Anti-Inflammatory/Anti-Aging Strategies
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One of the major complaints that people have is that “they are always tired”. “They just do not care anymore, they are just too tired.” [Kindly view a post that is relevant to this subject: Depression, Anhedonia and Run-Away Inflammation.]

In the past, scientists thought that there was a blood-brain barrier that “isolated” the brain from the actions of the immune system. They labeled the brain “immune privileged”; because studies suggested that a healthy brain had few, if any inflammatory cells in it. Only when there was a brain infection did scientists think that immune cells migrated into the brain.

Researchers failed to take into account that chronic inflammatory diseases are associated the brain. For example conditions such as inflammatory bowel disease, psoriasis, liver disease, and rheumatoid arthritis may result in a lack of social interest, feelings of being unwell and unremitting fatigue—all which are governed by brain function.

Inflammation is activated when the body encounters pathogens and cancerous cells. The inflammatory response is a primary means by which the body will destroy these threats. Inflammation is basically a controlled “burn”.  Firefighters will often have a “controlled burn” in a forest to get rid of dead trees and limbs.  They strive to keep the fire limited to a specific area.  Sometimes however firefighters are unable to control the fire and acres of forest are burned in error.

Similarly, once immune cells have taken care of a threat to the body, for example cancer cells, pathogens, etc., it is essential that the immune system “turn” down the inflammatory “flame”. Chronic, unnecessary inflammation leads to many autoimmune diseases that destroy their own organs, such as diabetes, Crohn’s bowel disease, multiple sclerosis, and lupus

Inflammation is all about location, location, location. If one has inflammation in the insulin-producing cells that control blood sugar, the person may get diabetes. If their intestines are inflamed they may suffer from Crohn’s.  If there is too much destruction and inflammation of nerve cells, they may suffer from multiple sclerosis.

Let us hypothesize that an individual has two trillion immune white blood cells and that half of these cells are out of control and producing too strong an inflammatory response. This inflammation is destroying previously healthy tissues and organs.  Since the body is always striving to balance inflammation, the other half a trillion of cells are working towards lowering the amount of inflammation and destruction that is going on in the body

Each of these cells is expending a trivial amount of energy trying to accomplish its task, but a tiny amount of energy multiplied by two trillion cells is a great deal of “wasted energy”. Is it any wonder why these people complain of being tired?

Individuals who have been diagnosed with autoimmune conditions have higher levels of inflammatory cytokines, immune messages, than people without disease. In heart failure patients, significant fatigue is associated with poor recovery and a higher risk of death. Patients with high levels of anti-inflammatory cytokines, molecules that decrease inflammation, recover more fully and rapidly than patients with high amounts of inflammatory cytokines. When patients are treated for their heart problems, their cytokine levels begin to resemble the cytokine ratios of healthy individuals, and their energy returns.

In mice with liver inflammation, immune cells from the liver travel to the brain and trigger other specialized immune cells called microglia releasing a biochemical that attracts more inflammatory cells into the brain, which in turn produces more inflammation.

In individuals with multiple sclerosis, a nervous system disease with a major inflammatory component, patients had less fatigue when they took anti-inflammatory medications.

The association of appropriate levels of inflammation with a healthy brain and high energy reserves is clear; the key is being in immunological balance. Once individuals balance inflammatory and anti-inflammatory cells they typically regain their energy and focus.

Aren’t you tired of being tired all the time? Don’t wait any longer. Contact Dr. Hellen to talk bout enhancing your quality of life.  There is no fee for consulting with her for the first 30 minutes.  She may be contacted by using this form or at: 302.265.3870 (ET, USA).

http://www.ncbi.nlm.nih.gov/pubmed/25905315
http://www.ncbi.nlm.nih.gov/pubmed/25905315
www.ncbi.nlm.nih.gov/pubmed/26589194
http://www.the-scientist.com/?articles.view/articleNo/43120/title/Brain-Drain/
http://www.ncbi.nlm.nih.gov/pubmed/26705751
http://www.ncbi.nlm.nih.gov/pubmed/25682012

 

Depression, Anhedonia and Run-Away Inflammation

Posted on Sunday, November, 29th, 2015 by Dr. Hellen in Uncategorized

Without the ability to produce inflammation we die.  The inflammatory response is the main weapon that the immune system uses to protect us from infection, keep cancer cells from growing out of control, and help tissues heal when they are damaged.

