New Information

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New Information

Postby Annesse » Sat Apr 07, 2012 2:41 pm

Hi Everyone,

My name is Annesse and I have just written a book on MS and other autoimmune diseases. I was diagnosed with lupus, CFS and fibromyalgia over 20 years ago. I believe that MS, lupus, fibromyalgia, RA, CFS etc. share a common cause. Every symptom and valid scientific finding in each of these diseases can be traced directly back to missing enzymes in the pancreas. Specifically, protease and DNase 1. By looking at these diseases as symptoms of one disease, which is PEDD (Pancreatic Enzyme Deficiency Disease) I believe we can solve the MS puzzle. If you can only explain one finding in MS, such as mitochrondrial dysfunction, then you have only one piece of the puzzle. You will know you have solved the puzzle when all of the pieces are in place and a clear picture emerges. These diseases all share many common findings and if you develop one of these diseases, you are far more likely to develop another one. For instance, reporting in the May 2006 issue of the Journal of Rheumatology, researchers identified an association between rheumatoid arthritis and MS. They state, "Since a great proportion of our patients developed MS first and subsequently RA, the best explanation for these cases is a predisposition in MS patients to develop another autoimmune disease."

Arthritis Today also states, "People with other rheumatic diseases, such as rheumatoid arthritis or lupus, are at greater risk for fibromyalgia. For example, about 20 to 30 percent of people with rheumatoid arthritis also develop fibromyalgia, although no one knows why."

Imagine if you could trace every single symptom and valid scientific finding not just of MS, but of these other diseases as well, directly back to DNase 1 or protease. We can start with lupus. Researchers from around the world have discovered a causative factor of lupus. It is a lack of the enzyme DNase 1. DNase 1 originates in the pancreas. Its job is to break down dietary proteins and DNA. If you are unable to break down dietary proteins, unbroken down bits of proteins and DNA will end up in your bloodstream and the immune system will target them. The immune system will form "NETS" and these NETS can become lodged in organs and tissues. Here is a picture of one of these NETS. Pay special attention to the last paragraph where it states lupus patients lack the enzyme DNase 1. Additional studies from around the world confirm the lack of DNase 1 in lupus. If this enzyme is removed in mice for instance, the mice developed lupus. If the enzyme is genetically modified in humans, lupus is the result.

http://www.sciencedaily.com/releases/20 ... 161423.htm
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Re: New Information

Postby jam » Sat Apr 07, 2012 3:43 pm

Annesse, just out of interest, my sister has lupus and I have ppms. I had rheumatics as a child, which was terrible pain, and I use to wake up crying in pain, this continued well into my adulthood and then I developed ms. I had to constantly take pain killers for the pain.

Hope this will be of some interest to you.


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Re: New Information

Postby Annesse » Sat Apr 07, 2012 3:58 pm

Thank you Jam~ I think the evidence will show that these diseases are clearly connected.

The lack of DNase 1 would explain one of the findings in MS-low uric acid.

http://www.ncbi.nlm.nih.gov/pubmed/16202511

Low levels of uric acid also explains why MS patients rarely get gout. As this information shows, in a review of 20 million patient records, MS and gout were found to be almost virtually exclusive. High levels of uric acid can lead to gout.

http://www.nhfw.info/multiple-sclerosis.html

As I previously stated, DNase 1 breaks down dietary DNA and proteins. As the following information shows, uric acid is the final breakdown product of DNA. If you lack DNase 1, you would not be able to properly digest proteins and DNA, and this would result in low levels of uric acid.

http://www.science-autism.org/Urate.htm

There is not a symptom or valid scientific finding in MS that we will not be able to trace directly back to pancreatic enzymes in just this way.
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Re: New Information

Postby cheerleader » Sat Apr 07, 2012 4:51 pm

It's an interesting theory, Annesse...but I'm not sure the research in MS will agree with your claims.

