Probably the most important part of healthy living is getting good sleep. Without it we will get diseases of all sorts. -Dr. A
Sleep disturbance is a frequent and serious complication of hemodialysis (HD). Low serum vitamin D levels have been associated with sleep quality in non-HD subjects. Our aim was to examine the possible association between serum vitamin D levels and the presence of sleep disturbance in HD patients. We recruited 141 HD patients at the HD center of the First Affiliated Hospital of Jiaxing University during 2014–2015. Serum levels of 25-hydroxyvitamin D (25(OH)D) were determined by the competitive protein-binding assay. Sleep quality was measured using the Pittsburgh Sleep Quality Index (PSQI). Demographic, clinical and laboratory data were recorded. Meanwhile, 117 healthy control subjects were also recruited and underwent measurement of 25(OH)D. Eighty-eight patients (62.4%) had sleep disturbance (PSQI scores ≥ 5). Patients with sleep disturbance showed lower levels of 25(OH)D as compared to those without sleep disturbance (85.6 ± 37.4 vs. 39.1 ± 29.1 nmol/L, p < 0.001). In multivariate analyses, serum levels of 25(OH)D (≤48.0 nmol/L) were independently associated with sleep disturbance in HD patients (OR 9.897, 95% CI 3.356–29.187, p < 0.001) after adjustment for possible variables. Our study demonstrates that low serum levels of vitamin D are independently associated with sleep disturbance in HD patients, but the finding needs to be confirmed in future experimental and clinical studies.
Deficits in riboflavin availability, imbalances in the intracellular ratio of FAD to FMN, and mutations that affect flavin binding domains and/or interactions with client proteins result in marked structural alterations within the skeletal and central nervous systems similar to those of disorders (inborn errors) in the biosynthetic pathways that lead to cholesterol, steroid hormones, and vitamin D and their metabolites. Studies of riboflavin deficiency during embryonic development demonstrate congenital malformations similar to those associated with genetic alterations of the flavoenzymes in these pathways. Overall, a deeper understanding of the role of riboflavin in these pathways may prove essential to targeted therapeutic designs aimed at cholesterol and vitamin D metabolism.
A major source of vitamin D for most humans is synthesized from the exposure of the skin to sunlight typically between 1000 h and 1500 h in the spring, summer, and fall.[1,29,33,60] Vitamin D produced in the skin may last at least twice as long in the blood compared with ingested vitamin D. When an adult wearing a bathing suit is exposed to one minimal erythemal dose of UV radiation (a slight pinkness to the skin 24 h after exposure), the amount of vitamin D produced is equivalent to ingesting between 10,000 and 25,000 IU. A variety of factors reduce the skin’s production of vitamin D3, including increased skin pigmentation, aging, and the topical application of a sunscreen.[1,36,37] An alteration in the zenith angle of the sun caused by a change in latitude, season of the year, or time of day dramatically influences the skin’s production of vitamin D3.[1,33]
Around 100,000 people in the UK are battling the disease, so the new study suggests that upping their intake of vitamin D could have a major impact.The disease destroys the fatty myelin sheath that insulates nerve fibres and assists the transmission of electrical signals. It can cause symptoms ranging from mild tingling or numbness to full-blown paralysis.
“These results are exciting, as vitamin D has the potential to be an inexpensive, safe and convenient treatment for people with MS,” said lead scientist Dr Peter Calabresi, from Johns Hopkins University School of Medicine in Baltimore.”More research is needed to confirm these findings with larger groups of people and to help us understand the mechanisms for these effects, but the results are promising.
“The body makes vitamin D when the body is in direct sunlight. Vitamin D is known to be important for bone health and it can nautrally be obtained by eating cheese, eggs and fish oil, as well as direct exposure to sunlight. For the new study, 40 patients with relapsing-remitting MS – a form of the disorder characterised by active and passive periods – received either 10,400 or 800 international units (IU) of vitamin D3 supplements every day for six months.The first dose was significantly higher than the recommended daily allowance for vitamin D of 600 IU.Patients taking the high dose experienced a reduction in the percentage of specific immune system T-cells related to MS activity.
Above a certain threshold, every five nanograms per millilitre increase in vitamin D blood levels led to a 1 per cent reduction of the T-cells, the researchers reported in the journal Neurology. It suggests that the maxim dose could reduce dangerous immune cells by eight per cent.
