Plastics, Pesticides, Triclosan, Flame Retardants, Oh My… Poor Immune System!!

Labs

The Complex Connection

For the past few weeks, I’ve been listening and taking notes from presentations in the Digestion Sessions and Autoimmune Summit. Along with the role that the microbiome and various critters play in immune disorders, many of the speakers also discussed the complex role that toxicants played in contributing to autoimmunity.

Due to the fact that approximately 70% of our immune system is in our digestive tract, it acts to modulate our susceptibility to various diseases and how we respond to various insults, including chemicals. Specifically, for autoimmunity to take hold, a genetic predisposition, a trigger, and intestinal permeability all are needed. The authors of the 2006 article in Gut explained the connection in the following way:

As discussed previously, there are data available suggesting that abrogation of epithelial barrier function can induce inflammatory disease, either locally or remotely. We will offer a hypothesis to explain this observation and then provide experimental data to support this. In order to do this we will consider type 1 diabetes as a model disease and then extend these observations to several other diseases that we believe have similar aetiologies.

We hypothesise that many diseases have a pathogenesis that consists of three main features, represented diagrammatically in fig 55.

  1. A genetically susceptible immune system (the mucosal immune system), that allows the host to react abnormally to an environmental antigen.
  2. An environmental product that triggers the disease process.
  3. The ability for the environmental agent to interact with the mucosal immune system. Since the purpose of the epithelial barrier is to keep these two factors separate, and we measure this function of the barrier by permeability, the corollary of this is that an increase in permeability is a requirement for disease expression. (3)

 

The Chemical Connection

Specific chemicals have been linked to various autoimmune diseases in the past. For example, systemic sclerosis has been linked to occupational silica dust exposure. In 2012, Dr. Piligian presented at the SLE Workshop at Hospital for Special Surgery. He discussed how environmental triggers were involved with autoimmunity, along with inflammation, epigenetic control, and infections. Below is an excerpt from the summary of the presentation:

Dr. Piligian reported that a disease similar to scleroderma has been associated with silicone implants, with the accompanying severe pain and chronic fatigue. Lupus antibodies (anti-Sm& anti-RNP) have been detected in patients with silicone implants, and these antibodies disappeared once the implant was removed. Hydrazines (colorless and flammable liquid, with an ammonia like scent) occurs in tobacco, and is commercially used in making plastics, anti-corrosives, rubber products, herbicides, photographic supplies, preservatives, textiles, and dyes, have been associated with drug-induced lupus in some studies. Certain metals, such as mercury, have also been identified as possible triggers of autoimmune processes in the body. Epidemiologic data is still accumulating on these associations and it’s possible they will be disproved with more evidence. (4)

 

Playing a tough basketball game.

Autoimmunity & Triggers- The Smoking Guns of Chemicals and Gluten

In a 2011 article in Environmental Health Perspective, the connection between the environmental triggers for autoimmunity including gluten, pharmaceuticals, and cigarette smoke were discussed. This provides further evidence that what we are exposed to can affect our immune system in negative ways:

According to Pollard, the best evidence linking environmental exposures to autoimmune diseases so far comes from pharmaceutical drug studies. That’s not surprising, he says, given that patients in such studies are closely monitored with respect to dose, clinical outcome, and confounding from other factors. Two drugs in particular have been linked conclusively to SLE in a minority of patients, Pollard says: procainamide, a treatment for cardiac arrhythmia, and hydralazine, used for high blood pressure.9 “And when you take patients off the drugs, their lupus symptoms go away,” Pollard says.

Apart from pharmaceutical exposures and SLE, solid evidence also links gluten ingestion with celiac disease; indeed symptoms disappear upon gluten’s removal from the diet, according to Alessio Fasano, director of the Center for Celiac Research at the University of Maryland School of Medicine. However, human evidence for other environment–disease links is more tenuous, in part because of inherent limitations in environmental epidemiology, Pollard says: people tend to be mobile, they’re exposed to many environmental agents at once, and there’s often a significant time delay before the onset of autoimmune symptoms.

Proposed links also tend to suffer from conflicting study results. For instance, cigarette smoking was linked to SLE in studies from the United Kingdom, Sweden, and Japan,10,11,12 but three U.S.-based studies failed to show a similar connection.13,14,15 (2)

It’s All About the Stochastic Events

“Stochastic”, involving a random variable or due to chance or probability. 

As noted in the above abstract, finding one root cause or trigger per autoimmune disease is nearly impossible. It’s stochasmic, meaning its a combination of factors  and various triggers interacting with our genetics that can ignite the process. For some people it may be plastics that create the final contribution to set the stage for an autoimmune response, others it may be mercury, some it may be gluten.

For example, in the Autoimmune Summit and Digestion Sessions, Dr. Datis Kharrizian discussed how the top three chemicals that cross-react with the thyroid in Hashimoto’s Thyroiditis include BPA (Bisphenol A, a chemical in plastic), latex, and fire retardants. One person may react to one or all three!

