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CSU 3/2008: LOW BIRTHWEIGHT AND ADULT MORBIDITY AND MORTALITY

Thursday, 10th of January 2008

CSU 3/2008: LOW BIRTHWEIGHT AND ADULT MORBIDITY AND MORTALITY

 The effects of low birthweight on infants are widely understood; the  effects of LBW on adults, less so.
 
 
 The last few decades have seen work from Europe and North America
 linking low birthweight to adult morbidity and mortality as well. Writing
 in the International Journal of Epidemiology, Kajantje and colleagues wrote
 as follows; see main conclusion in boldface (full text available online at
 http://ije.oxfordjournals.org/cgi/content/full/34/3/655 ).
 
 Size at birth as a predictor of mortality in adulthood: a
 follow-up of 350 000 person-years, Int J Epidemiol. 34(3):655-63
 
 
 Kajantie E, Osmond C, Barker DJ, Forsén T, Phillips DI, Eriksson  JG.
 
 
 National Public Health Institute, Helsinki, Finland.
 eero.kajantie@helsinki.fi
 
  BACKGROUND: Small body size at birth, as a marker of an adverse
 intrauterine environment, has recently emerged as an important
 risk factor for death from cardiovascular disease. Our aim was to
 study the relationship between small size at birth and all-cause
 and non-cardiovascular mortality, which has been poorly
 documented.

METHODS: We studied 13 830 individuals born between
 1924 and 1944 in Helsinki, Finland, at term as singletons. Dates
 and primary causes of death between 1971 and 1998 were obtained
 from the Finnish National Death Register. RESULTS: 1668 men and
 671 women died during the follow-up at the mean age of 56.0
 (range 26.7-74.9) years. Lower birthweight was associated with
 increased all-cause mortality in females (Odds ratio (OR) for 1
 kg decrease in birthweight 1.25, 95% CI 1.05-1.49; P = 0.01) but
 not in males (OR 1.08; 0.96-1.19; P = 0.2; P for sex-birthweight
 interaction = 0.09). Similarly, short length at birth was a
 predictor of all-cause mortality in females (OR for 1 cm decrease
 1.10; 1.05-1.15; P < 0.0001) but not in males (OR 1.01;
 0.98-1.02; P = 0.4; P for sex-length at birth interaction =
 0.002). Low birthweight and short length at birth predicted
 premature death in adulthood (<55 years) in both sexes. In males,
 death from cardiovascular disease (n = 654) was associated with
 lower birthweight (OR for 1 kg decrease 1.33; 1.12-1.59; P =
 0.001), and length (OR 1.05; 1.00-1.10; P = 0.03), and in females
 death from cardiovascular disease (n = 179) was associated with
 short length at birth (OR 1.11; 1.02-1.20; P = 0.02). In females
 death from non-cardiovascular diseases was predicted by low
 birthweight (OR 1.25; 1.01-1.54; P = 0.04) and short length at
 birth (OR 1.09; 1.03-1.15; P = 0.003) (n = 475), but not in males
 (n = 975; P for interaction = 0.02 and 0.004, respectively).
 Cancer-related death was associated with higher birthweight (OR
 for 1 kg decrease 0.76; 0.61-0.95; P = 0.02) and ponderal index
 (OR for 1 kg/m(3) increase 0.95; 0.91-0.99; P = 0.01) in males (n
 = 361) but not in females (n = 269). CONCLUSIONS: Small size at
 birth is associated with increased all-cause mortality at all
 ages among adult women but only with premature death in adult
 men. Among women death from both cardiovascular and
 non-cardiovascular causes is associated with small body size at
 birth. Among men an association between small birthsize and later
 cardiovascular disease is counterbalanced by an association
 between large body size at birth and later cancer.
 
 Summarizing the results of work from Finland, Clive Osmond, one of the
 researchers from the numerous Finnish studies, said "our best estimate is
 that every one kilogram increase [in birth weight] reduces heart disease
 by about seventeen per cent. The effect with diabetes seems a bit
 stronger." ("Medical Dispatch: Small and Thin," The New Yorker, 19 Nov
 2007, 52-27).
 
 
 Writing in the International Journal of Epidemiology, David Barker, a major
 researcher in this field, referred to "concerns about what the United
 Nations refer to as the ‘double burden’ of malnutrition. ‘While
 undernutrition kills in early life, it also leads to a high risk of disease
 and death in later life.’"
  
 
 This leads to the question of why we do not invest more resources in fetal
 nutrition in the developing world, now that the effects of low birthweight
 are well understood in both children and adults. Two underused
 interventions in pregnancy are the use of antihelminthics from second
 trimester to reduce both maternal and fetal undernutrition, and, in
 countries with stable malaria, intermittent malaria prophylaxis of the
 mother.
 
 
 Good reading.
 
 
 
 
 
 BD
 
 
 PS This update was inspired by a recent article in The New Yorker,
 summarized below.
  
 Stephen S. Hall, Medical Dispatch, "Small and Thin," The New Yorker,
 November 19, 2007, p. 52
  
 ANNALS OF EPIDEMIOLOGY about David J.P. Barker’s theory that adult disease
 is linked to pre-natal and early post-natal life. In the early
 nineteen-eighties, a group of British epidemiologists compiled an atlas of
 the common causes of death in various parts of England and Wales. The map
 charting heart disease was difficult to interpret. The poorer areas of
 England indicated higher-than-average death rates, and the prosperous areas
 indicated below-average death rates. David J.P. Barker, one of the authors
 of the “Atlas of Mortality from Selected Diseases in England and Wales,
 1968-1978,” used this data to question whether the cause of this disease
 was adult behaviors or something from early childhood. Barker and a
 statistician named Clive Osmond discovered that the areas with the highest
 death rates from heart disease had the highest rates of infant mortality
 about fifty years earlier. Barker questioned whether vulnerability to heart
 disease was rooted in adulthood, in childhood—or did it go all the way back
 to life in the womb? And, was the trajectory toward disease perhaps set by
 how healthy the mother had been even before her child-bearing years? In
 1986, when Barker’s basic claim that heart disease was “related to
 nutrition during prenatal and early postnatal life” —now known as the
 Barker hypothesis—was first published in The Lancet, it was regarded as
 heretical. Barker thought birth weight could tie an individual’s prenatal
 development with his health as an adult. At the beginning of the twentieth
 century, Britain began to keep records of infant health. It took two years
 for Barker and his colleagues to find the adults whose birth records they
 now possessed. Men who had weighed 5.5 pounds or less at birth had the
 highest rates of death from coronary heart disease. This paper appeared in
 The Lancet in 1989. Many doctors disliked the idea, in part because it
 undermined a decades-long public-health message that linked heart disease
 to adult behavior. Mentions several scientists who tried to prove the
 theory wrong, but ended up convinced that it was accurate. In 1997, a
 Finnish doctor named Johan Eriksson and his colleague Tom Forsen further
 proved the Barker hypothesis. A biologist named Tom Fleming was among the
 earliest to test the Barker hypothesis in rats. Barker makes sure to say
 that no child is doomed by low birth weight; rather, such knowledge should
 allow doctors to identify heightened vulnerability in certain children, for
 whom preventative measures can make a great deal of difference. The Barker
 hypothesis has, gradually, acquired its own air of orthodoxy.