To determine whether antibody reactivity with the cell surface was DNA dependent, we pretreated the oligodendrocyte and neuroblastoma cells with DNaseI and again measured antibody binding. We found cell-surface recognition of neuroblastoma cells by each of the antibodies was abolished by DNaseI treatment. In contrast, however, although DNaseI treatment prevented binding of mAbs MS-A and SI-1 with oligodendrocytes, the binding of MS-B with these cells was largely unaffected by DNase treatment. The data indicate that, whereas surface binding of mAbs MS-A and SI-1 to both cell types and MS-B to neuroblastoma cells was DNA dependent, the binding of MS-B to oligodendrocytes seemed to be largely independent of DNA.

http://www.pnas.org/content/98/4/1793.full

If you take one step back, and look at endothelial dysfunction-which is independent of DNA--there may be more of a connection to MS and other autoimmune diseases.
http://ccsvi.org/index.php/helping-myse ... ial-health

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Re: New Information

Postby Annesse » Sat Apr 07, 2012 4:59 pm

Hi Cheer~ We are just getting started. We will clearly be able to explain the endothelial cell dysfunction as well and we will be able to trace it directly back to missing protease.
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Re: New Information

Postby cheerleader » Sat Apr 07, 2012 5:06 pm

Endothelial dysfunction is not dependent on one missing protease, Annesse...it is multi-factorial, and comes from oxidative stress, high homocysteine levels, low vitamin D, high c reactive protein, virsues, bacteria and a host of other environmental and epigenetic situations.
Claiming that one specific enzyme is behind all autoimmune disease is a big statement.
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Re: New Information

Postby Annesse » Sat Apr 07, 2012 8:51 pm

I agree Cheer, it is a very big statement. We will take one symptom and finding at a time and in the end, we will have traced them all directly back to missing protease and DNase 1. Proteases digest dietary proteins.

You mentioned low vitamin D. This is a common finding in MS and in other autoimmune diseases as well. Explaining the lack of vitamin D will also explain other features of these diseases, such as abnormal calcium metabolism, blood that does not clot readily, and osteoporosis. Here is some information from my book.

"Arthritis and Adequate Protein Digestion

Lita Lee Ph.D., a chemist and enzyme nutritionist explained the connection well when she wrote, "All forms of arthritis involve abnormal calcium metabolism. Ninety-nine percent of the body calcium is in the bones and teeth. The other one percent, found in the blood, is just as important because it is essential in the BLOOD CLOTTING MECHANISM, muscle and nerve function, VITAMIN D FUNCTION, and the function of hormones that control calcium metabolism (called parathyroid hormones). Of the one percent of calcium in the blood, half is PROTEIN BOUND and half is IONIZED. Both require ADEQUATE PROTEIN DIGESTION. If you are deficient in protein because you can't digest it, you cannot carry protein-bound calcium. If you lack optimum acidity from inadequate digestion of protein, you will not have enough ionized calcium. In either case, you are a candidate for arthritis.

The abnormal deposit of calcium is one of the factors involved in arthritis and arthritic inflammation. Soft tissue, any kind of body tissue other than bones and teeth, is a target for depositing calcium. Wherever this happens, pathology occurs:in the joints, around inflamed areas (osteoarthritis), in the arteries (arteriosclerosis), in the kidneys (kidney stones), in the soft lenses of the eyes (cataracts), in the brain (stroke) and so on," (Lee, 2009).

According to the National Rheumatoid Arthritis Society, "Osteoporosis is a common feature in adults with rheumatoid arthritis". Osteoporosis is also commonly found in MS. In a 2006 British study, it was found that people with RA are 50% more likely to develop osteoporosis. The study, of approximately 30,000 people with RA, found that the risk of osteoporosis existed even if no other risk factor, such as the long-term use of corticosteroids or smoking was present. In fact, the risk posed by RA alone was as great as the risk caused by taking corticosteroids.

When the blood cannot carry protein-bound calcium because it lacks protein, it withdraws the necessary calcium from the bones to maintain homeostasis or internal balance. The bones need sufficient calcium to develop and maintain bone structure.

