Commentary: Modifying body weight not birthweight is the key to lowering blood pressure

Rachel Huxley

Institute for International Health, 144 Burren Street, Newtown, Sydney, NSW 2042, Australia. E-mail: rhuxley{at}iih.usyd.edu.au

The fetal-origins hypothesis suggests that an adverse early life environment can have a profound and long-lasting impact on an individual’s health in later life.1 A central tenet of the hypothesis is a reported inverse association between birthweight, which is often used as a surrogate measure of fetal nutrition, with subsequently raised blood pressure or hypertension.2 This inverse association between birthweight and blood pressure (but less so with hypertension) has been reported widely in the literature and is considered to provide some of the strongest evidence for an association between an adverse early life environment and chronic disease,3 although a recent overview of the evidence casts doubt on whether there is any association at all.4 An additional feature of the fetal-origins hypothesis, which sprang initially from studies which had information on body size in childhood or adult life, suggests that ‘catch-up’ growth in childhood5 (defined as being above average height or weight or both, combined with a low birthweight), further predisposes to raised blood pressure in later life, as well as with increased rates of insulin resistance and coronary heart disease. However, an increased risk of coronary heart disease and type 2 diabetes has also been reported to be associated with a reduced catch-up growth in childhood.

It is in this context that the study by Zhao and colleagues was conducted.6 In this large population-based study of 13 467 Chinese women, the authors firstly examined the relationship of birthweight with hypertension, which they defined either as ‘confirmed’ (n = 1433) or ‘possible’ (n = 940) on the basis of past or current use of antihypertensive medication. Secondly, the authors proceeded to investigate the effects of growth in adolescence and young adulthood in conjunction with birthweight on the risk of developing hypertension in later life. Rather than relying on height and weight measurements to assess adolescent growth, innovatively, the authors used self-reported perceptions of body size relative to their peers. As with some, but not all, previous studies, a dose-response association of birthweight with the prevalence of ‘early-onset’ hypertension (but not with ‘late-onset’ hypertension) was reported. Moreover, the risk of developing ‘early-onset’ hypertension was far higher in those individuals who were both born with a low birthweight (<2500 g) and who exhibited some measure of ‘catch-up’ growth in adolescence (but not in young adulthood). Findings which would seem to be in general accord with the fetal-origins hypothesis.5

However, the evidence for a ‘dose-response’ relationship of birthweight with hypertension in this population is at best, limited. Although individuals who were born with a birthweight <=2500 g had an increased risk of hypertension, there was only weak evidence for a ‘dose-response’ trend with birthweight in women with confirmed cases of hypertension (P = 0.16). Even after the inclusion of possible cases of hypertension, the evidence for an inverse trend, although strengthened, remained weak (P = 0.07), which suggests that the increase in prevalence of hypertension was largely confined to those women born weighing <2500 g. In these individuals, the association between low birthweight and increased prevalence of hypertension may have been confounded by genetic factors that are associated with both low birthweight and with raised blood pressure in later life, e.g. maternal hypertension.

Furthermore, only in an analysis of the relationship between birthweight and blood pressure, stratified by age of onset of hypertension, did the relationship with birthweight reach conventional levels of significance, but interestingly, only in those individuals diagnosed with ‘early onset hypertension’ (20–40 years) (P = 0.01). In women who were diagnosed with hypertension between 41 and 70 years (i.e. ‘late-onset’ hypertension) there was no evidence of an association with birthweight (P = 0.70) (Figure 1Go). This is at odds with the widely held view of an inverse relationship between birthweight and blood pressure at all ages2 as well as with the suggestion that the strength of the inverse association is ‘amplified’ with age.5



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Figure 1 Association of birthweight with the probability of ‘early-onset’ hypertension (black squares) (P for trend = 0.01) and with ‘late-onset’ hypertension (black diamonds) (P for trend = 0.70). Adapted from Zhao et al.6

