Trigger VII-Identify Individual Nutritional Deficiencies
In order to effectively combat autoimmune disease, it’s vital to nourish your body with a healthy supply of vitamins and nutrients. These are the building blocks to repairing cells from a molecular level and restoring healthy organs, tissue, and systemic health.When it comes to autoimmune disease, there are certain nutrients that are integral to supporting immune function. When deficiencies are present, susceptibility to autoimmune response and inflammation increases. This is especially apparent in intestinal permeability, or leaky gut.
“Vitamin D deficiency may compromise the mucosal barrier, leading to increased susceptibility to mucosal damage and increased risk of IBD (inflammatory bowel disease)”8
“There is growing appreciation of the importance of the pleiotropic hormone vitamin D in the development of tolerance, immune system defenses, and epithelial barrier integrity.”9
“These observations suggest that vitamin D plays a critical role in mucosal barrier homeostasis by preserving the integrity of junction complexes and the healing capacity of the colonic epithelium.”10
There is also growing evidence that vitamin D regulates immune function and acts on the immune system in many ways to suppress systemic inflammation:
“The common denominator that rises from these studies is that vitamin D affects the immune system at many levels and by a number of mechanisms. It takes part in the genetic regulation of cytokine production, VDR expression and affects important biological processes by which these cells interact. On the whole, vitamin D confers an immunosuppressive effect.”11
“Vitamin D down-regulates nuclear factor-kB (NF-kB) activity, increases IL-10 production and decreases IL-6, IL-12, IFN-c, and TNF-a production, leading to a cytokine profile which favors less inflammation”13
“VDR plays a critical role in mucosal barrier homeostasis by preserving the integrity of junction complexes and the healing capacity of the colonic epithelium”14
EPA-DHA Essential Fatty Acids (Fish Oils)
“EPA appears to exert much of its anti-inflammatory benefit by suppressing NF-kappaB activation via activation of PPAR-alpha and thus reducing elaboration of proinflammatory mediators”15
“When endoscopic endpoints were used to evaluate the role of fish oil in the treatment of ulcerative colitis, 3 of 3 studies showed statistically significant improvement in the study group that received fish oil supplementation”16
The following compounds support:
-repair and regeneration of intestinal lining
-reduction of autoimmune onset and subsequent flare-ups
“Regarding intestinal permeability, Zinc Carnosine caused an approximate threefold increase in gut integrity and repair”17
“Curcumin, a component of turmeric, has been shown to be non-toxic, to have antioxidant activity, and to inhibit such mediators of inflammation as NFB, cyclooxygenase-2 (COX-2), lipooxygenase (LOX), and inducible nitric oxide synthase (iNOS)”18
“In a larger, randomized, double-blind, multicenter trial involving patients with quiescent ulcerative colitis, https://drhagmeyer.com/wp-content/uploads/2022/08/pexels-karolina-grabowska-5904094-1.pngistration of 1 g of curcumin twice daily resulted in both clinical improvement and a statistically significant decrease in the rate of relapse”19
“In various chronic illnesses in which inflammation is known to play a major role, curcumin has been shown to exhibit therapeutic potential. These diseases include Alzheimer’s disease (AD), Parkinson’s disease, multiple sclerosis, epilepsy, cerebral injury, CVDs, cancer, allergy, asthma, bronchitis, colitis, rheumatoid arthritis, renal ischemia, psoriasis, diabetes, obesity, depression, fatigue, and AIDS”20
Generated in the liver, Glutathione is one of the body’s key antioxidants and guards our cells’ energy producing powerhouse, the mitochondria. Ultimately it is glutathione that takes on any free radical so that the mitochondria is not affected. When this system breaks down, the immune system is activated and the body’s ability to produce cellular energy is compromised. As the immune response is triggered, inducible nitric oxide synthase (iNOS) is also activated which leads to tissue destruction and begets further autoimmunity. A functional glutathione system is mandatory in autoimmune prevention.
One study found that tissue destruction was higher in participants with a lower glutathione status. Conversely, those with the most glutathione activity were also found to have the least amount of tissue destruction. Fundamental to autoimmunity modulation, glutathione aides in supporting T-cell regulation and tissue regeneration.As the glutathione recycling system breaks down, the body cannot properly regulate T-cells which are key players in modulating autoimmune attacks and systemic inflammation. Glutathione reinforces GI function by supporting the formation of tighter junctions in intestinal lining.
The other system that is important in autoimmune modulation is the nitric oxide system. Nitric oxide is an important messenger molecule involved in many physiological and pathological processes. Depending on which isomer is indicated it’s effect on autoimmunity can be either destructive, causing inflammation in the tissue, or protective, supporting tissue regrowth. There are many isomers of nitric oxide that affect the body in various ways.
Nitric Oxide Synthase Isomers
-Enhances neuronal synapses
-Safeguards the neurons
-Aides in tissue recovery and regeneration
-Optimizes blood flow
-Dissolves endothelium plaques
-Dilates blood vessels
-Encourages tissue destruction
-Ignites AI attack
Destruction of tissue in autoimmune disease can be caused by:
• Elevated iNOS (increased tissue destruction)
• Decreased eNOS (cold hands, feet, decreased blood flow)
• Decreased nNOS (decreased brain function)
How these isomers are manipulated or modulated will determine how much destruction of tissue or ability to recover from autoimmune flare-ups a person has.
“Based on these data, it appears that the isoforms of NOS contribute to pathophysiology, and that induced NOS and NO may function, in part, in a protective pathway.”2
“Collectively, these data implicate discrete roles for the NOS isoforms in the emergence of local tissue pathology and underscore the need to define the specific pathways that are being targeted.”3
Increased iNOS promotes intestinal permeability
The literature suggests a correlation between up-regulation of iNOS isomers and increased intestinal permeability:
“iNOS up-regulation and oxidation/nitration of intestinal cytoskeletal proteins, promotes intestinal leakiness. We hypothesized that iNOS inhibitors will inhibit the liver and intestinal barrier cascade.”4
“We conclude that NO plays a critical immunoregulatory role and NO modulation may prevent the onset of autoimmune reactions.”5
“Together, these data indicate that antioxidant modulation of nitric oxide might be a feasible therapeutic tool to interfere with development of autoimmune diabetes.”6
“Interleukin-17 is a proinflammatory cytokine involved in autoimmune disorders. The proinflammatory action of IL-17 depends considerably on its ability to trigger the expression of inducible nitric oxide (iNOS). We propose IL-17 and NO modulation could be relevant forms of therapy for autoimmune disorders.”7
Citation for some of the content included in this article:Datis Kharrazian, D.C., Autoimmune Regulation of the Nitric Oxide and Glutathione Systems, 11/4/10
Take Away Points
•Vitamin D is an important modulator of autoimmunity and intestinal permeability
•Vitamin D regulates immune function and acts on the immune system in many ways to suppress systemic inflammation
•Glutathione is the body’s most important anti-oxidant
•Glutathione plays a significant role in preventing and modulating autoimmune disease
•Lower glutathione status equates to more tissue destruction in AI patients
•When the glutathione recycling system fails, there is increased flare ups of autoimmune disease
•Nitric Oxide is critical in autoimmune modulation
•Some isomers have protective or destructive qualities based on which is expressed
•The modulation of these isomers determines how much tissue damage takes place and the recovery of the tissue
•Upregulation of iNOS (inducible nitric oxide synthase) increases intestinal permeability
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