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Welcome to Achieve True Health

This is the post excerpt.

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Hello there!

Many of you know I have been struggling with Interstitial Cystitis for almost 10 years. Through my search for an answer, I have learned that all chronic illnesses share 2 things in common: A dysfunctional gut and a dysregulated immune system. To help educate others, I have created a blog. If you know anyone who is struggling with any CHRONIC illness such as IC, Fibromyalgia, Hashimotos, Ulcerative Colitis, Celiac…and the list goes on and on…PLEASE SHARE. The info can save their life!

This is my first post on my new blog.  Honestly, I should have started this blog sooner. If you know what I have been through, you too will wonder why I waited so long to share with you my story.  It has been..well, interesting to say the least.  For those of you who know Carowinds, I equate this with the “Fury”.  Some parts are exciting, but when they are bad, they are downright miserable to the core!

I also have to thank a few people for inspiring me to begin this aggressive journey.  My wonderful partner in crime, Terry, who has been my backbone and support !  He has been a blessing in our lives, and has really pushed me get answers and not just “accept it”, as the doctors would have you.  The other people I have to thank are my team of practitioners: Dr. Bagwell with Maximized Living, Dr. Porter with Novant Health, Bre Walker with Dominion Integrative, and Andrew and Mallorie with On Point Acupuncture!  They have all opened my eyes to a different way of thinking about health and functional medicine.

I don’t want to bore you with too much of my life’s details, but I think it is important that you know how this started and where I am today.

A little about me:  I am 38 years old, divorced, and have 2 beautiful children.  An 8 year old girl and 4 year old boy.  I live in Charlotte, NC.  I am originally from NJ, where I was married and finished college.  We moved here in 2007 to “have a better life”, FWIW.

Fast forward to 2007, and the birth of my first born, via C-section.  About 1.5 to 2 years later, I am afflicted with this condition.  It really came on suddenly. I have always noticed I urinated more frequently, especially during times of high stress.  But the pain came on fast, less than two years after she was born. How can I describe this pain ?  Burning, stabbing, fire, heat, throbbing.  There were times I cried when I had to urinate, and my poor daughter, two years old, would witness my misery.  I felt like I was in an INFERNO.

I immediately went to the gynocologist, figuring this is a UTI. I never had one before, but this is how it feels, right ladies?  Well, to my demise, the lab result was…..NEGATIVE.  What?  How could this be?  Where is this pain coming from.  The doctor proceeds to tell me he is diagnosing me with IC using diagnosis of exclusion, and that I can use a new drug called Elmiron. Ok great doc, gimme the medicine and I see you later.  Well , not so fast.  The catch is, the longer you take this medicine, the better you will feel……………….

What?

Do you mean I have to take this drug forever?

Yes, that is what I am saying.  The drug’s action works better if you take it longer.

Thank you doctor, but no thank you.

I left and did not fill the $500 prescription. Oh and I found out it makes your hair fall out! One thing I know, I have beautiful hair, no way I am going to go bald.

This was the start of my journey.  I would like to call this a journey from hell, but that would be unfair to label that so poorly. I have had some really rough times with this, as you will see in this blog.  But the journey has allowed me to grow in many ways.  It has humbled me at times. It has force me to educate myself, and learn about my body.  Along the process, I continued with my education, and pursued a Masters Degree in Biology. During my studies, I was able to correlate the things i learned in class with my disease.  It has taught me compassion, patience, and prioritization. It has also forced me to appreciate my life. Yes, that means stop and smell the flowers.

I am still on this journey. I am not cured.  But I am getting pretty damn close.

Welcome to my blog!

 

 

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Mast Cell Activation and Inflammation

strawberries

I love strawberries!  They are high in Vitamin C and just delicious on salads.  Sadly, they also can cause pain in many people who have mast cell activation disorder. Read below….

I have recently become very interested in histamine intolerance and mast cells, and strawberries is on the list of foods high in histamine. There is some significant research being done on mast cell activation, autoimmune disease and the immune system.  Histamine intolerance is the disequilibrium between accumulated histamine and histamine degradation (Manzotti, Breda, Di Gioacchino, & Burastero, 2016).  Histamine degradation is dependent on the primary enzyme, diamine oxidase (DAO). Histamine is a biogenic amine found in foods such as pickles, matured cheese, fermented foods and leftovers.  Some foods are histamine liberators and that includes fruits such as pineapples, bananas, citrus fruits, papayas and strawberries.  The ingestion of histamine rich foods can provoke a variety of symptoms such as digestive, arrhythmia, flushing, asthma, hypotension, rhinoconjunctivitis, and headaches.  Impaired DAO production is often the culprit, which can result in increased enteral histamine uptake and increased plasma histamine concentrations (Manzotti et al., 2016).  Interesting the study by Manzotti demonstrated that 71% of patients reported functional bloating after consuming high histamine foods.

The latest research indicates that mast cells that release histamine and other inflammation in the bloodstream are active participants in autoimmune disease related tissue damage.  Increased mast cell activity, release of histamine and other inflammatory agents are frequently seen in autoimmune conditions such as MS, RA and many others (Healing Histamine, n.d.).   A variety of receptors including those engaged by antibody, complement, pathogens, and intrinsic danger signals are implicated in mast cell activation in disease.  A variety of receptors including those engaged by antibody, complement, pathogens, and intrinsic danger signals are implicated in mast cell activation in disease (Brown & Hatfield, 2012).  Mast cells can also recruit other immune cells such as neutrophils, to the sites of autoimmune destruction.  “Mast cells can only act as accessory cells to the self-reactive T and/or antibody driven autoimmune responses” (Brown & Hatfield, 2012).  This includes mast cells among one of the major contributors to autoimmunity and should definitely be considered.