The inability to metabolize vitamin D would also play a role. Vitamin D helps the bones absorb calcium and hold onto minerals. The higher a bone's mineral content, the stronger it is.

There are other factors involved in osteoporosis and we will be discussing these as well.
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Re: New Information

Postby cheerleader » Sat Apr 07, 2012 10:06 pm

Make sure you have research proving MS is an autoimmune disease, Annesse, before you put it in your book in the same category as Lupus (where there is an identifiable antigenic target).

However, direct proof of an autoimmune cause of MS is lacking, as no specific autoantibody or autoreactive T-cell directed against a self-antigen in the nervous system can passively transfer MS to experimental animals. EAE itself is an imperfect model of MS, as it does not exactly parallel the clinical or pathological features of MS [1,3,23]. In addition, EAE is responsive to many drugs directed against T-cells (eg, azathioprine, cyclosporine, and monoclonal antibodies directed at CD4 cells). These same drugs have failed to demonstrate consistent effectiveness as therapy for MS.

http://www.uptodate.com/contents/epidem ... -in-adults
http://www.expert-reviews.com/doi/pdf/10.1586/ern.10.69
http://www.springerlink.com/content/y352380v17u17r4j/
http://archneur.ama-assn.org/cgi/conten ... 61/10/1610

I found research linking the lack of DNase1 to Lupus and other autoimmune conditions, but there is nothing linking it in MS research....MS is a very different disease.
take care,
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Re: New Information

Postby Annesse » Sat Apr 07, 2012 11:11 pm

I think the information I present will redefine the definition of "autoimmune disease". Researchers are discovering that the immune system is actually targeting unbroken down proteins and DNA, such as what we saw in the picture of the lupus NETS. Also, the immune system is targeting abnormal peptides. If your body is unable to properly digest proteins, you will not be able to form normal peptides, as peptides are made from amino acids that are derived from dietary proteins.

Researchers from UCLA, for instance, have discovered that 100% of rosacea patients have abnormal peptides on their skin and this is what the immune system is targeting. Here is what the lead researcher Dr. Gallo stated: "In rosacea, peptides are made abnormally. And the peptides were processed into an abnormal form that we found only in rosacea patients skin, not in normal skin. This abnormal form triggers the body's inflammatory immune system, which normally activates when you have a cut or injury."

Researchers from National Jewish Health and the University of Colorado Anshutz Medical Center have discovered the precise abnormal peptide that can trigger diabetes. In an article from Science Daily they stated the findings support, "An emerging theory about the origins of autoimmunity."

An abnormal peptide has also been discovered in Interstitial Cystitis (IC). IC is a common condition in many autoimmune sufferers.

It is called Antiproliferative Factor (APF). It is a glycopeptide.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC511055/


Here is a study on CFS that found CFS patients lack the amino acids found in proteins and the specific amino acid necessary for forming glycopeptides. The study also states, "The majority of studies, including the present investigation, have noted reductions in urine and plasma amino acid levels in patients with CFS compared with healthy controls."

A very important finding in this study was that CFS patients lack the amino acid asparagine. The study states,"The reduction in the urinary output of asparagine in CFS patients noted in this study may be consistent with "impaired protein synthesis", since asparagine is an important amino acid in protein structures, required for forming GLYCOPEPTIDES."

http://ebm.rsmjournals.com/content/232/8/1041.full

Please bear with me. I have a great deal more evidence to present.
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Re: New Information

Postby Annesse » Sun Apr 08, 2012 12:20 pm

The lack of protease and DNase 1, and the resulting inability to digest proteins, has so far explained the formation of "immune complexes", low uric acid, low vitamin D, blood that does not clot readily, one of the features of arthritis;abnormal calcium metabolism, osteoporosis, and the formation of abnormal peptides. Lack of DNase 1 has even been determined to be a "causative factor" of lupus.

