Heal Your Gut to Reverse Autoimmune Disease

Heal Your Gut to Reverse Autoimmune Disease

Source: GreenMedInfo.com
Ali Le Vere, B.S., B.S.
June 13, 2017

Health Begins In the Gut.  From a clinical standpoint, insofar as functional medicine is concerned, whether you present with rheumatoid arthritis, multiple sclerosis, ulcerative colitis, or systemic lupus erythematosus—the fundamental objective is the same: heal the gut.

Hippocrates understood the inextricably intertwined relationship between the systemic health of the organism and the nine-meter tube from mouth to anus when he famously uttered, “All disease begins in the gut” over two thousand years ago. The ancient Greek physician also illuminated his understanding of the therapeutic role of nutrition when he championed holistic medicine with his proclamation, “Let food be thy medicine and medicine be thy food”.

After all, covering an average surface area of thirty-two square meters, the size of half a badminton court, the gut represents the second largest interface between the external environment and the internal biochemical milieu of the body (Helander & Fandriks, 2014). Over sixty tons of food will pass through our gastrointestinal tract in our lifetime.

Why is gut health so paramount in prevention and treatment of autoimmune disease? If you are a savvy consumer of holistic health information, you probably already know how important our microbiome—the collection of one hundred trillion commensal bacteria that inhabit our colon, plus their genetic material—is to our health. Although the widely cited 10:1 ratio has been revised, researchers estimate that we have at least as many bacterial cells as human cells, which has led some scientists like Stanford’s Dr. Justin Sonnenberg to hypothesize that humans may merely be elaborate vessels designed for the propagation of bacterial colonies (Sender, Fuchs, & Milo, 2016).

At any single moment, two to six pounds of bacteria resides within us. Even more awe-inspiring is that a single person contains 3.8×10^13 bacteria (38,000,000,000,000 colony forming units)—a number representing more than all the stars in the galaxy (Sender, Fuchs, & Milo, 2016).

Following the advent of germ theory and the discovery of vaccinations, scientists were under the impression that all bacteria were bad bugs, and speculated that specific microbes were the causative agents behind particular disease entities. This led to the reductionist, pill-for-every-ill therapies that predominate in Western medicine, as well as to the maligning of all bacteria as organisms to be feared and eradicated. Thus the age of antibiotics, triclosan-laden anti-bacterial soaps, hand sanitizer, chemical cleaners, and the “there’s a shot for that” mentality was inaugurated.

Ironically, it is rumored that on his deathbed, Louis Pasteur, the father of immunization and pasteurization himself, admitted that it is the terrain—the gut ecology and biochemical milieu—that matters, rather than the infecting pathogen (Tracey, 2017). In other words, our bodies, like plants, are more susceptible to pests, or infection, when our ecosystem is in a state of disharmony—when our microbial soil is depleted and our micronutrient status is compromised.

The magic bullet approach initially introduced by Pasteur, however, was misguided, and has the potential to produce dire consequences for immune health. In fact, the hygiene hypothesis, embraced by many scientists, purports that the reason that autoimmune diseases and atopic disorders (eczema, allergies, asthma) are epidemic in the Western world while virtually absent from developing nations is the hyper-sanitized, antibiotic-ridden society in which we live, which has decimated our gut microflora and thus obliterated their beneficial effects on our immune systems (after all, 70% of our immune system resides within our gut) (Vighi et al., 2008).

According to the hygiene hypothesis, the immune system acquires self-tolerance, or the ability to distinguish self from stranger and safety from danger, and thus prevent overreactions against our own tissue, based on repeated infectious exposures (Eschler, Hasham, & Tomer, 2011). Further, “Some pathogens have the potential to prevent or abrogate rather than induce an autoimmune process,” such that annihilating them with antibiotics results in improper maturation of the immune system and a tendency towards autoimmune reactions (Christen, 2014).

However, antibiotics are not only harmful in that they prevent infections from instructing development of the immune system. They also disrupt the finely tuned symphony of actions orchestrated by our microbiota, or those friendly bugs that inhabit our gut. The microbiota serve innumerable roles, including competing for attachment sites with potentially pathogenic microbes, reducing their virulence, inhibiting the effects of bacterial toxins, and generating anti-microbial substances such as bacteriocidins and hydrogen peroxide that can selectively suppress pathogenic bacteria and fungi (Corr et al., 2009; Castagliuolo et al., 1999).

