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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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Borrelia burgdorferi, is a bacterial infection that results from an infected tick, originally from mammals or birds, biting and injecting the microorganism into a human host. Individuals treated early in infection are likely to recover completely; however, delaying treatment may result in long recovery times, or result in disease that will last for years, or for life.

Infection Affects Multiple Organ Systems
Lyme disease can affect any organ or multiple systems including, skin, joints, nervous system, muscles, and skin. Early symptoms are a red, expanding rash, erythema migrans, that often appears at the tick bite site, and flu-like symptoms such as body aches, fever, chills, headache, and fatigue.

Left untreated, unfocused severe pain may, irregular heart beat and other heart problems, chronic inflammation of the joints (especially the knees, i.e., Lyme arthritis), liver inflammation (hepatitis) and eye problems. Unremitting fatigue, memory problems, and brain “fog” may also accompany the disease.

Incomplete recovery from Lyme disease may result in significant neurological problems, including Bell’s palsy (paralysis of one side of the face), weakness or numbness of limbs, impaired muscle movement, and meningitis (inflammation of brain membranes).

Twenty to fifty percent of patients with neurological issues may continue to experience difficulties for years.

Immune Responses to Lyme Infection
The extent of recovery from Lyme disease depends on factors such as the numbers of bacteria initially injected and the types of immune responses triggered by the infection.

As with healing from most infections, recovery from Lyme disease is a highly complex process requiring the correct interplay of inflammatory and anti-inflammatory cytokines, immune regulating molecules. Successful recovery requires a homeostatic, a balanced immune attack with enough inflammation to kill the organism without damaging by-stander cells and organs.

For example, the cytokine interleukin-6 (IL-6) stimulates inflammation but is also, depending on what the body needs, able to decrease inflammatory responses. (IL-6 is also triggers pain receptors and helps nerve cells regenerate.) Transforming growth factor-β (TGF-β) is another cytokine that helps the body control the amount of inflammation produced in response to infection.

Another cytokine, tumor necrosis factor-α (TNF-α) is an inflammatory cytokine that stimulates certain immune cells to find, engulf, and digest invading organisms. Mice susceptible to Lyme disease are unable to manufacture enough of this factor which may account for their susceptibility.

In humans as well, patients that were recovering well had significantly higher levels of tumor necrosis factor-α compared to those with on-going disease. Once again, these responses likely reflect the powerful inflammatory response that helps the body eliminate the disease.

Additionally, recovering infected individuals had higher levels of transforming growth factor than individuals with severe symptoms. These findings suggest that transforming growth factor was successfully limiting the amount of inflammation being produced in response to infection.

Similarly, in mice with Lyme arthritis, animals that did best were those in which high TNF-α cytokine levels helped kill the bacteria, followed by an aggressive IL-6 response that dampened the inflammatory response.

In further support of these findings, patients with rashes (early infection) had high levels of the anti-inflammatory cytokine, transforming growth factor, as compared to those who had more severe neurological involvement.

Conclusion:
The body uses inflammatory responses to protect itself from infection and heal itself. Inflammation helps the body destroy organisms, almost as if the body was “burning” the infection out. However, just like a forest fire, if inflammation is not well controlled the person with Lyme disease may suffer symptoms for years or for life. This is why it is essential for the body to produce a balanced, immune inflammatory response to infection.

 

Contact Dr. Hellen at: 302.265.3870 (ET), DrHellen@DrHellenGreenblatt.info, or by using the contact form: http://drhellengreenblatt.info/contact-dr-hellen.


www.mayoclinic.org/diseases-conditions/lyme-disease/basics/definition/con-20019701
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www.youtube.com/watch?v=xuTlC_0KzGU VIDEO
www.ncbi.nlm.nih.gov/pmc/articles/PMC2991005/

When I ask people for their typical dietary intake, many people “shamefully” tell me that they drink coffee.  It  surprises them when I ask “what is wrong with that”?  Coffee is a healthy addition to one’s diet because it can help the body regulate its  immune inflammatory responses.

Studies have shown that coffee consumption reduces the risk of conditions such as diabetes, neurological diseases, cardiovascular disease, certain cancers, depression,and back and neck pain to mention a few.

 Diabetes
Phytonutrients, plant compounds, other than caffeine, found in coffee, are reported to reduce blood sugar levels, and decrease the way the body stores carbohydrates and fats.  Data from over 450,000 people found that every additional cup per day of caffeinated or decaffeinated coffee lowers the risk of diabetes by 5 to 10%.  Heavy consumers of coffee, 12 cups/day, have a 67%  lower risk of getting diabetes.  The effect is not due to the caffeine found in coffee, but to other compounds in coffee.

 Parkinson’s Disease
In Parkinson’s disease, caffeinated coffee may protect nerve cells from destruction, decrease the incidence of Parkinson’s, and the improve mobility of individuals with Parkinson’s disease. In the case of Parkinson’s, the caffeine in coffee is the “magic ingredient”, since decaffeinated coffee does not have the same affect.  Women with Parkinson’s Disease, that were on hormonal replacement therapy, showed less benefit from coffee.  

