Clinical and Epidemiologic Research Vitamin D and Macular Thickness in the Elderly: An Optical Coherence Tomography Study

PURPOSE. Vitamin D insufficiency is associated with age-related macular degeneration. Our objective was to determine whether low serum 25-hydroxyvitamin D (25OHD) concentration was associated with macular thickness among older adults with no signs of macular dysfunction. METHODS. Sixty-two French older community-dwellers with no patent macular dysfunction (mean 6 SD, 71.2 6 5.0 years; 45.2% female) included in the Gait and Alzheimer Interaction Tracking (GAIT) study (ClinicalTrials.gov number, NCT01315717) were separated into two groups according to serum 25OHD level (i.e., insufficient < 50 nmol/L or sufficient ‡ 50 nmol/ L). The macular thickness was measured on 1000 lm central macula with optical coherence tomography, and further binarized according to normal values of macular thickness (i.e., 267.74 lm for males, and 255.60 lm for females). Age, sex, number of comorbidities, cognitive disorders, body mass index, mean arterial pressure, visual acuity, intraocular pressure, serum calcium concentration and season of testing were considered as potential confounders. RESULTS. The mean serum 25OHD concentration was 61.2 6 26.3 nmol/L. Patients with vitamin D insufficiency had a reduced macular thickness compared to those without (232.9 6 40.4 lm vs. 253.3 6 32.1 lm, P ¼ 0.042). After adjustment for potential confounders, vitamin D insufficiency was associated with a decreased macular thickness (b ¼ À59.4 lm, P ¼ 0.001). Consistently, the participants with vitamin D insufficiency had a 3.7-fold higher risk of having abnormally low macular thickness compared with those with sufficient 25OHD level (P ¼ 0.042). CONCLUSIONS. Vitamin D insufficiency was associated with reduced macular thickness among older patients with no patent macular dysfunction. This implies that vitamin D insufficiency may be involved in macular thinning, and provides a scientific base for vitamin D replacement trials in age-related macular degeneration. Keywords: macular thickness, vitamin D, neuroendocrinology, older adults, age-related macular degeneration, retina B eyond its classical contribution to bone health, vitamin D is a secosteroid hormone involved in several target tissues expressing vitamin D receptors, 1,2 including the retina. MATERIALS AND METHODS Participants We studied 73 community dwellers (mean age 70.9 6 4.9 years; 42.9% female) followed in the Memory Clinic of Anger

Fall prevention and vitamin D in the elderly: an overview of the key role of the non-bone effects

Preventing falls and fall-related fractures in the elderly is an objective yet to be reached. There is increasing evidence that a supplementation of vitamin D and/or of calcium may reduce the fall and fracture rates. A vitamin D-calcium supplement appears to have a high potential due to its simple application and its low cost. However, published studies have shown conflicting results as some studies failed to show any effect, while others reported a significant decrease of falls and fractures. Through a 15-year literature overview, and after a brief reminder on mechanism of falls in older adults, we reported evidences for a vitamin D action on postural adaptations - i.e., muscles and central nervous system - which may explain the decreased fall and bone fracture rates and we underlined the reasons for differences and controversies between published data. Vitamin D supplementation should thus be integrated into primary and secondary fall prevention strategies in older adults

Test-retest reliability of stride time variability while dual tasking in healthy and demented adults with frontotemporal degeneration

Although test-retest reliability of mean values of spatio-temporal gait parameters has been assessed for reliability while walking alone (i.e., single tasking), little is known about the test-retest reliability of stride time variability (STV) while performing an attention demanding-task (i.e., dual tasking). The objective of this study was to examine immediate test-retest reliability of STV while single and dual tasking in cognitively healthy older individuals (CHI) and in demented patients with frontotemporal degeneration (FTD)

Maternal and Neonatal Vitamin D Binding Protein Polymorphisms and 25-Hydroxyvitamin D Cutoffs as Determinants of Neonatal Birth Anthropometry