Our gut microbes also promote the de-conjugation and detoxification of proliferative, carcinogenic estrogen species and other exogenous toxins, reducing their enterohepatic recirculation (Gorbach, 1984). Commensal bacteria likewise aid in nutrient extraction and assimilation, as the secondary bile acids and short-chain fatty acids they produce from fermentation of indigestible carbohydrates lead to liberation of compounds like peptide YY from cells, which decreases intestinal transit, encourages satiety, maximizes nutrient absorption, and increases energy harvested from food (Boulange et al., 2016).

Critically, gut bacteria reinforce the intestinal barrier, preventing metabolic endotoxemia, a process which contributes to metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), coronary heart disease, stroke, and polycystic ovarian syndrome (PCOS) (Neves et al., 2013; Lindheim et al., 2017). The products of microbial fermentation of prebiotic carbohydrates also increase insulin sensitivity and improve glucose balance, which prevents the pathologic insulin resistance, oxidative stress, and endothelial dysfunction that lead to diabetes and cardiovascular disease (Boulange et al., 2016).

The maintenance of the intestinal lining by the microbiota similarly prevents autoimmune disease. For instance, a decrease in bifidobacteria populations leads to intestinal hyperpermeability, or leaky gut, which in turn leads to the translocation of metabolic byproducts, food antigens, bacteria, and lipopolysaccharide (also known as LPS, an immunogenic cell wall component from Gram-negative bacteria) across the gut barrier into systemic circulation (Rapin & Wiernsperger, 2010). This activates the mesenteric lymph nodes and gut-associated lymphoid tissue (GALT) and instigates a downstream inflammatory cascade.

Medications Compromise Gut Barrier Integrity

A single course of antibiotics can lead to perturbations in microbiota lasting up to 16 months on average, or 18 to 24 months for Clindamycin and up to four years following triple therapy for Helicobacter pylori (Hawrelak & Myers, 2004; Jernberg et al., 2010; Cotter et al., 2012). Even worse, novel molecular analysis techniques using 16S rRNA have demonstrated that antibiotic-resistant microbes are present up to four years post-antibiotic (Jernberg et al., 2010; Cotter et al., 2012).

Other commonly used medicinal agents, non-steroidal anti-inflammatory drugs (NSAIDs) such as Motrin, Ibuprofen, and Naproxen, increase concentrations of gram-negative bacteria, which produce lipopolysacchide (LPS), the endotoxin that can traverse the gut barrier and generate a milieu favoring insulin resistance, type 2 diabetes, NAFLD, PCOS, coronary heart disease and stroke (Marlicz et al., 2014).

In addition to inducing gastrointestinal ulcers, increasing risk of myocardial infarction by a third, and doubling risk of congestive heart failure, NSAIDs have also been demonstrated to decrease concentrations of bifidobacteria and lactobacilli—beneficial commensal flora populations in our gut (Bhala et al., 2013; Montenegro et al., 2014). Because bifidobacteria are responsible for butyrate production, the short chain fatty acid that heals and seals the gut lining, a decrease in bifidobacteria can perpetuate leaky gut syndrome.

What’s more, acid-blocking drugs, or proton pump inhibitors (PPIs) such as Prilosec and Nexium, used for gastroesophageal reflux disease (GERD), are associated with a decrease in small bowel beneficial bifidobacteria and a significant decline in microbial diversity within seven days of beginning therapy (Seto et al., 2014; Wallace et al., 2011). PPIs have likewise been shown to increase the risk of small intestinal bacterial overgrowth (SIBO) and the potentially fatal infection, Clostridium difficile (Lo & Chan, 2013; Janarthanan et al., 2012).

With antibiotics in particular, however, there is evidence of localized permanent extinction—in other words, some species of microorganisms never recover post-antibiotic, and cannot be “reinoculated” unless you undergo the arduous and expensive process of fecal microbiota transplant (FMT).

Furthermore, even food preparation and processing can influence intestinal permeability. When food is browned or caramelized as part of the Maillard reaction, reducing sugars spontaneously react with lipids, nucleic acids, and aminopeptides, creating advanced glycation end products (AGEs) in a process that generates free radicals, inflammation, and ensuing intestinal permeability (Vlassara & Uribarri, 2004; Bengmark, 2007).

The Leaky Gut – Autoimmune Connection

The intestinal barrier is a mucosal surface wherein epithelial cells known as enterocytes are separated by tight junction proteins, desmosomes, and adherens junctions that function as architectural scaffolding and selective gates, opening and closing to allow fluid and nutrients to be absorbed and waste products to be excreted (Groschwitz & Hogan, 2009). According to Turner (2009), epithelial cells “establish a barrier between sometimes hostile external environments and the internal milieu” (p. 799). This barrier is critical because “The mucosa is directly exposed to the external environment and taxed with antigenic loads…at far greater quantities on a daily basis than the systemic immune system sees in a lifetime” (Mayer, 2003).