Autoimmune and allergic diseases share fundamentally important features in that both are the result of “hypersensitive” immune responses directed toward inherently harmless antigens (Brown & Hatfield, 2012).  An early progress of autoimmune disease involves the activation and expansion of T and/or antibody producing B cells that wear autoreactive receptors.  These autoreactive T or B cells can then enter the bloodstream and migrate to sites of inflamed tissues expressing relevant autoantigens (Brown & Hatfield, 2012). “T cells, through the elaboration of cytotoxic mediators, and antibodies, through complement fixation or their ability to activate resident accessory cells such as macrophages and mast cells via Fc receptor engagement, can play direct roles in tissue destruction at these sites” (Brown & Hatfield, 2012)

In addition to eliciting the above described adaptive immune response, antigens can engage a class of danger- associated receptors on both adaptive and innate immune cells, including mast cells.  These receptors include toll-like receptors (TLRs) and Nacht-LRRs (NLRs) (Brown & Hatfield, 2012).  Activation of immune cells through TLRs and NLRs induces the expression of multiple inflammatory mediators that can ultimately result in local tissue damage causing the release of normally sequestered tissue antigen (Brown & Hatfield, 2012). Subsequent recognition of these antigens by T or B cells will induce activation and initiate autoimmunity. Alternatively, infection-induced activation of accessory immune cells, including mast cells, macrophages, and neutrophils, can boost inflammation and transform a relatively modest autoreactive response.

There is evidence that other TLRs are expressed on mast cells.   For example, activation of mature mast cells through TLR2 results in their production of several pro-inflammatory cytokines critical in autoimmunity including IL-17, IFNγ, TNF, and IL-1β.  Mast cells also express multiple IgG Fc receptors. This is significant because IgG autoantibodies are hallmarks of many autoimmune diseases and have been detected in multiple autoimmune diseases.

 

References

Brown, M. A., & Hatfield, J. K. (2012). Mast Cells are Important Modifiers of Autoimmune Disease: With so Much Evidence, Why is There Still Controversy? Front Immunol, 3, 147. doi:10.3389/fimmu.2012.00147

 

Healing Histamine (n.d.).  Histamine Intolerance, Mast Cells & Autoimmunity.  Retrieved (2018, May 15) from https://healinghistamine.com/histamine-mast-cells-autoimmune-disorders/

 

Manzotti, G., Breda, D., Di Gioacchino, M., & Burastero, S. E. (2016). Serum diamine oxidase activity in patients with histamine intolerance. Int J Immunopathol Pharmacol, 29(1), 105-111. doi:10.1177/0394632015617170

Erectile Dysfunction and Inflammation

viagra-pills

Cytokines, are small secreted proteins released by cells have a specific effect on the interactions and communications between cells. Different cytokines are associated with different diseases or conditions(Zhang & An, 2007). One particular cytokine, TNF-α, has been shown to play an important role in ED as well as cardiovascular disease (CVD), due to the effect it has on the vascular system.  Patients with ED often show high levels of TNF-a, which is a cytokine that is often secreted by white blood cells in response to inflammatory stimuli.  In addition, the presence of a low-grade inflammatory process is associated with many cardiovascular diseases (CVD). Cytokines levels, such as TNF-α, are increased in response to inflammation and contribute to the changes in vascular reactivity observed in CVD (Carneiro et al., 2010). Two distinct surface receptors mediate the effects of TNF-α. These include TNFR-1, and TNFR-2.  Gene expression of TNFR-1 has been demonstrated in cavernosal tissue of the penis (Carneiro et al., 2010).  It has been pretty well established that this cytokine is an important contributor of many cardiovascular diseases related to endothelial dysfunction. Additionally, endothelial function is impaired in inflammatory conditions and conditions with increased oxidative stress.  In vivo laboratory administration of TNF-α demonstrates impairment of endothelium-dependent vasorelaxation in a variety of vascular beds and decreases the release of nitric oxide (NO), which is required for erectile function. TNF-α has the ability to increase arterial reactive oxygen species generation, which likely accounts for some of the reduction in NO levels.

So the question is, what is causing the TNF-α to be elevated?  I found the link to environmental toxins to be quite intriguing.  Could exposure to these toxins induce elevations in inflammatory cytokines, like TNF-α, that leads to downstream effects such as vascular dysfunction?  Some environmental toxins, such as endocrine disrupting chemicals (EDCs) interfere with the synthesis of cytokines, immunoglobulins, and inflammatory mediators, and they also affect the activation and survival of immune cells (Yang et al., 2014).  The dysfunction of the immune system caused by some EDCs may lead to immunity immunodeficiency against infection, or to hyperreactivity of immune responses, as seen in allergy and autoimmune disease (Yang et al., 2014).  Nonylphenol (NP), one of the alkylphenols, is the most important metabolite of a group of nonionic surfactants, is a common EDC that can bioaccumulate through the diet.  It is structurally similar to estrogen, which can feminize male animals and may be linked to infertility.  Some in vitro or ex vivo studies suggest that NP skews T cells towards Th2 responses through its influence on dendritic cells (DCs), resulting in increased expression of IL-6 and TNF-α, but not IL-10 and IL-12, in response to LPS stimulationNP increases the expression of TNF-α, but suppressed anti-inflammatory cytokine IL-10 production in a range of physiological doses, burning both ends of the candle.