However, one has to have the right balance of inflammation to be healthy.  We need enough inflammation to protect us, but  too much of an inflammatory response leads to increased risk of developing diseases such as irritable bowel disease, multiple sclerosis, arthritis, lupus, and diabetes.

The mind as well as the body is negatively affected by run-away inflammation. Emotional problems such as depression, spikes of high or low moods (bipolar disorders), or schizophrenia are accompanied by uncontrolled inflammation.

Genes control the amount of inflammation that the body produces. When “inflammatory” genes are turned on, up-regulated, immune cells produce cytokines, inflammatory immune messengers, along with biological compounds such as C-reactive protein (CRP).

LONELINESS AND ANHEDONIA

Loneliness and feelings of isolation are linked to an increased risk of chronic disease and death and are associated with increased levels of inflammation.

Some depressed individuals experience anhedonia, a condition in which they   lack motivation and do not enjoy  life.  These people find no joy in food,   spending time with their family or friends, concerts, or activities that others find pleasurable.

Individuals with anhedonia experience persistent brain inflammation, among other biological events and typical treatments for depression are often not helpful.

BRAIN REGIONS COMMUNICATE WITH ONE ANOTHER

Different parts of the brain communicate with one another as they control a person’s response to pleasure and rewards such as social interactions, food and sex.  Reacting positively to these stimuli motivates one to repeat them in the future.  The ability of these regions to communicate with one another is called “connectivity”.

Individuals with low connectivity have increased inflammation and deeper feelings of anhedonia.  High CRP (an inflammatory marker) levels were also correlated with the inability to experience pleasure.

One of the medications used for individuals suffering with anhedonia is infliximab.  This medication is prescribed for patients with inflammatory conditions such as bowel disease and arthritis.  Additionally, administrating cytokines, immune messengers of inflammation, changes the reward-related regions of the brain.

DOPAMINE
style=”text-align: justify;”>Dopamine, which is produced brain cells, is strongly associated with the brain’s pleasure/reward regions. Dopamine helps us feel enjoyment and motivates us to participate in or continue to engage in activities that give us pleasure.

Decreased production of dopamine is associated with heighted inflammation and decreased connectivity between the pleasure centers of the brain. Administering inflammatory cytokines over a long period of time may lead to decreases in dopamine production.

THE LINK BETWEEN PHYSICAL ACTIVITY AND DEPRESSION

Every time muscles contract, they release anti-inflammatory molecules that help the body balance the amount of inflammation it produces.  Additionally, exercise activates the brain’s pleasure centers. The evidence shows that there is a strong link between physical activity and mental and physical health.

Regular physical activity decreases one’s risk of depression.  Researchers tracked individuals that experienced their first heart attack and had been physically active for 10 years prior to the event. Heart attack survivors who exercised for years prior to the event had a 20% lower risk of developing depression compared to individuals that had not been physically active.

Also, people who had become physically active before their first heart attack had a better protection against depression compared to those who had been active at one time,  but then became inactive.

SUMMARY

Increased inflammation has been associated with depression and other negative emotional states.  Maintaining the body’s balance of inflammatory and anti-inflammatory responses helps support healthy emotional responses.

Dr. Hellen’s major passion in life is helping people to enjoy life at its fullest. She may be contacted by using this form, at  drhellen@drhellengreenblatt.info, or at:  302.265.3870 (ET, USA).

 

http://www.npr.org/sections/health-shots/2015/11/29/457255876/loneliness-may-warp-our-genes-and-our-immune-systems
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www.pnas.org/content/early/2015/11/18/1514249112.full.pdfcause-illness-and-early-death.html
www.psychologytoday.com/blog/the-compass-pleasure/201104/exercise-pleasure-and-the-brain
http://www.pnas.org/content/early/2015/11/18/1514249112.abstract
www.psychologistworld.com/biological/neurotransmitters/dopamine.php

Asthma: An Inflammatory Syndrome

Posted on Wednesday, October, 28th, 2015 by Dr. Hellen in Allergies | Chronic Disease | Inflammation

Asthma is an inflammatory condition which affects the lungs in negative ways. It is not a single disease, but a group of symptoms that arise from the abnormal immune responses to environmental triggers.