Another feature of these diseases that would need to be explained is why hypothyroidism commonly occurs with the other diseases we have been discussing. For instance, Healthy Divas, a resource center for autoimmune disease states,"An estimated 85% of Chronic Fatigue Syndrome sufferers also have hypothyroidism." The Archives of Neurology states, "Myasthenia gravis has been associated with disorders of the thyroid gland."

An abstract from the Annals of the Rheumatic Diseases found that, "Clinical hypothyroidism was observed three times more often in female RA patients than females in the general population." The John Hopkins Lupus Center states, " Autoimmune thyroid disease is common in lupus."

In this next study entitled, "Association of MS with thyroid disease", it states, "We found that thyroid disorders were at least three times more common in women with MS than in female controls."

http://www.neurology.org/content/53/4/883.abstract

If you lack protease, you would not be able to digest dietary proteins and release essential amino acids, since they are derived from dietary proteins. One of the essential amino acids that you would lack is phenylalanine. In the study I posted above on CFS, it was found that CFS sufferers have "significantly lower levels of phenylalanine." Here is a study that confirms fibromyalgia patients also have significantly lower levels of phenylalanine and also numerous other amino acids found in high protein foods.

http://www.ncbi.nlm.nih.gov/pubmed/19281806

And here is a cerebrospinal fluid study that found tryptophan, tyrosine and phenylalanine were all diminished in the plasma of patients with MS. It states," By far the greatest decrease was in the tryptophan level as well as tyrosine and phenylalanine."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC490278/

The lack of the essential amino acid phenylalanine would lead to a lack of both of the thyroid hormones.
Phenylalanine converts into tyrosine. Tyrosine is then used in the synthesis of thyroxine and triiodothyronine. Both of these thyroid hormones are tyrosine-based.
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Re: New Information

Postby Annesse » Mon Apr 09, 2012 7:07 am

The lack of phenylalanine also explains another important finding in MS. Following is a quote from an article in US News & World Report.

"Multiple Sclerosis is associated with reduced levels of an important neurotransmitter, noradrenaline. There is evidence of damage to the Locus Coerulius (LC) in Alzheimer's and Parkinson's disease, but this is the first time it has been demonstrated that there is stress involved to the neurons of the LC of MS patients, and that there is a reduction in brain noradrenaline levels,' said the study's first author, Paul Polak, a research specialist at the University of Chicago." The study was published online February 4, 2011 in Brain. (University of Illinois at Chicago,2011)

In order to produce noradrenaline, you would need to be able to digest dietary proteins. Just like the thyroid hormones, both of the adrenal hormones, adrenaline and noradrenaline are derived from phenylalanine. Phenylalanine converts into tyrosine and tyrosine is used in the synthesis of dopamine. Dopamine is the precursor to adrenaline and noradrenaline.
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Re: New Information

Postby Annesse » Mon Apr 09, 2012 8:13 pm

Dopamine is also derived from phenylalanine. Low dopamine levels are associated with the following symptoms: Stiff, rigid, achy muscles, cognitive impairment, impaired motor skills, tremors, inability to focus attention, poor balance and coordination,and strange walking pattern (gait), frequently with small steps.

The previous cerebrospinal fluid study I posted on MS found that tryptophan, another essential amino acid derived from dietary proteins, is also found lacking in MS. Tryptophan is needed to make serotonin, a mood-determining brain chemical. Both serotonin and tryptophan shortages have been linked to depression, insomnia, confusion and anxiety.

Adequate production of the hormone melatonin is necessary to achieve sound refreshing sleep. Melatonin is also derived from tryptophan. The lack of the essential amino acids, phenylalanine and tryptophan, accounts for many of the symptoms of MS.
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Re: New Information

Postby Annesse » Mon Apr 09, 2012 9:14 pm

Another finding in MS, RA, lupus, Sjogrens, and fibromyalgia that would need to be explained is dysautonomia or autonomic nervous system dysfunction. The study entitled, " Autonomic Dysfunction in Multiple Sclerosis: Correlation with Disease-Related Parameters", states, "Ninety percent of the patients had symptoms related to autonomic dysfunction."

