OBJECTIVE—While high parity is hypothesized to be associated with insulin resistance and type 2 diabetes, few studies have examined this association in diverse racial samples or geographical areas. Our objectives were to estimate the magnitude of association between parity and diabetes and to determine if higher parity is predictive of future risk of diabetes.

RESEARCH DESIGN AND METHODS—This was a population-based, prospective cohort study of 7,024 Caucasian and African-American women from the Atherosclerosis Risk in Communities study, a prospective epidemiological study of men and women aged 45–64 years, with 9 years of follow-up. Incident diabetes was defined by the 1997 American Diabetes Association diagnostic criteria. Parity was defined as the number of live births (no live births [nulliparity], one to two live births, three to four live births, and five or more live births [grandmultiparity]). Parity and risk of diabetes was estimated for 754 incident cases of diabetes with Cox proportional hazard regression models, adjusting for sociodemographic, clinical, and lifestyle factors and inflammatory markers.

RESULTS—Incidence rates were highest among women with five or more live births (23/1,000 person-years [95% CI 20.3–26.7]) and lowest among women with one to two live births (11/1,000 person-years [9.6–12.5]). Adjustment indicated that much of the risk was due to sociodemographic factors and higher obesity, but after adjustment for all covariates, grandmultiparity (five or more) was still associated with a 27% increased risk for diabetes (hazard ratio 1.27 [95% CI 1.02–1.57]).

CONCLUSIONS—Grandmultiparity is predictive of future risk of diabetes after adjustment for confounders.

There is growing interest in the effect of childbearing on the development of chronic medical conditions, including cardiovascular disease (1) and diabetes (24). Earlier investigations have suggested that parity, particularly five or more live births, might be associated with diabetes (2,4,5), whereas other investigations have found no association (68). Potential mechanisms include the influence of multiple pregnancies on postpartum weight retention (9,10) and development of obesity (6,7,11) or the influence of multiple exposures to the metabolic changes of pregnancy (2), including impaired insulin sensitivity and central obesity (12), both of which parallel the mechanisms underlying the development of diabetes. Other studies (5,13,14) suggest that nulliparity (no live births) may be associated with diabetes. Potential mechanisms include underlying insulin resistance and β-cell dysfunction (5) related to infertility and pregnancy loss (15).

While these studies offer important, useful information, the effect of parity on diabetes is not completely understood. Prior studies are relatively limited to one geographical region (4,8) or population (7,14). While some studies have adjusted for measures of obesity, fewer studies have adjusted for potentially modifiable lifestyle factors, such as physical activity and caloric intake (7), and limited laboratory data, such as markers of obesity or inflammation (5,16), have been presented. It is important for clinicians to be aware of potential associations between childbearing and diabetes in order to counsel women about potential long-term consequences of the metabolic and lifestyle changes associated with pregnancy (17).

The Atherosclerosis Risk in Communities (ARIC) study is a community-based cohort of men and women with currently 9 years of follow-up (18). Our goal was to determine the relation of parity with diabetes, accounting for the contribution of sociodemographic, clinical, and physiologic factors using a longitudinal approach. Our hypothesis was that parity is independently associated with diabetes. The study objectives were to 1) determine the incidence of diabetes across parity groups in a community-based sample, 2) describe the association between parity and established risk factors for diabetes, and 3) determine whether parity is independently associated and predictive of diabetes after adjustment for sociodemographic and clinical factors and measures of inflammation.

We conducted a longitudinal analysis of data from the ARIC study to examine the presence and strength of an association between parity and diabetes in a sample of African-American and Caucasian women. This study was approved by the institutional review boards of each participating institution.

The ARIC study is a prospective, population-based study of 15,792 adult men and women, aged 45–64 years, who were recruited between 1986 and 1989 from four U.S. communities: Forsyth County, North Carolina; Jackson, Mississippi; Washington County, Maryland; and surburban Minneapolis, Minnesota (18). Baseline examinations were conducted between 1986 and 1989 (visit 1), with follow-up and clinic visits every 3 years (1990–1992 [visit 2], 1993–1995 [visit 3], and 1996–1998 [visit 4]), for a total of 9 years of follow-up. Response rates for the second, third, and fourth follow-ups were 93, 86, and 81%, respectively. We limited our analysis to Caucasian and African-American women (n = 8,579) due to small numbers of women in other racial groups. Participants who had diabetes at baseline (n = 1,096) and never returned for follow-up (n = 436) or whose information on parity was missing (n = 23) were excluded. The final sample size for the analysis was 7,024 women.