Another interesting association with increased levels of TNF-α is associated with intestinal parasites such as Entamoeba histolytica.  Although TNF can be synthesized and secreted by many other cell types, such as neutrophils, eosinophils, and mast cells, the main source of TNF is activated macrophages.  Usually, TNF contributes to the control of parasitic and bacterial infection like in the case of Trypanosoma infection or by triggering an immune response. E. histolytica activates the inflammatory process by promoting TNF production, which is thought to be crucial for guiding E. histolytica towards TNF-producing cells of the host. One may speculate that this behavior is triggered by its need of nutrients that cannot be satisfied in the inflamed tissues. Inflammation causes change in the gastrointestinal microbiota, and these changes may provoke E. histolytica to search for alternative sources of nutrients.

Other intestinal parasites have been associated with HPA axis dysfunction, since the immune and neuroendocrine systems are interconnected by a network in which hormones, antigens, receptors, cytokines, antibodies and neuropeptides modulate immune response. This indicates that intestinal parasites can influence sex hormone production, such as testosterone.  Low testosterone levels often go hand in hand with erectile dysfunction, but that will be discussed in a future blog.

The bottom line; get to the bottom of the problem. Find the source of the inflammation that is ruining your sex life. Run functional labs such as a stool test to rule out intestinal parasites.  An HPA axis test, such as the Dutch Complete, can determine the hormone imbalance and potentially identify the root cause. An environmental toxin test can reveal if toxins are ruining contributing to your immune dysfunction.  Running these labs will allow you to get on a healing path so you can get off the purple pill and regain your life back. You should work with a practitioner who is knowledgeable about the tests and can work with you to find your path to wellness.

 

References

Ankri, S. (2015). Entamoeba histolytica – tumor necrosis factor: a fatal attraction. Microb Cell, 2(7), 216-218. doi:10.15698/mic2015.07.216

Carneiro, F. S., Webb, R. C., & Tostes, R. C. (2010). Emerging role for TNF-alpha in erectile dysfunction. J Sex Med, 7(12), 3823-3834. doi:10.1111/j.1743-6109.2010.01762.x

Yang, S. N., Hsieh, C. C., Kuo, H. F., Lee, M. S., Huang, M. Y., Kuo, C. H., & Hung, C. H. (2014). The effects of environmental toxins on allergic inflammation. Allergy Asthma Immunol Res, 6(6), 478-484. doi:10.4168/aair.2014.6.6.478

Zhang, J. M., & An, J. (2007). Cytokines, inflammation, and pain. Int Anesthesiol Clin, 45(2), 27-37. doi:10.1097/AIA.0b013e318034194e

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Microbiome & Immune Connection

The-human-microbiome-and-human-health.jpg

Microbiome and the Influence on the Immune System-it’s more important than you think!

The composition of the microbiome can influence the function of your IMMUNE SYSTEM.  For example, numerous studies indicate that your microbiome can influence  your susceptibility to certain bacteria such as Campylobacter, which is often seen in anxiety disorders.  In fact, a book by Martin Blaser called “Missing Microbes” discusses that the alteration of the human microbiome could be one of the factors attributed to the rise of conditions such as food allergies, asthma, celiac disease and intestinal disorders such as IBD.  His theory is that the modern medical practices, that includes overuse of antibiotics, may have negatively shifted the microbiome in a way that is affecting human health detrimentally.  The use of antimicrobial drugs is known to be associated with the development of certain infectious diseases, such as colitis and candida overgrowth, through disruption of this delicate microbiome balance (Casadevall and Pirofski, 2018).

It is hypothesized that the establishment of your microbiome occurs during the first 3 years of your life, and disruptions in this establishment during this time can have long term implications (Blaser, 2016).  According to Blaser, 50% of babies in the US are born by C-section, and this can be the beginning of some of the various disruptions in the delicate microbiome balance. This is not limited to bacteria, but also fungal and viral elements of the microbiome, that are also demonstrating a role in human health as well.

Nutritional intervention: Probiotics
A nutritional intervention to address the microbiome is the use of probiotics.  Probiotics are live organisms that, when ingested in adequate quantities, exert a health benefit on the host.  Probiotics can directly stimulate the growth of beneficial bacteria and competitively exclude the number of more harmful, toxin producing microbiota (Zhou & Foster, 2015).  Lactobacillus, Bifidobacterium, and Saccharomyces are three extensively studied and commonly used probiotics in humans and animals.

Probiotics are demonstrating to directly affect your gut immune system, which is responsible for

Three main beneficial effects of probiotics on your gut defense system include the following:

  1. Probiotics can block pathogenic bacteria by producing substances that directly compete with pathogens for adherence to the intestinal epithelium.
  2. Probiotics can enhance intestinal barrier function and stimulate protective responses from epithelial cells. This can lower the chance of bacteria translocating into the blood stream and entering systemically. This function may decrease infections and immune related reactions, thus supporting the health of the immune system (Enviormedica, n.d).
  3. Probiotics are able to modulate the immune system and pathogen induced inflammation through various immune regulated signaling pathways.

Immune Cells

Probiotics can regulate host innate and adaptive immune responses by modulating the functions of your very immune cells.    For example, a probiotic mixture consisting of L. acidophilus, L. casei, L. reuteri, B. bifidium, and Streptococcus thermophilus stimulated regulatory proteins involved in your immune system that are responsible for both inflammatory and anti-inflammatory mechanisms.