Alzheimer’s and Dementia
As mentioned above, caffeine may help the body protect nerve cells. Consuming caffeinated coffee over a long period appears to decrease the risk of dementia or Alzheimer’s.

Heart Disease
In other studies, although coffee may raise blood pressure for a brief time, after two months of daily coffee consumption, blood pressure is reduced. It also lowers the risk of heart disease and reduces stroke incidents.

Cancer
Drinking one cup of coffee a day has been associated with a 42% lower risk of liver cancer.  Women that drank two or more cups of coffee per day had a delayed onset of a hard-to-treat cancer.  Individuals drinking three cups of coffee a day had a 40% lower risk of developing pharyngeal, esophageal, and oral cancers. Men who drank over six cups of caffeinated or non-caffeinated coffee a da,y had an 18% lower risk of prostate cancer, and a 40% lower risk of aggressive prostate cancer. Individuals that were heavy coffee drinkers had a 30% lower risk of colorectal cancer.

 Depression
A study of over 50,000 women, found that 4 cups of coffee daily lowered their risk of depression by 20%.

Coffee and Pain Responses
Subjects who consume coffee while working at the computer, report less pain in their back and necks than those that abstain from drinking coffee

Inflammatory Responses  and Coffee:
Regular coffee consumption affects the production of cytokines, such as IL-1 and IL-10 that regulate immune inflammatory responses. The data suggests that the benefits of coffee consumption are due to the phytonutrients, plant nutrients, and caffeine found in coffee. The adage that “coffee is not good for you”, should be re-examined.

 

Reach out to Dr. Hellen Greenblatt for simple steps to help the body balance inflammatory responses. 


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Alzheimer’s and IVIG Rx
Last week John Gever, Senior Editor, MedPage Today brought attention to the results of a small study presented at the 2012 Alzheimer’s Association International Conference held in Vancouver, British Columbia.  In this study, patients with mild to moderate Alzheimer’s were given antibody preparations, immunoglobulin preparations, which were obtained by pooling plasma from numerous blood donors.  This sterile, medical product, IVIG, intravenous immunoglobulin, consists mostly of immunoglobulins, antibodies,  and is administered intravenously (IV). 

After receiving IVIG twice a month for three years, patient’s ‘ ability to function or think, their mood, or memory did not worsen over the three years. [Untreated Alzheimer’s disease patients typically show measurable declines in 3 to 6 months.]

The FDA, The U.S. Food and Drug Administration, has approved the use of IVIG for only six conditions.  However, it has been used “off-label”, to try and treat about 50 other conditions, including infectious diseases, a wide-range of autoimmune conditions, organ transplant and cancer patients, blood, and neurological conditions to mention a few.

When practitioners are asked how s/he thinks IVIG works, the response is typically, except for infectious diseases, “we are not sure”.

 IVIG Contains Immunoglobulins and Smaller Immune Factors
IVIG contains antibodies to organisms such as streptococcus, hepatitis, measles, polio, etc., that can specifically neutralize infectious agents.  Other immunoglobulins may be directed  against specific immunological factors. 

However, viewing reported results in chronically ill populations, I have always been of the opinion that IVIG also contains cytokines, or cytokine-like immune molecules, with potent immune system-modulating properties, which help the body return to immune homeostasis, immune balance. 

 I suggest that the reason that Alzheimer’s patients receiving IVIG saw a stabilization of their symptoms, is that IVIG limited inflammatory responses and thus slowed the progression of disease.

 Alzheimer’s and Inflammatory Cytokine Levels
This supposition is further supported by the fact that animal models suggest that excessive production of inflammatory cytokines, inflammatory messages, are implicated in Alzheimer’s disease. These animals have a condition similar to human Alzheimer’s, and also have higher levels of inflammatory cytokines in their blood.  When a drug was administered that inhibited the cytokines, there was less damage to nerve cells and neurological outcomes in the animals improved.  

 The scientists suggest that blocking production of high amounts of inflammatory cytokines may be beneficial for any number of brain conditions, such as “Alzheimer’s and Parkinson’s disease, multiple sclerosis (MS), motor neurone disease, frontotemporal dementia, and complications from traumatic brain injury.” (1)

 Immune Homeostasis, Immune Balance the Key to Health
Thus improvements, or at least delay in the onset of Alzheimer’s, or other brain –associated conditions, may be associated with the body achieving immune homeostasis.  A body in inflammatory balance controls the immune system’s  inappropriate inflammatory responses which otherwise may lead to damage of bystander tissues.

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.medpagetoday.com/MeetingCoverage/AAIC/33780
http://emedicine.medscape.com/article/210367-overview#aw2aab6b3
www.alz.org/aaic/tues_1030amct_ivig_trial.asp
www.jneurosci.org/content/32/30/10201.abstract?sid=349221d1-e12f-411a-80a6-80285ed5db54
www.ncbi.nlm.nih.gov/pubmed/22806462

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