### Exposure

The independent variable, parity, was defined as the total number of live births and was based on data collected at entry into the study. We classified parity into four categories: no live births (nulliparity), one to two live births, three to four live births, and five or more live births (grandmulliparity). We did not include spontaneous miscarriages or pregnancy terminations. We also constructed an additional category, nulligravida, for women who reported that they had never been pregnant and had not undergone any type of delivery.

### Outcome: type 2 diabetes

Individuals were classified as having diabetes based on the 1997 American Diabetes Association criteria (19): 1) a reported history of physician-diagnosed diabetes, 2) current use of antidiabetes medications, or 3) fasting serum glucose levels ≥126 mg/dl and nonfasting serum glucose levels ≥200 mg/dl. Individuals without diabetes at study entry who subsequently met any of these criteria at visits 2, 3, or 4 were considered to have incident diabetes.

### Incidence of type 2 diabetes

Over 9 years of follow-up, there were 224, 280, and 205 incident cases of type 2 diabetes among women with one to two live births, three to four live births, and five or more live births, respectively (Table 2). Approximately 44% of the sample was diagnosed with type 2 diabetes by a clinician. Incidence rates ranged from 11.0/1,000 person-years (95% CI 9.6–12.5) in women with one to two live births to 13.8/1,000 person-years (12.3–15.6) in women with three to four live births, and 23.3/1,000 person-years (20.3–26.7) in women with five or more live births. The incidence of diabetes among women with prior pregnancies but no live births was 19.8/1,000 person-years (12.1–32.3).

### Parity and incident diabetes

After adjustment for sociodemographic factors, women with five or more live births had a 44% increased rate of developing diabetes compared with women with one to two live births (RH 1.44 [95% CI 1.18–1.77]) (Table 3). After the addition of lifestyle factors, five or more live births were still associated with the risk of diabetes. The association between five or more live births and diabetes was attenuated but remained significant after an additional adjustment for BMI and waist circumference (RH 1.24 [1.00–1.53]). In the fully adjusted model, including markers of inflammation, women with five or more live births had a 27% increased rate of developing diabetes compared with women with one to two live births (RH 1.27 [1.02–1.57]).

Further adjustment for time-dependent variables (income, smoking status, waist circumference, BMI, caloric intake, sports index, and leukocyte count) did not change the RHs of development of diabetes in any parity group compared with women with one to two live births.

Figure 1 shows the association of parity with type 2 diabetes stratified by race and BMI subgroups. The hazard ratio for developing type 2 diabetes was similar between African-American and Caucasian women for each parity category (Fig. 1A) and for each BMI category (Fig. 1B). There were no significant interactions with educational or income levels (data not shown).

We estimated the magnitude of association of parity with diabetes and identified behavioral, clinical, and laboratory factors that might account, in part, for the association of parity with diabetes. We then described the independent association between parity and diabetes, adjusting for covariates.

There are several possible mechanisms to explain the association between parity and type 2 diabetes. First, women of higher parity have a higher caloric intake and lower physical activity than women of lower parity. These sedentary lifestyle behaviors can lead to higher BMI, insulin resistance, and development of diabetes (10,25). In our study population, women of higher parity had a higher mean BMI and waist circumference at baseline than women of lower parity. Thus, postpartum weight retention with multiple births coupled with a sedentary lifestyle among highly parous women may also lead to diabetes. These findings suggest the need to further explore patterns of postpartum weight retention. Incorporating effective educational initiatives focused on nutrition and physical activity into standard prenatal and postnatal care may be a reasonable strategy to promote healthy lifestyle behaviors among women.

Second, socioeconomic status might lead to both higher parity and risk of diabetes. Both income and education were strong confounders of the association between parity and diabetes in our study. The addition of these variables to the multivariable models markedly attenuated the association between parity and diabetes. Lower socioeconomic status is associated with higher parity and can also affect lifestyle behaviors and risk of diabetes.

