gut bacteria

Environmental Pollutants and the Microbiome

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The pollution we release into the environment affects all of us, not least of all the delicate ecosystem of gut microbes that keep us healthy. The gut microbiome plays a pivotal role in our health – from energy production and immune function, to cognitive development and homeostasis. In fact the metabolic activities of our gut microbes are so vital to health that the gut is now considered an organ in its own right. It should be no surprise then that the hundreds of environmental pollutants our bodies are exposed to every day have profound adverse effects on our microbiome.

This article focuses on three categories of environmental pollutants and their effects on our microbiome – air pollutants, pesticides and heavy metals. 

Air Pollution Linked to Obesity and Diabetes

Air pollution is the fourth leading cause of death worldwide. The particulate matter in air pollution can alter the gut’s composition and function by either inhibiting or promoting the growth of certain microbes. 

Air pollution greatly influences the rate of obesity and type 2 diabetes. In fact, the geographic distribution of diabetes globally correlates with air pollution. In 2016 alone, air pollution (particularly PM2.5) contributed to 3.2 million cases of diabetes globally. The mechanism by which air pollution drives these diseases is through particulate matter altering the gut microbiome and its metabolic activities as illustrated:

Pollution and Gut Bacteria

Reference: Bailey et al, Exposure to air pollutants and the gut microbiota: a potential link between exposure, obesity, and type 2 diabetes, 29 April 2020.

A number of studies demonstrate elevated levels of air pollution exposure are associated with several gastrointestinal diseases, including inflammatory bowel disease (IBD), irritable bowel syndrome, appendicitis, and GI disorders in infants. Cigarette smoke, which contains particulate matter that is also present in air pollution, has also been shown to alter gut composition in human and animal studies. 

A 2020 study of 101 young Southern Californians (averaging 19.6 years old) found that exposure to air pollutants was associated with alterations in gut bacterial diversity. The variation in diversity was significant with 4.0% variation for total Nitrogen Oxide (NOx) exposure, 4.4% for Nitrogen Dioxide and 11.2% for Ozone. This study also found that higher ozone exposure influenced gene pathways involved in fatty acid synthesis/degradation, all of which may play a role in gut barrier integrity, obesity and Type 2 diabetes. 

Another study of young people (aged 17-19) in Southern California, found that increased exposure to nitrogen oxide pollution near roadways influenced the abundance of gut bacteria (Bacteroidaceae and Coriobacteriaceae) that have been associated with obesity and altered metabolism. 

In a 2013 study of mice exposed to PM10 (very small particulates found in dust and smoke), for just 7-14 days, researchers found that the pollution altered the mice’s immune gene expression, enhanced pro-inflammatory cytokine secretion in the small intestine, increased gut permeability, and reduced white blood cell activity. When this exposure was increased to 35 days, even more inflammation in the colon was observed together with altered short chain fatty acid concentrations and changes in microbial composition. 

A 2019 epidemiological study in China found that gut microbes (particularly Firmicutes, Proteobacteria and Verrucomicrobia bacteria) play an important role in mediating the effects of particulate matter when it enters the body. However, both PM2.5 and PM1 reduce gut microbial diversity, in turn increasing the risks of developing Type 2 diabetes.

In summary, it is clear that air pollution negatively alters gut bacteria, setting the scene for increased disease risk in animals and humans, particularly Type 2 diabetes and obesity. Efforts to address the global obesity epidemic therefore should not overlook the role of our environment in driving disease, together with lifestyle and psycho-social factors.  

Pesticides Affect Gut Bacteria

Several studies demonstrate that gut microbiota help protect us against the toxicity of pesticides but once overwhelmed, disease can set in. For example, ingesting the broad-spectrum pesticide chlorpyrifos alters the gut microbiota of mice, contributing to obesity and insulin resistance

Some people (largely those connected to chemical companies) argue that certain pesticides are not harmful to humans because the pathways that they target do not exist in the human body. This is the argument made for glyphosate (RoundUp) in relation to the shikimate pathway. However this ignores the fact that many of these pathways do exist in the microbes living in our gut, thereby explaining the harmful effects that pesticides can have on our health. 

