Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- 1 The developmental origins of health and disease: an overview
- 2 The ‘developmental origins’ hypothesis: epidemiology
- 3 The conceptual basis for the developmental origins of health and disease
- 4 The periconceptional and embryonic period
- 5 Epigenetic mechanisms
- 6 A mitochondrial component of developmental programming
- 7 Role of exposure to environmental chemicals in developmental origins of health and disease
- 8 Maternal nutrition and fetal growth and development
- 9 Placental mechanisms and developmental origins of health and disease
- 10 Control of fetal metabolism: relevance to developmental origins of health and disease
- 11 Lipid metabolism: relevance to developmental origins of health and disease
- 12 Prenatal hypoxia: relevance to developmental origins of health and disease
- 13 The fetal hypothalamic–pituitary–adrenal axis: relevance to developmental origins of health and disease
- 14 Perinatal influences on the endocrine and metabolic axes during childhood
- 15 Patterns of growth: relevance to developmental origins of health and disease
- 16 The developmental environment and the endocrine pancreas
- 17 The developmental environment and insulin resistance
- 18 The developmental environment and the development of obesity
- 19 The developmental environment and its role in the metabolic syndrome
- 20 Programming the cardiovascular system
- 21 The role of vascular dysfunction in developmental origins of health and disease: evidence from human and animal studies
- 22 The developmental environment and atherogenesis
- 23 The developmental environment, renal function and disease
- 24 The developmental environment: effect on fluid and electrolyte homeostasis
- 25 The developmental environment: effects on lung structure and function
- 26 Developmental origins of asthma and related allergic disorders
- 27 The developmental environment: influences on subsequent cognitive function and behaviour
- 28 The developmental environment and the origins of neurological disorders
- 29 The developmental environment: clinical perspectives on effects on the musculoskeletal system
- 30 The developmental environment: experimental perspectives on skeletal development
- 31 The developmental environment and the early origins of cancer
- 32 The developmental environment: implications for ageing and life span
- 33 Developmental origins of health and disease: implications for primary intervention for cardiovascular and metabolic disease
- 34 Developmental origins of health and disease: public-health perspectives
- 35 Developmental origins of health and disease: implications for developing countries
- 36 Developmental origins of health and disease: ethical and social considerations
- 37 Past obstacles and future promise
- Index
- References
29 - The developmental environment: clinical perspectives on effects on the musculoskeletal system
Published online by Cambridge University Press: 08 August 2009
Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- 1 The developmental origins of health and disease: an overview
- 2 The ‘developmental origins’ hypothesis: epidemiology
- 3 The conceptual basis for the developmental origins of health and disease
- 4 The periconceptional and embryonic period
- 5 Epigenetic mechanisms
- 6 A mitochondrial component of developmental programming
- 7 Role of exposure to environmental chemicals in developmental origins of health and disease
- 8 Maternal nutrition and fetal growth and development
- 9 Placental mechanisms and developmental origins of health and disease
- 10 Control of fetal metabolism: relevance to developmental origins of health and disease
- 11 Lipid metabolism: relevance to developmental origins of health and disease
- 12 Prenatal hypoxia: relevance to developmental origins of health and disease
- 13 The fetal hypothalamic–pituitary–adrenal axis: relevance to developmental origins of health and disease
- 14 Perinatal influences on the endocrine and metabolic axes during childhood
- 15 Patterns of growth: relevance to developmental origins of health and disease
- 16 The developmental environment and the endocrine pancreas
