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Vasoactive Intestinal Peptide and NeuroInflammation

Alzheimer’s Disease, perhaps the illness most feared by people as they grow older, is increasingly recognized as a neuroinflammatory condition.  One of the most common causes of neuroinflammation is insulin resistance caused by excess sugar, and some have begun to wonder if Alzheimer’s is actually Diabetes Type III (1,2).  In addition cytokines such as TGF beta, a hallmark of biotoxin induced neuroinflammation, are elevated in Alzheimer’s (3).

Vasoactive Intestinal Peptide is a neuropeptide which allows immunomodulation of the innate immune response.  The innate immune response is a function of our more primitive immune system that people with “mold or multi” haplotypes must use in order to defend against biotoxins. Unfortunately the primitive immune system depends on cytokines which end up promoting widespread inflammation everywhere in the body, including the brain (4).  Dr. Shoemaker uses VIP as the last step in his Biotoxin Protocol.  He has shown that regular use of VIP over a 6 month period decreases many of the inflammatory markers associated with biotoxin illness as well as increasing the ability to tolerate some mold exposure (5).

What many people using VIP on a regular basis don’t realize is that VIP also has widespread and potent neuroprotective effects. VIP has such potent neuroinflammatory properties that it has even been proposed as a promising agent for neuroinflammatory conditions such as Alzheimer’s, Parkinson’s and Autistic Spectrum Disorders (7) It has been shown to decrease neuroinflammation,  excitotoxicity, and perhaps even protect against Alzheimer’s . Although VIP is primarily known as a gut hormone it also acts as a neurotransmitter in the CNS.    VIP is widely expressed throughout numerous brain regions, with the highest expression levels found in the cerebral cortex, hippocampus, amygdala, and hypothalamus, regions where biotoxins such as mold have been shown to damage.

The neuroprotective properties of VIP are facilitated by promoting the expression and secretion of astroglia-derived factors in the presence of toxins. VIP has protected the cells from neurotoxic effects of ethanol, hydrogen peroxide (H2O2, beta-amyloid and glycoprotein 120 (gp120).  VIP has even been shown to limit microglia activation and the release of inflammatory neurotoxins such as Tumor Necrosis Factor and nitric oxide (8)

1.  Monte S andWands JR, Alzheimer’sDisease Is Type 3 Diabetes–Evidence Reviewed  

2.    Eikelenboom P, van Exel E, Hoozemans JJ, Veerhuis R, Rozemuller AJ, van Gool WA. Neuroinflammation – an     early event in both the history and pathogenesis of Alzheimer’s disease Neurodegener Dis. 2010;7(1-3):38–41.

3.   SwardfagerW, Lanctôt K, Rothenburg L, Wong A, Cappell J, Herrmann N. A meta analysis of cytokines in   Alzheimer’s Disease. Biol Psychiatry 2010; 68: 93041

4.    S G R Smalley, P A Barrow, N Foster  Immunomodulation of innate immune responses by vasoactive intestinal peptide (VIP): its therapeutic potential in inflammatory disease Clin Exp Immunol.2009 August; 157(2): 225–234

5.    Shoemaker R, House D, Ryan J. Vasoactive intestinal polypeptide (VIP) corrects chronic inflammatory response syndrome (CIRS) acquired following exposure to water-damaged buildings. Health 2013; 3: 396-401.

6.    VIP Enhances Phagocytosis of Fibrillar Beta-Amyloid by Microgliaand Attenuates Amyloid Deposition   the Brain of APP/PS1 Mice PLoS One. 2012; 7(2): e29790. Published online 2012 February 6

7.  Therapeutic potential of vasoactive intestinal peptide and its receptors in neurological disorders  Dejda A1, Sokołowska P, Nowak JZ Neuroprotective potentialof three neuropeptides PACAP, VIP and PHI. Pharmacol Rep. 2005 May-Jun;57(3):307-20.

8.   DelgadoM, Nieves V, Gonzalez-Rey E. Vasoactive intestinal peptide protects againstβ-amyloid-induced      neurodegeneration by inhibiting microglia activation atmultiple levels. Glia. 2008;56(10):1091–1103.

 

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