BACKGROUND: Vitamin D-binding protein (VDBP) is a vital regulator of optimal vitamin D homeostasis and bioavailability. Apart from its well-documented role as a key component in vitamin D dynamic transfer and circulation, it has a myriad of immunoregulatory functions related to innate immunity, which becomes particularly critical in states of increased immunological tolerance including pregnancy. In this regard, VDBP dyshomeostasis is considered to contribute to the development of several fetal, maternal, and neonatal adverse outcomes. However, precise physiological pathways, including the contribution of specific VDBP polymorphisms behind such phenomena, are yet to be fully deciphered. Our aim was to assess the combined effect of maternal and neonatal VDBP polymorphism heterogeneity in conjunction with different maternal and neonatal 25(OH)D cutoffs on the neonatal anthropometric profile at birth. METHODS: The study included data and samples from a cohort of 66 mother-child pairs at birth. The inclusion criterion was full-term pregnancy (gestational weeks 37-42). Neonatal and maternal 25(OH)D cutoffs were included according to vitamin D status at birth and delivery. Concentrations of 25(OH)D2 and 25(OH)D3 were measured using liquid chromatography-tandem mass spectrometry. RESULTS: The upper arm length of neonates with 25(OH)D ≤ 25 nmol/L was higher in neonate CC carriers for rs2298850. The upper thigh neonatal circumference was also higher in the ones with either 25(OH)D ≤ 50 or ≤75 nmol/L in rs2298850 CG + GG or rs4588 GT + TT carriers. We did not observe any significant effect for maternal VDBP polymorphisms nor for birth maternal 25(OH)D concentrations, on birth neonatal anthropometry. CONCLUSIONS: Our findings emphasize a potential role for neonatal VDBP genotypes rs2298850 and rs4588, in conjunction with specific neonatal 25(OH)D cutoffs, in the range of sufficiency on neonatal growth and development

Investigating the role of functional polymorphism of maternal and neonatal vitamin D binding protein in the context of 25‐hydroxyvitamin D cutoffs as determinants of maternal‐neonatal vitamin D status profiles in a sunny mediterranean region

Recent results indicate that dysregulation of vitamin D‐binding protein (VDBP) could be involved in the development of hypovitaminosis D, and it comprises a risk factor for adverse fetal, maternal and neonatal outcomes. Until recently, there was a paucity of results regarding the effect of maternal and neonatal VDBP polymorphisms on vitamin D status during pregnancy in the Mediterranean region, with a high prevalence of hypovitaminosis D. We aimed to evaluate the combined effect of maternal and neonatal VDBP polymorphisms and different maternal and neonatal 25‐hy-droxyvitamin D (25(OH)D) cut‐offs on maternal and neonatal vitamin D profile. Blood samples were obtained from a cohort of 66 mother–child pairs at birth. Our results revealed that: (i) Maternal VDBP polymorphisms do not affect neonatal vitamin D status at birth, in any given internationally adopted maternal or neonatal cut‐off for 25(OH)D concentrations; (ii) neonatal VDBP polymor-phisms are not implicated in the regulation of neonatal vitamin D status at birth; (iii) comparing the distributions of maternal VDBP polymorphisms and maternal 25(OH)D concentrations, with cutoffs at birth, revealed that mothers with a CC genotype for rs2298850 and a CC genotype for rs4588 tended to demonstrate higher 25(OH)D (≥75 nmol/L) during delivery (p = 0.05 and p = 0.04, respec-tively), after adjustments for biofactors that affect vitamin D equilibrium, including UVB, BMI and weeks of gestation. In conclusion, this study from Southern Europe indicates that maternal and neonatal VDBP polymorphisms do not affect neonatal vitamin D status at birth, whereas mothers with CC genotype for rs2298850 and CC genotype for rs4588 demonstrate higher 25(OH)D concen-trations. Future larger studies are required to establish a causative effect of these specific polymor-phisms in the attainment of an adequate (≥75 nmol/L) maternal vitamin D status during pregnancy

Associations between total, free and bioavailable 25-hydroxyvitamin D forms with adiponectin and irisin in maternal-neonatal pairs at birth from Greece

Background: Apart from the well-established skeletal effects, vitamin D has been explored as a secretagogue influencing various adipokines, including adiponectin and irisin. Recent evidence suggests that specific forms of 25-Hydroxyvitamin D (25(OHD), such as free and bioavailable 25(OH)D, may provide more accurate measurements of vitamin D status. The relationship between vitamin D status and serum irisin and adiponectin concentrations remains largely unexplored, particularly during pregnancy. Methods: We analyzed data from 67 healthy maternal-neonatal pairs from Northern Greece at birth. Biochemical and hormonal tests were conducted on each maternal-neonatal pair. The vitamin D forms were estimated using validated mathematical models. Subsequently, regression analyses were conducted to determine the association between the vitamin D forms and adipokine levels. Results: Bioavailable maternal 25(OH)D was inversely associated with neonatal irisin concentrations [β=-73.46 (-140.573 to -6.341), p=0.034]. No other associations were observed between maternal vitamin D status and neonatal adipokine concentrations. Conclusion: In conclusion, maternal bioavailable vitamin D concentrations are inversely associated with neonatal serum irisin concentrations, warranting further studies to evaluate the underlying mechanisms for this finding