For example, herbicides like 2,4-D (used for lawn and weed control), may affect gut bacteria because not only plants but also bacteria can synthesize plant hormones. Both pure glyphosate and glyphosate-based formulations alter the bacterial makeup of the gut microbiome in rodents and honeybees.

Further, the fungicide imazalil (used as a preservative and to prevent decay and control fungal infections in fruits and vegetables) induces microbiota dysbiosis and hepatic metabolism disorder in zebrafish and causing adverse alterations to the microbiota of mice

Another study showed that the insecticide diazinon damaged the microbiomes and metabolic profiles of mice. Interestingly, exposure to diazinon and another insecticide called malathion influences the ability of gut bacteria to modulate gene expression (through a process called quorum sensing), yet another sign of the ways in which pollutants can drive disease through alterations to gut microbiota. 

Whilst there are fewer studies examining the effects on the gut of agro chemicals beyond glyphosate and chlorpyrifos, studies in adults across multiple species using a wide range of agro chemicals find gut microbiome alterations as well as impaired lipid metabolism, oxidative stress, and inflammation among other things. 

The Heavy Metals Toxins

Heavy metals are elements found in the Earth’s crust which are highly toxic even at low concentrations. Gut bacteria play an important role in metabolizing and eliminating heavy metals from the body. For example, human gut bacteria can transform inorganic arsenic into less toxic organic arsenic, whereas demethylation of methyl mercury by gut bacteria creates more toxic inorganic mercury. 

A 2014 study of mice exposed to arsenic in drinking water for four weeks, found disturbed gut microbiota and metabolic activities. A 2017 study of mice found similar results from lead exposure, with vitamin E, bile acid, and nitrogen metabolism all impaired. Similar results were found in a 2018 study that exposed rats to a range of heavy metals including arsenic, cadmium, cobalt, chromium, and nickel. In a 2019 study of frogs, cadmium exposure also altered gut microbiota, and so too with fish.

A 2018 study of fish (fathead minnows) and mice exposed to mercury found that it damaged their guts and impaired lipid metabolism and neurotransmission. Nutritional supplementation may help to soften these effects however, with selenium reversing some of the gut damage in mercury-poisoned rats. 

Like mercury, studies show that magnesium chloride damages the gastrointestinal tracts of mice and chickens, causing thicker muscle walls, wider submucosa, a decrease in goblet cells and necrosis in gut enterocytes. In chickens, magnesium chloride exposure also adversely altered the metabolism of xenobiotics (any substance that is foreign to animal life), and PAHs (chemicals found in coal, oil and gas).

A 2018 study found that protein rich diets can alter the microbiome, in turn assisting with mercury elimination, in humans. A 2019 study of adult Bangladeshis reported that arsenic exposure altered the gut microbiome and resulted in an overproduction of the Citrobacter bacteria, which can cause a range of health problems including urinary tract infections, respiratory diseases, gastrointestinal inflammation, and sepsis in immunocompromised individuals. Citrobacter is also associated with higher vascular intima-media thickness (IMT), a subclinical marker of atherosclerosis. As such, arsenic exposure may play a key role in the development of atherosclerosis.

A Fundamental Rethink Is Required

In conclusion, it is clear that pollutants profoundly influence the gut bacteria of humans and animals, impairing healthy metabolism and therefore increasing the risk of disease. Just as the pollution we create is damaging our environment, so too it is damaging us, yet another sign that we are more intimately connected with the environment than our extractivist economies acknowledge. Whilst there are many steps we can take as individuals to protect ourselves against environmental pollution, such as eating organic/chemical-free nutrient-dense whole foods, exercising, reducing stress, minimizing our exposure to known pollutants, and supplementing to strengthen our immune systems, ultimately it is the systems that drive this pollution which need to change. That requires a fundamental rethink of our politics and economies so that they no longer treat the earth and us as expendable resources to fuel unfettered growth. 

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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This article was published originally on May 3, 2021. 

