Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS
Posted: Wed Apr 23, 2014 9:42 am
An interesting approach to understanding Vit D and MS would be use the episodic or TM (transverse Myelitis of the brain) form of MS and test regularly to establish if the relapse faze is the reason that Vit D is required or if the process of having a relapse uses hi amounts of Vit D. Many diseases draw high amounts of Vit D either by the cause of the disease or by the healing.
Another angle that is often debated with Vit D is the levels and the bodies ability to use the Vit D. A recent article;
From www.chronicillnessrecovery.org
The Compromised Immune System
Persistent intracellular bacterial infection compromises the immune system
and causes a chronic inflammatory response.[1, 2] Cell-wall-deficient
bacteria parasitize nucleated cells in order to escape host defenses, thus
contributing to failures of treatment.[3, 4] The concept that intracellular
bacteria are protected from the host's immune response was first proposed by
Rous in 1916.[5] In an essay on the renin-angiotensin system and the immune
response, Smith postulates that unresolved cellular stress is caused by
infectious agents, with the deliberate intent to avoid adaptive immune
responses.[6] The host immune system has developed many mechanisms to
neutralize and remove pathogenic bacteria. In turn, bacteria have developed
mechanisms to alter and evade the host immune response.[7] For example,
regulation of the vitamin D receptor (VDR) is a common mechanism used in the
host defense against pathogens, but certain microbes have been shown to slow
innate immune defenses by down-regulating the VDR:
Mycobacterium tuberculosis down-regulates VDR activity.[8]
Mycobacterium leprae inhibits VDR activity through down-regulation of
CYP27B1 in monocytes.[9]
Aspergillus fumigates secretes a toxin capable of down-regulating VDR in
macrophages.[10]
Epstein-Barr virus lowers VDR activity.[11]
HIV completely shuts down VDR activity.[12]
In VDR knockout mice, a circumstance that closely mimics extreme VDR
dysregulation, 1,25-D levels increase by a factor of ten.[13]
Slowing the ability of the VDR to express elements of innate immune function
allows intracellular bacteria to persist in the cytoplasm of nucleated cells
and increases susceptibility to co-infections that are commonly found in
patients with chronic illnesses (e.g., viruses, fungi, parasites and
cell-walled bacteria).[14]
Elevated 1,25(OH)2D is evidence of the dysregulated immune system's attempt
to activate the VDR to produce antimicrobial peptides (e.g., cathelicidin)
to combat infection.[15] Studies have found elevated 1,25(OH)2D and reduced
cathelicidin in chronic diseases:
Sarcoidosis patients are deficient in cathelicidin despite healthy vitamin
D3 levels.[16]
1,25(OH)2D is elevated (>60 pg/ml) in 42% of Crohn's patients and the source
of the active vitaminD production appears to be the inflamed intestine.[17]
1,25(OH)2D is elevated in the synovial fluid of patients with RA.[18]
Crohn's disease decreases expression of cathelicidin.[19]
1,25(OH)2D is a marker of vitamin D endocrine function.[20] Down-regulation
by bacterial ligands may prevent the VDR from expressing the enzymes
necessary to keep 1,25(OH)2D in a normal range. Elevated 1,25(OH)2D also
reduces VDR competence, suppresses macrophage function, and inhibits the
Nuclear Factor kappa-ß cytokine pathway, thus further compromising the
immune system.[21-23]
Another angle that is often debated with Vit D is the levels and the bodies ability to use the Vit D. A recent article;
From www.chronicillnessrecovery.org
The Compromised Immune System
Persistent intracellular bacterial infection compromises the immune system
and causes a chronic inflammatory response.[1, 2] Cell-wall-deficient
bacteria parasitize nucleated cells in order to escape host defenses, thus
contributing to failures of treatment.[3, 4] The concept that intracellular
bacteria are protected from the host's immune response was first proposed by
Rous in 1916.[5] In an essay on the renin-angiotensin system and the immune
response, Smith postulates that unresolved cellular stress is caused by
infectious agents, with the deliberate intent to avoid adaptive immune
responses.[6] The host immune system has developed many mechanisms to
neutralize and remove pathogenic bacteria. In turn, bacteria have developed
mechanisms to alter and evade the host immune response.[7] For example,
regulation of the vitamin D receptor (VDR) is a common mechanism used in the
host defense against pathogens, but certain microbes have been shown to slow
innate immune defenses by down-regulating the VDR:
Mycobacterium tuberculosis down-regulates VDR activity.[8]
Mycobacterium leprae inhibits VDR activity through down-regulation of
CYP27B1 in monocytes.[9]
Aspergillus fumigates secretes a toxin capable of down-regulating VDR in
macrophages.[10]
Epstein-Barr virus lowers VDR activity.[11]
HIV completely shuts down VDR activity.[12]
In VDR knockout mice, a circumstance that closely mimics extreme VDR
dysregulation, 1,25-D levels increase by a factor of ten.[13]
Slowing the ability of the VDR to express elements of innate immune function
allows intracellular bacteria to persist in the cytoplasm of nucleated cells
and increases susceptibility to co-infections that are commonly found in
patients with chronic illnesses (e.g., viruses, fungi, parasites and
cell-walled bacteria).[14]
Elevated 1,25(OH)2D is evidence of the dysregulated immune system's attempt
to activate the VDR to produce antimicrobial peptides (e.g., cathelicidin)
to combat infection.[15] Studies have found elevated 1,25(OH)2D and reduced
cathelicidin in chronic diseases:
Sarcoidosis patients are deficient in cathelicidin despite healthy vitamin
D3 levels.[16]
1,25(OH)2D is elevated (>60 pg/ml) in 42% of Crohn's patients and the source
of the active vitaminD production appears to be the inflamed intestine.[17]
1,25(OH)2D is elevated in the synovial fluid of patients with RA.[18]
Crohn's disease decreases expression of cathelicidin.[19]
1,25(OH)2D is a marker of vitamin D endocrine function.[20] Down-regulation
by bacterial ligands may prevent the VDR from expressing the enzymes
necessary to keep 1,25(OH)2D in a normal range. Elevated 1,25(OH)2D also
reduces VDR competence, suppresses macrophage function, and inhibits the
Nuclear Factor kappa-ß cytokine pathway, thus further compromising the
immune system.[21-23]