Asthmatics suffer from limited air flow, difficulties in breathing, heightened sensitivity to particles or toxins in the air, wheezing, coughing, and tightness of the throat and chest.

Asthma can be triggered by allergens, air-borne pollutants, upper respiratory infections (like a cold or the flu), exercise, and nonsteroidal anti-inflammatory drugs, such as acetaminophen.

The cells that line the airways, the epithelium, are the first point of contact when particles are inhaled. Until recently, scientists were unaware that these cells contribute to inflammatory responses within the lungs.

Scientists are busily trying to clarify the role of over 50 different cytokines that are involved in regulating the amount of lung inflammation that asthmatics experience. When challenged with antigens, lung cells produce great numbers of inflammatory cytokines, immune messages. These immune factors regulate the activity of genes that result in inflammation and the body’s efforts to control inflammation.  Inflammatory cytokines increase the levels of inflammation to help the body remove the antigens, while other cytokines dampen excessive immune responses, trying to bring inflammatory responses back to balance.

Structural changes in the airways result from the actions of different classes of inflammatory cells and their immune proteins and biologically active molecules. Lung cells can also release molecules that cause the muscles and blood vessels in the airways to become stiff and narrow.

The lungs become overly sensitive to environmental stimuli triggering the production of excessive levels of mucus, perhaps to help dilute and wash antigens out. These fluids can clog the airways of the lungs making it even more difficult to breathe. The hypersensitivity of the lungs results in a vicious cycle of over-active immune reactions, inflammation, and more mucus production.

10.28.15 Ashma PNG grpahic

 

As always the key to healthy immune support is balance. The body needs to produce enough inflammation to help us heal and protect us from external and internal challenges, but the inflammatory response must be well balanced and controlled.

Dr. Hellen’s major passion in life is helping people get more energy, become more productive, and enjoy life at its fullest. She may be contacted by using this form, drhellen@drhellengreenblatt.info, or at: 302.265.3870 (ET, USA).

www.gluegrant.org/inflammation-asthma.htm
http://jaoa.org/article.aspx?articleid=2094079
http://www.worldallergy.org/professional/allergic_diseases_center/cytokines/
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Delirium is an under-reported condition that may affect up to 56% of older individuals after surgery, patients that have been heavily sedated for a length of time, burn, cancer, and patients on ventilators for long periods. Patients experience vivid hallucinations that may be part of a vicious cycle if doctors attempt to control the delusions with larger amounts of sedatives; the medications may disorient and confuse the patient even more.

The delusions and accompanying cognitive issues can persist for months after patients leave the hospital and can lead to a misdiagnosis of dementia, rather than delirium. [Dementia develops gradually and gradually worsens, while delirium may be of sudden onset.]

Delirium is associated with excessive inflammation in the brain resulting from triggering specialized immune cells the microglia. If stimulated over a long time, the cells release inflammatory cytokines, molecules that damage nerve cells and contribute to damage and break down of the capillaries in the brain, the blood-brain barrier.

C-reactive protein, CRP, is one measure of inflammation. CRP levels were measured in elderly surgical patients who had ended up with complications such as delirium, cardiovascular issues, or infection. The levels of CRP in their blood were predictive as to how fully they recovered.

A recent study measured the levels of 12 different inflammatory and anti-inflammatory cytokines in older patients undergoing surgery. Those having episodes of delirium had consistently high levels of inflammatory cytokines as compared to patients that did not have high levels of cytokines. Similar results were seen in patients that developed delirium after procedures such as open-heart surgery and hip fracture repair.

Conclusion

In order for the body to heal after it is hurt, or to fight an infection successfully, a delicate balance of cytokines, immune messages are required. Too little of an inflammatory response and the individual may not survive an infection. Too much of an inflammatory response and healthy tissue is destroyed. Homeostasis, balance, is what the body strives for every moment.

Dr. Hellen would be pleased to provide guidance to helping enhance your quality of life.  She may be contacted by using this form or at: 302.265.3870 (ET, USA).

