- Design
- Prospective birth cohort with mediation analysis (ALSPAC)
- Population
- 1,933 offspring followed to age 24, UK
- Primary outcome
- MASLD at 24 by transient elastography plus cardiometabolic risk factor
- Effect
- Maternal BMI OR 1.10/unit; paternal 1.09/unit; biparental overweight OR 3.73 (2.43–5.73)
An analysis of the UK ALSPAC birth cohort in Gut (7 September) followed 1,933 offspring to age 24, when MASLD was assessed by transient elastography plus a cardiometabolic risk factor.
At 24, 10.4% had MASLD. Each 1 kg/m² higher maternal pre-pregnancy BMI was associated with 10% higher odds (OR 1.10), and each 1 kg/m² higher paternal BMI with 9% higher odds (OR 1.09), independently. When both parents were overweight or obese, the odds were 3.7 times those with two normal-weight parents (OR 3.73, 95% CI 2.43 to 5.73). About two-thirds of that association ran through excess BMI during childhood, from 7 to 17.
This is observational and cannot separate genes from shared environment. But the large share carried by childhood weight suggests a window where family-based weight management may matter for liver health decades later.
- Ask about parental obesity when assessing young adults for MASLD risk.
- Childhood excess weight carried most of the parental association; family-based prevention is a reasonable target.
- Paternal as well as maternal weight was independently associated with offspring MASLD.
- One in ten 24-year-olds in this cohort already had MASLD.
Why it matters
It extends MASLD risk back before birth and highlights childhood weight as the main pathway.
Don't overread it
Observational data; it cannot show that parental weight loss before pregnancy would prevent MASLD in children.
The statistics, in plain English
An odds ratio of 1.10 per unit BMI compounds: a mother 5 kg/m² heavier corresponds to roughly 60% higher odds. Mediation analysis estimates how much of the link runs through childhood BMI (67%), but it rests on assumptions about unmeasured confounding.
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