Higher pre-pregnancy weight tracks with offspring heart disease decades on

A pregnancy is increasingly studied not just for its immediate outcome but as a possible setting of a child's long-term health. A cohort study in JAMA Network Open, published 1 September, asks whether a mother's weight in early pregnancy and how much she gains during it are associated with her child's risk of cardiovascular disease years later — and finds a graded association that survives, in attenuated form, a demanding test for family confounding [s1].

The study

The researchers used Swedish national registers covering everyone born between 1 January 1982 and 31 December 2014, following them from birth to a first cardiovascular diagnosis, death, emigration or the end of 2023 [s1]. The cohort was large: 2,496,335 offspring, 51.4% male, with a mean age of 23.3 years (SD 9.8) at the end of follow-up, over a median 22.0 years (IQR 14.7–30.4) [s1]. During that time 22,510 offspring — 0.9% — were diagnosed with cardiovascular disease [s1].

Maternal body mass index in early pregnancy was categorised from underweight through obesity classes 1 to 3, and gestational weight gain was standardised for gestational age into z scores [s1].

The numbers

Compared with offspring of mothers with normal BMI, the hazard ratios for cardiovascular disease rose step by step with maternal weight: 1.29 (95% CI 1.24–1.33) for maternal overweight, 1.66 (1.57–1.75) for obesity class 1, 2.16 (1.96–2.39) for obesity class 2, and 2.74 (2.29–3.28) for obesity class 3 [s1]. Greater gestational weight gain was independently associated with higher risk across BMI groups; among offspring of normal-weight mothers, a high weight gain (z score ≥ 1) carried a hazard ratio of 1.16 (95% CI 1.09–1.22) [s1].

A dose-response pattern like this — risk climbing in order with the exposure — is one of the features that makes an association more credible than a single point estimate. But it does not, by itself, establish cause.

The sibling test

The study's most important design feature addresses exactly that gap. In sibling analyses — which compare children of the same mother, holding constant the genetics and shared home environment that could confound a simple population comparison — the associations for higher maternal BMI and weight gain were attenuated, but remained generally evident [s1]. That is a meaningful result in both directions: part of the population-level association appears to reflect shared familial factors rather than pregnancy itself, yet a signal persists even after those factors are stripped out, which is harder to explain away [s1].

How to read it

This is observational, and the outcome is early-onset disease. With a cohort whose mean age is only 23, most participants have not reached the age when cardiovascular disease is common, so the events captured here are the unusually early ones and the findings speak to relative risk in young adults, not to lifetime absolute risk [s1]. Residual confounding is never fully excluded even by sibling designs, and the registers cannot capture everything about diet, activity or paternal factors. An accompanying editorial situates the work within the broader debate over how much "eating for two" shapes a child's cardiovascular trajectory [s2].

The absolute numbers are the antidote to over-reading the hazard ratios. Across the whole cohort, 0.9% of offspring were diagnosed with cardiovascular disease over a median 22 years of follow-up, so even a hazard ratio of 2.74 in the highest maternal-BMI group is a multiplication of a still-small baseline risk in young adulthood [s1]. The gestational-weight-gain finding is the more novel half of the paper, because it points to something potentially modifiable during pregnancy rather than a mother's weight before it: even among women who started pregnancy at a normal BMI, gaining substantially more than expected was associated with a 16% higher offspring risk [s1]. But "associated with" is doing real work in that sentence — the sibling analysis is what keeps the result from being dismissed as pure family confounding, and it is also what shows a chunk of the crude association was exactly that [s1].

What to watch

The clinically live question is whether modifying maternal weight — before or during pregnancy — changes offspring risk, which an observational cohort cannot answer. What this study strengthens is the rationale for treating maternal cardiometabolic health as a two-generation issue, while being careful not to convert a hazard ratio in young adults into alarm or blame directed at mothers.

This article is informational and does not constitute medical advice.

Sources

• [s1] Maternal Body Mass Index, Gestational Weight Gain, and Cardiovascular Disease in Offspring. JAMA Network Open, 1 September 2026. https://doi.org/10.1001/jamanetworkopen.2026.31324
• [s2] Your Child's Cardiovascular Health—Can Eating for Two Be Too Much? JAMA Network Open, 1 September 2026. https://doi.org/10.1001/jamanetworkopen.2026.31215