Intestinal Epithelial Cells

Probiotics can repair damaged epithelial barrier while producing antibacterial substances and protective proteins, as well as regulate intestinal epithelial immune function (such as cytokine production) (Yan & Polk, 2011).  For example, l. johnonsii has the ability to upregulate various receptors on your immune cells,  which may indicate that the probiotic is able to stimulate the gut immunity. “These findings suggest that probiotics regulation of innate immunity in intestinal epithelial cells may serve as a mechanism for disease prevention and treatment” (Yan & Polk, 2011).

References:

American Society for Microbiology. (2016, September 6).  Missing Microbes with Dr. Martin Blaser.  Retrieved 2018, May 4 from https://www.youtube.com/watch?v=KwK_O0ahDKo

Environmedica. (n.d.). Probiotics for Immune System Support. Retrieved 2018, May 3 from https://www.enviromedica.com/probiotics-immune-system (Links to an external site.)Links to an external site.

Yan, F., & Polk, D. B. (2011). Probiotics and immune health. Curr Opin Gastroenterol, 27(6), 496-501. doi:10.1097/MOG.0b013e32834baa4d

Zhou, L., & Foster, J. A. (2015). Psychobiotics and the gut-brain axis: in the pursuit of happiness. Neuropsychiatr Dis Treat, 11, 715-723. doi:10.2147/ndt.S61997

Endocrine Disruptors and your Health

endocrine.disrupturs.png

Our world is toxic, and lately endocrine disruptors have been the focus of the health industry.  New products are popping all over the market, and may new companies are launching in the market, claiming to be free of endocrine disrupting chemicals.

I just encountered a new product line called Poofy Organics that looks promising with products that are clean and free of these dangerous and pesky chemicals.  They have a diverse product line and best of all, they are affordable! Read on about what these chemicals are, what they do to your body and I will share the link to where you can order if you wanted to try for yourself.

I first encountered the topic of endocrine disruptors from one of my friends a few years ago who started making her own hair and skin care products using cleaner, phthalate free ingredients.  At the time, I did not know much about endocrine disruptors, but it was also around the time that BPA was being removed from baby bottles.

What are endocrine disruptors?

They are chemicals that may interfere with the body’s endocrine system and are showing to have adverse developmental, reproductive, neurological, and immune effects in both humans and wildlife (Endocrine Disruptors, n.d.).  They can be found in a wide range of every day products such as pharmaceuticals, pesticides, plastics, metal food cans, detergents, toys, and cosmetics.  Currently there are numerous studies, supported by the NIEHS, to determine if exposure to endocrine disruptors may result in human health effects, particularly infertility and cancer (Costa, Spritzer, Hohl, & Bachega, 2014).  Studies indicate that endocrine disruptors can affect multiple areas of reproduction, development and metabolism.

Endocrine disruptors primarily exert their effects by binding to hormone receptors and transcriptional factors. (Costa et al., 2014)  There are 3 main methods that affect the hormone levels in the body (Endocrine Disruptors, n.d.):

  1. They can mimic naturally occurring hormones such as estrogens, androgens, and thyroid hormones, potentially over-stimulating (called the agonistic effect)
  2. They can bind to a receptor within a cell and block the endogenous hormone from binding, such as anti-estrogens and anti-androgens (called the antagonistic effect)
  3. They can interfere with the way natural hormones or their receptors are made or controlled, by altering metabolism in the liver.

However, recent studies are showing that they can also alter the enzymes involved in the synthesis or catabolism of steroids (Costa et al., 2014).  I find most alarming is that the highest incidence of reproductive disorders that were observed in the second generation of the women exposed to endocrine disruptors, such as diethylstilbestrol (DES).  This suggests that the epigenetic changes can affect subsequent generations.

Where are endocrine disruptors found?  Everywhere!  They are ubiquitous in our modern society, unfortunately.  Research indicates many places where they can be found to accumulate. There are 3 main categories that they are listed in, which are BPA, DEHP, and phytoestrogens.  However, I felt the EWG did a fairly good job summarizing them down to the Deadly Dozen.   I will summarize 5 of them below:

  1. BPA-biphenol A-It is one of the chemical compounds of highest production worldwide; more than 6 billion pounds are produced annually. (Costa et al., 2014) . It has been identified in 95% of urine samples of the American population and also found in serum of pregnant women. BPA is most recognized on its effects on thyroid hormones, particularly its estrogenic and adipogenic activities, which could definitely linked to metabolic diseases such as hypothyroidism, diabetes, obesity, and cardiovascular disease.  One way to minimize exposure is to eat fresh foods and avoid canned foods.  Also I found it interesting that BPA is found in cashier receipts.  In fact, levels of BPA in cashiers who handle receipts were higher after their shifts than in between shifts. (Our Chemical Lives, 2015)
  2. Phthalates-These are plasticizers used as softeners, but are also found in paints, solvents, toys, personal and medical care products, and cosmetics and blood transfusion bags (Costa et al., 2014) The main routes of human exposure are food and skin absorption, and it can occur during trans placental route and during breastfeeding.  DEHP, Di (2-ethylhexylphthalate), are implicated in the toxicity of the reproductive system and also increased proliferation of fat cells, which predisposes you to visceral obesity (Costa et al., 2014).  Also epidemiological studies have correlated phthalates in cord blood and lower gestational age at delivery. Other areas where studies link their effects in with male fertility, lower sperm counts and defects in male reproductive system  (Deadly Dozen Endocrine Disruptors, 2013). Exposure to DEHP can alter DNA methylation patterns in both the prostate and testicular cells (Sweeney, Hasan, Soto, & Sonnenschein, 2015).  These epigenetic patterns seen are also heritable, meaning DNA methylation patterns and histone modifications have been observed in successive generations (Sweeney et al., 2015).  “Interruption of hormonal function within the developing tissues have been shown to lead anatomical changes in new born male babies as well (Sweeney et al., 2015).
  3. Dioxins-These compromise a group of organochlorine compounds that include PCBs (polychlorinated biphenyls). They are found in insulators, flame-retardants, lubricants, and machine and transformer fluids.  They can disrupt both male and female sex hormone signaling, and if exposed in the womb, they can permanently affect sperm quality and lower the sperm count in men  (Deadly Dozen, 2013).  They are fat soluble and can easily contaminate the food chain because they accumulate in fat cells. They are also not readily metabolized and excreted and half a half-life of 8 years (Costa et al., 2014).  They are found in products like meat, fish, milk, eggs and butter, so the best wait to limit exposure is to cut back on eating animal products.
  4. Pesticides- A recent study in UK reported there are approximately 127 pesticides identified with endocrine disrupting activity. Among the classes of pesticides that stand out are organophosphates, carbamates, and organochlorines (Costa et al., 2014).  Also, there is still some contamination of DDT found in some developed countries despite being banned.  Atrazine is the most commonly detected pesticide found in ground and surface water (Costa et al., 2014).  It is linked to breast tumors, delayed puberty and prostate inflammation in animals, and even prostate cancer in humans (Deadly Dozen, 2013).  Organophosphates can effect brain development, behavior and fertility. They can also interfere with testosterone communication, lowering both testosterone and thyroid hormone levels.  Ways to limit exposure is to buy organic, use EWG’s Shoppers guide to pesticides in produce to assist in finding fruits and vegetables with fewest pesticide residues.
  5. PFC-perflourinated chemicals used in non-stick cookware. I chose this one because I love to cook, but accumulation of this chemical makes home cooked meals not as healthy as they should be! Perfluorochemicals are so widespread and extraordinarily persistent that 99 percent of Americans have these chemicals in their bodies (Deadly Dozen, 2013).  One particular compound, PFOA, has been shown to be resistant to biodegradation, which mean it will never break down in the environment. PFOA is linked to decreased sperm quality, low birth weight, kidney disease, thyroid disease, cholesterol, etc.  It seems to affect the thyroid and sex hormones the most.  One way to minimize exposure is to eliminate the usage of non-stick pans.  There is a pan called the “Green Pan” that is non-stick, ceramic based pan that is made from a sand derivative that does not use PFOA or PFAS during the production process.  It also is heat resistant to temperatures up to 450C and it will not release any toxic fumes if you accidentally overheat it.

Here is some information about the Green Pan:

https://www.greenpan.us/why-ceramic (Links to an external site.)

Here is the link to the EWG 2017Shopper’s Guide to Pesticides in Produce

https://www.ewg.org/foodnews/#.Wfy0prpFxfw (Links to an external site.)

One thing I found was interesting was that licorice (Glycyrrhiza glabra) root extract (LRE) may help alleviate the toxicity of endocrine disruptors (Chu, de la Cruz, Hwang, & Hong, 2014) IT is commonly called “gamcho” in Korea exhibits anti-oxidative, chemo-protective, and detoxifying properties.  In recent studies, special attention has been given to the study of plant and their isolates for the prevention of diseases.  Licorice root has been used in over 70% of Chinese medicines and has been used by human beings for over 4000 years.   According to a study in 2014, there is some promising evidence that licorice root extract can be used as a potential toxicity-alleviating agent to prevent the occurrence of endocrine disrupting-induced tumors and can help modulate the risk of cancer to excessive exposure to endocrine disruptors. Furthermore, licorice root has other healing properties and can act as an adaptogenic agent for modulating adrenal insufficiency, and is definitely worth exploring further.

So for the best part, here is the link to order Poofy.  POOFY ORGANICS was founded in 2006 after a family member was diagnosed with breast cancer.  The family was determined to stop using products laden with toxic chemicals. With no suitable alternatives to turn to, they made it their mission to find the safest and most effective ingredients for our products.  I am waiting for a box of samples to arrive, I can’t wait to try these products out!!!

Poofy logo

https://dena.poofyorganics.com/

References

Chu, X. T., de la Cruz, J., Hwang, S. G., & Hong, H. (2014). Tumorigenic effects of endocrine-disrupting chemicals are alleviated by licorice (Glycyrrhiza glabra) root extract through suppression of AhR expression in mammalian cells. Asian Pac J Cancer Prev, 15(12), 4809-4813.

 

Costa, E. M., Spritzer, P. M., Hohl, A., & Bachega, T. A. (2014). Effects of endocrine disruptors in the development of the female reproductive tract. Arq Bras Endocrinol Metabol, 58(2), 153-161.

Dirty Dozen Endocrine Disruptors. (2013, October 28). Retrieved from https://www.ewg.org/research/dirty-dozen-list-endocrine-disruptors#.WfykCrpFxfw

Endocrine Disruptors.(n.d.)  Retrieved from http://www.ewg.org/research/dirty-dozen-list-endocrine-disruptors (Links to an external site.)Links to an external site. (Links to an external site.)

