Body mass index at different life stages: Why it matters

Introduction

Body mass index (BMI) is a widely used tool in clinical practice to assess weight relative to height. Originally coined by Belgian mathematician Adolphe Quetelet in the 1830s to study patterns of body size, BMI is calculated by dividing a patient’s weight (in kg) by the square of their height (m²). This calculation provided a simple, standardized way to compare body size across individuals and populations, enabling early identification of weight-related health risk at a population level. In the 1970s, BMI began being used to categorize American patients as underweight (<18.5 kg/m²), normal weight (18.5–24.9 kg/m²), overweight (25–29.9 kg/m²), or obese (≥30 kg/m²). The obese category is further stratified into classes I (30.0–34.9 kg/m²), II (35.0–39.9 kg/m²), and III (≥40.0 kg/m²), reflecting both increasing disease severity and the growing public health burden of obesity. Despite its limitations, BMI plays a significant role in predicting risks for a variety of health conditions, including cardiometabolic disease and several cancers. Understanding BMI’s

role across different stages of life is crucial, as it plays a predictive role in and outside of obstetric and gynecological pathologies. This review explores the significance of BMI in childhood, adolescence, reproductive years, menopause, and beyond, and debunks fact from fiction.

BMI in childhood (3-13 years of age)

Children with higher BMI experience menarche earlier: Fact

Childhood and adolescent obesity in 3- to 11-year-old female patients shows a correlation with early menarche and ovarian dysfunction.¹ Increased BMI in girls and adolescents ages 7 to 13 prior to menarche can predict early menarche.² Large cross‑sectional studies of adolescents at ages 11, 13, and 15 have shown that overweight girls reach menarche approximately 6 to 9 months earlier (at ages 11.5-11.9 years) vs their normal‑weight peers (at 12.1 -12.4 years).³

Children with higher BMI may be at higher lifelong risk for endometrial cancer: Fact

A greater BMI during childhood (measured at 10 years of age) increases the risk of developing endometrial carcinoma (EC) later in life.⁴ The specific age at which a BMI increase occurs shows little impact.4 Regarding specific endometrial cancer subtypes, adult obesity demonstrates increased risk overall for EC and the endometrioid EC subtype.⁵ In contrast, studies show childhood BMI (measured at 10 years of age) increases risk for the non–endometrioid EC subtype, which is generally thought of as faster growing and carries a poorer prognosis.⁴ Intentional weight loss, even without normalization of BMI and especially with bariatric surgery, decreases the risk of EC by roughly half that of adults with obesity.⁶

Children with higher BMI may be at higher risk for breast cancer: Fiction

In contrast with EC, recorded BMI in childhood and adolescence (measured at the age of 7-13 years) is found to be inversely correlated with breast cancer risk.⁷ Women reporting a larger body size in childhood and adolescence had a 10% to 16% dose-response reduction risk of breast cancer in adulthood, when compared with women who reported being smaller as children, and this pattern holds across menopausal status and hormone receptor status.⁷

BMI in the reproductive years

BMI can affect fertility: Fact

In reproductive years (post menarche until menopause), BMI plays a pivotal role in fertility and pregnancy outcomes.⁸ Obesity is a leading cause of infertility due to its role in hormonal balance, ovulation, and endometrial function.⁸ In a study of anovulatory women with obesity, modest weight loss of approximately 5% to 10% of body weight through diet, exercise, and/or weight‑lowering drugs produced a marked increase in ovulation rates.⁸ The obesity effect on the hypothalamic-pituitary-ovarian axis in women mechanistically occurs through changes in luteinizing hormone and estrone.⁹ Leptin also plays a significant role in gonadotropin-releasing hormone pulses, which control ovulation.⁹ Patients who qualify as obese according to BMI have higher levels of leptin and show decreased rates of success with in vitro fertilization and fertility.⁹

Obesity during reproductive years affects polycystic ovary syndrome (PCOS): Fact

Perhaps the most common gynecologic pathology in reproductive age associated with elevated BMI is PCOS as a result of insulin resistance.¹⁰ The relationship between obesity and PCOS is cyclical; PCOS facilitates weight gain, and obesity exacerbates PCOS symptoms.¹⁰ Addressing BMI in the treatment of PCOS or infertility can be crucial in the treatment of symptom relief.¹⁰ In adolescents and young women with obesity and PCOS, modest weight loss of approximately 5% to 10% of body weight is associated with improvements in menstrual irregularity, hyperandrogenism, body composition, and metabolic profile, with larger (about 8%) BMI reductions linked to greater drops in testosterone levels.¹⁰