Tight junctions, regulated by a molecule called zonulin, as well as by conformational changes in the proteins occludin and claudin, are dynamic intercellular structures that modulate the trafficking or passage of macromolecules from the intestinal lumen to the submucosa and into systemic circulation (Fasano, 2012). According to Rapin and Wiernsperger (2010), “Tight junctions play a major role in regulating the paracellular passage of luminal elements” (p. 635).

Under normal circumstances, solutes exceeding a certain size, or molecular radius, are prohibited from absorption across the gut barrier by competent tight junctions (Fasano, 2012). However, when insults such as gluten, dysbiosis, pathogens, toxins, over-exercising, chemotherapy, radiation, and medications such as NSAIDs and steroids disrupt the tight junctions, microbial products and intact food proteins that have not been degraded into their constituent parts translocate across the paracellular space into the body (Fasano, 2012).

Macrophages embedded in the GALT are part of the innate immune system, or the non-specific, first line of defense against infection (Fasano, 2011; Yu & Yang, 2009). These cells, along with dendritic cells, recognize the incoming undigested food particles, toxic agents, and bacterial components as foreign invaders, and present them to cells of the adaptive immune system called T and B lymphocytes, leading to clonal expansion (proliferation or multiplication of specific subsets of T and B cells) and recruitment of more pro-inflammatory immune cells to the gut through a process called leukocyte homing.

The release of inflammatory cytokines, or intercellular signaling molecules such as interleukin-1 (IL-1), interleukin-2 (IL-6), and tumor necrosis factor alpha (TNF-α) at the site of immune activation causes other immune cells migrating throughout the lymphatic vessels of the body to express more cell adhesion molecules (CAMs). CAMS enable white blood cells to stick to and roll along blood vessels and extravasate, or navigate across, the blood vessels made leaky by histamine and other local vasodilators, into the inflamed intestinal tissue. Cytokines contribute to this vicious process of leaky gut syndrome, as they also play a prominent role in compromising tight junction integrity (Watson, Duckworth, Guan, & Montrose, 2009). This culminates in a massive inflammatory response that can become systemic and lead to autoimmunity.

When the amino acid sequence is homologous between the target antigen, such as gluten, against which the immune system is mounting a response, and tissue proteins, such as the thyroid tissue, a case of mistaken identity occurs, and the immune response can become directed against self tissues, manifesting as autoimmune disease (Hashimoto’s thyroiditis in this instance). Summarized by Suzuki (2013), “Disruption of the intestinal tight junction barrier, followed by permeation of luminal noxious molecules, induces a perturbation of the mucosal immune system and inflammation, and can act as a trigger for the development of intestinal and systemic diseases” (p. 631).

A protein called zonulin is responsible for induction of tolerance and orchestration of immune responses by modulating intercellular tight junctions in the gastrointestinal epithelium in a rapid, reversible, and reproducible fashion (Fasano, 2011). Zonulin evolved as an adaptive mechanism to flush out microorganisms as part of the innate immune response against bacterial colonization of the small intestine (Fasano, 2011).

Specific gliadin-permeating peptides can initiate intestinal permeability via MyD88-dependent release of zonulin, which causes conformational changes in tight junction architecture and cytoskeletal assembly that leads to paracellular entry of gliadin (a gluten sub-fraction) into the intestinal submucosa (Thomas, Fasano, & Vogel, 2006). Signaling through the CXCR3-mediated, MyD88-dependent pathway generates a Th1-dominant, pro-inflammatory cytokine milieu that recruits mononuclear cells into the submucosa (Fasano, 2011). After gliadin infiltrates the lamina propria, the barrier function can be further disrupted by the persistence of inflammatory mediators such as TNF-α and interferon-gamma (IFN-γ) (Fasano, 2011).

In those individuals predisposed to celiac disease, gliadin is presented by HLA-DQ and HLA-DR major histocompatibility complex (MHC) molecules, leading to abrogation of oral tolerance and a transition to a Th1/Th17 response (Fasano, 2011). Dendritic cells home to pancreatic and mesenteric lymph nodes and present gliadin, leading to “migration of CD4−CD8−γδ and CD4−CD8+ αβ T cells to the target organ (gut and/or pancreas) where they cause inflammation” (Fasano, 2011). This results in the interaction between T cells and antigen-presenting cells, producing the adaptive immune response that causes profound villous atrophy in celiac disease (Fasano, 2011). Celiac disease patients have higher concentrations of serum zonulin during the acute phase of disease compared with their healthy counterparts, and also have over-expressed CXCR3, the intestinal receptor for gliadin (Fasano, 2011).

