PEDD (Pancreatic Enzyme Deficiency Disease)

What are the symptoms / diagnositics ?

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I can't find any really good articles, but here's a pretty good one:

The main symptoms are lots of fat in the stools ("steatorrhea") and weight loss. The fatty stools can lead to diarrhea, foul smelling stools, etc. The failure to absorb fat properly can result in a number of deficiencies of fat-soluble vitamins, leading to anemia, bleeding disorders, and bone problems.

Diagnosis isn't straight-forward, since a number of other diseases of absorption will produce similar symptoms. A number of fairly involved absorption tests may be required, and MRI scans will likely be done to look for signs of pancreatitis.

Treatment involves adjusting diet to limit fats, supplementing for vitamins that are poorly absorbed, and the use of pancreatic enzyme supplements. In addition, the underlying cause of the condition (eg, pancreatitis) will be treated if possible.

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This is a good article explaining each of the enzymes the pancreas produces and how it affects digestion.

There are prescription pancreas enzyme medications that can be given to replace any you are deficient in.

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You can literally trace every symptom of every autoimmune disease directly back to missing enzymes in the pancreas. Specifically protease and DNase1. The information that the previous posters provided show that without protease, your body will not be able to break down immune complexes. These immune complexes consist of unbroken down proteins and DNA also due to a lack of protease, since you would not be able to digest dietary proteins. Your immune system targets these protein fragments and DNA and forms "NETS" that become lodged in your organs and tissues. The lack of the pancreatic enzyme DNase1 has been determined to be a "causative" factor of lupus. Here is a picture of these "NETS" in a lupus patients bloodstream. In the last paragraph, the researchers state lupus patients lack the enzyme DNase1.

So, that would be one symptom of PEDD, immune complexes that become lodged in organs and tissues, causing organ failure and damage. Other symptoms of PEDD would be the same a lupus patient would suffer, since the lack of DNase1 has been determined to be a causitive factor of lupus. Here are some symptoms and scientific findings of lupus: Autonomic nervous system dysfunction, hypothyroidism, restless legs syndrome, arthritis, osteoporosis, spinal cord degeneration, migraines, hypermobility, low adrenal function, chemical sensitivity, low cortisol, anemia, lack of vitamin B12, iron, and magnesium, joint and muscle pain, fatigue, insomnia, depression, neuropathy, swollen glands, low grade fever, high C-reactive protein, rashes, itchiness, vision complications, dry eyes and mouth, increased risk of heart attack and stroke, easy bruising, brain fog, porphyria, mitochrondrial dysfunction, POTS, heat intolerance, and the list goes on. You can trace each of these symptoms directly back to these missing enzymes.

For instance, lupus patients have an increased risk of developing restless legs syndrome. So do fibromyalgia, diabetes, MS, Sjogrens patietns etc. Studies have linked restless legs syndrome to low iron and dopamine. Here is one such study.

Dopamine and Iron in The Pathophysiology of Restless Legs
Syndrome (Rls)
Allen, R. 2004. Sleep Med. 5(4):385-91.

Results: The pharmacological treatment data strongly support a dopaminergic
abnormality for RLS. Other pharmacological data and some imaging data also support
this, although the data are not entirely consistent. The secondary forms of RLS strongly
support an iron deficiency abnormality for RLS, further documented by several other
studies. Some animal studies have shown a relation between iron deficiency and
dopaminergic abnormalities that have some similarity to those seen in the RLS patient.
Conclusions: It is concluded that there may be an iron-dopamine connection central
to the pathophysiology of RLS for at least some if not most patients with this disorder.

Here is how PEDD would lead to RLS (and anemia) Protease regulate iron absorption in the body. Here is a study that shows this.
Hörl, W.H. 2008. Nephrol. Dial. Transplant. 23(10):3063-3064.

New Insights Into Intestinal Iron Absorption…Du et al. described the novel and exciting finding that the transmembrane serine
protease 6 (TMPRSS6) senses iron deficiency [1]. In their study, Du et al. described a
mutant mouse, which is characterized by progressive loss of body hair and microcytic
anaemia. The phenotype was found to result from reduced intestinal iron absorption
caused by high levels of hepcidin. Iron deprivation and anaemia suppressed hepcidin
mRNA levels in the livers of wild-type mice, whereas high mRNA levels persisted in the
livers of anaemic mutant mice. The high hepcidin levels in the mutant mice resulted
from a splice defect in the Tmprss6 gene. This suggests that TMPRSS6 physiologically
downregulates hepcidin mRNA transcription and thus promotes iron uptake [1].
Take home message: Iron deficiency activates the serine protease TMPRSS6. The
protease then inhibits hepcidin transcription and thereby allows intestinal iron
absorption and cellular iron release.

PEDD would also lead to a lack of dopamine. Protease break down dietary proteins and release essential amino acids. One of the amino acids found lacking in MS, lupus, Fibromyalgia, CFS etc is phenylalanine. Phenylalanine breaks down into tyrosine and tyrosine breaks down into dopamine. The lack of dopamine and iron would then lead to RLS. Here is a study that shows fibromyalgia patients lack phenylalanine.

Altered Amino Acid Homeostasis in Subjects Affected by
Bazzichi, L., L. Palego, G. Giannaccini, A. Rossi, F. De Feo, C. Giacomelli, L. Betti, L. Giusti,
G. Mascia, S. Bombardieri, A. Lucacchini. 2009. Clin Bioche, 42(10-11):1064-70.
The objectives were to evaluate plasma amino acid (AA) concentrations in patients
affected by fibromyalgia (FM) and to study the relationships between their levels and
FM clinical parameters.
Significant lower plasma taurine, alanine, tyrosine (Tyr), valine, methionine,
phenylalanine and threonine concentrations, and the sum of essential AAs were
observed in FM patients vs. healthy controls (P<0.05). Tyr CAA’ ratio and the sum of
AAs competing with tryptophan for brain uptake were significantly reduced in FM
(P<0.05). A significant correlation was found between FM clinical parameters and
certain AAs.

You can trace every single symptom (and every valid scientific finding) back to PEDD in just the same way as you can RLS. If you have any doubts, just pick a symptom off the list (or come up with another symptom of autoimmune disease) and we will trace it back.

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If this is so, then what is the solution. How does one improve pancreatic function? Through diet?

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Yes, through diet and healing the GI tract. Also, avoidance of things that can destroy these enzymes. Here is some more information on the connection to these enzymes and autoimmune disease and cancer. ase

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Beware of panaceas.

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Wow, so much information! Thanks you guys!

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Annesse, what destroys these enzymes???? I checked that linked, but maybe it's my brain fog today..but didn't see it or maybe just don't understand it...I'm not doing very well today!

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Hi sickofcrest~Lots of things will deplete your enzymes, beneficial bacteria etc. In order to properly digest proteins, you need protease and DNase1, sufficient amounts of HCI (stomach acid), intrinsic factor, and beneficial bacteria. Along with protease, adequate HCI is needed to break down protein fragments in foods (including gluten and cow's milk protein) to avoid an immune response. One study found allergenic antigens were reduced up to 10,000-fold by adequate HCI.

Many medications, antibiotics, fluoride, acid-blocking medications, steroids etc. will damage your GI and destroy enzymes and intestinal flora. For instance, the top three drugs that are known to induce lupus are procainamide (Pronesty), hydralazine (Apresoline), and quinidine(Quinaglute). All three of these drugs are "enzyme inhibitors".

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