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Hormones, Gut Bacteria, and Autoimmune Disease

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Women disproportionately suffer from autoimmune diseases at a rate of 3 to 1 compared to men. Most believe hormones influence the risk of autoimmune disease but determining the mechanisms has eluded researchers for some time. In animal research, when male rats are castrated, the incidence of autoimmune disease goes up, but when female rats are castrated – their ovaries are removed, the results are mixed. New research finds that the bacteria in the gut interact with hormones and provide the key to understanding the sex differences in the risks for and onset of autoimmune disease.

In a study published in the journal Immunity, Gender Bias in Autoimmunity is Influenced by Microbiota, researchers tested the potential signals between hormones and immune function, gut microbes and immune function, and hormones plus gut microbes and immune function in male and female mice. They wanted to delineate the relationship between hormones, specifically testosterone, gut bacteria and autoimmune factors. Is it solely the hormone signal that influences the types and distribution of gut bacteria that then initiates or regulates the immune response or do the gut microbes regulate the hormones which then influence the immune response, or is it some combination of the two? It appears to be the latter; hormones and gut microbiota interact synergistically to regulate the expression of various immune factors and each other.

In a series of experiments, researchers were able to show that the gut bacteria in post pubescent male mice, both quantitatively and qualitatively differed from those of the female mice and testosterone was the key. In male mice, there appeared to be a feedback loop in which testosterone increased gut bacteria and the gut bacteria in turn increased testosterone, to some degree. Once the minimum threshold was reached, higher concentrations of testosterone did not influence gut bacteria any longer. Because these bacteria in turn control the balance between inflammatory and anti-inflammatory factors researchers postulate that the relationship between gut microbiota and testosterone may be key in understanding the gender bias in autoimmune disease.

Questions remain. Testosterone is not the only androgen within the hormone pathway. There are other androgens that have noted and direct influence on immune factors. Moreover, while testosterone may be implicated that does not necessarily rule out a role for the estrogens, as testosterone is the precursor hormone for estrone, estradiol and the other estrogens. The downstream conversion from testosterone to estrone or estradiol may be an important consideration for future research. Nevertheless, this study highlights the importance of hormones in disease, and more specifically, the critical cross-talk between hormones, gut bacteria and inflammatory/anti-inflammatory factors.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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This article was originally published on September 12, 2013. 

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Glyphosate Induced Obesity?

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Are you struggling with your weight? Are you eating well and exercising but still not losing weight? Well then, it might be time to consider what’s on or in what you are eating or what you are eating eats. Sound complicated? It’s not. An emerging body of evidence shows a strong link between eating foods sprayed with commercial herbicides and eating meats raised on commercial feedlots (that are born and bred on a cocktail of chemicals) and obesity.

After years of eating highly processed and chemically laden fruits, vegetables and meats, the bacteria in our guts shift radically towards a species that emit what are called endotoxins. These endotoxin releasing bacteria induce inflammation, which then shifts a series biochemical pathways that favor fat storage as a protective and compensatory reaction to the steady state of chemicals coming from our diet and the lack of nutrients contained within these foods. Indeed, what we now call autoimmune reactions, the continued elevation in inflammation and antibodies, may be a result of the food we eat (and the other pharmacological and environmental chemical exposures). It turns out, that the constant state of inflammation many of us find ourselves in is the body’s way of trying to clear those toxins.

With obesity in particular, there have been several interesting studies published over the last couple years providing clear links between chemical exposures and fat storage. Whether the body stores fat or uses fat depends upon the balance of good and bad bacteria in the gut and that balance is predicated heavily upon nutrient availability and toxic exposures. High calorie, low nutrient, chemically dosed foods, shift bacterial communities that increase fat storage and inflammation. Not only that, but since gut bacteria metabolize dietary vitamins and even synthesize vitamins from scratch on their own, the high fat, low nutrient, chemically laden diet downregulates the vitamin producing bacteria, in favor of the more pathogenic and opportunistic bacteria. This further depletes nutrient stores while enhancing inflammation. The cycle becomes very difficult to end, as anyone struggling to lose weight knows all too well. There is hope, however. New research from disparate sources demonstrates how reducing the toxic load and increasing nutrient availability can re-calibrate fat usage and storage parameters.

