As an adendum to the other post on sunlight sensitivity:

Here's a paper which touches upon chronic inflammation, and the mechanism of hyper vit D, and the subsequent hormone scew up this disregulation causes - (sun light sensitivity).
The cycle of chronic inflammation.
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Endocrinology. 1996 Oct;137(10):4514-7. Related Articles, Links

Autoregulation of 1,25-dihydroxyvitamin D synthesis in macrophage mitochondria by nitric oxide.

Adams JS, Ren SY.

Department of Medicine, Burns and Allen Cedars-Sinai Research Institute, UCLA School of Medicine 90048, USA.

Tissue macrophages from patients with granuloma-forming disease, most notably sarcoidosis, express a 25-hydroxyvitamin D-1-hydroxylase which can produce in vivo sufficient quantities of the active vitamin D metabolite 1,25-dihydroxyvitamin D to cause hypercalcemia. In contrast to the NADPH-dependent cytochrome P450-linked mixed function oxidase which is normally only expressed in significant quantity in proximal renal tubular cells and regulated in an endocrine fashion, the mitochondrial-based 1-hydroxylase in the macrophage [1] is stimulated in a paracrine mode by cytokines (i.e., IFN-gamma) and lipopolysaccharide (LPS) [2] requires an extracellular source of L-arginine for full basal expression and [3] can be regulated in an intracrine fashion by nitric oxide (NO). In these experiments we employed inducible nitric oxide synthase (iNOS)-free, intact mitochondria preparations from the avain macrophage-like cell line HD-11, which constitutively express the 1-hydroxylase, and nonenzymatically-generated NO to investigate NO-mediated autoregulation of the macrophage 1-hydroxylase. Sodium nitroprusside (SNP)- or S-nitroso-N-acetyl-penicillamine (SNAP)-induced up-regulation of the 1-hydroxylase required the presence of either NADPH or NADP in the reaction mixture, while NO-induced inhibition of mitochondrial 1,25-(OH)2D3 synthesis was NO-dependent and NADP/NADPH-independent. These data suggest NO has bifunctional effects on the macrophage 1-hydroxylase. At relatively high concentrations NO competes with O2 for enzyme binding, inhibiting hormone synthesis. At lower production levels, NO serves as a source of reducing equivalents for the enzyme by providing for the reduction of NADP to NADPH.

PMID: 8828516 [PubMed - indexed for MEDLINE]

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Mayo Clin Proc. 2003 Dec;78(12):1463-70.

Comment in:
Mayo Clin Proc. 2003 Dec;78(12):1457-9.

Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain.

Plotnikoff GA, Quigley JM.

Department of Internal Medicine, University of Minnesota Medical School, Minneapolis, Minn, USA. [email protected]

OBJECTIVE: To determine the prevalence of hypovitaminosis D in primary care outpatients with persistent, nonspecific musculoskeletal pain syndromes refractory to standard therapies.

PATIENTS AND METHODS: In this cross-sectional study, 150 patients presented consecutively between February 2000 and June 2002 with persistent, nonspecific musculoskeletal pain to the Community University Health Care Center, a university-affiliated inner city primary care clinic in Minneapolis, Minn (45 degrees north). Immigrant (n = 83) and nonimmigrant (n = 67) persons of both sexes, aged 10 to 65 years, from 6 broad ethnic groups were screened for vitamin D status. Serum 25-hydroxyvitamin D levels were determined by radioimmunoassay.

RESULTS: Of the African American, East African, Hispanic, and American Indian patients, 100% had deficient levels of vitamin D (< or = 20 ng/mL). Of all patients, 93% (140/ 150) had deficient levels of vitamin D (mean, 12.08 ng/mL; 95% confidence interval, 11.18-12.99 ng/mL). Nonimmigrants had vitamin D levels as deficient as immigrants (P = .48). Levels of vitamin D in men were as deficient as in women (P = .42). Of all patients, 28% (42/150) had severely deficient vitamin D levels (< or = 8 ng/mL), including 55% of whom were younger than 30 years. Five patients, 4 of whom were aged 35 years or younger, had vitamin D serum levels below the level of detection. The severity of deficiency was disproportionate by age for young women (P < .001), by sex for East African patients (P < .001), and by race for African American patients (P = .006). Season was not a significant factor in determining vitamin D serum levels (P = .06).

CONCLUSION: All patients with persistent, nonspecific musculoskeletal pain are at high risk for the consequences of unrecognized and untreated severe hypovitaminosis D. This risk extends to those considered at low risk for vitamin D deficiency: nonelderly, nonhousebound, or nonimmigrant persons of either sex. Nonimmigrant women of childbearing age with such pain appear to be at greatest risk for misdiagnosis or delayed diagnosis. Because osteomalacia is a known cause of persistent, nonspecific musculoskeletal pain, screening all outpatients with such pain for hypovitaminosis D should be standard practice in clinical care.

PMID: 14661675 [PubMed - indexed for MEDLINE]

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Minn Med. 2003 Jan;86(1):43-5.

Vitamin D--the steroid hormone prescription for every patient.

Plotnikoff GA.

University of Minnesota, USA.

Physicians in the United States rarely screen for hypovitaminosis D and rarely prescribe vitamin D, even when medically indicated. This is of particular concern in Minnesota. The sun's intensity at Minnesota's latitudes limits vitamin D production, at best, to March through October. A variety of lifestyle situations, including long work hours, may preclude adequate sun exposure. Additionally, people of Northern European background may avoid sun exposure to reduce risk of skin cancer and premature aging. And people of Asian and African heritage may not have sufficient vitamin D production due to increased skin pigmentation. This brief article summarizes key points regarding the importance of vitamin D, including its action as a steroid hormone and its role in cancer, hypertension, and autoimmune disease as well as in perinatal and prenatal health. The potential benefit of hypovitaminosis D screening and vitamin D supplementation is discussed, as are the populations most likely to need screening and supplementation.

PMID: 12585559 [PubMed - indexed for MEDLINE]

Now, one consideration might be the following, and I'll admit that I haven't taken time to look into it. Supposedly, there are different forms of vitamin D and its precursors. So, maybe the body isn't metabolizing it correctly. Also, it could be that these researchers are measuring it in a different way or are measuring a different form of it, since there's supposedly an active form and an inactive form of Vit D (I think).

PS - Since you didn't give the link to the previous topic on sunlight, I'll add it here, for benefit of folks who might have trouble finding it later.

http://flash.lymenet.org/ubb/Forum1/HTML/024684.html

Inflammation causing the inability to process the hormones correctly (mis regulation of Vit D.)

It's not understood by most Drs. correctly.

Chronic Lyme = chronic inflammation = overlap in symptoms with other inflammatory diseases.

The results are the same to the patient, regardless of the name of the disease.

This ties toether the previous discussions on Nitric Oxide, lippopolysacharides and hyper sensitivities.