Control brains did not contain the spirochetes.

Allen had recently proposed a novel role for biofilms—colonies of bacteria that adhere to surfaces and are largely resistant to immune attack or antibiotics—in eczema....  Allen knew of recent work showing that Lyme spirochetes form biofilms, which led him to wonder if biofilms might also play a role in Alzheimer’s disease. When Allen stained for biofilms in brains from deceased Alzheimer’s patients, he found them in the same hippocampal locations as amyloid plaquesToll-like receptor 2 (TLR2), a key player in innate immunity, was also present in the same region of the Alzheimer’s brains but not in the controls. He hypothesizes that TLR2 is activated by the presence of bacteria, but is locked out by the biofilm and damages the surrounding tissue instead.

Spirochetes, common members of the oral microbiome, belong to a small set of microbes that cross the blood-brain barrier when they’re circulating in the blood, as they are during active Lyme infections or after oral surgery. However, the bacteria are so slow to divide that it can take decades to grow a biofilm. This time line is consistent with Alzheimer’s being a disease of old age, Allen reasons, and is corroborated by syphilis cases in which the neuroinvasive effects of spirochetes might appear as long as 50 years after primary infection.

Allen’s work contributes to the revival of a long-standing hypothesis concerning the development of Alzheimer’s. For 30 years, a handful of researchers have been pursuing the idea that pathogenic microbes may serve as triggers for the disease’s neuropathology..... In light of continued failures to develop effective drugs, some researchers, such as Harvard neurobiologist Rudolph Tanzi, think it’s high time that more effort and funding go into alternative theories of the disease. “Any hypothesis about Alzheimer’s disease must include amyloid plaques, tangles, inflammation—and, I believe, infection.”

Herpes simplex virus type 1 (HSV1) can acutely infect the brain and cause a rare but very serious encephalitis. In the late 1980s, University of Manchester molecular virologist Ruth Itzhaki noticed that the areas of the brain affected in HSV1 patients were the same as those damaged in patients with Alzheimer’s disease. Knowing that herpes can lie latent in the body for long periods of time, she began to wonder if there was a causal connection between the infection and the neurodegenerative disorder.

Around the same time, neuropathologist Miklossy, then at the University of Lausanne in Switzerland, was detailing the brain damage caused by spirochetes—both in neurosyphilis and neuroborrelia, a syndrome caused by Lyme bacteria. She happened upon a head trauma case with evidence of bacterial invasion and plaque formation, and turned her attention to Alzheimer’s. She isolated spirochetes from brain tissue in 14 Alzheimer’s patients but detected none in 13 age-matched controls. In addition, monoclonal antibodies that target the amyloid precursor protein (APP)—which, when cleaved, forms amyloid-β—cross-reacted with the spirochete species found, suggesting the bacteria might be the source of the protein.

Meanwhile, in the U.S., a third line of evidence linking Alzheimer’s to microbial infection began to emerge. While serving on a fraud investigation committee, Alan Hudson, a microbiologist then at MCP-Hahnemann School of Medicine in Philadelphia, met Brian Balin.... Soon, Balin began to send Hudson Alzheimer’s brain tissue to test for intracellular bacteria in the Chlamydia genus. Some samples tested positive for C. pneumoniae: specifically, the bacteria resided in microglia and astrocytes in regions of the brain associated with Alzheimer’s neuropathology, such as the hippocampus and other limbic system areas. Hudson had a second technician repeat the tests before he called Balin to unblind the samples. The negatives were from control brains; the positives all had advanced Alzheimer’s disease. "We were floored,” Hudson says.

Thus, as early as the 1990s, three laboratories in different countries, each studying different organisms, had each implicated human pathogens in the etiology of Alzheimer’s disease. But the suggestion that Alzheimer’s might have some microbial infection component was still well outside of the theoretical mainstream. Last year, Itzhaki, Miklossy, Hudson, and Balin, along with 29 other scientists, published a review in the Journal of Alzheimer’s Disease to lay out the evidence implicating a causal role for microbes in the disease.

The microbe theorists freely admit that their proposed microbial triggers are not the only cause of Alzheimer’s disease. In Itzhaki’s case, some 40 percent of cases are not explained by HSV1 infection. Of course, the idea that Alzheimer’s might be linked to infection isn’t limited to any one pathogen; the hypothesis is simply that, following infection, certain pathogens gain access to brain, where immune responses result in the accumulation of amyloid-β, leading to plaque formation.