However, even in healthy individuals, biopsies reveal a transient zonulin release upon gluten ingestion accompanied by an increase in intestinal permeability that does not reach the level observed in celiac disease (Drago et al., 2006). The authors of the in vitro study state, “Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules” (Drago et al., 2006, p. 408). Furthermore, when intestinal biopsies were examined from celiac patients with active disease, celiac patients in remission, non-celiac gluten-sensitive patients, and non-celiac controls, intestinal permeability was found to occur after gliadin exposure in all individuals (Hollon et al., 2015).

The same mechanism is implicated in all autoimmune diseases—leaky gut leading to molecular mimicry and/or the bystander effect—biochemical processes that could be characterized as “friendly fire” that are responsible for the resultant tissue damage and symptom expression (Fasano, 2012). Thus, compromised gut integrity, or dysfunctional intestinal permeability, is a precursor and essential trigger for all autoimmune disease, including celiac disease, type 1 diabetes, rheumatoid arthritis, multiple sclerosis, Crohn’s disease, ulcerative colitis, and ankylosing spondylitis, and can also appear in allergic syndromes such as asthma (Fasano, 2012; Drago et al., 2006; Westall, 2007; Edwards, 2008; Yacyshyn & Meddings, 1995; Martinez-Gonzalez et al., 1994; Schmitz et al., 1999; Hijazi et al., 2004).

Moreover, intestinal permeability, as assessed by a lactulose-mannitol test, may predispose a patient to the development of food reactions, as increased intestinal permeability is associated with food allergy (Laudat et al., 1994; Andre, 1986). However, food allergy itself may inflict “mucosal damage caused by local hypersensitivity reactions to food antigens,” creating a pattern in which an individual becomes sensitive to more and more foods (Tatsuno, 1989).

An Ounce of Prevention is Worth a Pound of Cure

For people resistant to dietary and lifestyle modifications to resolve intestinal permeability, I will share that I am a living testament to the consequences of dysfunctional intestinal permeability, which leads to a domino scenario where autoimmune conditions are developed one after another. This scenario is far from uncommon, as a fourth of patients with autoimmune disease tend to develop additional autoimmune diseases, leading to multiple autoimmune syndrome. It is often cited that an individual is three times as likely to develop another autoimmune disease after acquiring one (Cojocaru, Cojocaru, & Silosi, 2010). Hence, my mission is to save others from the heartache I have endured as a consequence of these devastating chronic illnesses.

The succession of autoimmune diseases I developed due to a confluence of environmental triggers, genetic susceptibilities, and compromised gut barrier speak to the importance of preserving tight junction integrity and acting as a guardian of your gut epithelium. The gravity of leaky gut syndrome is illustrated by Brandtzaeg (2013), who states, “Increased epithelial permeability for antigens is a crucial primary or secondary event in the pathogenesis of several disorders” (p. 67).

In my case, a multitude of factors converged to produce autoimmunity—intestinal hyper-permeability, dysbiosis, food sensitivities, mitochondrial dysfunction, genetic polymorphisms, histamine intolerance, mycotoxins, adrenal dysfunction, heavy metal toxicity, micronutrient deficiencies, hormonal imbalances, and a host of recalcitrant and stealth infections. Reversing an autoimmune disease is magnitudes of order more complex than preventing one, which is why educating the public at large about how intestinal permeability serves as a prelude to autoimmunity is of the utmost importance.

However, if you go to a conventional physician complaining of a leaky gut, your concerns are likely to be dismissed and more often than not, you will leave with a recommendation to spend less time on the internet—or even worse, your symptoms will be branded psychosomatic and your doctor will label you a hypochondriac, as almost half of autoimmune patients experience in the subclinical stages of their disease (AARDA, 2017).

Despite the litany of peer-reviewed studies in the scientific literature on pathologic paracellular intestinal hyper-permeability, the biomedical establishment is by and large ignorant to this condition and its implications. Ironically, although Western medicine relegates leaky gut syndrome to the realm of fanciful fairy tales, the pharmaceutical industry is actively investigating drugs to reverse it (Kato et al., 2017). Only when there is a financial incentive and a pharmaceutical approach developed for a disorder is it anointed with legitimacy in the eyes of the allopathic physician.

If health is your objective, however, restoration of gut barrier integrity should be prioritized, since, “The autoimmune process can be arrested if the interplay between genes and environmental triggers is preventing by re-establishing intestinal barrier function” (Fasano & Shea-Donohue, 2005). Because gluten is pivotally implicated in intestinal hyper-permeability, its exclusion from the diet, along with an oligoantigenic elimination-provocation diet, should be a first line of treatment in any patient on the autoimmune spectrum.