Obesity in reproductive years increases risk for having a child with congenital anomalies: Fact

Research has found that any extreme of maternal BMI (underweight or obese) is associated with an increased risk of congenital anomalies in the fetus. There has not been shown to be an increase in congenital anomaly risk when comparing normal BMI (18.5-24.9 kg/m²) groups to the overweight BMI (25-29.9 kg/m²) groups however, there was an increase in risk when comparing the normal BMI (18.5-24.9 kg/m²) group with the obese BMI (≥30 kg/m²) group.¹¹ In other words, a marginal increase in BMI did not increase the risk for congenital anomalies, but a significant increase in BMI does.

Specifically, maternal obesity was associated with ventricular septal defect, cleft lip, neural tube defects and eye anomalies, whereas being underweight was associated with atrial septal defects and genital anomalies.11 While the relative risk of congenital anomalies is increased in mothers with obesity, the overall likelihood of congenital anomalies at a population level remains low, and as such, most infants born to mothers with obesity are unaffected.

Pelvic pain is more severe in obese patients: Fiction

Chronic pelvic pain is defined as persistent, noncyclic pain associated with dyspareunia and dysmenorrhea. It is a common condition in women of reproductive age stemming from a variety of causes, including gynecologic, musculoskeletal, urologic, or neurologic.¹³ Studies find no significant difference in pain reported on the Visual Analogue Scale or numerical categorical pain scale in patients with normal vs elevated BMI.¹⁴ Patients with overweight or obesity do not rate their chronic pelvic pain worse than patients with normal BMI.¹⁴

BMI in pregnancy

Patients overweight or obese have increased risk for complicated pregnancies: Fact

Compared with patients of normal weight, cumulative live birth rates were lower in women who were overweight.¹⁵ The same study demonstrated that a reduction of BMI (from obesity to overweight or overweight to normal) could be beneficial in cumulative live birth weight.¹⁵ In a meta-analysis including 86 studies, patients overweight or obese are at increased odds of cesarean delivery, gestational diabetes, hypertension, preeclampsia, postpartum hemorrhage, and premature rupture of membranes.¹⁶ Helping patients achieve a healthy weight prior to conception can thus improve fertility and reduce pregnancy complications.¹⁵

Increased BMI can lead to increased rates of miscarriage: Fact

Obese maternal BMI carries an increased risk of miscarriage. Primigravidas with class II to III obesity (BMI > 34.9 kg/m²) had an 11.3% miscarriage rate compared with 2.7% in normal‑BMI primigravidas.¹⁷ Miscarriage rates for class I obese (BMI 30-34.9 kg/m²) primigravidas was 3.7%, which is not significantly different from rates for normal BMI.¹⁷ Increased risk appears confined to first‑pregnancy women with class II to III obesity, with miscarriage rates around 4 to 5 times higher than normal‑BMI primigravidas in that subgroup.¹⁷

BMI is an important consideration in comprehensive prenatal care: Fact

Treatment of patients who are overweight or obese should differ from that of patients with normal BMI during their prenatal care. Multiple clinical practice guidelines have been suggested regarding the care of patients with an obese or overweight BMI in pregnancy. The various guidelines generally agree on nutritional advice, weight gain parameters, exercise, and risk counseling.¹⁸ Agreement is limited regarding the timing of screening tests, ideal postpartum care, and management of adverse outcomes.¹⁸ The 2013-created, 2020-reaffirmed, American College of Obstetricians and Gynecologists recommendations for weight gain in pregnancy are depicted in the Table, and demonstrate the difference in weight gain recommendations for different BMI categories.¹⁹ Additional research is needed for the different classes of obese BMI.

