B-vitamins and bone in health and disease: the current evidence

Clarke, M.; Ward, Mary; Strain, JJ; Hoey, Leane; Dickey, William; McNulty, Helene

doi:10.1017/s0029665114000044

Cited by 32 publications

(36 citation statements)

References 95 publications

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“…Zanchi et al demonstrated that children diagnosed with CD at a younger age showed the most robust BMD recovery versus older children and adolescents. 7 Even though vitamin deficiencies, presumably the result of malabsorption, are common in CD at diagnosis and may contribute to fracture risk 3, 38 , despite the initially depressed BMD 39 , following treatment with a GFD both adults and young patients with CD will show improvements in BMD. 12, 13 Risks of falls 40 and bone loss 41 increase with age, resulting in the overwhelming majority of osteoporotic fractures occurring in the elderly, particularly women.…”

Section: Discussionmentioning

confidence: 99%

Celiac Disease Does Not Influence Fracture Risk in Young Patients with Type 1 Diabetes

Reilly

Lebwohl

Mollazadegan

et al. 2016

The Journal of Pediatrics

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Objectives To examine the risk of any fractures in patients with both type 1 diabetes (T1D) and celiac disease (CD) vs patients with T1D only. Study design We performed a population-based cohort study. We defined T1D as individuals aged ≤30 years who had a diagnosis of diabetes recorded in the Swedish National Patient Register between 1964–2009. Individuals with CD were identified through biopsy report data between 1969–2008 from any of Sweden’s 28 pathology departments. Some 958 individuals had both T1D and CD and were matched for sex, age and calendar period with 4,598 reference individuals with T1D only. We then used a stratified Cox regression analysis, where CD was modeled as a time-dependent covariate, to estimate the risk of any fractures and osteoporotic fractures (hip, distal forearm, thoracic and lumbar spine, and proximal humerus) in patients with both T1D and CD compared with that in patients with T1D only. Results During follow-up, 12 patients with T1D and CD had a fracture (1 osteoporotic fracture). CD did not influence the risk of any fracture (adjusted Hazard Ratio=0.77; 95%CI=0.42–1.41) or osteoporotic fractures (adjusted Hazard Ratio=0.46; 95%CI=0.06–3.51) in patients with T1D. Stratification for time since CD diagnosis did not affect risk estimates. Conclusion Having a diagnosis of CD does not seem to influence fracture risk in young patients with T1D. Follow-up in this study was, however, too short to ascertain osteoporotic fractures which traditionally occur in old age.

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Section: Discussionmentioning

confidence: 99%

Celiac Disease Does Not Influence Fracture Risk in Young Patients with Type 1 Diabetes

Reilly

Lebwohl

Mollazadegan

et al. 2016

The Journal of Pediatrics

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“…The importance of the maternal intake of folate and other methyl donors during pregnancy on DNA methylation patterns and offspring phenotype was established more than a decade ago using the agouti (A(vy)) mice which have a transposable element in the agouti gene (19) . Maternal supplementation with folic acid, vitamin B 12 , choline and betaine increased CpG methylation at the A(vy) locus in the offspring and increased the proportion of leaner offspring with darker coats (19) . The agouti locus is an example of a metastable epiallele (ME) that is variably expressed in genetically identical individuals due to epigenetic modifications that were established during early development (20) .…”

Section: Epigenetics As a Mechanism Linking Early Life Nutrition Withmentioning

confidence: 99%

Maternal folate deficiency and metabolic dysfunction in offspring

McKay

Mathers

2015

Proc. Nutr. Soc.

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Conference on 'Diet, gene regulation and metabolic disease' Symposium 3: Nutrition, epigenetics and the fetal origins of metabolic disease Maternal folate deficiency and metabolic dysfunction in offspring The importance of folate during pregnancy was established more than 80 years ago by Lucy Wills' ground-breaking studies of tropical macrocytic anaemia. More recently, it has become apparent that the adverse consequences of inadequate nutrient supply during early developmental may be exacerbated by over-nutrition postnatally. The present paper aims to review recent evidence that maternal methyl donor (notably folate) supply peri-conceptually and during pregnancy has long-term effects on offspring (metabolic) health. In addition, we propose the hypothesis that epigenetic mechanisms, especially DNA methylation, may mediate the effects of these early life nutritional insults. We discuss evidence from a natural experiment in human subjects which provides proof of principle for the hypothesis. We describe an attempt to test this hypothesis using a mouse model in which female C57Bl/6 mice were randomised to low or normal folate diets prior to, and during, pregnancy and lactation. Low maternal folate supply resulted in offspring that were more susceptible to detrimental metabolic effects of a high-fat diet fed from weaning, manifested as increased circulating TAG concentration. Interestingly, this metabolic phenotype in adult offspring occurred without any detectable change in adiposity, suggesting a different aetiological origin from the more commonly reported observation that maternal undernutrition leads to increased offspring adiposity and to symptoms of the Metabolic Syndrome. The widespread prevalence of overweight and obesity and of folate deficiency among women of child-bearing age highlights the possibility that this double nutritional insult may exacerbate the risk of metabolic disease in their offspring.

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“…Several cohort reports indicated that B-vitamins could play protective roles in bone health [56]. Homocystinuria is a rare autosomal recessive disease in which the metabolism of homocysteine is severely impaired, leading to excessive accumulation of homocysteine in the blood and urine (Fig.…”

Section: Snps In the Homocysteine And Folaterelated Genes And Fracturesmentioning

confidence: 99%

Recent genetic discoveries in osteoporosis, sarcopenia and obesity [Review]

Urano

Inoue

2015

Endocr J

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Abstract. Osteoporosis is a skeletal disorder characterized by low bone mineral density (BMD) and an increased susceptibility to fractures. Evidence from genetic studies indicates that BMD, a complex quantitative trait with a normal distribution, is genetically controlled. Genome-wide association studies (GWAS) as well as studies using candidate gene approaches have identified single-nucleotide polymorphisms (SNPs) that are associated with BMD, osteoporosis and osteoporotic fractures. These SNPs have been mapped close to or within genes including those encoding WNT/β-catenin signaling proteins. Understanding the genetics of osteoporosis will help to identify novel candidates for diagnostic and therapeutic targets. Genetic factors are also important for the development of sarcopenia, which is characterized by a loss of lean body mass, and obesity, which is characterized by high fat mass. Hence, in this review, we discuss the genetic factors, identified by genetic studies, which regulate the body components related to osteoporosis, sarcopenia, and obesity.

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B-vitamins and bone in health and disease: the current evidence

Cited by 32 publications

References 95 publications

Celiac Disease Does Not Influence Fracture Risk in Young Patients with Type 1 Diabetes

Celiac Disease Does Not Influence Fracture Risk in Young Patients with Type 1 Diabetes

Maternal folate deficiency and metabolic dysfunction in offspring

Recent genetic discoveries in osteoporosis, sarcopenia and obesity [Review]

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