Main Findings
We found that women born small or premature may have future risk of GDM.
However, the evidence certainty was low, and the presented findings may
be overestimated, as we observed some evidence of publication bias.
These findings were approximately consistent across the subgroups,
including different populations, exposures, and studies of varied
methodological quality; these findings were robust in sensitivity
analyses.
Our finding that the mother’s size at birth or premature birth may
affect GDM risk was consistent with that of a previous narrative review20. The strength of this association was
similar to that observed in women with a family history of diabetes
mellitus, an established risk factor for GDM42-44. However, the importance of the risk
factor in clinical decision depends on the absolute risk difference. Our
findings suggested that careful review of the mother’s birth status may
indicate her risk of GDM and guide pregnancy management in moderate to
high prevalence settings. The mother’s preterm birth status and size at
birth are not currently considered risk factors for GDM in any of the
major guidelines or risk models 43-46. Our
findings may help further refine these guidelines and models or to
develop new ones.
The certainty of evidence for the association between premature birth or
SGA status and GDM was low due to the high risk of publication bias, as
shown by funnel-plot analysis. The
contour-enhanced funnel plot suggests that studies with non-significant
findings may not have been published. Although we did not identify any
ongoing or unpublished studies, this did not eliminate the risk of
publication bias, as observational studies are less likely to be
registered than clinical trials 47. Thus, the
reported estimates may be overestimates. The studies included in this
review tended not to adjust for confounders, such as smoking, obesity,
socioeconomic status, and family history of diabetes. Future studies
should adjust for these factors.
The main result of this review was subject to substantial between-study
heterogeneity, as shown by the I 2 statistic27. This heterogeneity may be due to the
different types of exposure (LBW, SGA, or preterm birth) considered in
this study. However, as all exposure types were associated with
increased GDM risk, the high I 2 statistic may
be due to the large number of participants and narrow CIs of the primary
studies 48. Given these findings, we did not
assign a low rating to the inconsistency domain of the GRADE criteria29.
The underlying mechanism of the association between preterm birth or SGA
status and subsequent GDM may be gestational malnutrition due to
maternal malnutrition or placental insufficiency49. Findings from animal studies have
suggested that malnutrition in utero is associated with reduced β-cell
counts, pancreas weight, and pancreatic insulin content50-52. According to the Barker foetal origin
hypothesis, these foetal programming events may affect the future risk
of disease 17. A review of epidemiological
studies has suggested that LBW and preterm birth are associated with the
risk of type 2 diabetes in adulthood; a similar mechanism is possible
for GDM 16.