Gut Bacteria and Obesity

Just a few years ago, researchers from Shanghai, China identified one of the gut bacterial over growths associated with obesity and published their results in a paper entitled: An opportunistic pathogen isolated from the gut of an obese human causes obesity in germfree mice. Called enterobacter clocae, the endotoxin producing bacteria was found overpopulated in the gut of a severely obese patient who was also insulin resistant, hypertensive and suffered from the array of obesity related health issues. The enterobacter clocae pathogens made up 35% of the total bacterial content in this patient’s gut; a huge bacterial load. Knowing that enterobacter emitted endotoxins and that endotoxins were associated with inflammation and insulin dysregulation, the researchers speculated that a reduction in the enterobacter population would correspond with a reduction in weight and the other health issues. They were correct. With a special diet and traditional Chinese herbs, weight loss and health parameters changed along with the reduction in toxic load. After 9 weeks, enterobacter represented only 1.7% of the total gut bacteria and at 23 weeks, .32%. The total weight loss during that period was 50kg or 110lbs.

Could something as simple as reducing the opportunistic enterobacter via diet be the solution to obesity? To answer this question, the researchers went back to lab and designed an experiment to test the hypothesis, only they did it in the reverse. They asked if enterobacter was a causative factor in obesity, could they induce obesity in mice bred specifically to resist excessive weight gain simply by increasing the bacterial load?

From the fecal matter of the obese patient, the researchers isolated the particular strain of enterobacter clocae called B29. They took the B29 and inoculated four groups of seven, germ-free mice; B29 inoculated plus normal diet or high fat diet and non-inoculated normal or high fat diet. Germ-free mice are a strain of mice that are microorganisms free and raised in isolates. They are resistant to obesity even when fed a high fat diet.

One mouse from each of the inoculated groups died immediately after the inoculation indicating the toxic nature of this bacteria. Remember, this strain of bacteria represented 35% of the original patient’s gut bacteria, likely acquired gradually over the course of lifetime. During the first week, all of the inoculated mice lost weight, again indicating the mounting immune response. Anorexia, is often a sign of illness as the body reallocates resources towards fighting an infection.

Subsequently, and after the immediate anorexic responses, both groups of inoculated mice gained excessive weight, whereas the non-inoculated mice did not. The inoculated plus high fat diet group not only gained significantly more weight but expressed higher levels of enterobacter inflammatory markers and insulin resistance showing an interaction between diet and bacterial growth. The researchers speculate that the high fat diet facilitates the transfer of this bacteria to the bloodstream and increases the systemic inflammatory reaction. The inflammation then shifts the body towards fat storage via a range biochemical cascades meant to fight the infection but that also induces other reactions along the way; reactions we consider hallmarks of metabolic disease including high cholesterol, insulin resistance, liver damage, decreased adiponectin (satiety hormone – low adiponection means one is always hungry) and even increased amyloid A proteins associated with Alzheimer’s. This study, albeit small and in need of replication, shows us that when the balance of good to bad bacteria shifts, obesity is induced. It doesn’t tell us, however, how environmental chemicals in and on food impact this bacterial shift. For that we have to go to a couple other reports.

Nutritional Perils of the Western Diet

The Western diet has become a synonymous with highly processed foods that barely resemble actual food in nutrient and DNA composition. Indeed, in our efforts to produce the largest and prettiest produce, we’ve cultivated out 95% of the genetic variation from food crops; reducing to almost nothing the ~200,000 plant metabolites that provide nutrition. To make matters worse, we have substituted nutritionally rich and diverse crops with ones that originate from plant seeds engineered with bacterial RNA and DNA and are laced with glyphosate, adjuvants and other chemicals. In addition, all commercial meat production relies heavily on genetically modified, glyphosate-doused feed to grow the cattle, combined with prophylactic antibiotics, growth hormones and a cocktail of other chemicals that compensate for the deplorable conditions under which Western foods are produced. The genetically modified, chemically laden food stuffs are then sold to the consumer as fruits, vegetables, meats and dairy or processed even further into other food-like products. From beginning to end of the food chain are exposures to chemicals and foreign bacterial DNA that our bodies cannot accommodate and that provide only limited nutrients.

