Anti-Inflammatory Strategies–Achieving Homeostasis
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Ebola virus disease (EVD), formerly known as Ebola hemorrhagic fever, is a severe, often fatal illness in humans. As of this post, the virus has spread through many African nations, and is the worst Ebola outbreak every recorded. The virus has infected over 1200 people and abuot 60% of these individuals have died from the disease.

Health practitioners have put themselves at great risk caring for those who have become infected. According to the BBC, one hundred health workers have been affected and half of them have died. At least three high-profile physicians in the forefront of care have succumbed to the virus, and three nurses who worked in the same treatment center as one of the physicians, are believed to have died from the virus.

Two Americans working to battle Ebola in Liberia, one a physician, have tested positive for the virus and are undergoing intensive treatment and workers from Doctors without Borders and the Red Cross are “overwhelmed” for the virus that has no cure.

Depending on the type of Ebola virus, up to 90% of those infected can die a rapid and difficult death. The onset of symptoms may be characterized by a sudden spiking fever, headache, joint, muscle, and stomach pain, diarrhea, vomiting, and in some cases, uncontrolled internal and external bleeding. Infected individuals die from failure of multiple organs in the body such as the nervous system, liver, and kidneys.

The disease is characterized by abnormal immune responses in which the Ebola viruses appear to evade attack of immune cells; dramatic immune imbalances occur in response to infection. There is evidence that the immune system responds with a “cytokine” storm during which certain immune cells “dump” large amounts of pro-inflammatory molecules, cytokines, into the body. Other biological compounds are released as well that contribute to the confused immune response.

Additionally, specialized cells produce insufficient amount of anti-viral cytokines, while at the same time, there is a significant increase in death of other types of immune cells. Scientists at the National Institute of Allergy and Infectious Diseases call this “a mixed anti-inflammatory response syndrome (MARS)”, and suggest that this “catastrophic uncontrolled immunological status contributes to the development of fatal hemorrhagic fever”.

Perhaps some of the symptoms that patients experience are due to autoimmune responses against individual classes of lymphocytes. This would account for the loss of certain immune cells, such as CD4 and CD8 cells. If they were available in higher numbers, they might be able to help the body fight the infection.

Many immunological factors contribute to Ebola virus fatalities. It is my contention that if  individuals were able to achieve immune homeostasis, immune balance, they would be better equipped to mount  controlled inflammatory responses which might help control the course of the disease.

 www.cdc.gov/vhf/ebola/pdf/fact-sheet.pdf
www.cdc.gov/media/releases/2014/t0728-ebola.html
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Over the last 18 months, at least 25 children have been affected in the California area by a “polio-like” illness resulting in partial paralysis of five of the children.  As of this week, two out of five of these children have tested positive for enterovirus.  According to the news media, Australia and Asia have also report similar cases.

A commonly found virus, enteroviruses typically result in only mild symptoms such as runny nose, coughing, muscle aches, and sneezing. However, there are 60 different varieties of enteroviruses, and infection with certain types of these viruses results in spontaneous abortion, stillbirth, and congenital anomalies.  Infection with other varieties of enteroviruses can lead to damage of various tissues including skin, muscles, brain, spine, nerve cells, liver, and heart.

Some enteroviruses appear to specifically target the brain and the nervous system, leading to short- or long-term paralysis affecting mobility. So for example, polio enteroviruses attack the nervous system triggering an inflammatory response to destroy the viruses.  The resulting inflammation may lead to mild paralysis, or to an individual becoming completely paralyzed within hours.

Some persistent enteroviruses survive in the body for a prolonged time with continued inflammation and damage to tissues.   So for example, polio patients that initially recover from their disease may continue to experience damage of nerve and muscle cells by inflammatory processes.  This resurgence of symptoms can result in a post-polio syndrome (PPS) years after their original exposure to the virus.

Individuals with post-polio syndrome have high levels of inflammatory cytokines, immune factors, in the spinal fluids between the thin layers of tissues that protect the spinal cord.  Other conditions resulting from enterovirus infection are often associated with the production of inflammatory molecules. Even patients with relatively mild symptoms and no nervous system complications may show increased blood levels of inflammatory immune factors.  This suggests that excessive inflammatory responses are occurring throughout the body.

A delicate balance exists between inflammatory and anti-inflammatory responses of the body.  The immune system is always on alert defending itself against infection.  However, once the process is triggered, the inflammation must be a measured, controlled response that does not destroy healthy tissue.

www.decodedscience.com/polio-like-virus-california-enterovirus-68-paralyzing-kids/43034
www.ncbi.nlm.nih.gov/pubmed/18219253
www.ninds.nih.gov/disorders/post_polio/detail_post_polio.htm
www.ncbi.nlm.nih.gov/pubmed/24367714
www.enterovirusfoundation.org/associations.shtml
www.ncbi.nlm.nih.gov/pubmed/22776106
 

Gut-associated lymphoid tissues are found in the walls of the intestine and contain billions of immune cells.  The white blood cells control the levels and types of bacteria that naturally populate the intestines.  The bacteria help to digest food that provides energy to the body,  and are part of the immune/bacterial ecosystem of the intestine.

 Interestingly, both immune cells and bacteria, protect the intestines from attack by pathogenic microorganisms, and cancer cells, and help heal the intestines when they are damaged.  Cross talk between the bacteria, and immune cells help the intestines maintain homeostasis, balance.  Each keeps the other in check.

 CELIAC DISEASE
Celiac disease is an intestinal, inflammatory, autoimmune (against oneself) disorder.  Individuals with celiac disease suffer from a wide-range of symptoms including diarrhea, fatigue, weight loss, inability to focus, skin and neurological issues, constipation, a feeling of being “bloated”, gas, anemia, headaches, osteoporosis (loss of bone density), and depression. 