 

www.theatlantic.com/health/archive/2015/06/the-overlooked-danger-of-delirium-in-hospitals/394829/
www.mayoclinic.org/diseases-conditions/delirium/basics/definition/con-20033982
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www.ncbi.nlm.nih.gov/pubmed/17504139

 

 

For over two decades I have noticed that individuals in immune homeostasis, immune balance, are on fewer medications or no medications than their cohorts, and the majority of them look and feel 10 years younger than other people their age. Comparing photos of how these individuals look now with photos as how they looked 10-20 years ago, it is amazing how great they look! Their youthfulness is especially apparent when I compare these photos to those of individuals that have not made the effort to control inflammation.

Too many older individuals suffer from chronic inflammatory diseases such as arthritis, diabetes, cognition deficits, Parkinson’s disease, lung, kidney, and bladder problems. Over the years there have been numerous studies associating chronic (long-term) inflammation with the development of mutating cells and cancers. However because of the time it takes to do longevity studies it is difficult to prove that limiting inflammation makes a difference in how well people age.

Just this month, a team of scientists from Keio University School of Medicine, Tokyo, Japan and the Newcastle University’s Institute for Ageing in the UK published a study of the immune status of over 1500 individuals ranging in age from 100-115 years.

The study group was divided into two: centenarians, 100-104 years of age, and semi-supercentenarians aged 105 and above. The result was that these long-lived individuals had lower levels of inflammation as compared to the general public.  

Dr. von Zglinicki, one of the investigators, said, “Centenarians and supercentenarians are different – put simply, they age slower. They can ward off diseases for much longer than the general population… it’s only recently we could mechanistically prove that inflammation actually causes accelerated ageing in mice…This study, showing for the first time that inflammation levels predict successful ageing even in the extreme old….”

Dr. Yasumichi Arai, the first author on the study said, “Our results suggest that suppression of chronic inflammation might help people to age more slowly…However, presently available potent anti-inflammatories [medications] are not suited for long-term treatment of chronic inflammation because of their strong side-effects. Safer alternatives could make a large difference for the quality of life of older people.

As I have pointed out for decades, controlling the delicate balance of inflammatory responses, i.e., achieving immune homeostasis, makes all the difference in one’s youthfulness and quality of life.

P.S.  My post of May 20, 2013 also discusses the role of inflammation in longevity.

Please contact me directly if you would like to learn simple approaches to making a difference in your health.
http://www.ncl.ac.uk/press.office/press.release/item/scientists-crack-the-secret-of-the-centenarians
http://www.ebiomedicine.com/article/S2352-3964(15)30081-5/fulltext
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Idiopathic pulmonary fibrosis (IPF) is a disease in which the tiny air sacs or “alveoli” that make up the lungs become inflamed and are gradually replaced by scar tissue (fibrosis).  As the amount of scar tissue increases, the lungs stiffen and are unable to transfer oxygen from the lungs to the blood stream. This results in the brain and other organs becoming oxygen deprived.

As  IPF progresses, day-to-day activities such as walking short distances, climbing stairs, dressing, or even talking on the phone become a problem because the person cannot catch their breath (dyspnea).  The person feels as if they are suffocating and may require supplemental oxygen.

Advanced idiopathic pulmonary fibrosis makes people more susceptible to getting and fighting infections.

The term “ idiopathic” suggests that clinicians do not know what causes the disease.  Lung inflammation may be triggered by infection with pathogens, airborne hazards, or certain types of medical treatments.  Exposed to these types of challenges, the immune system boosts its inflammatory response to attack the pathogens and remove hazards or damaged tissues.  In a vicious cycle, the uncontrolled inflammation results in greater lung damage.

Idiopathic pulmonary fibrosis may be considered an inflammatory autoimmune disease.  Autoimmune (meaning against oneself) conditions result from the body’s overactive, defensive, inflammatory reactions to an immune challenge.  The  body’s own immune cells mistakenly attack and destroy previously healthy by-stander tissues or organs, very much like a forest fire damages healthy trees.

The body responds to injury by forming scar tissue, made mainly of the key protein collagen. Pulmonary fibrosis results in inflammation and scarring that occurs again and again.  It is an imbalance between the build-up of scars, and the breakdown of collagen that is needed for tissue repair.  In IPF, lungs with old scar tissue is found layered over old damage, while fresh scarring is seen over more recent damage.

 Lung damage in IPF patients is due to imbalances between inflammatory and anti-inflammatory cytokines, immune messengers generated in response to substances or circumstances that initiated the lung damage in the first place.  Imbalances of cytokines results in more and more fibrosis.

