ReadYourDNA

Birth Weight

Where your DNA places you among other people, and the studies behind it.

General information

Not tailored to your result, and not medical advice

Stop Smoking Early In Pregnancy: Maternal smoking is one of the best documented behavioral influences on birth weight. A Swedish sibling analysis of national register data compared pregnancies within the same mother, which holds family genetics and social background constant, and found that smoking throughout pregnancy lowered birth weight by about 162 g at 1 to 9 cigarettes a day and about 226 g above that. Mothers who stopped after the first trimester showed reductions of only about 29 g and 1 g, so stopping early recovers most of the difference. PLOS One (PMC)

Watch Weight Gain In Pregnancy: Both ends of gestational weight gain move birth weight. A meta-analysis of 23 cohorts covering 1,309,136 pregnancies found that gaining less than national guidance was associated with higher odds of a small-for-gestational-age baby (OR 1.53, 95% CI 1.44 to 1.64), while gaining more was associated with higher odds of macrosomia (OR 1.95, 95% CI 1.79 to 2.11) and of a large-for-gestational-age baby (OR 1.85, 95% CI 1.76 to 1.95). In that pooled population 47% gained above guidance and 23% gained below it, so both directions are common. Diet quality and regular activity sit underneath those numbers, and what weight gain suits a particular pregnancy is a question for the clinician following it. JAMA (PMC)

Keep Caffeine Intake Modest: Caffeine crosses the placenta and is cleared more slowly as pregnancy progresses. The data are observational, and caffeine intake tracks with smoking and with the absence of pregnancy nausea, so some of the association may not be caffeine itself. Tea, cola, energy drinks and chocolate all count toward the daily total. BMC Medicine (PMC)

Treat Birth Weight As Fixed: Your own birth weight cannot be changed, so what matters is reading it correctly. In 237,631 UK Biobank participants, lower birth weight tracked with higher rates of type 2 diabetes and coronary artery disease, and a Mendelian randomisation analysis supported a causal contribution that was not explained by adult obesity or high blood pressure. The effect sizes are modest and sit alongside much larger adult influences, so smoking status, physical activity, diet and adult body weight are where the changeable risk actually lies. Circulation: Genomic and Precision Medicine (PubMed)

Expect Only Modest Lifestyle Effects: Behavior change programs in pregnancy move a mother's weight gain more reliably than they move the baby's size. An individual participant data meta-analysis of 36 randomised trials covering 12,526 women found that diet and physical activity interventions reduced gestational weight gain by 0.70 kg (95% CI 0.48 to 0.92), but showed no significant effect on large-for-gestational-age births (OR 0.90, 95% CI 0.76 to 1.07) or small-for-gestational-age births (OR 1.06, 95% CI 0.94 to 1.20). The honest summary is that avoiding clear exposures such as tobacco matters, while fine-tuning birth weight through lifestyle is not something the trials have shown to work. The BMJ (PMC)

Genetics vs Environment

How much of this is genetic?

Genetics explains 31% of why people differ in this trait. The rest is environment, daily habits and chance.

Heritability estimate: Lunde et al. 2007, Am J Epidemiol — fetal genetic factors explained about 31% of the variation in birth weight

About Birth Weight

Background and further reading

Birth weight is one of the most-studied human anthropometric traits and a marker of fetal growth. In most populations the typical range at term is roughly 2.5 to 4.5 kg (about 5.5 to 10 lb), with an average near 3.3 to 3.5 kg. It reflects the combined influence of the baby's own genes, the mother's genes and metabolism, gestational length, and the intrauterine environment. This score summarises only the contribution of common variants carried in the fetal (your own) genome that nudge growth before birth. It is not a measure of adult body size and does not diagnose anything.

Genetic Basis: Large genome-wide association studies from the Early Growth Genetics (EGG) Consortium and UK Biobank have identified around 190 independent signals associated with birth weight. Many of these loci sit in or near genes involved in glucose regulation and growth signalling, including ADCY5, CCNL1, the CDKAL1 region, HHEX-IDE, and the insulin/IGF pathway. Birth weight is highly polygenic: each variant shifts weight by only a few grams, and it is the accumulation across the whole genome that produces a measurable tendency. A distinctive feature of birth weight is that both the fetal genome and the maternal genome contribute, sometimes in opposing directions, because the mother's genes shape the environment the baby grows in.

Environmental Factors: Non-genetic factors account for the majority of variation in birth weight. Gestational age at delivery is the single largest determinant, followed by maternal nutrition, pre-pregnancy weight, gestational diabetes and glucose levels, maternal smoking (which lowers birth weight), altitude, birth order, and the sex of the baby. Because so much of birth weight is set by the intrauterine environment and by the mother's own genes rather than the baby's DNA, the tendency captured by this fetal-genome score is only a modest part of the full picture. Researchers study birth weight partly because variants that lower it overlap with genes linked to adult metabolic traits, an observation known as the fetal insulin hypothesis, though this is a population-level association and not a personal prediction.

How this was calculated

The published research behind your score, and the variants it draws on.

Study Details

6 published scores from 5 studies

The birth weight score combines 6 polygenic scores drawn from 5 published studies.

Arehart CH (2025). Modeling the genomic architecture of adiposity and anthropometrics across the lifespan. Nat Commun: 711k

Jung H (2024). Integration of risk factor polygenic risk score with disease polygenic risk score for disease prediction. Commun Biol: 1.1M

Ding Y (2022). Polygenic scoring accuracy varies across the genetic ancestry continuum in all human populations bioRxiv: 980k

Privé F (2022). Portability of 245 polygenic scores when derived from the UK Biobank and applied to 9 ancestry groups from the same cohort Am J Hum Genet: 828k

Tanigawa Y (2022). Significant sparse polygenic risk scores across 813 traits in UK Biobank. PLoS Genet: 6k

Further reading

Warrington NM, et al. Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors. Nature Genetics (2019)

Horikoshi M, et al. Genome-wide associations for birth weight and correlations with adult disease. Nature (2016)

Lunde A, et al. Genetic and environmental influences on birth weight, birth length, head circumference, and gestational age by use of population-based parent-offspring data. American Journal of Epidemiology (2007)

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Content updated August 2026.

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