Third, we explored the role of inflammation as a possible connection between parity and diabetes risk. Other research indicates that fibrinogen levels (26) and white blood cell counts (27) can be related to incident diabetes and obesity, respectively. In our study population, higher parity was associated with an increase in these inflammatory markers. Higher parity may lead to obesity or weight retention, as evidenced by a concurrent rise in inflammatory markers and development of diabetes. Also, it may be that some of the association of inflammation with parity is explained by socioeconomic factors (28).

While some investigators propose that hormone levels might heighten insulin sensitivity (29), others propose that hormones might adversely affect insulin resistance and increase the risk of diabetes (30). Our findings do not support menopausal status, oral contraceptive use, or hormonal use as potential mediators of the association between parity and diabetes.

Our study has several strengths. The ARIC study is a large sample of individuals in which there was a standardized method of identifying incident diabetes for up to 9 years of follow-up. Because there are standardized measures of exposures, outcomes, behavioral factors, and laboratory measures (e.g., inflammatory markers) used at each recruitment site in an observational study design, the ARIC study provides an opportunity to examine potential mechanisms of the association between parity and diabetes.

There are also limitations to this study. Our results may have limited generalizability to other racial groups with higher rates of diabetes, such as Native Americans. We did not have data on pregnancy-related confounders, such as a history of gestational diabetes, gestational weight gain, or postpartum weight retention. Because most practitioners did not practice universal screening at the time of ARIC study recruitment, data on gestational diabetes was not ascertained. Women with prior gestational diabetes are known to be at high risk for the development of type 2 diabetes. Also, we did not have information on breast-feeding practices, which may affect the incidence of type 2 diabetes (31). Data on these parameters could broaden our understanding of the association between childbearing and lifestyle behaviors related to diabetes. Because we were unable to discern between nonlive births due to spontaneous miscarriage and intrauterine fetal death, we could not characterize potential pathways between parity and diabetes based on nonlive birth pregnancy outcomes.

The main implication of our study is that the association of pregnancy with development of diabetes, whether through biological mechanisms or lifestyle behaviors, deserves further study. After adjustment for all covariates, grandmultiparity is associated with a higher risk of diabetes. While further study is warranted, this work suggests the need for physicians to discuss the potential long-term effects of pregnancy to their patients. Our study serves as a basis for additional longitudinal studies of young women in which specific pregnancy-related weight gain measures, lifestyle factors, and changes in socioeconomic status can be prospectively measured. Additional studies should also include laboratory measures of insulin resistance, glucose tolerance, and adiposity as women progress through their reproductive years.

Figure 1—

The association of parity with incident type 2 diabetes among racial subgroups (A) and categories of BMI (B). A: Dotted line represents African-American women and solid line represents Caucasian women. Vertical line represent 95% CIs. B: Solid line represents normal/underweight, dotted line represents overweight, and dashed line represents obesity.

Figure 1—

The association of parity with incident type 2 diabetes among racial subgroups (A) and categories of BMI (B). A: Dotted line represents African-American women and solid line represents Caucasian women. Vertical line represent 95% CIs. B: Solid line represents normal/underweight, dotted line represents overweight, and dashed line represents obesity.

Table 1—

Baseline demographic, behavioral, clinical, and physiological characteristics of 7,024 adult women by parity