Individuals with IPF may find that if they are able to control the amount of inflammation produced by their immune systems, if they can stay in homeostasis, balance,  their quality of life may change for the better.

Please contact Dr. Hellen if you wish her assistance in changing your quality of life. There is no fee for her services.  She may be contacted by using this form or at: 302.265.3870 (ET, USA).

 

www.coalitionforpf.org/cytokine-functions/
www.nhlbi.nih.gov/health/health-topics/topics/ipf
www.ncbi.nlm.nih.gov/pubmed/26132817
www.immuneworks.com/autoimmune-lung-diseases/idiopathic-pulmonary-fibrosis-ipf-treatments
www.ncbi.nlm.nih.gov/pubmed/26150910
faculty.ksu.edu.sa/hadilalotair/Chests%20Library/IPF.pdf

 

 

Middle East Respiratory Syndrome (MERS) is a viral disease of the lungs that was first reported in Saudi Arabia in 2012 and has now spread to several other countries, including South Korea and the United States. Genetic material isolated from an individual that died of MERS was identical to genetic material found in one of his own camels. The infected camel possibly infected the owner and is responsible for the death of the man.

 People infected with the virus initially report mild symptoms of a cold, chills, body aches, sore throat, fever, difficulty in breathing, and a cough.  Some individuals report gastrointestinal issues such as diarrhea, nausea, and vomiting.  When symptoms become severe, death may follow failure of the lungs and kidneys.

Most of individuals that have succumbed to infection with MERS suffered with other medical conditions, such as diabetes, cancer, chronic lung conditions, heart, or kidney disease.

MERS and SARS

There is limited scientific information on MERS.  However, the MERS virus is in the same family of viruses as SARS, the virus that causes severe acute respiratory syndrome. Infection with this virus results in severe breathing difficulties which too frequently results in death. (Both the traveling businessman and his World Health Organization physician, Dr. Carlo Urbani who identified the infection as a new disease in the business person, died of the virus.)

 Although there are similarities in symptoms, two major differences between MERS and SARS are: a) MERS progresses to lung failure more rapidly than SARS and b) MERS affects older individuals more than it does younger people. [The high numbers of fatalities from MERS may be related to the older age of infected persons and the fact that individuals with other conditions are more susceptible to respiratory failure].

 Since so little is understood about the disease, people with diabetes, lung, kidney, and immune disorders should take precautions if they are exposed to infected individuals.

The Immune System and Infections

The only part of the body that protects us from infection is our immune system. The role of the immune system is to recognize threats from pathogens, stop, and then up regulate inflammatory responses to destroy the pathogens before they can multiply.

 When the immune system is recognizes invasion by pathogens, immune cells are triggered to produce antibodies and other immune factors, such as cytokines. Cytokines are proteins that help recruit immune cells into an area to help fight the battle, and orchestrate the protective immune responses.In SARS, an over-response of the immune system,  a “cytokine storm” occurs that too often results in the deaths of infected persons.  It is likely that infection with MERS triggers the production of high levels of cytokines, resulting in excessive inflammation and death.

Summary:

People with unbalanced immune systems are at higher risk of having severe symptoms when infected with pathogens.  It is essential that the immune system always be in balance, in homeostasis for optimal protection from disease.

The inflammatory response to infection has to be a controlled, limited response. There must be enough of an immune response to defend the body against disease, but not so great an inflammatory response that the body is harmed.


www.cdc.gov/coronavirus/mers/
www.nejm.org/doi/full/10.1056/NEJMoa1401505
www.nlm.nih.gov/medlineplus/ency/article/007192
www.cdc.gov/coronavirus/mers/
www.nejm.org/doi/full/10.1056/NEJMoa1401505

Mutating cells and invasion by pathogens triggers inflammatory responses in the body.  Inflammation consists of a series of events involving cytokines (immune messages), other immune factors, and circulating white blood cells. Uncontrolled levels of inflammation damages healthy tissues and organs.

Excessive inflammation of the eyes may result in sight-threatening condition.

