Skeletal remodelling is a continuous process during life and is still active also in extreme senescence. In the elderly, bone resorption often prevails over bone formation, causing bone loss and fragility. Elderly subjects are exposed to the risk of fractures, and loss of self-sufficiency, if considering that the proximal femur is the most frequently involved site. Bone remodelling can maintain circulating calcium within physiological ranges, at the expense of a substantial loss of this ion from the skeleton, particularly during senescence.
Vitamin D has received tremendous amount of attention recently due to the ever-increasing reports of association between vitamin D deficiency and a wide range of conditions, from cancer to fertility to longevity. The fascination of disease association with vitamin D deficiency comes from the relatively easy solution to overcome such a risk factor, that is, either by increase in sun exposure and/or diet supplementation.
European researchers have observed that schizophrenia is 3 times more frequent in immigrants than in native-born subjects. This increased risk is even higher in dark-skinned immigrants, and the second generation is more affected than the first one. Immigrant status is an important environmental risk factor not only for schizophrenia but also for other psychoses. The explanations proposed to date have been mainly related to epidemiological biases and psychological reasons, such as racism or social defeat, but no biological hypotheses have been tested so far.
Observational studies document a positive relationship between vitamin D from the environment (sunlight or diet), circulating vitamin D status, and improved symptoms or prevention of multiple sclerosis (MS). Experimental animal models of MS reproduce the beneficial effects of vitamin D and 1,25(OH)(2)D(3). The geographical distribution of MS can be explained by both the hygiene hypothesis and the vitamin D hypothesis.
OBJECTIVE: Inadequate vitamin D status is related to increased adiposity, risk of falls, and muscle weakness, particularly in older people. We hypothesized that serum 25-hydroxyvitamin D [25(OH)D] is related to physical fitness indices (androidal fat, whole body lean mass, balance, strength) in healthy postmenopausal women. METHODS: Covariates for fitness indices included age or years since menopause, weight, 25(OH)D, energy expenditure, and calcium intake.
BACKGROUND: Vitamin D deficiency has potential adverse effects on neurocognitive health and subcortical function. However, no studies have examined the association between vitamin D status, dementia, and cranial MRI indicators of cerebrovascular disease (CVD). METHODS: Cross-sectional investigation of 25-hydroxyvitamin D [25(OH)D], dementia, and MRI measures of CVD in elders receiving home care (aged 65-99 years) from 2003 to 2007. RESULTS: Among 318 participants, the mean age was 73.5 +/- 8.1 years, 231 (72.6%) were women, and 109 (34.3%) were black.
Vitamin D and the vitamin D receptor (VDR) have been shown to be important regulators of the immune system. In particular, vitamin D and VDR deficiency exacerbates experimental autoimmune diseases such as inflammatory bowel disease (IBD). IBD develops due to an immune-mediated attack by pathogenic T-cells that overproduce IL-17 and IFN-gamma and a few regulatory cells. VDR knockout mice have twice as many T-cells making IL-17 and IFN-gamma than wild-type mice.
Vitamin D status changes with season, but the effect of these changes on immune function is not clear. In this study, we show that in utero vitamin D deficiency in mice results in a significant reduction in invariant NKT (iNKT) cell numbers that could not be corrected by later intervention with vitamin D or 1,25-dihydroxy vitamin D(3) (active form of the vitamin). Furthermore, this was intrinsic to hematopoietic cells, as vitamin D-deficient bone marrow is specifically defective in generating iNKT cells in wild-type recipients.
Epidemiologic studies link vitamin D deficiency to onset of type 1 diabetes mellitus (T1DM). T1DM exhibits increased inflammation, which is pronounced with microvascular complications (T1DM-MV). However, there are a paucity of data on vitamin D in T1DM-MV in relation to biomarkers of inflammation, and this formed the aim of the study. Healthy control subjects (n = 36), patients with T1DM (n = 24), and patients with T1DM-MV (n =26) were recruited. Serum vitamin D levels, monocyte toll-like receptor (TLR) 2 and TLR4 expression and nuclear factor-κB (NFκB) activity were assessed.
Multiple pathways converge to result in the overexpression of T(h)17 cells in the absence of either vitamin D or the vitamin D receptor (VDR). CD4(+) T cells from VDR knockout (KO) mice have a more activated phenotype than their wild-type (WT) counterparts and readily develop into T(h)17 cells under a variety of in vitro conditions. Vitamin D-deficient CD4(+) T cells also overproduced IL-17 in vitro and 1,25 dihydroxyvitamin D(3) inhibited the development of T(h)17 cells in CD4(+) T-cell cultures.