- 17 The developmental environment and insulin resistance
- 18 The developmental environment and the development of obesity
- 19 The developmental environment and its role in the metabolic syndrome
- 20 Programming the cardiovascular system
- 21 The role of vascular dysfunction in developmental origins of health and disease: evidence from human and animal studies
- 22 The developmental environment and atherogenesis
- 23 The developmental environment, renal function and disease
- 24 The developmental environment: effect on fluid and electrolyte homeostasis
- 25 The developmental environment: effects on lung structure and function
- 26 Developmental origins of asthma and related allergic disorders
- 27 The developmental environment: influences on subsequent cognitive function and behaviour
- 28 The developmental environment and the origins of neurological disorders
- 29 The developmental environment: clinical perspectives on effects on the musculoskeletal system
- 30 The developmental environment: experimental perspectives on skeletal development
- 31 The developmental environment and the early origins of cancer
- 32 The developmental environment: implications for ageing and life span
- 33 Developmental origins of health and disease: implications for primary intervention for cardiovascular and metabolic disease
- 34 Developmental origins of health and disease: public-health perspectives
- 35 Developmental origins of health and disease: implications for developing countries
- 36 Developmental origins of health and disease: ethical and social considerations
- 37 Past obstacles and future promise
- Index
- References
Summary
Introduction
The ability to move, the protection of vital organs and stable support for the body are the principal roles of the musculoskeletal system (muscle, bone and cartilage) (Simkin 1994). This system accounts for a large proportion of the body mass; for example, the muscle mass of a healthy adult 70-kg individual is about 20 kg (Kreisberg et al. 1970). The musculoskeletal system develops embryonically from the mesodermal layer, differentiating into dermatomes containing skeletal and muscle cell precursors in the first trimester. At this stage the embryo is only a few millimetres long. The growing fetus usually obtains nourishment at the expense of the mother, who tends to suffer in periods of adversity, but placental size and unrestricted blood flow through placental vessels to and from the fetus are important for optimal growth, especially during the last trimester. Fetal nutrition and the uterine environment are likely to play a part in the transcription of the genomic blueprint acquired at conception into the phenotypic newborn. Some of these developmental adaptations are now known to have long-term effects on the later risk of osteoporosis, sarcopenia and osteoarthritis. During early childhood, growth is rapid and there are windows of opportunity for environmental or lifestyle factors to have long-term effects, especially on the skeleton.
Puberty, which occurs much earlier in girls, brings growth to an end and its timing will have long-term consequences for adult stature.
- Type
- Chapter
- Information
- Developmental Origins of Health and Disease , pp. 392 - 405Publisher: Cambridge University PressPrint publication year: 2006
References
, , et al. (1998). Are rates of ageing determined in utero?Age Ageing, 27, 579–83.CrossRefGoogle Scholar
, , et al. (2002). Polymorphism of the IGF-2 gene, birthweight and grip strength in adult men. Age Ageing, 31, 468–70.CrossRefGoogle Scholar
, and (1997). Calcium-regulating hormones and parathyroid hormone-related peptide in normal human pregnancy and postpartum: a longitudinal study. Eur. J. Endocrinol., 137, 402–9.CrossRefGoogle ScholarPubMed
and (1992). The changing profile of joint troubles with age: findings from a postal survey of the population. Ann. Rheum. Dis., 51, 366–71.CrossRefGoogle Scholar
(1995b). The fetal origins of adult disease. Proc. R. Soc. Lond. B, 262, 37–43.CrossRefGoogle Scholar
(1998). Programming the baby. In Mothers, Babies and Health in Later Life (ed. ). Edinburgh: Churchill Livingstone, pp. 13–41.Google Scholar
