The association between low birth weight and raised blood pressure has been
extensively replicated. Little is known about the way childhood growth mod
ifies the effects of low birth weight. We report on the fetal and childhood
growth of 1958 men and women who received treatment for hypertension and b
elong to a cohort of 7086 people born in Helsinki, Finland, during 1924-193
3. As expected, the men and women who developed hypertension had low birth
weight (P = 0.002), They were also shorter in body length at birth (P = 0,0
2). After birth they experienced accelerated growth, so that by 7 years the
ir heights and weights were approximately average. In a simultaneous regres
sion, both birth length and tall height had statistically significant altho
ugh opposing effects on hypertension (P = 0.003 for birth length and 0.009
for height at 7 years). Accelerated postnatal growth was associated with be
tter childhood living conditions. Children who later developed both hyperte
nsion and type 2 diabetes, rather than hypertension alone, had small placen
tal size as well as small body size at birth, and their accelerated postnat
al growth continued beyond 7 years. We suggest that hypertension may origin
ate through retarded growth in utero followed by accelerated postnatal grow
th as a result of good living conditions. Retarded fetal growth leads to pe
rmanently reduced cell numbers in the kidney and other tissues, and subsequ
ent accelerated growth may lead to excessive metabolic demand on this limit
ed cell mass.