So, in addition to the direct exposure to chemical toxicants, conventionally grown Western foodstuffs also impair health by reducing vital nutrient content required for even the most basic cell functioning. By disrupting the balance between good gut bacteria and bad or pathogenic bacteria conventionally grown further disrupts nutrient availability while increasing inflammation and the cascade of ill-health is set in motion.

Metabolic Starvation in the Face of Obesity

As we’ve covered previously, every cell in the body requires energy to exist and function. That energy comes in the form of mitochondrial adenosine triphosphate or (ATP). The production of ATP requires nutrients as co-factors and for enzyme functioning. Many of these nutrients come from diet and others are produced de novo or from scratch by the bacteria in our gut. Glyphosate grown foods attack both. Glyphosate reduces the nutrient availability of foodstuffs, even in the less processed, presumed healthy fruits and vegetables, while simultaneously killing the good bacteria in our guts. Glyphosate is a potent bactericide that in a perverse twist of design preferentially targets the beneficial bacteria while leaving untouched the opportunistic and pathogenic bacteria, like enterobacter clocae. So while eating a healthy diet might lead to weight loss and improved health outcomes under normal circumstances, when that diet consists of conventionally grown foods, with genetically engineered seeds capable of withstanding the toxic insults of glyphosate and its adjuvants, neither the diet nor the disrupted intestinal flora can produce the nutrients required to enable healthy cellular metabolism. The GM-glyphosate combo induces a state of metabolic starvation and through a number of survival pathways and shifts towards fat storage rather than fat loss as a secondary source of energy.

Critical to this entire equation is the fact that the bactericidal properties of glyphosate disrupt normal gut microflora.  Glyphosate directly shifts the balance of power away from the healthy, vitamin and mineral factories that feed the body’s enzymes and mitochondria, towards more pathogenic bacteria that are resistant to glyphosate and may even feed on it, further evoking metabolic starvation. As the bacterial balance continues to shift, disease appears and inflammation ensues. Those diseases are then treated pharmacologically with drugs that also disrupt gut bacteria, deplete nutrient stores and damage mitochondria. The cascade of ill-health becomes more and more difficult to end using traditional approaches. Moreover, where and how disease appears is as much based upon individual predispositions as it is on nutrition and other exposures, making the complexity of modern illness something modern medicine is not accustomed too. In other words, these diseases do not fit neatly into the one disease, one medication model, and thus, very rarely respond favorably to treatment.

To Lose Weight, Feed the Body What it Needs: Nutrients.

Despite the complexity of the interactions that come together and create the chronic health issues we face today, there is one variable that can be controlled that will mitigate obesity and ill-health directly: eating, or more specifically, what is eaten. The simple act of cleaning up one’s diet, of moving away from processed foods and away from conventionally grown foods towards organics, can have a tremendous effect on reducing the body’s toxic load and subsequent inflammation, weight gain, and disease. Similarly, replacing needed micronutrients so that bacterial and mitochondrial functioning can come back online and switch from fat storage to fat/energy burning will be critical. This will take time, however, and the transition towards health may be slow. Obesity and ill-health did not emerge overnight and they will not disappear overnight. Finally, we have to recognize that there is no one-size-fits-all, silver bullet, diet vitamin or diet pill. Each of us adapts to chemical exposures and the lack of nutrition individually and uniquely. So each of us requires a different cocktail of nutrients to move forward. Which nutrients and at what doses should be determined individually and may involve some degree of trial and error. As the Western diet is devoid of critical vitamins, minerals and amino acids, it is likely many individuals are suffering from broad based deficiencies. It is also likely, that restoring what has been absent chronically will go a long way towards health and healing, regardless of one’s particular health issues. So if you are struggling with obesity and other health issues, feed your body what it needs to function – nutrients.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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This post was published originally on Hormones Matter on July 28, 2014. 