BMI during menopause

High BMI can increase risk for pelvic organ prolapse: Fact

Elevated BMI is a generally accepted risk factor for pelvic organ prolapse (POP), along with parity, pelvic muscle weakness, and smoking.²⁰ POP recurrence risk is also increased in high BMI.20 Waist circumference over 88 cm was also cited as a risk factor for POP.²⁰

Obesity in peri or post menopause can exacerbate menopausal changes: Fact

Hypertension and dyslipidemia are often perpetuated by menopause if there is an increase in BMI.²¹ Hot flashes and sleep disturbances may also be exacerbated by high BMI.²¹ Normal BMI prior to menopause has shown some protection against potential health issues during menopause, such as cardiometabolic risk factors and vasomotor symptoms.²¹

Postmenopausal obesity decreases the risk of breast cancer: Fiction

In contrast with childhood obesity, the risk for breast cancer increases with high BMI in postmenopausal women.²² Among premenopausal women with obesity, increased waist circumference during menopausal transition increased the risk of breast cancer.²³ High levels of aromatase-expressing adipose tissue represent a major source of endogenous estrogens in the postmenopausal period that affect breast cancer risk.²²

Limitations

Although BMI is a widely used screening tool, it has several limitations. BMI does not fully account for the differences in body composition, such as muscle mass vs fat mass.²⁴ This is particularly relevant for athletes or individuals with high muscle mass.²⁴ BMI is most studied in Caucasian populations, which can further limit its use across different ethnicities and races. BMI also lacks insight into fat distribution, which waist circumference can compensate for.²⁴

In contrast with BMI alone, abdominal obesity and waist circumference measurements have shown a correlation for identifying metabolic syndrome and cardiovascular disease rates.²⁴ These measurements better reflect visceral adiposity, which is metabolically active and strongly associated with insulin resistance, and do not undergo false elevations for increased muscle mass. They also reflect ethnic and geographical trends that BMI may omit: demographics that are more predisposed to metabolic syndromes with higher rates of abdominal obesity.²⁴ The presence of central obesity is more likely to be detrimental to health and cardiometabolic risk than BMI alone and shows promise as a tool to use in conjunction with BMI to improve cardiometabolic risk stratification.²⁴

Conclusion

These recommendations underscore the important and nuanced role of BMI in women’s health. The described BMI-related risks and trends help inform future risk assessments and patient education. Overall, its utility as an accessible screening tool and its ability to interpret across key reproductive and hormonal transitions—childhood, adolescence, pregnancy, and menopause—support individualized recommendations and longitudinal clinical care.

References:

1. Laru J, Nedelec R, Koivuaho E, et al. BMI in childhood and adolescence is associated with impaired reproductive function—a population-based cohort study from birth to age 50 years. Hum Reprod. 2021;36(11):2948-2961. doi:10.1093/humrep/deab164

2. Aarestrup J, Pedersen DC, Thomas PE, et al. Birthweight, childhood body mass index, height and growth, and risk of polycystic ovary syndrome. Obes Facts. 2021;14(3):274-282. doi:10.1159/000515294

3. Marconi D, Lipari D, Pammolli A, et al. How does BMI correlate with menarche onset? evidence from the Italian HBSC cross-sectional study. BMC Womens Health. 2025;25:39. doi:10.1186/s12905-025-03572-y

4. Fang X, Wang X, Song Z, et al. Causal association of childhood obesity with cancer risk in adulthood: a Mendelian randomization study. Int J Cancer. 2021;149(7):1421-1425. doi:10.1002/ijc.33691

5. Dougan MM, Hankinson SE, De Vivo I, Tworoger SS, Glynn RJ, Michels KB. Prospective study of body size throughout the life-course and the incidence of endometrial cancer among premenopausal and postmenopausal women. Int J Cancer. 2015;137(3):625-637. doi:10.1002/ijc.29427

6. Ruffini ML, Fraga BL, Moraes CEAG, et al. Weight loss measures and their impact on the risk of developing endometrial cancer: a systematic review and meta-analysis. Int J Gynaecol Obstet. 2025;171(2):613-620. doi:10.1002/ijgo.70219

7. Pedersen DC, Jensen BW, Tjønneland A, et al. Birthweight, childhood body size, and timing of puberty and risks of breast cancer by menopausal status and tumor receptor subtypes. Breast Cancer Res. 2022;24(1):77. doi:10.1186/s13058-022-01578-0

8. van den Brandt PA, Ziegler RG, Wang M, et al. Body size and weight change over adulthood and risk of breast cancer by menopausal and hormone receptor status: a pooled analysis of 20 prospective cohort studies. Eur J Epidemiol. 2021;36(1):37-55. doi:10.1007/s10654-020-00688-3

