Association between the number of live births and hazard of
all-cause premature mortality
Table 2 shows the results of the multivariate Cox proportional hazard
regression models between the number of live births and hazard of
all-cause premature mortality. After adjustment for age, race,
education, Townsend deprivation index, BMI, smoking statues, moderate
drinking, moderrate activity, we found that the nulliparous women
(HR0=1.17, 95% CI: 1.10-1.25) had higher risk of
premature all-cause death, and the women with two, three and four
childern had lower risk of premature all-cause death
(HR2=0.86, 95% CI: 0.82-0.92, HR3=0.87,
95% CI: 0.82-0.93, HR4=0.91, 95% CI: 0.83-0.99),
compared with the reference group. These results did not change
appreciably after further adjustment for diabetes, hypertension, asthma,
emphysema and chronic bronchitis, or female specific factors (use of
oral contraceptive pills, history of stillbirth, spontaneous miscarriage
or termination, age at menarche, age at menopause, and length of
menstrual). The HR (95%CI) of all-cause premature mortality across
groups were 1.17(1.09-1.25), 1.00(reference), 0.87(0.82-0.93),
0.88(0.82-0.94), 0.90(0.82-0.99) and 0.94(0.83-1.08), respectively
(P-trend<0.001). The hazard of all-cause premature mortality was higher
among childless women, comparied with those who had only one child, and
women with two, three, or four children have lower all-cause premature
mortality, and this is true across models 3 to 5.
The potential nonlinear association
between all-cause premature mortality and the number of live births was
intuitively described using restricted cubic spline (RCS) based on
model5. As shown in Supplementary Figure 1, there was a non-linear
relationship between the number of live births and all-cause premature
mortality (P for non-linear<0.001), which proves the above
conclusion. The nadir for all-cause premature death risk was estimated
from RCS to be at two live births, which was significantly lower than
one live birth. Also, the all-cause premature mortality of mothers with
three or four children was lower than mothers who had one child.
Moreover, women without child was signifcant increases in risk were
observed for premature all-cause death than women with one child.
Although the data for the women with five or more children was not
significant, there is a clear upward trend in the RCS curve. More
specifcally, we prefer to describe this nonlinear relationship with
approximates U-shape where women with none, one, or four children have
higher all-cause premature mortality than those with two or three
children.
Sensitivity analyses did not affect
the assessment of the relationship between parity and all-cause
premature mortality risk (Supplementary Table 1). Similar results were
observed after excluding participants with less than 1 and 2 years of
follow-up, respectively. To avoid the possible influence of biochemical
indicators on the results, we repeated our analyses by adjusting the
covariate biochemical indicators additionally. The results were barely
changed. The results of furthur adjusting for covariates dietary factors
showed the conclusion remains alomost the same.