In this longitudinal cohort of 97,291 male conscripts, we found that there was no association between elective or nonelective CS and young adulthood obesity when accounting for possible confounding factors and conducting several predefined sensitivity analyses as compared with vaginal delivery. To the best of our knowledge, we have presented the largest and most comprehensive differentiation between elective and nonelective CS so far.

Comparison with previous research

In contrast with previous research [10,13,15,16], we did not observe any association between CS and young adulthood obesity. This could be explained by previous studies’ limited ability to adjust for maternal prepregnancy BMI [16], small sample sizes [10,13,15,16], and/or inability to differentiate between elective/prelabor and nonelective/acute CS [10,16]. To the best of our knowledge, the largest previous study on CS and offspring overweight/obesity that differentiated between types of CS was conducted on children (5 years old), with only 145 exposed cases, and described a significant association between CS on maternal request and overweight/obesity (odds ratio [OR] 1.18, CI 95% 1.00–1.41) [64]. In contrast, a meta-analysis [13] suggested that there was no association between prelabor CS and obesity in adulthood. However, this analysis was limited to very few participants (prelabor CS = 252 and vaginal delivery = 17,506).

Although a majority of previous studies have had limitations, studies with less uncertainty have suggested that there may be an attenuation with age in the association between CS and obesity [15,23]. The attenuation by age could potentially explain our findings. However, childhood obesity not persisting into young adulthood or adulthood may be of less relevance for clinical manifestation of obesity-related consequences [65–67].

Contrary to our findings, a recent study [24] on very young children (12 months old) suggested a strong association between elective CS and overweight (OR 2.01, CI 95% 1.13–3.58) but no such association for emergency CS (OR 1.08, CI 95% 0.66–1.76). The authors hypothesize that this may be a function of lack of fetal stress exposure induced by the onset of labor, which may be absent in elective CS, and that emergency CS may be exposed to maternal microbiota to a greater extent than elective CS. However, adjusting for intrapartum antibiotics did not alter their findings, suggesting that microbiota exposure did not explain the low risk in the emergency CS [24]. Contrary to the suggestion that CS supports the hygiene hypothesis, there have been suggestions that CS is a risk factor for childhood obesity that is independent of second- and third-trimester antibiotic use [68], although antibiotic use may also independently influence childhood obesity [68].

In addition to the aforementioned discrepancies between our study and previous studies, it should be noted that our cohort was born between 1982 and 1987, which could have implications for the comparability to more recent birth cohorts [24]. However, several studies conducted on younger children with more recent birth years have suggested null associations similar to those we observed in our cohort [22,23,25].

In our cohort, only accounting for maternal prepregnancy BMI attenuated the association between elective or nonelective CS and obesity by 15% and 16%, respectively (RRR 1.14 versus 0.99 and 1.17 versus 1.01) (S11 Table). Indeed, this was the strongest confounder in the association between either form of CS and obesity in our study. As obesity has a high heritability [69] and/or could be a function of fetal programming [70], it is plausible that taking maternal prepregnancy BMI into account captures both genetic predispositions transferred from mother to offspring and the fetal exposure to an obesogenic state in the mother. Using our fixed-effects linear regression, which accounts for familial confounding shared between brothers (e.g., obesogenic familial environment and obesity-related genetic traits), we did not observe any association between any form of CS and offspring obesity. Notably, we observed an association between nonelective CS and overweight in our multinomial discordant sibling sample. However, this may be explained by the small number of exposed cases and the possibility of residual confounding. Hence, we suspect there to be an association between nonelective CS and overweight as a function of confounding by medical indication for CS [23]. Indeed, if there is a causal effect of CS on overweight/obesity, an association should be present in elective CS as well [23].

Despite unnecessary CS being subject to some criticism [71], it is of interest to further study unnecessary CS and its possible association to offspring morbidity [72]. Although Swedish registers enable us to differentiate between elective and nonelective CS, they do not enable us to perform detailed classifications of CS using such classifications as the Robson classification [73], which may provide further insight into the potential role of CS in offspring health.