9. Zheng L, Yang L, Guo Z, Yao N, Zhang S, Pu P. Obesity and its impact on female reproductive health: unraveling the connections. Front Endocrinol (Lausanne). 2024;14:1326546. doi:10.3389/fendo.2023.1326546

10. Calcaterra V, Verduci E, Cena H, et al. Polycystic ovary syndrome in insulin-resistant adolescents with obesity: the role of nutrition therapy and food supplements as a strategy to protect fertility. Nutrients. 2021;13(6):1848. doi:10.3390/nu13061848

11. Calcaterra V, Cena H, Sottotetti F, et al. Low-calorie ketogenic diet: potential application in the treatment of polycystic ovary syndrome in adolescents. Nutrients. 2023;15(16):3582. doi:10.3390/nu15163582

12. Stothard KJ, Tennant PWG, Bell R, Rankin J. Maternal overweight and obesity and the risk of congenital anomalies: a systematic review and meta-analysis. JAMA. 2009;301(6):636-650. doi:10.1001/jama.2009.113

13. Brite J, Laughon SK, Troendle J, Mills J. Maternal overweight and obesity and risk of congenital heart defects in offspring. Int J Obes (Lond). 2014;38(6):878-882. doi:10.1038/ijo.2013.244

14. Souza CA, Oliveira LM, Scheffel C, et al. Quality of life associated to chronic pelvic pain is independent of endometriosis diagnosis—a cross-sectional survey. Health Qual Life Outcomes. 2011;9:41. doi:10.1186/1477-7525-9-41

15. Gurian MB, Mitidieri AM, da Silva JB, et al. Measurement of pain and anthropometric parameters in women with chronic pelvic pain. J Eval Clin Pract. 2015;21(1):21-27. doi:10.1111/jep.12221

16. Langley-Evans SC, Pearce J, Ellis S. Overweight, obesity and excessive weight gain in pregnancy as risk factors for adverse pregnancy outcomes: a narrative review. J Hum Nutr Diet. 2022;35(2):250-264. doi:10.1111/jhn.12999

17. Vats H, Saxena R, Sachdeva MP, Walia GK, Gupta V. Impact of maternal pre-pregnancy body mass index on maternal, fetal and neonatal adverse outcomes in the worldwide populations: a systematic review and meta-analysis. Obes Res Clin Pract. 2021;15(6):536-545. doi:10.1016/j.orcp.2021.10.005

18. O'Dwyer V, Monaghan B, Fattah C, Farah N, Kennelly MM, Turner MJ. Miscarriage after sonographic confirmation of an ongoing pregnancy in women with moderate and severe obesity. Obes Facts. 2012;5(3):393-398. doi:10.1159/000336253

19. Simon A, Pratt M, Hutton B, et al. Guidelines for the management of pregnant women with obesity: a systematic review. Obes Rev. 2020;21(3):e12972. doi:10.1111/obr.12972

20. American College of Obstetricians and Gynecologists. ACOG Committee opinion no. 548: weight gain during pregnancy. Obstet Gynecol. 2013;121(1):210-212. doi:10.1097/01.aog.0000425668.87506.4c

21. Fitz FF, Bortolini MAT, Pereira GMV, Salerno GRF, Castro RA. PEOPLE: lifestyle and comorbidities as risk factors for pelvic organ prolapse—a systematic review and meta-analysis: PEOPLE: PElvic Organ Prolapse Lifestyle comorbiditiEs. Int Urogynecol J. 2023;34(9):2007-2032. doi:10.1007/s00192-023-05569-3

22. Opoku AA, Abushama M, Konje JC. Obesity and menopause. Best Pract Res Clin Obstet Gynaecol. 2023;88:102348. doi:10.1016/j.bpobgyn.2023.102348

23. Erdélyi A, Pálfi E, Tűű L, et al. The importance of nutrition in menopause and perimenopause—a review. Nutrients. 2023;16(1):27. doi:10.3390/nu16010027

24. Sweatt K, Garvey WT, Martins C. Strengths and limitations of BMI in the diagnosis of obesity: what is the path forward? Curr Obes Rep. 2024;13(3):584-595. doi:10.1007/s13679-024-00580-1