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Hijazi, Z., Molla, A.M., Al-Habashi, H., Muawad, W.M., Molla, A.M., & Sharma, P.N. (2004) Intestinal permeability is increased in bronchial asthma. Archives of Diseases in Children, 89, 227–229.

Hollon, J., Puppa, E.L., Greenwald, B., Goldberg, E., Guerrerio, A., & Fasano, A. (2015). Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity. Nutrients, 7(3), 1565-1576.  doi: 10.3390/nu7031565.

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Dr. Mercola and Dr. Chutkan on Gut Health

Source: Mercola.com
Dr. Mercola | Dr. Chutkan
February 3, 2017

http://articles.mercola.com/sites/art… In this video, Dr. Joseph Mercola, founder of Mercola.com, and Dr. Robynne Chutkan, author of the book, “The Microbiome Solution: A Radical New Way to Heal Your Body From the Inside Out,” talk about the importance of gut health to overall health.

Dr. Mercola and Dr. Chutkan on Gut Health

Source: Mercola.com
Dr. Mercola | Dr. Chutkan
January 24, 2017

http://articles.mercola.com/sites/cur… In this video, Dr. Joseph Mercola, founder of Mercola.com, and Dr. Robynne Chutkan, author of the book, “The Microbiome Solution: A Radical New Way to Heal Your Body From the Inside Out,” talk about the importance of gut health to overall health.

Your Health Begins Here, But Your Doctor Doesn’t Know It!

Source: iHealthTube
April 27, 2016

When you get sick, your doctor likely doesn’t look at this part of the body for answers, or solutions. But Dr. Edward Group says that your health starts with these organs and that almost any condition, including cancer, can often be traced back to them. Find out how your health begins here, but your doctor doesn’t know it.

An excellent book that addresses this issue is Gut & Psychology Syndrome by Dr. Natasha Campbell-Mcbride MD.

Before Microbirth- Symbiotic bacteria in pregnancy

Before Microbirth- Symbiotic Bacteria in Pregnancy
Source: GreenMedInfo.com
Eleni Roumeliotou
February 9, 2016

Alternative health communities praise the benefits of vaginal birth for establishing a health bacterial flora in the body of newborn babies. The documentary “Microbirth” presents up-to-date scientific evidence about the long-lasting health effects that babies reap when delivered as nature intended or during a positive c-section [In a positive c-section, a sterile gauze is inserted into the mother´s vagina for up to an hour and upon surgical delivery is used to wipe the newborn´s body and head, in an effort to simulate vaginal birth and donate maternal bacteria]. Understanding the importance of seeding the baby with maternal symbiotic bacteria should be basic knowledge for doctors, midwives and parents alike because it truly has the potential to improve the health of the future generations. “Microbirth” is a grand and very necessary step into pushing this essential knowledge into mainstream medical practice.

But in order to get the full picture of when and how bacterial seeding of babies happens we should really go a few steps further than the truths presented in “Microbirth”. Or more specifically a few steps backwards, at least in time. This is because seeding a baby with maternal symbiotic bacteria does not start with a vaginal birth or a positive C-section at all. It all begins with conception and pregnancy. Unlike the outdated notion that a baby is growing in a perfectly sterile environment until birth, we now know that the baby is surrounded and supported by several different bacterial communities, which reside in different organs of the mother. Research shows that when pathogenic bacteria dominate the maternal organs, pregnancy complications become more frequent.

If the first bacterial seeding happened during birth, then we would expect meconium (baby´s first poo) to be essentially sterile, which we already have scientific proof that is not true. Therefore, somewhere along pregnancy, the baby interacts with maternal bacteria and receives the first sample of these lifelong, tiny buddies. Instead of considering birth as the only seeding event that donates maternal symbiotic bacteria to the baby, we need to understand that populating the baby´s body with bacteria is a multi-step process that begins with implantation of the fertilized egg, progresses throughout pregnancy and is finalized when the baby stops breastfeeding.

The baby receives and interacts continuously for the duration of the pregnancy with maternal bacteria and, later, vaginal birth and hopefully breastfeeding further reinforce and stabilize the first phase of seeding. These are all important and necessary steps for creating a healthy baby; it takes many months and conscious diet and lifestyle choices. Therefore, maintaining a healthy flora in the mother during pregnancy (by actively optimizing pregnancy probiotic / prebiotic intake and supporting beneficial bacteria) is the very first step for ensuring a healthy flora for the baby. Encouraging a vaginal birth or a positive c-section come second and breastfeeding third.