Vitamin D and the risk of dementia and Alzheimer disease

OBJECTIVE: To determine whether low vitamin D concentrations are associated with an increased risk of incident all-cause dementia and Alzheimer disease. METHODS: One thousand six hundred fifty-eight elderly ambulatory adults free from dementia, cardiovascular disease, and stroke who participated in the US population-based Cardiovascular Health Study between 1992-1993 and 1999 were included. Serum 25-hydroxyvitamin D (25(OH)D) concentrations were determined by liquid chromatography-tandem mass spectrometry from blood samples collected in 1992-1993. Incident all-cause dementia and Alzheimer disease status were assessed during follow-up using National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria. RESULTS: During a mean follow-up of 5.6 years, 171 participants developed all-cause dementia, including 102 cases of Alzheimer disease. Using Cox proportional hazards models, the multivariate adjusted hazard ratios (95% confidence interval [CI]) for incident all-cause dementia in participants who were severely 25(OH)D deficient (<25 nmol/L) and deficient (≥25 to <50 nmol/L) were 2.25 (95% CI: 1.23-4.13) and 1.53 (95% CI: 1.06-2.21) compared to participants with sufficient concentrations (≥50 nmol/L). The multivariate adjusted hazard ratios for incident Alzheimer disease in participants who were severely 25(OH)D deficient and deficient compared to participants with sufficient concentrations were 2.22 (95% CI: 1.02-4.83) and 1.69 (95% CI: 1.06-2.69). In multivariate adjusted penalized smoothing spline plots, the risk of all-cause dementia and Alzheimer disease markedly increased below a threshold of 50 nmol/L. CONCLUSION: Our results confirm that vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer disease. This adds to the ongoing debate about the role of vitamin D in nonskeletal conditions.National Heart, Lung, and Blood InstituteNational Institute of Neurological Disorders and StrokeNational Institute on AgingAlzheimer's AssociationMary Kinross Charitable TrustJames Tudor FoundationHalpin TrustAge Related Diseases and Health TrustNorman Family Charitable TrustUK National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care (CLAHRC) for the South West Peninsul

O2‐03‐02: Vitamin D and the risk of developing neuroimaging abnormalities

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/152624/1/alzjjalz201507143.pd

Vitamin D and the risk of dementia and Alzheimer disease

Objective: To determine whether low vitamin D concentrations are associated with an increased risk of incident all-cause dementia and Alzheimer disease. Methods: One thousand six hundred fifty-eight elderly ambulatory adults free from dementia, cardiovascular disease, and stroke who participated in the US population?based Cardiovascular Health Study between 1992?1993 and 1999 were included. Serum 25-hydroxyvitamin D (25(OH)D) concentrations were determined by liquid chromatography-tandem mass spectrometry from blood samples collected in 1992?1993. Incident all-cause dementia and Alzheimer disease status were assessed during follow-up using National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer\u27s Disease and Related Disorders Association criteria. Results: During a mean follow-up of 5.6 years, 171 participants developed all-cause dementia, including 102 cases of Alzheimer disease. Using Cox proportional hazards models, the multivariate adjusted hazard ratios (95% confidence interval [CI]) for incident all-cause dementia in participants who were severely 25(OH)D deficient (\u3c25 nmol/L) and deficient (?25 to \u3c50 nmol/L) were 2.25 (95% CI: 1.23?4.13) and 1.53 (95% CI: 1.06?2.21) compared to participants with sufficient concentrations (?50 nmol/L). The multivariate adjusted hazard ratios for incident Alzheimer disease in participants who were severely 25(OH)D deficient and deficient compared to participants with sufficient concentrations were 2.22 (95% CI: 1.02?4.83) and 1.69 (95% CI: 1.06?2.69). In multivariate adjusted penalized smoothing spline plots, the risk of all-cause dementia and Alzheimer disease markedly increased below a threshold of 50 nmol/L. Conclusion: Our results confirm that vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer disease. This adds to the ongoing debate about the role of vitamin D in nonskeletal conditions