Age at any birth and breast cancer risk

Abstract

In an effort to assess the relative importance of age at first birth, age at subsequent births, and total parity to the occurrence of breast cancer, reproductive data from 4,225 women with breast cancer and 12,307 hospitalized women without breast cancer were analyzed by a multiple logistic regression model. Age at first birth was confirmed to be the most important reproductive risk indicator; it was associated with a 3.5% increase of relative risk for every year of increase in age at first birth (the 95% confidence interval of this estimate was 2.3 to 4.7% increase per year). However, age at any birth after the first was also an independent and statistically significant risk indicator; it was associated with a 0.9% increase of relative risk for every year of increase in age at any (and every) birth (the 95% confidence interval of this estimate was 0.4 to 1.5% increase per year). There is evidence that the age of approximately 35 years represents for every birth a critical point; before this age any full-term pregnancy confers some degree of protection; after this age any full-term pregnancy appears to be associated with increase in breast cancer risk. The effect of parity is determined by the age of occurrence of the component pregnancies. While most pregnancies occur under the age of 35, the distribution varies from population to population, and this may account for the differences between populations in whether or not a protective effect is seen for births after the first, and if it is seen, its extent.

Effect of parity and age at delivery on breast cancer risk in Slovenian women aged 25–54 years

“…The estimated increase in the odds of breast cancer associated with age at delivery of the first child of 4.4%/year is comparable to estimates reported by Trichopoulos et al (1983) (3.5%) and Decarli et al (1996) (4.7%). Age at subsequent deliveries was associated with a 1% increase in risk for every 1 year increase of age at any birth.…”

“…The dotted curve corresponds to nulli-parous women. Trichopoulos et al (1983) published a model for estimating the effects of age at any birth on breast cancer risk. The age at diagnosis for cases and age at interview for controls is denoted by t. We let t i represent the age at the time of the ith birth, and assume that there are s births.…”

Dietary fat and breast cancer risk in the Swedish women's lifestyle and health cohort

“…For total fat, we fitted a model including education categories: 0 -10, 11 -13, 413 years þ BMI categories: o25, 25 -29.9, X30 kg/m 2 þ Parity: 0, 1, 2, 3, X4 þ Age at menarche, years þ use of OC: never, former and current þ Age at first birth, years (Trichopoulos et al, 1983) þ breast cancer in first-degree relative: yes or no þ alcohol intake, in g/day þ non-alcohol energy intake, in kJ/day. Total fat (10 g/day) was then added to the model, alternatively, as: (1) a continuous covariate, (2) in quintiles of total fat and (3) through splines.…”

From milk to malignancy: the role of mammary stem cells in development, pregnancy and breast cancer

“…Women who are younger than 24 years old at the time of their first full-term pregnancy are protected against developing breast cancer much later in life, while women over the age of 35 are ultimately at an increased risk [88,89]. However, immediately following the first full-term birth, women are at an increased risk of developing breast cancer [90], which in younger women lasts around 10 years, but in older women lasts longer [91].…”

“…Again, if MaSCs are the targets for transformation, this could help explain the lower breast cancer rates in women having undergone a full-term pregnancy. Notably, this effect dissipates with increased age at the time of first pregnancy [88,104], and in the mouse model pregnancy in older mice did not result in decreased MaSC numbers [43]. However, unlike the tumors that form shortly after pregnancy, the protective effect long after pregnancy is against ER/PR(+) tumors, suggesting that in such cases mutations that occur in MaSCs may not directly lead to transformation, but could lead to tumor formation upon further oncogenic challenges in downstream progenitors ( Figure 2C).…”