Mast cells are significantly increased in number in both the mucosa and detrusor of the bladder. Their activation appears to contribute to the pathophysiology of bladder pain syndrome (BPS) formerly interstitial cystitis.

In some women, oestradiol activates the neuropeptide, substance P which in turn augments mast cell histamine secretion.

The tryptase-positive and chymase-negative mast cells MC(TC) may be the type of mast cell dominantly present in the bladder of IC patients. The MC(TC) in detrusor increases with the progression of contracted bladder.

In these patients mast cells create vasoactive and proinflammatory molecules. This is accompanied by altered bladder glycosaminoglycans lining and bladder mastocytosis a form of tryptase immunoreacitivity.

The primary sensory (afferent) neurons responsible for histamine induced itch are unmyelinated C-fibers. C-fiber nociceptors exist in two major classes: mechano-responsive nociceptors and mechano-insensitive nociceptors. Mechano-responsive nociceptors have been shown in studies to respond to mostly pain and mechano-insensitive receptors respond mostly to itch induced by histamine.

Tachykinins (TK), such as substance P, and their neurokinin receptors which are ubiquitously expressed in the human urinary tract, represent an endogenous system regulating bladder inflammatory, immune responses, and visceral hypersensitivity. Increasing evidence correlates alterations in the TK system with urinary tract diseases such as neurogenic bladders, outflow obstruction, idiopathic detrusor instability, and interstitial cystitis.

Biomarkers for IC include interleukin-6, histamine, and methyhistamine each of which is present in patients with interstitial cystitis.

DNA Reprogramming Class to Clear for and normalize:

• Mast Cells:Tryptase-positive and chymase-positive (MC(TC)
• Oestradiol + neuropeptide substance P, Histamine secretion
  • For itching unmyelinated C-fibers nociceptors: both mechano-responsive nociceptors and mechano-insensitive nociceptors
• Methyhistamine
• Interleukin-4, 5 and 6
• Bladder lining glycosaminoglycans
• Bladder mastocytosis
• All tachykinins such as substance P and neurokinin-1 (NK-1) receptors
• Tryptase immunoreactivity

Enhancers:
Nanocrystalline silver has anti-inflammatory properties.
It decreases urine histamine levels, bladder tumor necrosis factor-alpha and mast cell activation without any toxic effect.

Suplatast tosilate (IPD-1151T) is an immunoregulatory compound that suppresses the production of interleukin (IL)-4 and IL-5. It was recently recognized to improve the symptoms in patients with interstitial cystitis

IPD-1151T inhibits bladder release of histamine and tumor necrosis factor-alpha IPD-1151T inhibited the proliferation of mast cell progenitor cells, IC-2, but not that of splenocytes or mature mast cells. Through inhibition of chemotaxis, IPD-1151T might limit the number of eosinophils at the inflammation site.

Flavonoid quercetin as found in AlpineV.

Taurine protects against WAS-induced oxidant urinary bladder injury, and thus may be a possible therapeutic agent against interstitial cystitis, the symptoms of which are aggravated by stress conditions.

Chondroitin sulphate appears to be a potent mast cell inhibitor.

L-arginine (LA), a semi-essential amino acid, which has recently been shown as a physiological precursor of nitric oxide (NO). LA led to an improvement in interstitial cystitis symptoms

Activation of NK1R by substance P (SP) induces both NKx-2.5 and NF-kappaB translocations.Nkx2.5 is the unique discriminator of NK1R-modulated inflammation, it can be imagined that in the near future, new based therapies selective for controlling Nkx2.5 activity in the urinary tract may be used in the treatment in a number of bladder disorders.

Inflammatory models of cystitis result in increased levels of TNF-alpha, SP and NGF production in the bladder.

melatonin appears to exert a urothelial protective activity in a bladder injury model.

Clearing for Interstitial Cystitis

Interstitial cystitis (IC) is a chronic bladder disorder related to neurogenic inflammation, with symptoms including pelvic and or perineal pain, urinary frequency and urgency.

Increasing evidence suggests that sensory nerve dysfunction may underlie this disorder. Studies have determined that urine of interstitial cystitis (IC) patients contains antiproliferative factor that inhibits primary bladder epithelial cell proliferation. IC’ers urine also has significantly decreased levels of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and increased levels of epidermal growth factor (EGF).

In this clearing we intend to decrease bladder distention, decrease bladder vascular permeability and stop unneeded leukocyte influx.

We are clearing to normalize and eliminate any neurogenic inflammation or sensory nerve dysfunction related to:

• Abnormal Antiproliferative factor (APF) on frizzled 8 sialoglycopeptide which causes inhibition of thymidine incorporation
• Decrease levels of Epidermal growth factor (EGF)
• Balance IGF binding protein-3 and IL-6
• Increase levels of Heparin-binding epidermal growth factor-like growth factor (HB-EGF)
• Normalize cyclic guanosine monophosphate
• Restore function of bladder epithelial cells
• Inhibit release of neuropeptides Substance P and calcitonin gene-related peptide
• Normalize lipopolysaccharide in the bladder

Enhancers:

• Botulinum toxin type A (BTX-A)
• Kidney terrain, Bladder terrain, Neural terrain
• Rena-zyme