Uveitis
Uveitis describes a group of eye inflammatory diseases.  Symptoms can develop gradually over a few days, or occur suddenly. Symptoms may include: photophobia (sensitivity to light), cloudy or blurred vision, increased floaters, difficulty in vision focus, headaches, “red eye” with pain ranging from a mild ache to intense pain, and loss of peripheral vision (ability to see objects at the side of one’s field of vision). Severe uveitis may lead to permanent damage to vision.

Many cases of eye tissue inflammation are “idiopathic”, i.e., without a known trigger.  Some clinicians suggest that uveitis is caused by:  a) autoimmune responses in which the body’s immune system mistakenly targets and attacks its own eye tissues, b) infections or cancer, c) trauma to the eye, or d) exposure to toxins.  Uveitis is more likely to occur in individuals that have other immune and inflammatory conditions.

Ebola and Uveitis
Two months after an American physician was treated for Ebola, and despite the fact that the virus was no longer detectable in his blood, there were high levels of Ebola virus in his eye. His eye infection was accompanied by an intense inflammatory reaction, uveitis. After much effort, the physician was successfully treated and thankfully  did not lose his sight.

In a study of 85 Ebola Virus Disease survivors in Sierra Leone, 40% reported that they had some sort of “eye problem”. (It is not known whether they also had uveitits.)

Retinitis Pigmentosa
Retinitis pigmentosa is a genetic disorder in which the light-sensitive retina, the “screen” at the back of the eye that captures images, becomes damaged .  Its photoreceptors,  rods and cones, begin to die off resulting in a  loss of vision.  This condition may end in blindness.

There are conflicting opinions as to whether inflammation plays a major role in this disease.

One study that support the contention that immune responses are involved in retinitis pigmentosa measured the levels of TNF-alpha.  TNF-alpha is a cytokine, that among other functions, helps regulate immunological responses. Depending on when and how much of the cytokine is produced , TNF-alpha may be pro-inflammatory (initiate inflammation), or anti-inflammatory (inhibit inflammation).   In animals with uveitis-like conditions, the levels of TNF-alpha in the eye are  increased between 5-10 fold over control animals.

Also,  in retinitis pigmentosa, immune white blood cells are attracted to the retina, perhaps to clean up debris from dying cells. Some investigators suggest that when these immune cells are overly stimulated, they initiate an autoimmune response, destroying other light-sensing centers in the retina.

Immune Homeostasis, Immune Balance
Immune inflammation is essential to defend the body against cancerous cells and invading microorganisms.  However, the appropriate levels of  “protective” cytokines are needed to balance the “destructive” cytokines produced in the eye so that it can maintain immune homeostasis, immune balance. Unchecked inflammation results in tissue damage and an inability of the body to mount stable and proper immune responses in the face of various challenges.

Dr. Hellen is available at 302.265.3870 for discussion on the role of inflammation and immune homeostasis in one’s health.  There is no charge to speak with her.  She may be contacted at: drhellen@drhellengreenblatt.info, or use the contact form.  Thank you.

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www.ncbi.nlm.nih.gov/pubmed/24174679
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Parkinson’s is a disease of the nervous system that affects mobility, memory, and cognition.  Individuals may eventually experience rigid muscles, tremors of the limbs and head, loss of muscle control, monotonous speech levels, and a slow, shuffling gait.

Individuals tend to develop the disease as they age. Having a close relative with Parkinson’s disease (PD) increases the likelihood of developing Parkinson’s, with men more than 1.5 times more likely to develop the disease than females.

Although the causes of Parkinson’s disease are not clear, a recent study suggests that individuals with a specific gene are at a higher risk of getting Parkinson’s disease if they were exposed to pyrethroids, a class of chemicals found in the majority of household insecticides.  Exposure of individuals to these pesticides may result in brain tissue inflammation.

Inflammation and Autoimmune Responses

In Parkinson’s disease, the body mounts an inflammatory response against its own brain cells, its dopaminergic neurons. (An immune response against oneself is called an autoimmune response.)

These specialized brain cells produce a biochemical called dopamine with many functions including controlling bodily movements, memory, ability to think, mood, and learning.  The body’s long-lasting inflammatory response against its own nervous cells gradually destroys the dopaminergic neurons resulting in abnormal dopamine levels and brain activity, symptoms associated with Parkinson’s disease.

