Tuesday, November 7, 2017

Serracor and #Fibromyalgia Facts

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Fibromyalgia 


Before 1976, fibromyalgia was most commonly known as fibrositis, where “itis” implied an inflammatory component. Despite the understanding of inflammatory pathways to pain, clinical research was unable to identify the role of inflammation in fibromyalgia for many years.

Within the last decade, fibromyalgia research has once again been focusing on the possible contribution of inflammation to disease progression, and is finding some new and interesting results.

Clinical studies have produced evidence that fibromyalgia is associated with the immune system’s improper regulation of proinflammatory cytokines that circulate in the bloodstream, contributing to the dysfunction of the central nervous system and pain-related neurotransmitters. Cytokines, depending on their concentration, induce symptoms, such as fatigue, fever, sleep, pain, and muscle pain, all of which develop in fibromyalgia patients.

These findings are uncovering new possibilities in research for fibromyalgia causation, as well as treatment options. Some experimental pain reduction therapies have been examined and shown positive results, correlating with decreased proinflammatory cytokine levels.7 Anticonvulsant drugs, analgesics, opiods and anti-depressants are commonly prescribed to fibromyalgia patients, but tend to carry side effects reflective of the syndrome itself,and many of which lack evidence for effectiveness.

Limited treatment options have led to an increasing use of systemic enzyme therapy as a means to alleviate symptoms and improve quality of life. Certain proteolytic (protein digesting) enzymes have been identified to have extremely beneficial actions when applied to inflammation and pain related to this condition.
 

It has long been known that people with chronic muscle pain or fibromyalgia have more fibrin in their tissues and blood. This fibrin, while initially helpful in the early stages of healing after an injury, can become problematic if the body does not clear itself of the agent after it has done its work.

Fibromyalgia sufferers experience micro-tears in their muscles from the normal activity of daily living — each and every day. But because the average fibromyalgia patient does not achieve and stay in stage 4 delta sleep at rest, growth hormone is not produced in enough quantities to heal these tears, which leads to more fibrin buildup.

For the most part, people with fibromyalgia do not have a strong enzymatic capacity for producing enzymes that break down fibrin. This leads to a buildup of fibrin, which over time catches red blood cells in a web of restriction. This fibrin causes a restriction of blood flow. Red blood cells literally become stuck, disabling them from getting into the capillaries to oxygenate and nourish the muscles where the metabolic waste that causes pain is removed.

The body uses fibrin to help heal itself after an injury. However, if you have poor blood flow and a lack of enzyme activity, fibrin will start to accumulate. If the injured area is slow to heal, fibrin accumulation appears as clumps of scar tissue in the muscles or at a surgical site.

Ultimately, if excess fibrin is present throughout the circulatory system, blood flow is restricted to areas of the body that need it most. Over time, the body compensates for this restriction by increasing its blood pressure. People with excess fibrin suffer from chronic fatigue, slow healing, inflammation and pain, as well as elevated blood pressure.

Proteolytic enzymes taken on an empty stomach break down these proteins into their smallest elements. The enzymes pass through the stomach and intestinal lining, and enter the bloodstream where they begin the process of breaking down the buildup in the muscles, connective tissue and blood. These enzymes bring nutrition and oxygen-rich blood that can remove the metabolic waste produced by inflammation and excess fibrin.

Serrapeptase has been proven to be the strongest of the proteolytic enzymes, inducing anti-inflammatory, fibrinolytic and anti-edemic (prevents swelling and fluid retention) activity in a number of tissues.

Using enzymes to clear your body of fibrin takes time. It takes years to develop webs of fibrin in your tissues — so be patient, log your usage and, over time, notice how much less pain and how much more flexibility you have.

Serrapeptase has demonstrated anti-inflammatory and fibrinolytic activity, and acts rapidly on localized inflammation with no reports of adverse effects.


Bromelain, a proteolytic enzyme extracted from pineapple, has also been found to be effective in reducing inflammation by blocking cytokine production and activity


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Monday, November 6, 2017

The Role of #Fibrin in #Parkinson’s #Disease #Serrscor NK



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Parkinson’s disease is an irreversible nervous system disorder that primarily affects musculo-skeletal movement. While the progressive disorder can cause stiffness and slow movements, signs and symptoms vary greatly among patients.

Common symptoms include: 
Tremors
Slowed Movement
Rigid Muscles
Impaired balance
Impaired Posture 
Speech changes


Parkinson’s disease is caused by the gradual breakdown of brain cells called neurons. The loss of neurons leads to a decrease in dopamine levels, leading to abnormal brain activity. Only 5% of Parkinson’s cases occur before the age of 40, with incidence increasing with age. A majority of cases seem to be sporadic and of unknown origin – however, like most diseases, there is a significant genetic component.

Recent theories about the causes of Parkinson’s disease are based on abnormal fibrin production and deposition in the brain. Also known as the “amyloid hypothesis,” researchers have been looking at the role of abnormal protein aggregation in Parkinson’s and other neurodegenerative disorders, like Alzheimer’s disease. There seems to be a correlation between fibrin deposits and brain tissue degeneration, suggesting that the fibrin contributes to cellular death in these diseases. Similar to Alzheimer’s disease and Huntington’s disease, Parkinson’s disease involves the mis-folding of a specific protein, eventually leading to fibrin deposits.

There are several theories as to the underlying cause of Parkinson’s, from oxidative damage to environmental toxins – but the latest research seeks to understand why the dopamine-containing neurons are affected so greatly. In fact, by the time a Parkinson’s patient presents with symptoms, about 70% of the dopamine-containing neurons have already been lost. Current therapies aim to address dopamine deficiencies, but future therapies seek to address the prevention of neuron degeneration (cellular death of the brain cells).

Although systemic enzymes are implicated for the treatment of Alzheimer’s disease, their use in similar neurodegenerative diseases has yet to be studied. Specifically nattokinase, which has been shown to directly dissolve the aggregated protein found in Alzheimer’s disease, may be an option available to those suffering from Parkinson’s disease.

 Nattokinase is a natural systemic enzyme that helps to decrease fibrin levels in the blood. Nattokinase is also able to reach areas where fibrin has already accumulated – helping to restore blood flow and inhibiting cellular death due to oxidative damage. Perhaps the most promising aspect of systemic enzyme therapy is its ability to be used concurrently with other medications. The only restriction is upon the use of nattokinase, which should be discussed with a doctor prior to adding it to a regimen with prescription blood thinners. However, it should be noted that systemic enzymes do not cause adverse side effects or drug-drug/drug-nutrient interactions.


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