A Conspectus of Research on Calcium Requirements of Man

Irwin, M. Isabel; Kienholz, E. W.

doi:10.1093/jn/103.7.1019

Cited by 46 publications

(5 citation statements)

References 379 publications

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“…Conventional wisdom would have it that nutritional rickets is primarily due to vitamin D deficiency, although dietary calcium intake modulates the severity and rapidity of onset of the disease [210,211]. However, over the last three decades evidence has been accumulating which implicates low dietary calcium intakes as a cause of rickets in the face of serum 25(OH)D concentrations above values generally associated with vitamin D deficiency rickets (>25 nmol/l).…”

Section: Dietary Calcium Deficiencymentioning

confidence: 99%

Vitamin D Deficiency and Nutritional Rickets in Children

Pettifor

2011

Vitamin D

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Section: Dietary Calcium Deficiencymentioning

confidence: 99%

Vitamin D Deficiency and Nutritional Rickets in Children

Pettifor

2011

Vitamin D

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“…Until recently, it was generally accepted that nutritional rickets is caused by vitamin D deficiency alone and that dietary calcium deficiency might exacerbate the disease in the presence of vitamin D deficiency but by itself is not responsible for nutritional rickets (13). In the past 25 y, consensus regarding the pathogenesis of nutritional rickets has shifted as studies have suggested that, among older children in developing countries in particular, dietary calcium deficiency plays a pivotal role.…”

Section: Introductionmentioning

confidence: 99%

Nutritional rickets: deficiency of vitamin D, calcium, or both?

Pettifor

2004

The American Journal of Clinical Nutrition

239

157

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Nutritional rickets remains a public health problem in many countries, despite dramatic declines in the prevalence of the condition in many developed countries since the discoveries of vitamin D and the role of ultraviolet light in prevention. The disease continues to be problematic among infants in many communities, especially among infants who are exclusively breast-fed, infants and children of dark-skinned immigrants living in temperate climates, infants and their mothers in the Middle East, and infants and children in many developing countries in the tropics and subtropics, such as Nigeria, Ethiopia, Yemen, and Bangladesh. Vitamin D deficiency remains the major cause of rickets among young infants in most countries, because breast milk is low in vitamin D and its metabolites and social and religious customs and/or climatic conditions often prevent adequate ultraviolet light exposure. In sunny countries such as Nigeria, South Africa, and Bangladesh, such factors do not apply. Studies indicated that the disease occurs among older toddlers and children and probably is attributable to low dietary calcium intakes, which are characteristic of cereal-based diets with limited variety and little access to dairy products. In such situations, calcium supplements alone result in healing of the bone disease. Studies among Asian children and African American toddlers suggested that low dietary calcium intakes result in increased catabolism of vitamin D and the development of vitamin D deficiency and rickets. Dietary calcium deficiency and vitamin D deficiency represent 2 ends of the spectrum for the pathogenesis of nutritional rickets, with a combination of the 2 in the middle.

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“…This technique provides a measure of in vivo whole body protein synthesis and breakdown in a relatively non--invasive and rapid manner. This is compared to nitrogen--balance studies, which can take several days (Irwin and Hegsted, 1971;Zello et al, 1995), and tissue--specific measures such as arterio--venous techniques, which require invasive biopsies (Paddon--Jones et al, 2004). A drawback of IAAO is that it does not allow for the calculation of tissue--specific protein synthesis (Ks) in metabolically active organs such as the liver or skeletal muscle.…”

Section: General Conclusionmentioning

confidence: 99%

The effects of dietary methyl donors on methionine partitioning in the neonatal piglet

Robinson

2015

Appl. Physiol. Nutr. Metab.

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The metabolism of the indispensable amino acid methionine is critical during development. Methionine is used to synthesize protein for growth and, using the methionine cycle, it is the precursor of >50 critical nutrients and contributes to epigenetic regulation. Therefore, the dietary methionine requirement must factor all the potential roles of methioine. Three major processes summarize the methionine cycle: transmethylation (TM), which transfers methyl groups to nutrient precursors and DNA; transsulfuration (TS), which represents methionine disposal; and remethylation (RM), which resynthesizes methionine using the dietary methyl donors folate and choline (via betaine). Dietary intakes of folate vary drastically, and choline intakes are often below the adequate intakes during preganancy and in early life, which we hypothesized would influence the methionine requirement. To test our hypothesis, we fed 4--8 day old neonatal piglets a low--methionine diet that was either deficient (MD-), or replete (MS+), in dietary methyl donors. We evaluated how methionine was balanced between the major TM reactions and protein synthesis. The MD-group exhibited marked differences in TM as creatine synthesis was ≈30% less (p<0.05), and phosphatidylcholine synthesis was ≈60% more (p<0.05) during MD-feeding. Interestingly, while MD-feeding did not affect liver protein synthesis, the methionine availablity and protein synthesis were lower in skeletal muscle of the MD-vs. MS+ animals (p<0.05). Furthermore, whole body protein turnover was also reduced during MD-feeding (p<0.05), which is significant as protein turnover is especially critical during infancy. Next, we measured the effect of methyl donors on the rates of TM, TS, and RM. The rates of RM and TM were iii reduced by ≈75% in the MD-group (p<0.05), while TS was unchanged. In order to evaluate the effectiveness of individual methyl donors on RM, we 'rescued' a second group of MD-animals with betaine (MD+B), folate (MD+F) or both (MD+FB). The rate of RM and TM increased by ≈2--fold after rescue (p<0.05) and reduced protein breakdown (p<0.05). These studies showed that dietary methyl donors affect neonatal methionine metabolism, which should be considered when defining the dietary requirements of methionine during development.iv

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A Conspectus of Research on Calcium Requirements of Man

Cited by 46 publications

References 379 publications

Vitamin D Deficiency and Nutritional Rickets in Children

Vitamin D Deficiency and Nutritional Rickets in Children

Nutritional rickets: deficiency of vitamin D, calcium, or both?

The effects of dietary methyl donors on methionine partitioning in the neonatal piglet

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