 

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The Harmful Effects of Antibiotics on the Human Microbiome

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How many articles about the importance of the microbiome – and the relationship between microbiome health and chronic, devastating diseases – need to come out in order for the cognitive dissonance around antibiotic safety to stop?

People assume that all antibiotics are safe drugs, that they damage bacteria but leave people and animals unharmed.  People assume (soap commercials have conditioned us well) that bacteria are bad, that they are harmful and make us sick, and that human life is improved when they are killed.  Many also assume that all antibiotics are created equally and that the more powerful an antibiotic, the better.  Most people assume that there are no long-term consequences from taking antibiotics.

There is ample evidence that these assumptions are false, and that a microbiome that is disturbed by antibiotics makes people more anxious, intolerant of pain, and sick with a variety of diseases.

A disrupted microbiome has been connected with development of Parkinson’s Disease (PD), as shown in Gut microbiota are related to Parkinson’s Disease and clinical phenotype,” published in the journal Movement Disorder.  It was found that patients with PD had less Prevotellaceae (a type of gut microbe) than those in the control group, and that, “The relative abundance of Enterobacteriaceae was positively associated with the severity of postural instability and gait difficulty.”  It is also pointed out in the study that the reason for examining the relationship between PD and the gut microbiome is that:

“In the course of PD, the enteric nervous system (ENS) and parasympathetic nerves are amongst the structures most frequently and earliest affected by alpha-synuclein pathology. Accordingly, gastrointestinal dysfunction is an important non-motor symptom in PD and often present years before motor symptom onset. Recent research has shown that intestinal microbiota interact with the autonomic and central nervous system via diverse pathways including the ENS and vagal nerve.”

The microbiome profoundly affects neurotransmitters and thus mental health, as is shown in “The microbiome-gut-brain axis during early life regulates the hippocampal serotonergic system in a sex-dependent manner” published in Molecular Psychiatry, as well as “That Gut Feeling” published in the American Psychological Association magazine, Monitor on Psychology.  The article, “Altering your gut bacteria could ease anxiety and depression” on www.sciencealert.com is also interesting and informative.  All of the articles point to the finding that, “that tweaking the balance between beneficial and disease-causing bacteria in an animal’s gut can alter its brain chemistry and lead it to become either more bold or more anxious” (quote from “That Gut Feeling”) and that temperament changes were induced by gut microbiome alterations. If you’re feeling anxious or depressed, you may want to look at your past antibiotic use.  Our guts and our brains communicate through a variety of signaling mechanisms including “the autonomic nervous system (ANS), the enteric nervous system (ENS), the neuroendocrine system, and the immune system” as well as the vagus nerve.

The connection between microbiome health and Alzheimer’s Disease is described in “Alzheimer’s disease and the microbiome” published in Frontiers in Cellular Neuroscience (and the referenced articles are interesting too).  In it, it is noted that, “GI tract-abundant gram-positive facultative anaerobic or microaerophilic Lactobacillus, and other Bifidobacterium species, are capable of metabolizing glutamate to produce gamma-amino butyric acid (GABA), the major inhibitory neurotransmitter in the CNS; dysfunctions in GABA-signaling are linked to anxiety, depression, defects in synaptogenesis, and cognitive impairment including Alzheimer’s Disease.”

Rheumatoid Arthritis is connected to microbiome health in the article on the NIH web site, “Gut Microbes Linked to Rheumatoid Arthritis,” in which it is noted that, “The immune system is influenced by the microbiome, a network of microorganisms that live in and on the human body. These microbes outnumber the body’s cells by 10 to 1. Trillions of microbes—both helpful and harmful—reside in the digestive tract. The gut microbiome has been linked to arthritis in animal studies.”

Inflammatory bowel diseases (IBD) Crohn’s disease and ulcerative colitis are connected to microbiome health in “Dysfunction of the intestinal microbiome in inflammatory bowel disease and treatment” published in Genome Biology. In the article, it is stated that, “The inflammatory bowel diseases (IBD) Crohn’s disease and ulcerative colitis result from alterations in intestinal microbes and the immune system.”