CharacteristicsNever pregnant*Parity
P
Women with prior pregnancies and the number of live births
No live births1–2 live births3–4 live births≥5 live births§
n 442 112 2,630 2,609 1,231
Age (years) 54.1 ± 5.9 54.8 ± 5.9 53.2 ± 5.8 53.3 ± 5.5 54.4 ± 5.2 <0.01
African American (%) 17 46 19 21 48 <0.01
High school education or less (%) 11 22 14 17 40 <0.01
Annual household income <$16K (%) 19 26 17 19 43 <0.01 Caloric intake (kcal/day) 1,440 ± 541 1,522 ± 489 1,486 ± 538 1,501 ± 525 1,529 ± 550 0.03 Leisure-time physical activity score 2.37 ± 0.75 2.39 ± 0.73 2.38 ± 0.78 2.36 ± 0.77 2.23 ± 0.69 <0.01 Current/former/never smoker (%) 24/25/51 25/37/38 26/23/51 22/25/53 24/19/57 <0.01 Ever taken birth control pills (%) 28 36 47 52 44 <0.01 Menopausal (%) 71 76 68 68 78 <0.01 Ever used hormone replacement (%) 38 43 38 37 32 <0.01 Family history of diabetes (%) 12 13 13 14 13 0.61 BMI (kg/m226.1 ± 5.5 27.2 ± 5.5 26.3 ± 5.4 27.3 ± 5.5 29.3 ± 6.3 <0.01 Waist circumference 91.5 ± 14.8 94.1 ± 15.3 91.5 ± 14.1 93.5 ± 14.5 98.2 ± 15.7 0.01 Leukocyte count (cells/ml) 5.8 ± 1.7 6.0 ± 1.9 5.9 ± 1.8 5.9 ± 1.9 5.8 ± 1.9 0.07 Fibrinogen levels (mg/dl) 305 ± 62 306 ± 71 300 ± 60 300 ± 60 311 ± 67 <0.01 Glucose (mmol/l) 5.3 ± 0.5 5.4 ± 0.5 5.3 ± 0.5 5.4 ± 0.5 5.5 ± 0.5 <0.01 CharacteristicsNever pregnant*Parity P Women with prior pregnancies and the number of live births No live births1–2 live births3–4 live births≥5 live births§ n 442 112 2,630 2,609 1,231 Age (years) 54.1 ± 5.9 54.8 ± 5.9 53.2 ± 5.8 53.3 ± 5.5 54.4 ± 5.2 <0.01 African American (%) 17 46 19 21 48 <0.01 High school education or less (%) 11 22 14 17 40 <0.01 Annual household income <$16K (%) 19 26 17 19 43 <0.01
Caloric intake (kcal/day) 1,440 ± 541 1,522 ± 489 1,486 ± 538 1,501 ± 525 1,529 ± 550 0.03
Leisure-time physical activity score 2.37 ± 0.75 2.39 ± 0.73 2.38 ± 0.78 2.36 ± 0.77 2.23 ± 0.69 <0.01
Current/former/never smoker (%) 24/25/51 25/37/38 26/23/51 22/25/53 24/19/57 <0.01
Ever taken birth control pills (%) 28 36 47 52 44 <0.01
Menopausal (%) 71 76 68 68 78 <0.01
Ever used hormone replacement (%) 38 43 38 37 32 <0.01
Family history of diabetes (%) 12 13 13 14 13 0.61
BMI (kg/m226.1 ± 5.5 27.2 ± 5.5 26.3 ± 5.4 27.3 ± 5.5 29.3 ± 6.3 <0.01
Waist circumference 91.5 ± 14.8 94.1 ± 15.3 91.5 ± 14.1 93.5 ± 14.5 98.2 ± 15.7 0.01
Leukocyte count (cells/ml) 5.8 ± 1.7 6.0 ± 1.9 5.9 ± 1.8 5.9 ± 1.9 5.8 ± 1.9 0.07
Fibrinogen levels (mg/dl) 305 ± 62 306 ± 71 300 ± 60 300 ± 60 311 ± 67 <0.01
Glucose (mmol/l) 5.3 ± 0.5 5.4 ± 0.5 5.3 ± 0.5 5.4 ± 0.5 5.5 ± 0.5 <0.01

Data are means ± SD unless otherwise indicated. For continuous variables, the P value is from ANOVA; for categorical variables, the P value is from the χ2 test.

*

Women who reported never being pregnant;

number of live births;

women who reported prior pregnancies but no live births;

§

grandmultiparity.

Table 2—

Incidence rate of diabetes by childbearing categories, the ARIC study, 1986–1998

Incidence rate of type 2 diabetesNever pregnant*Parity
No live births1–2 live births3–4 live births≥5 live births
Number of incident diabetes 29 16 224 280 205
Incidence rate per 1,000 person-years (95% CI) 8.4 (5.8–12.0) 19.8 (12.1–32.3) 11.0 (9.6–12.5) 13.8 (12.3–15.6) 23.3 (20.3–26.7)
Incidence rate of type 2 diabetesNever pregnant*Parity
No live births1–2 live births3–4 live births≥5 live births
Number of incident diabetes 29 16 224 280 205
Incidence rate per 1,000 person-years (95% CI) 8.4 (5.8–12.0) 19.8 (12.1–32.3) 11.0 (9.6–12.5) 13.8 (12.3–15.6) 23.3 (20.3–26.7)
*

Women who reported never being pregnant;

number of live births among women who reported prior pregnancies.