Our Chemical Lives. (2015, March 31).  Retrieved from https://www.youtube.com/watch?time_continue=1553&v=J9SWBAUlAvw

Sweeney, M. F., Hasan, N., Soto, A. M., & Sonnenschein, C. (2015). Environmental endocrine disruptors: Effects on the human male reproductive system. Rev Endocr Metab Disord, 16(4), 341-357. doi:10.1007/s11154-016-9337-4

 

 

 

 

Exercise and Inflammation

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Exercise and Inflammation-it’s more than just vanity!

Having worked in the fitness industry for over 15 years and helping people with their weight loss goals, I always wondered what role exercise had on inflammation.  In obesity, various mechanisms are thought to contribute to a low grade inflammation within the fat tissue affecting the development of several secondary diseases such as metabolic syndrome, insulin resistance (IR), diabetes, arterial hypertension and asthma (Schmidt et al., 2015).

The study I examined look at levels role of exercise and how it influences the levels of pro-inflammatory cytokines in participants with high vs. low physical activity (Gleeson et al., 2011).  The study demonstrated a strong relationship to BMI that may indicate that the decrease in inflammatory molecules may be related to decrease in visceral fat.  Interestingly, calorie restriction and fasting has been shown to reduce visceral fat in numerous other studies, as well as subsequent reduction in inflammation (which is an area I am very interested in digging into more).  Additionally, physical activity may further mitigate inflammation by improving endothelial function, increasing insulin sensitivity, enhancing liver health and increasing blood vessel growth and blood flow.

An article by Gleeson et. al discusses the anti-inflammatory effects of exercise and explains 3 main mechanisms of action:

  1. Reduction in visceral mass-as mentioned early, a reduction in visceral mass has an indirect effect of being able to decrease inflammation, since accumulation of fat in the omentum, liver and muscles, as well as the expansion of adipose tissue, results in enhanced production of certain inflammatory mediators. Therefore loss of visceral fat can result in reduction in inflammation.
  2. Release of IL-6 from working muscles-A fall in muscle glycogen content with exercise signals the muscles to secrete IL-6 (a pro-inflammatory cytokine), which stays high during the duration of exercise. However, this also initiates a rise in anti-inflammatory cytokines IL-10 and IL-1RA to minimize the effects on the tissue.  Also, it was interesting that you really need 2.5 hours or more of strenuous exercise to get a significant elevation of IL-6, which may partially explain why marathon runners may have suppressed immune systems.
  3. Increased levels of cortisol and adrenaline-IL-6 stimulates the release of cortisol, which is smaller doses, can have anti-inflammatory effects. It should be pointed out that too much cortisol secretion from the adrenal glands can create a chronic state of inflammation as well, so this could also be a dose dependent phenomenon.

There also appears to be a strong relationship between exhaustive exercise, such as marathon running, and chronic low-grade inflammation induced by the massive systemic release of several pro-inflammatory cytokines and chemokines, such as IL6 and IL8, G-CSF, although host tissue damage may be restricted by compensatory mechanisms.  In conclusion, benefits of regular exercise and physical activity are well observed, but I think more clear direction is needed on the types and intensities as well as the health of the person doing the exercise to understand the impact it may have on inflammation.

References

Gleeson, M., Bishop, N. C., Stensel, D. J., Lindley, M. R., Mastana, S. S., & Nimmo, M. A. (2011). The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease. Nat Rev Immunol, 11(9), 607-615. doi:10.1038/nri3041

Part 2 of 2: Inflammation and Exercise: friend or foe?  (2011, August 25).  Retrieved 2018, May 2 from https://inscientioveritas.org/inflammation-and-exercise/ (Links to an external site.)

Schmidt, F. M., Weschenfelder, J., Sander, C., Minkwitz, J., Thormann, J., Chittka, T., . . . Himmerich, H. (2015). Inflammatory cytokines in general and central obesity and modulating effects of physical activity. PLoS ONE, 10(3), e0121971. doi:10.1371/journal.pone.0121971

IC and Histamine

allergy

I have been very interested in histamine and histamine intolerance from the time I was first diagnosed with IC and noticed that allergy medications helped me during flare ups.  It is well known that there is an involvement of mast cells and cystitis related pain. “Interstitial cystitis has been found in combination with some allergic or autoimmune disorders and histopathological abnormalities resembling allergic disorders, including mast cell activation, histamine release and eosinophil infiltration” (Lee, Doggweiler-Wiygul, Kim, Hill, & Yoo, 2006).  Clinical studies demonstrate elevated mast cell numbers in the lamina propria of IC bladder biopsies.  This may explain why neuromodulatory therapies suggests are partially effective in IC therapies, as “neural-immune interactions play a role in IC pathogenesis” (Rudick, Bryce, Guichelaar, Berry, & Klumpp, 2008).  Mast cells contain preformed stores of immune mediators, such as histamine and TNF, and can be activated to release these stores by neurotransmitters such as substance P, a polypeptide thought to be involved in the synaptic transmission of pain and other nerve impulses. It is hypothesized that that activation of bladder related circuits in the CNS initiate substance P by peripheral nerves in the bladder can promote mast cell activation, mediated by substance P (Rudick et al., 2008).  The mast cells are thought to induce bladder inflammation by acting on the bladder epithelium (lining). Also, increased levels of urinary histamine metabolites have been detected in IC patients.  This is thought to be due to accumulation of mast cells in the lamina propria.

