Rheumatology Advance Access originally published online on July 20, 2009
Rheumatology 2009 48(10):1181-1182; doi:10.1093/rheumatology/kep213
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Editorial |
Musculoskeletal health—how early does it start?
1University of Sydney Pain Management and Research Institute, Royal North Shore Hospital, 2School of Public Health, University of Sydney, St Leonards, Australia and 3Aberdeen Pain Research Collaboration (Epidemiology Group), School of Medicine, University of Aberdeen, Aberdeen, Scotland.
Correspondence to: Fiona M. Blyth, Pain Management and Research Institute, Royal North Shore Hospital, University of Sydney, St Leonards, NSW 2065, Australia. E-mail: fblyth{at}med.usyd.edu.au
Events that occur early in human development can influence adult health profoundly. For example, Norwegians who were born during the Winter Famine of World War Two had a strikingly lower risk of colorectal cancer as adults when compared with adults who were born either before or after the war [1]. Less starkly unfavourable intrauterine environments that result in low birth weight babies have been repeatedly linked to adverse health effects in adult life [2]. The greatest burden of musculoskeletal conditions is borne by adults in mid- and later life, and it may therefore come as a surprise to think that some of the aetiological factors that contribute to this burden are found decades before, in early life. Do early life factors influence musculoskeletal health in adult life? If they do, what are the potential implications of this?
A growing evidence base suggests that early life exposures influence later musculoskeletal health. These factors are both specific and general in nature. Growth patterns before birth and in childhood may be one pathway leading to sarcopenia and frailty in later life [2]. Early growth trajectories in males are positively related to physical performance measures at the age of 53 years, even after adjusting for adult body size, lifetime social class and physical activity and health status at 53 years of age [3]. In men, low birth weight predicts hand OA at the age of 53 years [4]. Midlife grip strength is predicted by birth weight and pre-pubertal height gain, independent of adult risk factors [2, 3]. Low birth weight and early growth trajectories also predict development of osteoporosis and hip fracture risk in adult life [5]. The accumulating epidemiological evidence supports the concept of early life programming of later musculoskeletal development and functional capacity. However, the extent to which these significant associations from epidemiological studies represent causal relationships remains unclear, and evidence from a wide range of scientific disciplines (including birth cohort studies) will be needed to inform preventive strategies.
Early life influences on adult musculoskeletal pain conditions have also been demonstrated. Children with multiple common symptoms (frequent headache, abdominal pain and vomiting), or who were hospitalized after a road traffic accident, are significantly more likely to report chronic widespread pain in midlife [6, 7]. It has also been shown recently that extremely premature babies who undergo repeated procedures after birth show sustained and modality-specific changes in sensory processing at the age of 11 years when compared with age-matched controls [8]. Therefore, evidence suggests that pain processing in childhood may be significantly influenced if painful environmental exposures occur when pain somatosensory processing pathways are establishing and are in periods of developmental plasticity. However, it cannot be said that these changes in pain processing result in a higher risk of adult pain, as the evidence for this causal link is lacking at this time.
These are specific findings relating to musculoskeletal health, but they occur in the context of a more general effect of early life influences on adult health that encompasses a wide range of diseases and health states [6, 9]. This means that the underlying mechanisms are likely to involve central biological pathways. Evidence from the fields of developmental and evolutionary biology points to a range of possible mechanisms by which these early life environmental exposures might act; these include epigenetic DNA changes, changes in tissue differentiation and alterations in homoeostatic control systems (notably the hypothalamic–pituitary axis) [10]. Whatever the mechanisms involved, the key underlying effect from an evolutionary perspective is the extent to which humans display developmental plasticity, or the ability to respond to environmental exposures during critical time windows in early life [10]. These responses may be adaptive, or maladaptive, and thus increase the risk of adult disease.
Studies of the developmental origins of adult disease face several formidable hurdles. They have to grapple with the problem of temporal ‘distance’—important exposures that occur during fetal development or early life may be hard to detect in the presence of adult-onset exposures that are closer in time to disease onset. As these early life exposures occur during periods of enormous developmental change, the timing of exposures in relation to critical periods of development must be accurately determined [9]. Decades of follow-up are required to allow adult-onset disease to occur. We live in fortunate times, at least in relation to the last difficulty, as long-running birth cohort studies are now reaching the stage where chronic disease outcomes are occurring often enough to produce new insights into the relationships between early life environmental exposures and adult-onset diseases. These findings from birth cohort studies are coming together with evidence from other diverse scientific disciplines—fields such as developmental and evolutionary biology, and animal physiology [10]—to help us understand how developmental trajectories and early environmental exposures affect health in later life. The complexities of these relationships mean that cross-disciplinary research that integrates findings from a range of studies is needed.
The big question is what to do with this accumulating evidence about early life influences on adult musculoskeletal health. We are in a period of demographic change, with the population as a whole ageing, which will in all likelihood contribute to a rising burden of ageing-related musculoskeletal diseases. At the other end of life, whereas in the past, poor survival meant that few very low birth weight and/or pre-term babies survived, greater numbers now survive into adult life. This raises the question of how best to optimize adult musculoskeletal health at a population level. Should this include attempts to promote a ‘best start’ to life in terms of fetal and early childhood growth? We propose that early life population-level interventions of this type may make a difference to adult musculoskeletal health trajectories and, ultimately, to the population burden of musculoskeletal diseases, and at least warrant further attention and study.
Acknowledgements
The editorial was written during an academic visit by F.M.B. to the University of Aberdeen, and that visit was funded by the Australian Academy of Sciences under their Scientific Visits to Europe scheme.
Disclosure statement: The authors have declared no conflicts of interest.
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