The microbiome has been shown to affect both Type 1 and Type 2 diabetes.  In “Intestinal microbiota and type 2 diabetes: From mechanism insights to therapeutic perspective” published in the World Journal of Gastrointerology the relationship to Type 2 diabetes is shown.  In “Type 1 diabetes: role of intestinal microbiome in humans and mice” published in the Annals of the New York Academy of Sciences the connection to Type 1 diabetes is shown.

More general information about the relationship between the microbiome and human health can be found on the National Institute of Health’s Human Microbiome Project web site.

Thousands of articles about the importance of the microbiome have come out.  Millions of dollars have been spent studying the microbiome and its relationship to human health.  Antibiotics indiscriminately destroy bacteria in the microbiome, and some even lead to oxidative stress in the microbiome. Yet misconceptions about antibiotic safety persist. Why is that?

Greg Spooner answered that question perfectly. He said:

“I think the reason for this is that the early antibiotics (like penicillin) were quite safe and they spared us from very serious infections that often lead to death. Our life expectancy jumped at this point, and they were rightly considered miracle drugs. But this was also their downfall, as they quickly became so overused that they lost their efficacy and killed off many people’s helpful biomes. When FQs (fluoroquinolones) came out, most docs probably thought they were just “better” antibiotics that were still effective. ‘All progress is precarious, and the solution of one problem brings us face to face with another problem.’ – Martin Luther King Jr”

Indeed.

Antibiotics, as a class of drugs, have saved millions of lives. That is undeniable. But their value in life-threatening situations does not negate their consequences. The increased risk of Parkinson’s, Alzheimer’s, depression, anxiety, inflammatory bowel diseases, diabetes and other diseases that result from microbiome disruption, should be weighed carefully and conscientiously against the risk of harm from the diseases that are treated with antibiotics. This analysis isn’t being done currently. Both patients and physicians will need to shift their thinking about antibiotic safety for a proper safety analysis to be conducted.  Unfortunately, the proper safety analysis involves comparing immediate and acute pain to potential future pain, and humans are horrible at doing that kind of analysis.

Also, as Greg pointed out, the value and safety of one antibiotic does not mean that all antibiotics are equally safe and valuable.  Though penicillin is not kind to the microbiome, it doesn’t cause multi-symptom, chronic illness like fluoroquinolones do.  Fluoroquinolones are broad-spectrum antibiotics that not only kill bacteria, they deplete mitochondrial DNA and induce a massive amount of oxidative stress, not only in the microbiome, but in the body generally.  Fluoroquinolones are related to the diseases mentioned above not only through the destruction of the microbiome inflicted by them, but also through the destruction of mitochondria and disruption of cellular mineral homeostasis.

It would be a good place to start for the dangers of fluoroquinolones to be considered before they are prescribed.  After all, fluoroquinolones have an extensive list of adverse effects (the Cipro warning label is 43 pages long) that include tendon ruptures and seizures, among hundreds of other adverse effects. There are thousands of patients screaming about how they have been hurt by fluoroquinolones, and demanding that they be used more prudently.

All antibiotics should be used with care and consideration of potential future consequences. Those antibiotics with the most severe adverse effects should be looked at most closely and immediately. Fluoroquinolones are not worth the harm that they cause in most cases. Restriction of the use of fluoroquinolones is a good place to start in thinking about antibiotics as dangerous, consequential drugs. They are, indeed, consequential, dangerous drugs.

The role that antibiotics and the microbiome play in the many chronic diseases of modernity is just starting to be recognized.  Though recognition has been slow to come about, there are thousands of articles about the importance of the microbiome. Perhaps it is time for us to consider more prudent use of antibiotics, especially the most potent and destructive ones (like fluoroquinolones).