 Ingesting grains, such as wheat, rye, and barley, which contain a component of protein called gluten, reportedly stimulate celiac disease.

 The presence of gluten stimulates sensitive immune cells to produce proinflammatory cytokines.  These immune messages drive inflammation, resulting in the destruction of the intestinal wall and symptoms.   Genetic, environmental, dietary, neuroendocrine, and immunological factors all contribute to disease progression.

 Currently, the primary guidance that celiacs get, is to go on a “gluten-free” diet.  Although it may be effective for some people,  such diets are restrictive, expensive, and do not work well for everyone.  In one study, every patient, 100% of those surveyed, in a cohort of 300 individuals, hoped for another option.

 OTHER APPROACHES
I often hear from people with autoimmune challenges such as celiac disease, “it’s genetic”.  Fine, so your genes are partially to blame. Meanwhile, what will you do? Continue to be uncomfortable?  So I ask those with inflammatory issues, why not consider short-term approaches until researchers discover longer-term solutions?  In three words: limit excessive inflammation.

 I like to describe inflammation as a way that the body “burns” out pathogenic microorganisms and cancer cells. The body must produce enough inflammation to protect itself from disease, and help the healing process, but not so much that healthy tissue, for example the intestinal lining, is damaged.

 Nutritional Approaches
Vitamin C and omega-3 fatty acids, from fish oil, inhibit the production of proinflammatory cytokines. (There is however,  evidence that vitamin A increases inflammatory processes.).

 Medical Approaches
Antibodies against specific inflammatory cytokines reduce intestinal injury in celiac disease, and the administration of corticosteroids, along with a gluten-free diet, was reported, in a small clinical trial, to provide benefit to celiac patients.

 Immunological Homeostasis/Balance
Hyperimmune egg, an ingredient that helps the body return to immunological balance, helps to support gastrointestinal health.  Many individuals with digestive issues report daily consumption of hyperimmune egg leads to major differences in their quality of life.

 LIMIT INFLAMMATION FOR BETTER HEALTH
The key to a higher level of quality of life in celiac and other autoimmune and autoinflammatory conditions, is to help the body limit its excessive inflammatory responses.  Removing gluten from one’s diet, using vitamin C, omega-3, corticosteroids, and hyperimmune egg, may contribute to helping the body regulate run-away inflammation.

Feel free to contact Dr. Hellen at DrHellen@DrHellenGreenblatt.info with questions or to consult with her. A message may also be left at: 1.302-265.3870 or click on: http://drhellengreenblatt.info/contact-dr-hellen/.


www.cell.com/cell-host-microbe/retrieve/pii/S1931312812000662

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Recently, a professional networking site directed me to a short note by Lisa Moreno-Dickinson, President of the stopcaidnow.org. The title of her article was “When Doctors Don’t Know How to Help From Misdiagnosis to No diagnosis … What Can a Parent Do?”.

CAID refers to Childhood Auto Inflammatory Diseases. These genetic disorders usually start in infancy or childhood and are reported to be the result of gene mutations. The periodic attacks of these conditions affect many different organ systems. They are characterized by sudden inflammation and fever onset, and symptoms such as rashes, headache, abdominal, chest, muscle, and joint pains, swollen joints and scrotum.

Much of the science suggests that these conditions are not autoimmune in nature. These individuals have no any significant elevations of autoantibodies, immunoglobulins, large immune molecules that are directed against self, nor activation of specific white blood cells.

Our knowledge of the complexities of the immune system, especially its inflammatory pathways, are still in their infancy as supported by the fact that cancer, colds, infectious, and chronic diseases are rampant.

I respectfully suggest that perhaps autoinflammatory investigators have not used the appropriate assay to find autoimmune responses because a) it does not exist yet, or b) it is difficult to “test for everything”.

A recent report suggests that there is an association between autoinflammatory conditions and mitochondrial health. Mitochondria are the power stations of a cell that provides it with the energy it needs to grow, divide, and “do its job”. They play major roles in healthy aging, degenerative diseases, cancer, and ultimately, cell death. The greater its metabolic or energy requirements, the more mitochondria a cell appears to have. As an example, a muscle cell may have thousands of mitochondria and a skin cell only a few hundred.

Antibodies to mitochondrial proteins have been reported in autism spectrum disorders, which are attributed to inflammatory conditions of the nervous system. Additionally children with severe autism have higher levels of inflammatory cytokines and certain immune molecules than controls.

In Blau’s syndrome, an autoinflammatory disease, symptoms are associated with the skin, joints, and eyes. It is often mistaken for sarcoidosis, a known autoimmune disease of the skin and other organs. Crohn’s disease is an inflammatory autoimmune bowel disease in which the immune system attacks its own digestive lining.

There are two genes, NOD1 and NOD2 that help regulate the production pro-inflammatory cytokines, immune molecules that cause inflammation. Mutations of these genes are found in a number of inflammatory disorders including Blau’s syndrome, sarcoidosis, and inflammatory bowel diseases.

Investigations of the pivotal role of gene regulation of inflammatory responses are underway; however, ways to neutralize the effects of such mutations may be years away.

Parents and clinicians do not have the luxury of just waiting. We know that inappropriate inflammatory responses are occurring in many, so why not determine whether the re-introduction of immune homeostasis, immune balance would make a difference in their quality of life?

 

www.parentsociety.com/parenting/when-doctors-dont-know-what-to-do-or-how-to-help/?goback=%2Egde_151241_member_74525704

www.ncbi.nlm.nih.gov/pmc/articles/PMC2735099/

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