The following study concludes, "SLE and RA are associated with severe autonomic dysfunction."
http://www.ncbi.nlm.nih.gov/pubmed/20422909

What is dysautonomia? Dysautonomia is a dysfunction of the autonomic nervous system. The Merck Manual states, " The autonomic nervous system is the part of the nervous system that supplies the internal organs, including the blood vessels, stomach, intestine, liver, kidneys, bladder, genitals, lungs, pupils, and muscles of the eye, heart, and sweat, salivary, and digestive glands. The autonomic nervous system controls blood pressure, heart and breathing rates, body temperature, digestion, metabolism (thus affecting body weight), the balance of water and electrolytes (such as sodium and calcium), the production of body fluids (saliva, sweat, and tears), urination, defecation, sexual response, and other processes.

A dysfunction in the autonomic nervous system can cause dizziness or light-headedness due to excessive decrease in blood pressure when a person stands (orthostatic hypotension). People may sweat less or not at all and become intolerant to heat. The eyes and mouth may become dry. After eating, a person with dysautonomia may feel prematurely full or even vomit because the stomach empties very slowly (gastroparesis). Some people pass urine involuntarily (urinary incontinence), often because the bladder is overactive. Other people have difficulty emptying the bladder (urine retention) because the bladder is underactive. Constipation may occur, or control of bowel movements may be lost. The pupils may not dilate and narrow (constrict) as light changes."

Urinary tract infections are a common symptom of MS. Autonomic dysfunction can cause the nerves of the bladder to no longer respond normally to pressure as the bladder fills with urine. As a result, urine stays in the bladder, which leads to urinary tract infections. Dysautonomia explains many of the other features of MS as well.

The autonomic nervous system is controlled by two neurotransmitters. They are adrenaline and acetylcholine. Adrenaline is the predominant sympathetic neurotransmitter, whereas acetylcholine acts in the parasympathetic periphery. Phenylalanine is necessary to produce adrenaline.
The lack of phenylalanine would explain one of the missing neurotransmitters. We will clearly show why MS patients would also lack acetylcholine, the other neurotransmitter, as we move forward.
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Re: New Information

Postby Annesse » Tue Apr 10, 2012 4:08 pm

There are five nutrients that are commonly found lacking or dysregulated in all of these diseases. They are vitamin D, iron, zinc, vitamin B12 and magnesium. Connecting these missing nutrients to a lack of protease will be additional evidence that we have found the source of these diseases.

We are already shown why an inability to digest proteins would lead to an inability to metabolize vitamin D. Next will be iron. Low iron and an inability to properly metabolize iron are both features of MS. As the following information from LIVESTRONG shows, a lack of iron affects the production of oligodendrocytes.

"Researchers at Penn State's Life Sciences Consortium discovered a connection between iron deficiency and multiple sclerosis in 2000. Oligodendrocytes are cells specifically designed to manufacture myelin. The researchers learned that an iron deficiency affects the production of oligodendrocytes, which limits the amount of myelin produced. In addition, a shortfall of iron during crucial stages of development results in a shortage of neural connections, according to neuroscientist James Connor, Ph.D. This research appeared in the May 2000 issue of "Research Penn State."

Here is the link from LIVESTRONG for some additional information on MS and the association to iron and B12.
http://www.livestrong.com/article/51095 ... sclerosis/

Protease are "essential regulators" of iron in the body as the following studies show. A lack of protease would lead to an inability to properly metabolize iron, which would result in either iron overload or an iron deficiency.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430097/
http://www.haematologica.org/content/94/6/840.full (proteolytic; also called proteinase or protease are enzymes that break down proteins)
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Gout and MS

Postby lovebug » Tue Apr 10, 2012 9:00 pm

Well folks I do have Gout probably for 4-5 yrs. and RRMS for 3 yrs. Is that weird or what...................
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