A role for histamine and histamine receptors in pain responses has been documented in both humans and animal models.  “However, histamine can be derived from various cell types, including mast cells, basophils, and histaminergic neurons” (Rudick et al., 2008). More recently, inflammatory cells such as neutrophils and dendritic cells have been shown to produce histamine.  In fact, it has been demonstrated in various clinical settings that antihistamine therapy improves IC-related pelvic pain, and the mechanism for this effect is unknown. However, it can be inferred that this is due to histamine activation.  Irritable bowel syndrome (IBS) is another chronic condition that resembles IC in the characteristics of pathology. “In IBS, pain is correlated with activated colonic mucosal mast cells in proximity to nerves” (Rudick et al., 2008). In fact in IBS, colonic tissue extracts often reveal elevated histamine.  These findings support the idea that mast cell histamine may mediate pain in multiple pelvic pain syndromes (Rudick et al., 2008).

With my clients, we have a test I run by Dunwoody that can test for histamine intolerance. This test will measure hitamine levels, DAO (an enzyme that breaks down histamine), and DAO: histamine ratio. Classic symptoms of histamine intolerance include gas, high blood pressure, arrhythmia, nausea, hives, stomach ache, itching, cramps, headache, sneezing, dizziness, congestion, runny nose, shortness of breath, especially after meals containing histamine.  Low DAO is also associated with the same symptoms along with inflammation, arthritis and certain neurological conditions such as MS.  Low DAO is also associated with leaky gut and poor gut function and immunity.  It can also be a trigger for depression and anxiety.  Individuals with inability to break down histamine seem to “react to everyting” or seem to improve on anti-histamines.   I have to mention that the low histamine diet, combined with DAO enzyme before meals, has been shown to be really helpful in managing IC pain related to mast cells.  To really get on the road to healing and run some of the key functional tests, contact me at mandy@naturalhealthachiever.com so I can better guide you!

References:

Lee, J., Doggweiler-Wiygul, R., Kim, S., Hill, B. D., & Yoo, T. J. (2006). Is interstitial cystitis an allergic disorder?: A case of interstitial cystitis treated successfully with anti-IgE. Int J Urol, 13(5), 631-634. doi:10.1111/j.1442-2042.2006.01373.x

Rudick, C. N., Bryce, P. J., Guichelaar, L. A., Berry, R. E., & Klumpp, D. J. (2008). Mast cell-derived histamine mediates cystitis pain. PLoS ONE, 3(5), e2096. doi:10.1371/journal.pone.0002096

Development of Interstitial Cystitis (IC) Risk Score for Bladder Permeability

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I want to summarize some research I conducted recently on a study that evaluated inflammatory cytokines in women with IC with and without Hunner’s Ulcers to see if this non-invasive test could be used to substitute the current method of evaluation which is a very invasive and painful cystoscopy.  First I am going to review what a cytokine is, and then briefly summarize my findings.

What is a Cytokine Anyway?
Cytokines are small secreted proteins released by cells have a specific effect on the interactions and communications between cells.  They are signaling molecules that aid cell to cell communication in immune response and stimulate the movement of cells towards the site of inflammation, infection or trauma (Mandal, n.d.).  The word cytokine is a general name, but other names include lymphokine (cytokines made by lymphocytes), monokine (cytokines made by monocytes), chemokine (cytokines with chemotactic activities), and interleukin (cytokines made by one leukocyte and acting on other leukocytes) (Zhang & An, 2007).  Cytokines have autocrine (by acting on cells that secrete them), paracrine (acting on nearby cells) and endocrine action (acting on distant cells).  We have both pro-inflammatory and anti-inflammatory cytokines.  “There is significant evidence showing that certain cytokines/chemokines are involved in not only the initiation but also the persistence of pathologic pain by directly activating nociceptive sensory neurons” (Zhang & An, 2007).  Cytokines are made by many different cell population, but the majority of them are produced by helper T cells (Th) and macrophages.  Cytokines can be recruited by macrophages, mast cells, endothelial cells and Schwann cells.

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The Role of Cytokines in Inflammation:

Pro-inflammatory cytokines are produced predominantly by activated macrophages and are involved in the up-regulation of inflammatory reactions.  The main pro-inflammatory cytokines are IL-1B, IL-6 and TNF-a. These are often involved in the process of pathological pain.  “There is evidence that pro-inflammatory cytokines (e.g., IL-1β, TNF-α) and chemokines (e.g., MCP-1) may directly modulate neuronal activity in various classes of neurons in the peripheral and central nervous system” (Zhang & An, 2007)

  1. IL-B-This cytokine is released mostly by monocytes and macrophages as well as nonimmune cells (fibroblasts and endothelial cells) during cell injury, infection, inflammation and invasion. IL-B was found tin increase the production of substance P and prstoaglandin E2 in a number of neuronal and glial cells (Zhang & An, 2007)
  2. IL-6 Plays a key role in the neuronal reaction to nerve injury, and the development of neuropathic pain behavior following a peripheral nerve injury. IN fact, suppression of IL-6 has been demonstrated to lead to reduced regenerative effects
  3. TNF-a-This is also known as a cachectin, in an inflammatory cytokine that plays a key role in pain models. “TNF acts on several different signaling pathways through two cell surface receptors, TNFR1 and TNFR2 to regulate apoptotic pathways, NF-kB activation of inflammation, and activate stress-activated protein kinases (SAPKs)” (Zhang & An, 2007). It has been show to play an important role in both inflammatory and neuropathic hyperalgesia (increased sensitivity to pain).