Table 3—

RHs (95% CI) of diabetes over 9 years of follow-up by category of parity for 7,024 women, the ARIC study

No live births*1–2 live births (reference)3–4 live births≥5 live births
Model 1: unadjusted 0.77 (0.52–1.13) 1.78 (1.07–2.96) 1.0 1.26 (1.06–1.50) 2.10 (1.73–2.53)
Model 2: sociodemographics 0.77 (0.51–1.14) 1.41 (0.85–2.35) 1.0 1.23 (1.03–1.47) 1.44 (1.18–1.77)
Model 3: model 2 factors + lifestyle behaviors 0.80 (0.54–1.20) 1.48 (0.89–2.46) 1.0 1.26 (1.05–1.50) 1.46 (1.19–1.80)
Model 4: model 3 factors + reproductive factors 0.82 (0.55–1.22) 1.39 (0.82–2.35) 1.0 1.18 (0.98–1.42) 1.42 (1.15–1.76)
Model 5: model 4 factors + waist circumference and BMI 0.79 (0.53–1.18) 1.31 (0.77–2.22) 1.0 1.11 (0.92–1.34) 1.24 (1.00–1.53)
Model 6: model 5 factors + markers of inflammation§ 0.80 (0.54–1.20) 1.31 (0.77–2.23) 1.0 1.11 (0.92–1.34) 1.27 (1.02–1.57)
No live births*1–2 live births (reference)3–4 live births≥5 live births
Model 1: unadjusted 0.77 (0.52–1.13) 1.78 (1.07–2.96) 1.0 1.26 (1.06–1.50) 2.10 (1.73–2.53)
Model 2: sociodemographics 0.77 (0.51–1.14) 1.41 (0.85–2.35) 1.0 1.23 (1.03–1.47) 1.44 (1.18–1.77)
Model 3: model 2 factors + lifestyle behaviors 0.80 (0.54–1.20) 1.48 (0.89–2.46) 1.0 1.26 (1.05–1.50) 1.46 (1.19–1.80)
Model 4: model 3 factors + reproductive factors 0.82 (0.55–1.22) 1.39 (0.82–2.35) 1.0 1.18 (0.98–1.42) 1.42 (1.15–1.76)
Model 5: model 4 factors + waist circumference and BMI 0.79 (0.53–1.18) 1.31 (0.77–2.22) 1.0 1.11 (0.92–1.34) 1.24 (1.00–1.53)
Model 6: model 5 factors + markers of inflammation§ 0.80 (0.54–1.20) 1.31 (0.77–2.23) 1.0 1.11 (0.92–1.34) 1.27 (1.02–1.57)

Model 2: adjusted for age, center, race, income, education, and family history of diabetes. Model 3: adjusted for age, center, race, income, education, smoking, family history of diabetes, caloric intake, and physical activity score. Model 4: adjusted for age, center, race, income, education, smoking, family history of diabetes, caloric intake, physical activity score, menopause status, age at menopause, ever use of birth control pills, and ever use of hormone replacement therapy. Model 5: adjusted for age, center, race, income, education, smoking, family history of diabetes, caloric intake, physical activity score, menopause status, age at menopause, ever use of birth control pills, ever use of hormone replacement therapy, waist circumference, and BMI. Model 6: adjusted for age, center, race, income, education, smoking, family history of diabetes, caloric intake, physical activity score, menopause status, ever use of birth control pills, ever use of hormone replacement therapy, waist circumference, BMI, fibrinogen levels, and leukocyte count.

*

No live births, nulliparity;

≥5 live births, grandmultiparity.

P < 0.05.

§

Fibrinogen and leukocyte count.

W.K.N. and N.R.P. are supported, in part, by the National Insitute for Diabetes and Digestive Kidney Diseases (grant 1K23 DK-067944 to W.K.N. and grant 2K24-DK-O2643-06A1 to N.R.P.). The ARIC study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute Grants N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, and N01-HC-55022.

The authors thank the staff and participants of the ARIC study for their contributions.

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A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

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