The Association of Parity / Number of Live Births with Incident Type 2 Diabetes in Women: Over 15 Years of Follow-up in Tehran Lipid and Glucose Study | BMC Women’s Health

This is the first population-based cohort study conducted in the MENA region to examine the effect of parity / number of live births on incidents of T2DM. During 15.4 years of follow-up, after adjusting for a wide range of important risk factors for T2DM, including age, level of education, family history of diabetes, SBP, DBP, use of antihypertensive drugs and reproductive factors, higher parity / life The birth number was associated with a higher risk of developing T2DM. After further adjustment for obesity and TG / HDL-C indices, the higher risk was mitigated; however, HR trends in parity / live birth categories were marginally significant, and those with parity ≥ 4 had a more than 60% higher risk of developing T2DM. In addition, each additional live birth was associated with a significantly higher 6% risk of T2DM.

Our results were in line with two previous meta-analysis studies [5, 9]. Li et al., In a meta-analysis of cohort, cross-sectional and case-control studies, found a non-linear association between parity and risk of T2DM in which the combined multivariable RR for the development of T2D was 1, 06 (95% CI: 1.02-1.09) per live birth, with strong heterogeneity (I2= 87.2%) [5]. In addition, in their sensitivity analysis for prospective studies only, the RR reached 1.09 [5]. Likewise, in another joint analysis of cohort studies by Guo et al., Each unit increase in parity number had a combined RR of 1.06 (95% CI 1.02–1.09); however, a strong heterogeneity was shown between the included studies (I2= 84.3%) [9]. Additionally, in both meta-analyzes, compared to those with lower parity (baseline = 0 or 1), prospective study participants who had higher parity (at least 4 live births) were at approximately 40 % higher development of T2DM. [5, 9]. Based on data from 126,721 middle-aged women from eight cohort studies, a U-shaped association was found between the number of children and the risk of diabetes, in which women with 2 live births had the lowest risk. [16]. A similar U-shaped relationship was also seen in Danish women over the age of 33 [17] and Canadians aged 18 to 50 [10].

In the CARDIA study (development of coronary artery risk in young adults), it was shown that childbearing did not increase the incidence of diabetes until the women had developed gestational diabetes mellitus (GDM). In other words, the association of maternity with the DM incident can be explained by the GDM [18]. On the other hand, in Canadian women, an increased risk of MD with increasing parity was observed, even after adjusting for GD [10]. Likewise, among Danish women without a history of GDM, a relationship between parity and incident MD was also found. [17]. In the present study, even after adjusting for macrosomia, as a surrogate for DG [19], the association parity / number of live births and incident T2DM remained significant.

During a 5-year follow-up on Japanese women, Nanri et al. found that the association of parity with the risk of developing T2DM was significantly attenuated after adjusting for BMI. They suggested that a higher risk of developing T2DM due to increased parity could be explained in part by weight retention after pregnancy. [20]. In our short-term follow-up of less than 10 years, we also found similar results that all P values ​​became insignificant after adjusting for obesity indices in Model 4. However, in our long-term follow-up (main analysis), similar to a cohort study in American women [21], although the effect sizes for greater parity / number of live births were prominently attenuated in Model 4, but remained significant for parity / number of live births ≥ 4. Moreover, when we considered the change in BMI during follow-up as another covariate, generally the effect sizes did not change, and the P the value of the HR trend across parity number categories remained marginally significant.

In addition to weight retention, another explanation for the association of parity / number of live births with incident T2D in women may be the insulin resistance (IR) pathway. During a normal pregnancy, the target tissues (liver, muscle or fatty tissue) of the mother become increasingly insensitive to insulin, mainly due to the production of hormones by the placenta that antagonizes insulin. . [22]. This IR can progress to GD or can be overcome by a sufficient increase in the production of insulin by the beta cells of the pancreas. [22]; however, this process can place an additional burden on β cell function and affect insulin secretion, even after childbirth. [9, 23]. In addition to GD, a well-established risk factor for the future development of T2DM [24], it is also known that mothers with milder degrees of dysglycemia during pregnancy (i.e. less severe than GDM) were at greater risk of developing prediabetes and T2DM in the future. [23, 25]. In addition, in a comprehensive multivariate analysis, Kramer et al., Found that insulin sensitivity (as assessed by the Matsuda index) decreased during the first 3 years postpartum, even in women who had had a normal glucose-tolerant pregnancy. [23]. In addition, the expected reduction in physical activity and certain cardiometabolic changes during pregnancy (weight gain and dyslipidemia) may exacerbate this IR pathway. [22]. By repeating pregnancy, the time of exposure to the IR condition increases and may lead to a higher risk of developing T2DM. In the current study, despite the lack of data on insulin measurement, after further adjustment for TG / HDL-C (substitute for IR [26, 27]), each additional live birth and parity ≥ 4 were generally associated with a higher risk. This means that other factors could also play a role in the association of procreation and the development of T2DM, in particular psychosocio-economic factors.

The present study has several strengths, including standardized measures of traditional risk factors and the use of an oral glucose tolerance test for definition of results, rather than relying on self-reported data. Moreover, in addition to the well-known risk factors for T2DM, we also considered the change in BMI to be a strong covariate in our analysis, which was not addressed in previous studies in this area. The present study also has several weaknesses. First, during follow-up, possible changes in risk factors, as well as parity / number of live births, were not taken into account. Second, we were unable to show the impact of nulliparity due to the limited number of participants without a live birth. Third, we did not have access to data on participants’ diet, occupational status, income, and psychiatric history, which are potential representative factors of socioeconomic status and lifestyle. They could affect the association between parity / live birth number and incident T2DM. Fourth, at the start of the present study, only 18 participants reported a positive history of GDM that was too low to be considered a covariate. In addition, at the time of enrollment of this study (1999-2001) and before, there was no routine screening program for GDM such as oral glucose tolerance test (OGTT) during antenatal care in Iran. Therefore, most of the cases of DSG were missed by this time. However, in the present study, we fitted our models for macrosomia, the main surrogate for DG. Finally, this study was conducted among residents of the city of Tehran, and its findings may not be extended to rural populations.


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