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Permalink Reply by Rose Marie' on April 16, 2010 at 11:12pm

From my understanding at this time there is no known cure for alopecia areata.

Rosy

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Permalink Reply by George Ortiz on April 18, 2010 at 10:02am

Hey there hope all is well,There is no known cure although there is new promising research currently being tested called the Marshal protocol, please read this article posted below for all its worth.
The Marshall Protocol is a medical treatment being used by physicians worldwide to treat a variety of chronic inflammatory and autoimmune diseases including (but not limited to) sarcoidosis, Chronic Fatigue Syndrome, fibromyalgia, Crohn’s Disease, and rheumatoid arthritis. While other treatments for chronic disease use palliative medications in an effort to cover up symptoms, the Marshall Protocol is a curative treatment, which strives to address the root cause of the disease process.

Information about the treatment can be found at the study site, marshallprotocol.com and also at autoimmunityresearch.org. The site is run by the staff of the Autoimmunity Research Foundation, a California-based non-profit agency. Over 200 health professionals are members of the site, and discussions are moderated by a group of volunteer nurses. There is no charge to use the website or the treatment and all patients are welcome to participate.

The Marshall Protocol is a phase II community-based internet study that is monitored by the FDA. The FDA has already granted orphan product designations for two of Autoimmunity Research Foundation’s six applications – Sarcoidosis, and Post Treatment Lyme Disease Syndrome (PTLDS, commonly known as chronic Lyme). The Foundation continues to work with the FDA to make effective therapies available in an even wider array of chronic diagnoses.

Chronic Disease
The Marshall Protocol is based on the hypothesis that chronic diseases (termed Th1 illnesses), are the result of infection by an intraphagocytic, metagenomic microbiota of chronic bacterial forms that are often referred to as the Th1 pathogens. The term intraphagocytic refers to the fact that these bacteria have developed the ability to remain alive and proliferate undetected inside the cytoplasm of the cells they infect. These cells include macrophages, the very cells of the immune system that the body uses to kill invading pathogens. Once inside these cells, they cause our own cells to release inflammatory cytokines (proteins that often generate pain and/or fatigue).

The term metagenomic indicates that there is a tremendous number of different species of these chronic bacterial forms. Finally, the term microbiota refers to the fact that these bacteria are also hypothesized to sustain themselves by grouping into communities called biofilms. The bacteria inside a biofilm produce a protective matrix that allows them to more effectively evade the immune system and develop resistance to antibiotics.

Many of the Th1 pathogens are also postulated to be in a chronic state referred to as the L-form. L-form bacteria simply represent part of the natural life cycles of classical bacteria. Under certain conditions, they mutate from classical bacteria, losing their cell walls in the process. Although researchers have known about L-form bacteria for over a century, up until recently they have not fully understood their role in causing chronic disease. Because they lack a cell wall, many antibiotics are unable to kill them directly and they cannot be detected by standard laboratory tests.

The ability of the Th1 pathogens to proliferate in the body is directly related to the vitamin D receptor (VDR). Critically important to the body, the Vitamin D Receptor (VDR) controls the innate immune system – the body’s first line of defense against infection. It’s also responsible for turning on/off a wide array of genes and chemical pathways. One of the VDR’s myriad jobs is to control expression of several families of antimicrobial peptides (AMPs), proteins that kill bacteria, viruses and fungi by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell.

Although casually referred to as a vitamin by some members of the medical community, molecular biologists have long realized that the precursor form of vitamin D (25-D) is really a secosteroid. Recent molecular modeling research (which has been confirmed by a large amount of clinical data) has shown that levels of 25-D over 20 ng/ml can bind and inactivate the VDR, which subsequently shuts down the innate immune system.

Certain species of bacteria also produce substances that can bind and inactivate the VDR in a manner similar to 25-D. Consequently, people who are infected with the Th1 pathogens and consuming vitamin D are no longer able to produce the AMPs or turn on the innate immune response. This allows their bacteria to proliferate and spread.

When the innate immune system can no longer function, people have a very hard time keeping other pathogens under control. They often find that childhood viral infections reactivate, or that they acquire Candida (pathogenic yeast) and Mycoplasma as well. Thus, every person who starts the MP has a different mix of pathogens to kill depending on what microbes they have encountered during various stages of life. A person’s unique mix of pathogens is often referred to as their “toxigenic pea soup.”