Microglial cells are specialized immune cells located in the brain. They are considered the “canary in the mine”.  When microglial cells sense a threat, they become “activated” and release immune factors that may, depending on the types and amounts of these molecules, be beneficial or cause damage to nerve cells.

Activated microglial cells are found in large numbers in the brains of Parkinson’s patients, along with high levels of cytokines, biochemical molecules responsible for inflammation.

The brain and spine of the nervous system are cushioned by cerebrospinal fluid. This fluid helps to provide nutrients to the nervous system and removes waste products from the brain.

Individuals with Parkinson’s disease have high levels of immune inflammatory molecules in their spinal fluid.  The more concentrated the molecules, the more likely the person is to severe fatigue, depression, and cognitive impairment.

Summary

Certain genes that control immune system responses are also strongly linked with the development of Parkinson’s disease.

Increasingly, scientific studies suggest that inflammation and autoimmune responses result in Parkinson’s disease.

Helping the body limit out-of-control inflammation, and achieving a more homeostatic, more balanced immune response, may go a long way towards changing the quality of life in individuals with Parkinson’s.

Feel free to contact Dr. Hellen. There is no fee for speaking with her. Dr. Hellen may be contacted by using this form or at: 302.265.3870 (ET).

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Immediately after the body is injured, it starts the processes of stopping blood loss, restoring function, and preventing infection from pathogens on the skin or objects that may have caused the damage. The microenvironment of the injured area is in constant flux with the host cells continuously responding to the fluids, bacteria, and the dead and dying cells at the wound site.

One of the first phases of the healing process is for circulating platelets to attach to a fibrous scaffold, a matrix, to stop blood flow. Platelets, recently defined as immune cells, release cytokines, immune messengers, which permit cells to communicate with one another.

 Once the flow of blood ceases, specialized immune cells enter the area setting up an inflammatory response that “cleans” the wound site and removes bacteria, damaged tissues, and foreign matter. In order to achieve the appropriate levels of inflammation, many complex cell-to-cell interactions occur in specific order.

Accumulation of fluids, exudates, results from inflammation, along with swelling at the wound site. Exudates are essential for the healing process and contain debris, inflammatory cells, bacteria, and a large variety of immune proteins. Depending on their concentrations, factors may enhance healing or interfere with the process. Proteins found in exudates have a variety of functions including regulation of inflammatory responses, triggering growth of new blood vessels, and stimulating growth of new cells.

A delicate balance of inflammatory and anti-inflammatory messengers is crucial and it determines the pace, and outcome of healing. Homeostatic, balanced, inflammatory responses are essential. Too little, too great, or too lengthy of an inflammatory response damages healthy tissue and delays healing.

The remodeling phase is one where tissues regenerate and close the wound. Closure occurs as cells cross-link and organize themselves attaching to a scaffold, a matrix that will draw edges of the skin closed and cover the area.

Poorly Healing Wounds

The presence of bacteria, foreign bodies, a lack of oxygen in the tissues, and/or fragments of necrotic, dead, tissue can stimulate inflammatory cells continuously, resulting in uncontrolled inflammation and wounds that heal poorly.

Infection of a wound site also interferes with proper healing. Communities of bacteria tend to organize themselves into a biofilm, a thin sheet of bacteria. Biofilms increase survival of bacteria colonies, reducing chances that inflammatory immune responses, or antibiotics, can control them.

Exudates in poor healing wounds contain an over abundance of inflammatory cells and immune mediators that increase inflammation. Sufficient anti-inflammatory factors to control the damaging effects of excessive inflammation may not be available.

Proteolysis is another one of the steps required for healthy healing. This is an event during which the body degrades necrotic tissue, and dead and dying pathogens. [Think of proteolysis as an acid/enzyme reaction that breaks down tissues.] When immune cells release too many proteolytic proteins over a longer period, they become destructive of healthy tissue, and the body’s ability to heal the wound is overwhelmed.

Individuals with non-healing skin ulcers, such as those found in diabetics, not only struggle with excessive inflammatory responses, but their proteolytic enzyme levels are significantly elevated giving rise to further imbalances in inflammatory responses and interference with the body’s repair mechanisms.

Summary

The sensitive balance between stimulating and inhibitory mediators during diverse repair of wound is crucial to achieving tissue homeostasis following injury. Once unbalanced and excessive inflammation is controlled, will healing begin.

 
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