Continue Reading At: GreenMedInfo.com

How Essential Oils Can Help Replace Overused Antibiotics & Stop Drug Resistant Superbugs

Essential oils

Source: NaturalNews.com
David Gutierrez
February 19, 2016

Antibiotic resistance is rapidly reaching the scale of a global health crisis. More and more people are being treated with “last resort” antibiotics, and the head of the World Health Organization, Margaret Chan, recently warned that the explosion of increasingly virulent drug-resistant microbes may eventually mean the “end of modern medicine.”

“The rise of antibiotic resistance is a global health crisis,” Chan said. “More and more governments recognize (it is) one of the greatest threats to health today.”

One thing that ordinary consumers can do to stem this tide, is to avoid unnecessary antibiotic treatments by using natural alternatives.

Why antibiotics are bad for your health

One of the most common misuses of antibiotics is when doctors prescribe them for viral problems, such as a cold or the flu, or minor bacterial infections that might otherwise have cleared up on their own.

Essential oils provide numerous benefits over antibiotics. They do not contribute to the evolution of drug resistance, preserving antibiotics for truly serious or life-saving uses – particularly if you avoid always using the same essential oil for every infection. In addition, essential oils do not cause wholesale destruction of your body’s good microbes – “microbiome” – the way antibiotics do. Antibiotic use is increasingly being linked with a variety of systemic health problems, probably due to disruption of the many subtle processes that our microbiomes perform for our bodies. Even taking probiotics after antibiotics is not enough to undo this damage.

So, for your health and for the health of society as a whole, here are some of the top antimicrobial essential oils. Studies have shown many of these to be as effective as antibiotics, and in some cases more so.

The top antibacterial oils

Tea tree oil is one of the easiest essential oils for a beginner to use. Unlike most essential oils, it can safely be applied directly to the skin, without first being diluted with a carrier oil. It has shown potent activity against viruses, bacteria and other microbes.

Eucalyptus oil, in addition to its antimicrobial effects, has been shown to speed wound healing and to protect injuries from exposure to air (much like a bandage).

Does your natural toothpaste contain peppermint essential oil, and not just peppermint flavor? It should! Peppermint is a potent antimicrobial and antiviral agent.

Lavender oil has shown antibacterial and antiseptic properties. It is particularly effective in speeding the healing of minor skin injuries including cuts, wounds, burns and sunburns, and keeping them from scarring. It is also an effective treatment for inflammatory and bacterial skin conditions including acne and psoriasis.

The common kitchen herbs oregano and thyme, in their essential oil form, are potent antibacterials that have both shown effectiveness against staph bacteria, including the MRSA superbug. Oregano has also been found to be effective against E. coli and salmonella.

Continue Reading At: NaturalNews.com

The Microbiome and the Vaccine Industry


Source: GreenMedInfo.com
Keith Bell

The microbiome is at the base of the pyramid of life. Scientists are acknowledging it with every new paper published. New books and articles are revealing its importance to the public at large.

This includes vaccine scientists who acknowledge vaccine response hinges on the microbiome. They know vaccines can’t work when confronted with intestines containing an imbalanced microbiome. A stark example is the sanitation-challenged developing world where there are no toilets and people defecate in fields. This open defecation leads to imbalanced flora and a compromised immune system where vaccines fail. Vaccines don’t stand a chance of working under such circumstances because microbes dictate our immune response.

But there’s still something missing.

Though the vaccine industry has fully acknowledged their products require a healthy microbiome to be effective, they haven’t come forward to ask if the microbiome may also be the source of vaccine injury. If the microbiome is the solution, then perhaps it’s also the problem.

But scientists aren’t asking.  It’s as if they aren’t interested in vaccine safety. They only want to develop new vaccines and improve vaccine response. And that’s pretty sad considering chronic childhood diseases on the rise and an apparent autism epidemic.

Continue Reading At: GreenMedInfo.com

GMOs & Health – The Scientific Basis For Serious Concern & Immediate Action

GMOs and Health: The Scientific Basis for Serious Concern and Immediate Action
Source: GreenMedInfo.com
Nathan Daley, MD, MPH

You might ask, “why all the fuss about agricultural genetically modified organisms (GMOs)?” After all, regulatory agencies have approved these technologies for widespread application and consumption, so they must be safe, right?  Well, the truth is that there is no agency and no industry that  works to protect our health.  At best, the EPA, USDA, and FDA attempt to respond to our disease after the cause is widespread.  At that point only risk reduction, rather than risk avoidance, can be achieved.  This has been the case historically with radium paint, tobacco, particulate air pollution, water pollution, asbestos, lead, food-borne illnesses, and DDT.  A number of the various 80,000 chemicals in production will likely be added to this list in the future while the majority of them that actually do contribute to disease (often in combination and in complex ways) will never be scientifically associated with disease.  This is because science is far from perfect, scientific methodology is always biased and often manipulated, and scientific interpretation by stakeholders and decision makers is alarmingly inept (I’m not being political or condescending, these are well known and easily observed facts).