and (1991). Differential effects of insulin-like growth factors I and II on growth, differentiation and glucoregulation in differentiating chondrocyte cells in culture. Acta Endocrinol. (Copenh.), 125, 201–11.Google ScholarPubMed
, , , and (2000). A detailed assessment of alterations in bone turnover, calcium homeostasis, and bone density in normal pregnancy. J. Bone Miner. Res., 15, 557–63.CrossRefGoogle ScholarPubMed
, , , and (1990). Development of cholesterol homeostatic memory in the rat is influenced by maternal diets. Metabolism, 39, 468–73.CrossRefGoogle ScholarPubMed
and (1964). Effect of dietary restriction of pregnant rats on body weight gain of the offspring. J. Nutr., 82, 10–18.CrossRefGoogle ScholarPubMed
Cooper, C. and Melton, L. J. (1996). Magnitude and impact of osteoporosis and fractures. In Osteoporosis (ed. , and ). San Diego, CA: Academic Press, pp. 419–34.Google ScholarPubMed
, , et al. (1995). Childhood growth, physical activity and peak bone mass in women. J. Bone Miner. Res., 10, 940–7.CrossRefGoogle ScholarPubMed
, , , , and (1997). Growth in infancy and bone mass in later life. Ann. Rheum. Dis., 56, 17–21.CrossRefGoogle ScholarPubMed
, , , , and (2001). Maternal height, childhood growth and risk of hip fracture in later life: a longitudinal study. Osteoporos. Int., 12, 623–9.CrossRefGoogle ScholarPubMed
, and (2000). Cellular interactions and signaling in cartilage development. Osteoarthritis Cartilage, 8, 309–34.CrossRefGoogle ScholarPubMed
, , et al. (1999). Profiles of endogenous circulating cortisol and bone mineral density in healthy elderly men. J. Clin. Endocrinol. Metab., 84, 3058–63.Google ScholarPubMed
, , et al. (2001). Birthweight, vitamin D receptor genotype and the programming of osteoporosis. Paediatr. Perinat. Epidemiol., 15, 211–19.CrossRefGoogle Scholar
, , , , , , and the Southampton Genetic Epidemiology Research Group (2004). Polymorphism in the growth hormone gene, weight in infancy, and adult bone mass. J. Clin. Endocrinol. Metab., 89, 4898–903.CrossRefGoogle ScholarPubMed
(2000). Cbfa1: a molecular switch in osteoblast biology. Dev. Dyn., 219, 461–71.3.0.CO;2-C>CrossRefGoogle ScholarPubMed
, , , , and (1998). Programming of growth hormone secretion and bone mineral density in elderly men: an hypothesis. J. Clin. Endocrinol. Metab., 83, 135–9.Google ScholarPubMed
, , and (1998). Familial resemblance for bone mineral mass is expressed before puberty. J. Clin. Endocrinol. Metab., 83, 358–61.Google ScholarPubMed
, , , and (1987). Blood chemistry of normal human fetuses at midtrimester of pregnancy. Pediatr. Res., 21, 579–83.CrossRefGoogle ScholarPubMed
, , , and (2001). Intrauterine programming of adult body composition. J. Clin. Endocrinol. Metab., 86, 267–72.Google ScholarPubMed
, , , , and (1995). Ultrasonographic bone characteristics during normal pregnancy: longitudinal and cross-sectional evaluation. Am. J. Obstet. Gynecol., 173, 890–3.CrossRefGoogle ScholarPubMed
, , , and (1991). Changes in vertebral bone density in black girls and white girls during childhood and puberty. N. Engl. J. Med., 325, 1597–600.CrossRefGoogle ScholarPubMed
, , et al. (2001). Neonatal bone mass: influence of parental birthweight, maternal smoking, body composition, and activity during pregnancy. J. Bone Miner. Res., 16, 1694–703.CrossRefGoogle ScholarPubMed
, and (1994). Disproportionate fetal growth and raised IGE concentration in adult life. Clin. Exp. Allergy, 24, 641–8.CrossRefGoogle ScholarPubMed
, , et al. (2004). Umbilical cord calcium and maternal vitamin D status predict different lumbar spine bone parameters in the offspring at 9 years. J. Bone. Miner. Res., 19, 1032.Google Scholar
(1996). Calcium homeostasis in pregnancy. Clin. Endocrinol. (Oxf.), 45, 1–6.CrossRefGoogle ScholarPubMed
, , et al. (1994). Lethal skeletal dysplasia from targeted disruption of the parathyroid hormone-related peptide gene. Genes Dev., 8, 277–89.CrossRefGoogle ScholarPubMed
, , et al. (1997). Polymorphisms of the vitamin D receptor, infant growth and adult bone mass. Calcif. Tissue Int., 60, 233–5.CrossRefGoogle ScholarPubMed
, , and (1998). Postnatal development of bone mineral status during infancy. J. Am. Coll. Nutr., 17, 65–70.CrossRefGoogle ScholarPubMed