This cool article abstract summarizes the link between the connection of events of chemicals, triggers, and autoimmunity:

Susceptibility to most autoimmune diseases is dependent on polygenic inheritance, environmental factors, and poorly defined stochastic events. One of the significant challenges facing autoimmune disease research is in identifying the specific events that trigger loss of tolerance and autoimmunity. Although many intrinsic factors, including age, sex, and genetics, contribute to autoimmunity, extrinsic factors such as drugs, chemicals, microbes, or other environmental factors can also act as important initiators. This review explores how certain extrinsic factors, namely, drugs and chemicals, can promote the development of autoimmunity, focusing on a few better characterized agents that, in most instances, have been shown to produce autoimmune manifestations in human populations. Mechanisms of autoimmune disease induction are discussed in terms of research obtained using specific animal models. Although a number of different pathways have been delineated for drug/chemical-induced autoimmunity, some similarities do exist, and a working model is proposed. (5)

 

Decreasing the Probability

If you’re a regular reader of BreakFree Medicine, you haven’t been able to escape my hodgepodge of headlines on the health hazards of the multitude of chemicals that exist in our toxic world. In fact, as we speak I’m (still) editing the last section of my book on this very topic.

For many of us health conscious consumers, living in our world is like starring in a modern day filming of Friday the 13th!  As wellness devotees, we are frantically trying to avoid getting our immune system stabbed by the unfriendly hand of toxic invaders.

So what do we do?

We can aim to avoid chemicals in our food by buying organic when possible, read labels for GMOs, avoid hormone and immune disrupting personal care products, filter our water and air, and take our supplements. This is so that we can avoid or mitigate our risks in this scary world of toxic soup. It is very frustrating to some, as no matter what we do, we can’t completely avoid chemical exposure. It’s in the gas we pump, the carpet we walk on, the paint in our house, the mattresses we sleep on, the dust balls on our shelf, the apple we eat, and the golf course we drive by. Therefore, even the most pure and obsessive can’t shelter themselves from exposure! However, these are some measures we can take to protect ourselves.

 

Reviewing the Importance of the Gut In Immunity

Bugs

One of the major themes in my training was how the gut modulates our immune system via the microbiome. I’ve discussed how stealth infections can trigger autoimmunity via molecular mimicry. Recently, Scientific American reported on recent evidence from a small study linking an altered gut microbiome to the incidence of multiple sclerosis.

Researchers have speculated for some time that the myelin degradation seen in MS is due, at least in part, to autoimmune activity against the nervous system. Recent work presented at the MS Boston 2014 Meeting suggests that this aberrant immune response begins in the gut.

Eighty percent of the human immune system resides in the gastrointestinal tract. Alongside it are the trillions of symbiotic bacteria, fungi and other single-celled organisms that make up our guts’ microbiomes. Normally everyone wins: The microorganisms benefit from a home and a steady food supply; we enjoy the essential assistance they provide in various metabolic and digestive functions. Our microbiomes also help calibrate our immune systems, so our bodies recognize which co-inhabitants should be there and which should not. Yet mounting evidence suggests that when our resident biota are out of balance, they contribute to numerous diseases, including diabetes, rheumatoid arthritis, autism and, it appears, MS by inciting rogue immune activity that can spread throughout the body and brain.

One study presented at the conference, out of Brigham and Women’s Hospital (BWH), reported a single-celled organism called methanobrevibacteriaceae that activates the immune system is enriched in the gastrointestinal tracts of MS patients whereas bacteria that suppress immune activity are depleted. Other work, which resulted from a collaboration among 10 academic researcher centers across the U.S. and Canada, reported significantly altered gut flora in pediatric MS patients while a group of Japanese researchers found that yeast consumption reduced the chances of mice developing an MS-like disease by altering gut flora. (1)

So a gut attack can lead to a brain attack! This means taking care of your belly bugs is an important way to keep our immune systems from being hit. In fact, an optimal microbiome can aid in helping us rid our bodies of unwanted exposures.

Recently, some new exposures have popped up for us to be aware of. You can review them here and learn about other ways of protecting yourself from some of the most harmful exposures.

If one wants to dig deeper, they can also get a functional medicine assessment to individualize cleansing protocols and environmental support. The important take home point is that knowledge is power and we don’t have to live in a bubble to stay healthy.

 

Sources:

(1) Stetka, B. Could Multiple Sclerosis Begin in the Gut? MS researchers are focusing on the content of the gut’s microbiome as a possible contributor to the body’s autoimmune attack on its nervous system. Scientific America. October 8, 2014. http://www.scientificamerican.com/article/could-multiple-sclerosis-begin-in-the-gut/

(2) Questions Persist: Environmental Factors in Autoimmune Disease. Environ Health Perspect. Jun 2011; 119(6): A248–A253. PMCID: PMC3114837

(3) Alterations in intestinal permeability. Gut. Oct 2006; 55(10): 1512–1520. doi: 10.1136/gut.2005.085373

(4) Lysa Silverstein (summary). Possible Environmental Triggers Associated with Autoimmune Diseases: Adapted from a presentation given at the SLE Workshop at Hospital for Special Surgery. Presented March 30, 2012, Posted September 25, 2012. http://www.hss.edu/conditions_environmental-triggers-associated-with-autoimmune-diseases.asp

(5) Toxicology of Autoimmune Diseases. Chem. Res. Toxicol., 2010, 23 (3), pp 455–466. DOI: 10.1021/tx9003787

images courtesy istockphoto.com