The situation with agricultural GMOs is unique compared to other technologies. While genetic engineering of food crops has been ongoing for 15 years, it is currently experiencing a major boom with the potential for widespread worldwide application.  Yet, few people understand how a GMO food could really be so much different than a non-GMO food in regard to health and disease effects.  GMO foods look like non-GMO foods and so we don’t experience the same hesitation and aversion to consuming them like we would, say, a clearly labeled bottle of virus and pesticide in tomato juice.  Therefore, the quality of public education, consumer awareness, and informed public discussion about this technology has the potential to alter the future of GMO agriculture for better or worse.

In this article, I’ll first briefly mention the relative paucity of risk assessment studies on GMOs and the unbelievable weaknesses of the industry studies that have been done.  Then, drawing from numerous independent studies, I will explore the routes by which agricultural GMOs may cause adverse health effects.

GMOs Have Never Been “Proven” Safe

Let me be clear; despite the following negative review of industry science, this article is not a hatchet job against the agricultural GMO industry but, rather, a vehicle for consolidated scientific information on the safety or risks of GMO foods intended to allow readers to make informed choices about this technology.  It is just that, well, the science coming from the industry tends to raise serious concerns and suggests that the agricultural GMO industry has little concern for protecting public and ecosystem health.  Before we dive into the independent non-industry studies which suggest potential harm from GMO crops and foods, we must first look at the studies which supposedly demonstrate the safety of GMO crops and foods.  A critique of these studies remained impossible for some time as the data was kept private, until French researchers obtained a court order for their release.  This team of researchers, lead by Joel Spiroux de Vendomois, then analyzed the raw data from studies on three varieties of GMO corn owned by Monsanto.  Yet, it immediately became apparent that this data was not extremely helpful as the study methodology was profoundly insufficient.  In a 2010 paper published in the International Journal of Biological Sciences[1], the researchers summarize several major flaws in the study.  I’ll list just a few of them here:

  1. For each of the three varieties of GMO corn tested, only a single study was done.  However, a central tenet of sound science is that the results are reproducible and replicated by other studies, preferably those done by different researchers.
  2. Only the rat was used as a toxicological model.  Rats are useful models for the human detoxification systems, but poor models for human reproductive and embryological systems.  Remember, rat studies “proved” that thalidomide was safe for pregnant women to use… but the rabbit studies done AFTER thousands of babies were harmed “proved” that it caused birth defects!  Scientific proof is only as good as the scientific studies, which are always limited and narrowly focused.
  3. The studies lasted only 3 months and were done on young adult rats.  Yet, captive rats live about 24 months.  No studies looking at late life outcomes from this brief exposure or studies which used lifelong exposure to GMOs were performed.  This is clearly a problem unless human consumers are only supposed to eat GMO foods for no longer than 9 years between the ages of 10 and 20.  Yet, GMO food technology has been released (without labeling) with the intention of lifelong consumption.
  4. No reproductive or developmental studies were done.  Yet GMO foods do not carry a label declaring that their safety during pregnancy has not been evaluated.  Instead, they are unlabeled and meant to be consumed by both genders, at all ages and developmental stages, including during pregnancy and infancy.
  5. Adverse outcomes were only considered if they occurred in both genders!  Clearly genders are different.  For instance, women are much more likely to get breast cancer than men, and one must have a prostate to get prostate cancer.  In the industry studies, increases in prostate cancer in male rats and increases in mammary tumors in female rats would apparently have been omitted since they differed between genders.  This explains exactly what happened to their findings that male rats eating GMO corn had an 11% increase in heart size while female rats eating GMO corn had a 40% increase in serum triglycerides[2].   It is not clear what to make of these findings, but they should not have been omitted and, instead, should have been used to encourage more numerous and longer duration (lifespan) studies before the worldwide release of GMO corn.
  6. Adverse outcomes which are consider “normal” in old rats were omitted in this young rat population.  For instance, the researchers did not consider “chronic progressive nephropathy”, a kidney disease common in older rats, to be a problem even though it was occurring in young, 5 month old, rats eating the GMO corn.