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

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Hormones MatterTM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

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Endometriosis and the Gut – What Monkeys Can Tell Us About the Disease

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Female monkeys bred in captivity develop endometriosis at rates similar, if not a little higher (~20%) than those of the general population of women. Histologically, the endometriotic tissue in monkeys is identical to that in human women. Clinically, however, by the time symptoms present in monkeys or are recognized by their caregivers, the endometriosis has fully invaded the peritoneal cavity and the severity of the disease is often significant. With similarities in disease expression and because full medical necropsy (autopsy) reports are kept on all animals raised in captivity, investigating endometriosis in monkey may provide insight into this complicated disease process. Indeed, the few studies that have addressed endometriosis in monkey populations demonstrate clues overlooked in human research.

Risk Factors for Endometriosis in Monkeys

Like women, the risk factors in monkeys include, familial history, age, estrogens and environmental exposures. The link between estrogens, specifically estradiol implants, increases significantly with repeated exposures. Monkeys who have had more than three estradiol implants over the course of their lifetimes were nine times more likely to have the disease than their counterparts. Similarly, connections between environmental toxin exposures and risk of endometriosis have been noted.

An interesting finding in monkeys, perhaps not identified in humans, is a link between uterine surgery (hysterotomy), such as c-section or abortion and increased risk of ectopic endometriosis, by as much as five-fold. The theory being that the surgery ‘seeds’ the disease process by releasing the endometrial cells into the peritoneal cavity. Laparoscopic surgeries do not appear to increase risk, but the data are limited.

Gut Microflora

Like human women, female monkeys with endometriosis often have intestinal involvement with bowel movement irregularity, and as the disease progresses, visible endometrial implants along the large and small intestines. The presumption is that the damage to intestines arrives from the outside in; that is, from the endometrial tissue growth bearing down on the intestines and other organs. What if, there are factors within the gut that predispose or at least increase the risk or severity of intestinal involvement?  It turns out, there may intestinal factors that influence disease progression – the intestinal microflora.

In recent decades, our understanding of the importance of gut bacteria has increased significantly. We know that there are good bacteria and bad bacteria and that shifting the balance between those bacterial populations can lead to a host of health problems. In monkeys with endometriosis, the balance of bacterial power is significantly shifted in favor of yeast over-growth, gram-negative microbes and general intestinal inflammation. Compared to healthy controls, monkeys with endometriosis had significantly lower concentrations of lactobacillus, the good bacteria combined with significantly higher concentrations of gram negative bacteria such as E.Coli, Salmonella, the families of Enterobacteria, Klibsiella and Proteus. Additionally, intestinal inflammation was more prevalent in monkeys with endometriosis than in healthy monkeys. Is there a connection between gut bacteria and endometrial pain or gut bacteria and IBS? With the former, there is still too little research to tell, but relationship between gut bacteria and IBS is becoming more clear.

Gut Microflora, Irritable Bowel Syndrome and Probiotics

Irritable bowel syndrome (IBS) and endometriosis often co-occur. IBS can be misdiagnosed or pre-diagnosed ahead of endometriosis. Research suggests altered intestinal microflora in IBS similar to that identified in the monkey research described above, with reduced lactobicillus bacteria in combination with increased gram-negative bacteria. Endometriosis was not a variable. Could probiotic treatment improve IBS and by extension endometriosis related intestinal symptoms? Possibly.

A recent double-blind, placebo controlled study investigated whether a six month treatment protocol with probiotics relieved the common IBS symptoms of abdominal pain, distension, bowel movements (diarrhea and constipation), flatulence and stomach rumble. The researchers found a median reduction of symptoms 42% in the probiotic group versus the placebo group. The largest and statistically significant reductions were observed in abdominal pain and distension with few significant improvements in the quality or constitution the the bowel movements.

Though probiotics are common supplements in complementary care, no studies that I can identify have looked at either the gut bacteria in human endometriosis patients or evaluated the use of probiotics with these patients. With limited research from the monkey studies, however, perhaps we ought to look at the role of intestinal microflora and in women suffering from endometriosis. At the very least, restoring the balance of gut microflora could improve overall health. Moreover, I can’t help but think that as more and more studies link endometriosis and autoimmune diseases to alterations in micronutrients like vitamins A, B and D, damage to and/or changes in gut microflora might be involved.

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