Research indicates that the Th1 pathogens have evolved mechanisms that allow them to both mutate and alter the expression of the genes inside the cells they infect. These effects on the genes result in changes in the cellular environment that make it easier for new pathogens to invade the cell – creating a snowball effect where, as a person acquires more pathogens, it becomes even easier for them to pick up a diverse array of other infectious agents. This process is known as successive infection.

Since the Th1 pathogens have been shown to survive in the sperm and egg, and evidence is growing that they can also pass through the placental barrier, they can be passed from parent to child – meaning that Th1 illnesses often run in families. In addition, the bacterial forms may be easily passed by human contact to an infant soon after birth, during the period before the adaptive immune system is up and running.

Unlike its inactive counterpart, 25-D, that inactivates the VDR in healthy individuals, 1,25-D binds and activates the VDR. But in individuals who have 25-D and bacterial proteins blocking the VDR, 1,25-D is forced out of the receptor and into the surrounding environment.

Furthermore, in healthy individuals, the VDR transcribes an enzyme called CYP24. CYP24 breaks down excess 1,25-D, ensuring that the level of 1,25-D in the body stays in the normal range. But in chronically ill individuals, the VDR (which is blocked by bacterial susbstances) can no longer transcribe CYP24. The level of 1,25-D in the body becomes significantly elevated since there is no CYP24 to keep it in check.

Another enzyme called CYP27B1 normally regulates the amount of 25-D converted into 1,25-D. When more CYP27B1 is produced, conversion occurs at a greater rate. The cytokines released by the immune system in response to the Th1 pathogens activate a protein called Protein Kinase A (PKA). PKA in turn activates CYP27B1, causing more 25-D to be converted to 1,25-D.

These processes cause 1,25-D to rise to an unnaturally high level. Unfortunately, when 1,25-D reaches a certain threshold, it binds not just the VDR, but many of the body’s other nuclear receptors, displacing the metabolites that are meant to be in the receptors under normal conditions.

The nuclear receptors affected by 1,25-D are receptors that regulate the body’s hormones – the glucocorticoid receptor, and the alpha and beta thyroid receptors, the adrenal receptors, and the progesterone receptors, among others.

This means that when 1,25-D is high, it competitively displaces cortisol, T3, and other metabolites from their target nuclear receptors, causing havoc on the body’s hormonal pathways. Thus, most people with chronic disease find they have difficulty tolerating stress, changes in temperature, and a variety of other hormone-related issues. Also, when levels of 1,25-D rise above 42 ng/ml, calcium begins to be leached from the bones, a process that results in osteoporosis and osteopenia.

When 1,25-D rises due to the processes described above, it also binds a receptor called the PXR. The PXR subsequently inhibits conversion of pre-vitamin D to 25-D, causing 25-D levels to drop. This means that low levels of 25-D – the form of vitamin D measured by most doctors – is not a sign of vitamin D deficiency. Instead, low levels of 25-D are a result of the disease process.

The body also produces 1,25-D in response to sunlight on the skin and bright light in the eyes. Excessive exposure to these sources of light helps drive the disease process. Most patients on the MP must take certain precautions, described on the web site, to avoid too much sun/bright light.

The Treatment
Patients on the Marshall Protocol take a medication called olmesartan (called Benicar in the United States), which is able to bind and activate the VDR by pushing 25-D and bacterial proteins out of the receptor. Patients also lower levels of 25-D in the body by avoiding the kinds of vitamin D present in various foods. These measures renew the body’s ability to turn on the innate immune system and produce the anti microbial peptides. The immune system is then able to kill the Th1 pathogens and is once again able to manage viral and other co-infections.

At the same time, MP patients take pulsed, low-dose antibiotics. Antibiotics taken in this manner are much more effective against bacteria in biofilms and are able to greatly weaken the Th1 pathogens so that the patient’s own immune system is then able to destroy them. The antibiotics weaken the bacteria by blocking their ribosomes, which they need to produce proteins that help them survive and reproduce. It’s important to understand that when the Th1 pathogens die, there is a temporary change in a patient’s immunopathology.

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