Now, I can attest that modern toxicology students training at respectable universities are taught to do much better work than this. We can only speculate about the reasons such limited study methodologies were chosen.  Nonetheless, these are the studies which the FDA determined to be sufficient for the approval of the three GMO corn varieties represented.  As if the major flaws in the study methodologies were not enough to warrant a different decision, the French team of researchers found a number of concerning associations upon re-analyzing the raw data[3].  They summarize:

Our analysis clearly reveals for the 3 GMOs new side effects linked with GM maize consumption, which were sex- and often dose-dependent. Effects were mostly associated with the kidney and liver, the dietary detoxifying organs, although different between the 3 GMOs. Other effects were also noticed in the heart, adrenal glands, spleen and hematopoietic system. We conclude that these data highlight signs of hepatorenal toxicity, possibly due to the new pesticides specific to each GM corn.

This is not the only group of researchers to demonstrate an association between GMO consumption and adverse health outcomes.  Despite the industries resistance to providing GMO varieties to outside researchers for independent studies, there are still dozens of studies available to the public for review.  I’ll synthesize the findings of several of these studies below in considering the possible mechanisms by which agricultural GMOs may cause problems.  In general, the health effects of agricultural GMOs are mediated through at least three routes; 1. Directly though ingestion, 2. Indirectly through GMO associated pesticide exposure and ingestion, and 3. Indirectly through environmental and ecosystem effects.

Effects of GMO ingestion:

Ingesting GMOs can affect both the microbiome and human cells.  The microbiome is the microorganism population which lives on and in the human body.  Most of it exists in or on the mouth, nose, stomach, intestines, and skin.  The gut microbiome has received considerable attention due to its apparently profound effect on the immune system, not to mention its effect on food digestion.  The gut microbiome is involved in determining the risk of autoimmune diseases, allergic diseases, cardiovascular disease, and some infectious diseases like osteomyelitis.  The microbiome can get out of balance (called dysbiosis) and produce severe diseases such as Clostridium difficile overgrowth and more mild disorders like small bowel bacterial overgrowth and irritable bowel syndrome.  The bottom line is that a balanced microbiome is critical for health and we are just now beginning to appreciate how serious the consequences of dysbiosis may be.

Continue Reading At: GreenMedInfo.com

We Now Know HOW Antibiotics Kill off Good Bacteria in the Gut

Leading To A Common And Often Fatal Health Problem

Bacteria

Source: NaturalSociety.com
Julie Fidler
January 25, 2016

A single course of antibiotics can cause Clostridium difficile, or C. diff – a bacterium that can lead to a condition known as Clostridium difficile colitis – to flourish in the gut, according to researchers at North Carolina State University.

The discovery was made during experiments with mice. The scientists say the antibiotics were found to kill off bacteria responsible for altering bile acid.

C. Diff is a dormant spore bacteria that must germinate and become growing bacteria to colonize the gut. Certain antibiotics lead to a higher risk of C. diff, especially in hospital patients. For the study, Casey Theriot, an assistant professor of infectious disease at NC State, sought to find out just how C. diff spores interacted with natural bacterial environment (microbiota) of the gut.

“We know that within a healthy gut environment, the growth of C. diff is inhibited,” Theriot says. “But we wanted to learn more about the mechanisms behind that inhibitory effect.” [1]

Primary bile acids are created in the liver from cholesterol and help the body to digest food and absorb fat. Bile also controls the metabolism of lipoproteins, drugs, glucose, and energy. These acids travel through the intestinal tract to the large intestine where they are converted into secondary bile acids by other bacteria.

Scientists identified 26 primary and secondary bile acids in mice and recorded their levels before and after treatment with an antibiotic.

The team added C. diff spores to concentrations of the acids and discovered that primary bile acids allow spores to germinate, regardless of antibiotic treatment, including the broad-spectrum antibiotics cefoperazone, clindamycin, and vancomycin. [2]

When the spores passed into the mice’s large intestine, where normal gut bacteria create secondary bile acids, the researchers found that those secondary bile acids stopped C. diff from growing. After antibiotic treatment – which killed those bacteria and the secondary bile acids – the C. diff was able to quickly grow.

“These findings are a first step in understanding how the gut microbiota regulates bile acids throughout the intestine,” says Theriot. “Hopefully they will aid the development of future therapies for C. difficile infection and other metabolically relevant disorders such as obesity and diabetes.” [3]

In a February 2015 press release, the U.S. Centers for Disease Control and Prevention (CDC) said that C. diff caused nearly half a million infections in the United States in a single year. About 29,000 people died within 30 days of diagnosis, and about 15,000 thousand deaths were believed to have been directly caused by C. diff infections.

Continue Reading At: NaturalSociety.com