Vitamin D Levels in ME/CFS and Other Diseases

percyval577

basal and ganglia
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Because ME/CFS triggering viruses either have an effect on the vitamin D receptor or can be associated with vitamin D (thread and lit.) it should be wise to have a look at deficiencies (although a simple relationship is hardly to be expected).
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Vitamin D status in chronic fatique syndrome/myalgic encephalomyelitis: a cohort study from the North-West of England
Earl et al 2017


from the Discussion (my paragraphing)
In conclusion, patients with CFS/ME do not exhibit insufficient concentrations of circulating 25(OH)D3 at any time of the year. Given that this cohort of patients with CFS/ME clearly displays symptoms, regardless of serum 25(OH)D concentration, these data indicate that vitamin D status may not be a major contributing factor to the pathophysiology of patient with CFS/ME symptoms, although further analyses of those individuals with lower circulating 25(OH)D and more detailed investigation into vitamin D metabolism is still warranted.

Current health guidelines in the UK state supplementation of vitamin D should be recommended to individuals with increased risk of deficiency and the findings from the present study suggest, in agreement with other studies, that a significant percentage of healthy individuals exhibit insufficient concentrations of circulating vitamin D during the autumn and winter months.

The current findings do not support the notion that vitamin D concentration contributes to the continuing symptoms of CFS/ME. However, it may be important for patients with CFS/ME to supplement with vitamin D during the winter months as it is well documented that non-supplemented individuals may typically present with insufficient serum 25(OH)D during the winter season.
from the Discussion
A further limitation to the study was that only the main marker of vitamin D status, that is, 25(OH)D, was measured. It has recently been shown that there is a need to assess all of the vitamin D metabolites.35 [Johnson et al 2014: "Serum free and bioavailable 25-hydroxyvitamin D correlate better with bone densitiy than serum total 25-hydroxyvitamn-D.] It may be more appropriate to measure the amount of serum-free and bioavailable 25(OH)D as a predictor of vitamin D status than serum total 25(OH)D, while controlling for vitamin D binding protein phenotype.36 Future studies assessing these aspects of vitamin D metabolism in patients with CFS/ME are warranted.
open access
BMJ Open. 2017 Nov 8;7(11):e015296. doi: 10.1136/bmjopen-2016-015296.
 
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percyval577

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Vitamin D3 Deficiency Results in Dysfunction of Immunity with Severe Fatique and Depression in a variety of Diseases
Anna D Höck 2014, Review

Especially physiological effects of Vitamin D are reviewed. The author is a physician.


from the discussion
Fortunately, an increasing number of authors acknowledge the importance of vitamin D in immunoregulation (168-180).

Epidemiological studies report a correlation between an insufficient level of 25OHD3 and several immune diseases, such as chronic pulmonary infections (168-170), multiple sclerosis (171-174), SLE (175, 180), diabetes and cardiovascular diseases (22, 176), and cancer (7, 177-179). Additionally, low 25OHD3 levels and elevated immunoreactivity against Epstein-Barr virus were found before the onset of multiple sclerosis (171), and up-regulation of VDR and CYP27B1 was found in active lesions (174). Low 25OHD3 levels also correlated with recurrence of spinal inflammatory lesions (172), and reduced survival in ovarian cancer (179). Genetic variations in enzymes of the vitamin D pathway were found to augment the risk for multiple sclerosis (173), and differentiated thyroid carcinoma (178).

Low 25OHD3 levels were also prevalent in patients with FMS and CFS (2, 6, 8, 9, 11, 12, 14, 15).
from the Discussion
In contrast to these epidemiological studies, interventional studies are still rare and small-sized. After one-year treatment with 2,000 IU (50 μg)/day cholecalciferol, inflammatory and hemostatic markers and disease activity in SLE improved (180). A dose of 800 IU (20 μg) cholecalciferol/day applied for 2.5-10 months improved fatigue in patients with myasthenia gravis (10). Rehabilitation outcomes improved after vitamin D supplementation in those with multiple illnesses (16). 4,000 IU (100 μcg) cholecalciferol/day for one year reduced recurrent infections of the respiratory tract significantly (169). Importantly, a pilot study showed clearly improved mitochondrial oxidative function after normalization of 25OHD3 levels in 12 severely vitamin D3-deficient patients with chronic fatigue and myopathy (166).

However, large interventional studies and clear evidence for usefulness of vitamin D3 treatment are still lacking. One cause of obvious reluctance to undertake larger interventional studies may be the ongoing debate and overall uncertainty about doses and possible side-effects of vitamin D3 treatment.

[original paragraph]​

Timely diagnosis of underlying vitamin D3 deficiency or insufficiency and adequate treatment, even at the stage of unexplained chronic fatigue, is warranted.

Measuring the blood levels of the precursor 25OHD3 is easy and cost-effective. In contrast, an elevated level of the active metabolite 1,25(OH)2D3 does not indicate vitamin D sufficiency, but might be an important clue to calcium deficiency, presumably associated with autoimmunity (2). Sufficiency is defined as 25OHD3 levels above 30-100 ng/ml (75-250 nmol/l). Levels of 10-30 ng/ml (25-75 nmol/l) indicate insufficiency, those below 10 ng/ml (25 nmol/l) clear-cut deficiency.

Therapy is equally easy. Cholecalciferol can be applied orally, and continuous daily substitution is recommended. The therapeutic dose ranges from 4,000 to 10,000 IU (100-250 μg)/day. Higher doses of about 10,000 IU/day, and concurrent mineral, or other co-factor substitution are warranted in order to overcome eventual vitamin D3 resistance, such as in calcium deficiency. In contrast to drugs usually recommended for chronic inflammatory, autoimmune or malignant diseases, cholecalciferol is very inexpensive.

[original paragraph]​

Early treatment of chronic fatigue and recurrent infections might prevent full-blown CFS/ME. Elevating 25OHD3 levels in early stages of diseases may ameliorate the course, and shorten the time needed for induction therapy, thus lowering total treatment costs. Deleterious side-effects, often life-threatening, of modern biological, cytostatic or immunosuppressive compounds may be avoided, or at least reduced. Incidence of relapse and treatment resistance may decrease, as well as the burden of disease, and therapy costs. However, usefulness and cost-effectiveness of vitamin D3 co-treatment needs further investigation from high-powered and carefully designed clinical studies.
open acces
In Vivo. 2014 Jan-Feb;28(1):133-45
 
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tyson oberle

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I had my vitamin D level checked and it tested low, so then I started taking vitamin D and I also started eating more foods with vitamin D naturally in them. Then I got it retested and it tested optimal, but I didn't feel any better.