, , , , and (1996). Parathyroid hormone-related peptide (PTHrP) regulates fetal–placental calcium transport through a receptor distinct from the PTH/PTHrP receptor. Proc. Natl. Acad. Sci. USA, 93, 15233–8.CrossRefGoogle ScholarPubMed
, and (1970). Measurement of muscle mass in humans by isotopic dilution of creatine 14C. J. Appl. Physiol., 28, 264–7.CrossRefGoogle ScholarPubMed
, , , , and (2002). Birthweight, childhood size and muscle strength in adult life: evidence from a birth cohort study. Am. J. Epidemiol., 156, 627–33.CrossRefGoogle ScholarPubMed
, , and (1989). Bone mineral content in black and white children 1–6 years of age. Am. J. Dis. Child., 143, 1346–9.CrossRefGoogle Scholar
Lucas, A. (1991). Programming by early nutrition in man. In The Childhood Environment and Adult Disease (ed. and ). New York, NY: Wiley, pp. 38–55.Google Scholar
, , et al. (1994). Timing of peak bone mass in Caucasian females and its implication for the prevention of osteoporosis. J. Clin. Invest., 93, 799–808.CrossRefGoogle Scholar
, , , and (1989). Connective tissue, mechanical, and morphometric changes in the lungs of weanling rats fed a low protein diet. Pediatr. Pulmonol., 7, 159–66.CrossRefGoogle ScholarPubMed
and (1974). The determinants of growth and form. Proc. R. Soc. Lond. B, 185, 1–17.CrossRefGoogle ScholarPubMed
, and (1972). The effect of maternal malnutrition on the progeny in the rat: studies on growth, body composition and organ cellularity in first and second generation progeny. Aust. J. Exp. Biol. Med. Sci., 50, 435–46.CrossRefGoogle ScholarPubMed
, , et al. (2002). Intrauterine exposure to a maternal low protein diet reduces adult bone mass and alters growth plate morphology in rats. Calcif. Tissue Int., 71, 493–8.CrossRefGoogle ScholarPubMed
, , , , and (1998). Low total body bone mineral content and high bone resorption in Korean winter-born versus summer-born newborn infants. J. Pediatr., 132, 421–5.CrossRefGoogle ScholarPubMed
and (1970). The loss of bone with age, osteoporosis and fractures. Clin. Orthop. Relat. Res., 71, 229–52.CrossRefGoogle ScholarPubMed
, , , and (2003). Maternal protein deficiency affects mesenchymal stem cell activity in the developing offspring. Bone, 33, 100–7.CrossRefGoogle ScholarPubMed
(1995). Relation of fetal growth to adult muscle mass and glucose tolerance. Diabetic Med., 12, 686–90.CrossRefGoogle ScholarPubMed
, , et al. (1998). Elevated plasma cortisol concentrations: a link between low birthweight and the insulin resistance syndrome?J. Clin. Endocrinol. Metab., 83, 757–60.Google ScholarPubMed
, and (1988). Bone histology and mineral homeostasis in human pregnancy. Br. J. Obstet. Gynaecol., 95, 849–54.CrossRefGoogle ScholarPubMed
, , and (1997). Modulation of commitment, proliferation, and differentiation of chondrogenic cells in defined culture medium. Endocrinology, 138, 4966–76.CrossRefGoogle ScholarPubMed
and (1979). Maternal–perinatal calcium relationships. Obstet. Gynecol., 53, 74–6.Google ScholarPubMed
Simkin, P. A. (1994). The musculoskeletal system. In Rheumatology, (ed. and ). London: Mosby, pp. 1.2.1–1.2.10.Google Scholar
, , and (1987). Effects of early life undernutrition in artificially reared rats: subsequent body and organ growth. Br. J. Nutr., 58, 245–55.CrossRefGoogle ScholarPubMed
, , and (1990). Effect of a low protein diet during pregnancy on the fetal rat endocrine pancreas. Biol. Neonate, 57, 107–18.CrossRefGoogle ScholarPubMed
Specker, B. L., Namgung, R. and Tsang, R. C. (2001). Bone mineral acquisition in utero, during infancy, and throughout childhood. In Osteoporosis, 2nd edn (ed. , and ). New York, NY: Academic Press, vol. 1, pp. 599–620.Google ScholarPubMed
, , , , and (2001). Characterization of PGE(2) receptors (EP) and their role as mediators of 1alpha,25-(OH)(2)D(3) effects on growth zone chondrocytes. J. Steroid Biochem. Mol. Biol., 78, 261–74.CrossRefGoogle ScholarPubMed
Widdowson, E. M., Southgate, D. A. T. and Hey, E. (1988). Fetal growth and body composition. In Perinatal Nutrition (ed. ). New York, NY: Academic Press, pp. 3–14.Google Scholar
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