Anti-inflammatory cytokines are a series of immunoregulatory molecules that control the pro-inflammatory cytokine response. “Cytokines act in concert with specific cytokine inhibitors and soluble cytokine receptors to regulate the human immune response” (Zhang & An, 2007). Major anti-inflammatory cytokines include IL-1 receptor antagonist, IL-4, IL-10, IL-11 and IL-13.  Leukemia inhibitory factor, interferon-alpha, IL-6, and transforming growth factor (TGF)-β are categorized as either anti-inflammatory or pro-inflammatory cytokines, under various circumstances. Specific cytokine receptors for IL-1, TNF-α, and IL-18 also function as inhibitors for pro-inflammatory cytokines (Zhang & An, 2007).

IL-10 has to most potent anti-inflammatory properties, being able to repress the expression of inflammatory cytokines such as TNF-α, IL-6 and IL-1 by activated macrophages (Zhang & An, 2007).  “Recent clinical studies also indicate that low blood levels of IL-10 and another anti-inflammatory cytokine, IL-4, could be key to chronic pain since low concentrations of these two cytokines were found in patients with chronic widespread pain” (Zhang & An, 2007).

What I found interesting:

There is debate among experts over whether certain molecules should be called hormones or cytokines, which I found particularly interesting.  Cytokines differ in classic proteins in that the concentrations of cytokines can increase in magnitude of almost a thousand-fold in response to an infection or inflammation, which is unlike proteins that do not differ in circulation by more than one order of magnitude (Mandal, n.d.).  Additionally, cytokines have a much larger distribution of sources for their production since nearly all cells with a nucleus has the ability to produce them, particularly IL-1, IL-6, and TNF-a. These include endothelial cells, epithelial cells and resident macrophages (Mandal, n.d.).  The classic hormones, however, are secreted from distant glands, as is seen in the secretion of insulin from the pancreas.  Additionally, cytokines can exert both systemic and local effects on the body, unlike hormones.  “A cytokine’s actions may affect the same cell it was secreted from, other cells nearby or may act in a more endocrine manner and produce effects across the whole of the body, such as in the case with fever, for example” (Mandal, n.d.)  Cytokines are often redundant in their activity, which means similar functions can be stimulated by different cytokines (Zhang & An, 2007).  They are often produced in a cascade, stimulating the production of additional cytokines, and can act both synergistically or antagonistically (Zhang & An, 2007).

Development of Interstitial Cystitis (IC) Risk Score for Bladder Permeability

I picked IC because this is an area of interest for me since I have been afflicted with this illness and work to support other women who are also dealing with the pain of IC.  IC is a painful bladder syndrome that is multifactorial consisting of severe pelvic and genitalia pain, as well as dysfunctional urination.  The disease is characterized by urinary frequency, urgency and severe pelvic pain.  IC can compromise sexual function, employment and quality of life (Lamb, Janicki, Bartolone, Peters, & Chancellor, 2017).  A percentage of patients also present with Hunner’s lesions or ulcers on their bladder walls (UIC), which is diagnosed by cystoscopy, a rather painful procedure.  The objective of this study was to determine if a calculated Bladder Permeability Defect Risk Score (BP-RS) based on non-invasive urinary cytokines could discriminate UIC patients from controls and IC patients without Hunner’s ulcers.  If successful, this may be used as a less invasive way to diagnose IC with UIC instead of the painful cystoscopy.

Pro-inflammatory cytokines such as IL-6 and IL-8 have been reported to be increased in IC patients and has been positively associated with pain scores (Lamb et al., 2017).  The study measured the expression of cytokines, chemokines and growth factors in urine samples of patients recruited for the study. For the validation set and a portion of the training set, only GRO, IL-6, IL-8, and MCP-1 were measured. In the study, 448 patients (96.1% women), 54 patients had IC with Hunner’s lesions and 394 had either no IC or IC without Hunner’s lesions.

These findings are consistent with previous characteristics of IC patients with and without the Hunner’s ulcers.  IC with Hunner’s lesions may have a more bladder-centric involvement whereas IC without Hunner’s lesions may be more systemic.  “Patients with NUIC can have other comorbid pain syndromes, such as pelvic floor dysfunction, and respond better to systemic therapy” (Lamb et al., 2017). In contrast, UIC respond to more localized therapy focused on the bladder when demonstrating the pathology consists of urothelial permeability defect. “As such, UIC and NUIC may have different disease etiologies and therefore differential biomarkers may be feasible” (Lamb et al., 2017).

Results:

L-8 contributed most significantly toward the predictions (48%), followed by GRO (33%) and IL-6 (19%).IL-6 also is a pro-inflammatory cytokine and has been previously reported to be elevated in IC, and may be reflective of general inflammation.  Additionally, although several groups have investigated the expression of IL-8 in IC, GRO has been less studied. It has also been reported to be increased in other urological disease, such as bacterial cystitis and bladder cancer.  This study also is a step forward in evaluating alternative methods of diagnosing IC that is less invasive, damaging and painful than the current methods available.

References

Lamb, L. E., Janicki, J. J., Bartolone, S. N., Peters, K. M., & Chancellor, M. B. (2017). Development of an interstitial cystitis risk score for bladder permeability. PLoS ONE, 12(10), e0185686. doi:10.1371/journal.pone.0185686

Mandal, Ananya. (n.d.)What are Cytokines? Retrieved 2018, April 30 from https://www.news-medical.net/health/What-are-Cytokines.aspx

Zhang, J. M., & An, J. (2007). Cytokines, inflammation, and pain. Int Anesthesiol Clin, 45(2), 27-37. doi:10.1097/AIA.0b013e318034194e