 
In this current study, the risk of ‘early onset’ hypertension in individuals born light at birth was further increased if the woman exhibited some measure of catch-up growth (defined as being either heavier or taller) at age 15 years (but not at 20 years). This is similar to the findings of a study that reported an increased risk of hypertension in Swedish middle-aged men who were light at birth but tall as adults,7 but conflicts with a recent study of more that 275 000 Swedish male conscripts,8 in which low birthweight in conjunction with short adult stature was associated with increased risk of high blood pressure. Moreover, the positive effect of excessive weight gain on hypertension in this current study was not limited to the lower birthweight group, suggesting that the harmful effect of excessive weight affect all individuals irrespective of birthweight. It therefore remains unclear what role, if any, catch-up growth has in the determination of later blood pressure.

From a public health perspective, more relevant findings from the study by Zhao and colleagues are that, regardless of birthweight, being above average weight in adolescence or young adulthood predisposes individuals towards an increased risk of hypertension in later life. Furthermore, the risk of hypertension in this population begins at much lower levels of body mass index compared with Western populations. Although overweight individuals, who are born light, may have the greatest relative risk of hypertension, birthweight, unlike current weight, is not so easily modified. Recent estimates suggest that a 2-kg reduction in body weight could reduce systolic blood pressure by 1%,9 which is equivalent to the expected reduction in blood pressure estimated for a 1-kg increase in birthweight.5 Obesity, a condition normally associated with prosperous developed countries, is becoming endemic in developing nations, including China, due in large part to the adoption of westernized dietary and lifestyle habits. Paralleling these trends is the alarming rise in chronic ‘western’ disorders including type 2 diabetes, dyslipidaemia and raised blood pressure. Combating these rising trends will require the implementation of simple and effective interventions aimed at preventing and reducing the overall prevalence of overweight and obesity in all individuals, irrespective of their childhood growth. Even modest, but achievable, reductions in weight across the population would have a significant and worthwhile impact on reducing blood pressure and overall incidence of coronary heart disease.10

Acknowledgments

Gary Whitlock for helpful comments on an earlier draft.

References

1 Barker DJP. Fetal origins of coronary heart disease. BMJ 1995;311:171–74.[Free Full Text]

2 Law CM, Shiell AW. Is blood pressure inversely related to birth weight? The strength of evidence from a systematic review of the literature. J Hypertens 1996;14:935–41.[ISI][Medline]

3 Robinson R. The fetal-origins of adult disease: no longer just a hypothesis and may be critically important in South Asia. BMJ 2001; 322:375–76.[Free Full Text]

4 Huxley R, Neil A, Collins R. Unravelling the ‘fetal origins’ hypothesis: is there really an inverse association between birth weight and subsequent blood pressure? Lancet (In press).

5 Huxley RR, Shiell AW, Law CM. The role of size at birth and postnatal catch-up growth in determining systolic blood pressure: a systematic review of the literature. J Hypertens 2000;18:815–31.[CrossRef][ISI][Medline]

6 Zhao M, Shu XO, Jin F et al. Birthweight, childhood growth and hypertension in adulthood. Int J Epidemiol 2002;31:1048–56.

7 Leon DA, Koupilova I, Lithell HO et al. Failure to realize growth potential in utero and adult obesity in relation to blood pressure in 50 year old Swedish men. BMJ 1996;312:401–06.[Abstract/Free Full Text]

8 Lundgren EM, Cnattingius SHM, Jonsson GB, Tuvemo TH. Linear catch-up growth does not increase the risk of elevated blood pressure and reduces the risk of overweight in males. J Hypertens 2001;19:1533–38.[CrossRef][ISI][Medline]

9 Anderson JW, Konz EC. Obesity and disease management: effects of weight loss on comorbid conditions. Obes Res 2001;9(S4):326S–34S.[Abstract/Free Full Text]

10 Whitlock G, Lewington S, Ni Mhurchu C. Coronary heart disease and body mass index: a systematic review of the evidence from large prospective cohort studies. Seminars in Vascular Medicine. (In press).





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