Previously, we demonstrated i) that ergocalciferol (vitamin D2) increases axon diameter and potentiates nerve regeneration in a rat model of transected peripheral nerve and ii) that cholecalciferol (vitamin D3) improves breathing and hyper-reflexia in a rat model of paraplegia. However, before bringing this molecule to the clinic, it was of prime importance i) to assess which form – ergocalciferol versus cholecalciferol – and which dose were the most efficient and ii) to identify the molecular pathways activated by this pleiotropic molecule. The rat left peroneal nerve was cut out on a length of 10 mm and autografted in an inverted position. Animals were treated with either cholecalciferol or ergocalciferol, at the dose of 100 or 500 IU/kg/day, or excipient (Vehicle), and compared to unlesioned rats (Control). Functional recovery of hindlimb was measured weekly, during 12 weeks, using the peroneal functional index. Ventilatory, motor and sensitive responses of the regenerated axons were recorded and histological analysis was performed. In parallel, to identify the genes regulated by vitamin D in dorsal root ganglia and/or Schwann cells, we performed an in vitro transcriptome study. We observed that cholecalciferol is more efficient than ergocalciferol and, when delivered at a high dose (500 IU/kg/day), cholecalciferol induces a significant locomotor and electrophysiological recovery. We also demonstrated that cholecalciferol increases i) the number of preserved or newly formed axons in the proximal end, ii) the mean axon diameter in the distal end, and iii) neurite myelination in both distal and proximal ends. Finally, we found a modified expression of several genes involved in axogenesis and myelination, after 24 hours of vitamin supplementation. Our study is the first to demonstrate that vitamin D acts on myelination via the activation of several myelin-associated genes. It paves the way for future randomised controlled clinical trials for peripheral nerve or spinal cord repair.
A group of young patients having multiple sclerosis was treated with dietary supplements containing calcium, magnesium and vitamin D for a period of one to two years. The experimental design employed self-pairing: the response of each patient was compared with his/her own case history as control. The number of exacerbations observed during the program was less than one half the number expected from case histories. No side effects were apparent. The dietary regimen may offer a new means of controlling the exacerbation rate in MS, at least for younger patients. The results tend to support a theory of MS which states that calcium and magnesium are important in the development, structure and stability of myelin.
It has been known for more than 20 years that vitamin D exerts marked effects on immune and neural cells. These non-classical actions of vitamin D have recently gained a renewed attention since it has been shown that diminished levels of vitamin D induce immune-mediated symptoms in animal models of autoimmune diseases and is a risk factor for various brain diseases. For example, it has been demonstrated that vitamin D (i) modulates the production of several neurotrophins, (ii) up-regulates Interleukin-4 and (iii) inhibits the differentiation and survival of dendritic cells, resulting in impaired allo-reactive T cell activation. Not surprisingly, vitamin D has been found to be a strong candidate risk-modifying factor for Multiple Sclerosis (MS), the most prevalent neurological and inflammatory disease in the young adult population.
The significant role of vitamin D compounds as selective immunosuppressants is illustrated by their ability to either prevent or markedly suppress animal models of autoimmune disease
Vitamin D intake and incidence of multiple sclerosisK. L. Munger, MSc, S. M. Zhang, MD ScD, E. O’Reilly, MSc, M. A. Hernán, MD DrPH, M. J. Olek, DO, W. C. Willett, MD DrPH and A. Ascherio, MD DrPH
ABSTRACT Background: A protective effect of vitamin D on risk of multiple sclerosis (MS) has been proposed, but no prospective studies have addressed this hypothesis.
Methods: Dietary vitamin D intake was examined directly in relation to risk of MS in two large cohorts of women: the Nurses’ Health Study (NHS; 92,253 women followed from 1980 to 2000) and Nurses’ Health Study II (NHS II; 95,310 women followed from 1991 to 2001). Diet was assessed at baseline and updated every 4 years thereafter. During the follow-up, 173 cases of MS with onset of symptoms after baseline were confirmed.
Results: The pooled age-adjusted relative risk (RR) comparing women in the highest quintile of total vitamin D intake at baseline with those in the lowest was 0.67 (95% CI = 0.40 to 1.12; p for trend = 0.03). Intake of vitamin D from supplements was also inversely associated with risk of MS; the RR comparing women with intake of ≥400 IU/day with women with no supplemental vitamin D intake was 0.59 (95% CI = 0.38 to 0.91; p for trend = 0.006). No association was found between vitamin D from food and MS incidence.
Conclusion: These results support a protective effect of vitamin D intake on risk of developing MS.Received July 22, 2003.Accepted September 17, 2003.