Association of parental characteristics with offspring anthropometric failure, anaemia and mortality in India

The study investigates how parental attributes—sociodemographic (age, age at marriage, education, employment), physical (height, BMI), behavioural (tobacco and alcohol use), and presence of non-communicable diseases (diabetes, hypertension)—are associated with offspring anthropometric failure, anaemia, and under-five mortality in India. Situated within evolutionary and public health perspectives on parent–child health pathways, the work addresses gaps in prior Indian studies that typically evaluated limited parental factors or single child health outcomes and seldom included parental NCDs. Understanding these associations can inform strategies to reduce undernutrition, anaemia, and mortality among under-five children in India.

Prior evidence indicates that early maternal age and child marriage are linked to adverse offspring outcomes including low birthweight, preterm birth, stunting, and higher infant mortality; evidence on boys’ child marriage is scarce but suggests constrained education and earnings. Younger parental age associates with higher risks of anaemia, stunting, and incomplete immunisation. Both maternal and paternal education consistently show protective associations against child mortality and anthropometric failures across LMICs; effects of each parent’s education may be comparable, warranting inclusion of both. Parental employment, particularly professional maternal employment, relates to better child health, though findings are mixed for anaemia/stunting. Parental phenotypes: taller maternal and paternal stature associate with reduced child stunting; increases in maternal height associate with lower offspring mortality and undernutrition; higher parental BMI correlates with higher offspring BMI and lower undernutrition risks. Behavioural risks: parental tobacco use (including second-hand exposure) is associated with adverse birth outcomes, infections, and higher child mortality; alcohol misuse by parents relates to poorer child health, development, and adverse behaviours. Parental NCDs: maternal diabetes relates to poorer glycaemic outcomes and higher blood pressure in offspring; parental hypertension relates to adverse child outcomes, potentially via genetic pathways. Few Indian studies have jointly examined a comprehensive set of parental sociodemographic, behavioural, phenotypic, and NCD characteristics across multiple child outcomes, motivating this study.

Data source: India’s National Family Health Survey 2015–2016 (NFHS-4; DHS-7), a cross-sectional, nationally representative survey of 640 districts across 37 states/UTs using a stratified two-stage design (rural PSUs=villages; urban PSUs=CEBs) with PPS selection and high response (household response rate 97.6%). Sample: 699,686 women (15–49) and 112,122 men (15–54). Parent–child dyads were constructed by merging children’s, men’s, and household-member files using appropriate identifiers. Children aged 0–59 months had n=259,627 records (247,743 living; 11,884 deceased). After linkage to both parents, 33,047 children had complete parental info; eligible analytical samples: anthropometric failure n=25,429 (0–59 months), anaemia n=24,022 (6–59 months), under-five mortality n=28,693 (0–59 months). Selection bias assessment via chi-squared tests on child sex, maternal education, maternal age at birth, household head sex, social group, wealth index indicated no significant differences (p>0.05) between included and excluded samples. Outcomes: Primary—any anthropometric failure (stunting, wasting, or underweight), any anaemia (Hb<11.0 g/dL, ages 6–59 months, altitude-adjusted, HemoCue Hb 201+), and under-five mortality (death before age 5; neonatal and postneonatal by standard cut-offs). Complementary outcomes included severity strata for anthropometry (severe underweight/stunting/wasting), anaemia (mild–moderate, severe), and mortality timing (neonatal, postneonatal). Anthropometry measured with SECA devices (874 U scale; 213 Stadiometer; 417 Infantometer); definitions followed WHO 2006 standards. Predictors: Parental attributes grouped as—sociodemographic (age 15–29, 30–39, ≥40; age at marriage <18, 18–20, 21–25, ≥26; education none/incomplete primary, primary/incomplete secondary, secondary or higher; years of schooling; employment unemployed, non-manual, agricultural, manual/others); physical (height <145, 145–149.9, 150–154.9, 155–159.9, ≥160 cm; BMI <17.00, 17.00–18.49, 18.50–23.49, 23.50–24.99, 25.00–29.99, ≥30.00 kg/m²); behavioural (current tobacco use, alcohol use); NCDs (clinically assessed diabetes and hypertension using DHS biomarker protocols). Covariates: maternal age at birth (<17, 17–19, 20–24, 25–29, 30–49), child age (0–4 years; for anthropometry and anaemia models), sex, birth order (1,2,3,4,≥5), urban/rural residence, religion, social group (SC, ST, OBC, Others), wealth index (asset-based PCA), and state high-focus vs non-high-focus grouping. Statistical analysis: Survey-weighted multivariable logistic regressions with three model specifications per outcome: Model I (paternal characteristics + covariates), Model II (maternal characteristics + covariates), Model III (both parents’ characteristics + covariates). Multicollinearity assessed via VIF (<5 threshold). Analyses conducted in Stata 14 ‘svy’ framework with DHS weights. Results reported as odds ratios (OR) with 95% confidence intervals (CI).

• Fathers aged 30–39 years (vs 15–29) had lower odds of: any anthropometric failure (Model III OR=0.87, 95% CI: 0.77–0.97) and any anaemia (OR=0.88, 95% CI: 0.79–0.98). Fathers ≥40 also showed reduced odds for anthropometric failure (e.g., OR≈0.80, 95% CI: 0.65–0.97).
• Paternal age at marriage <18 years was associated with worse child survival; compared with <18, marriage at ages 18–25 was associated with lower under-five mortality in narrative results.
• Parental education exhibited protective associations across outcomes: relative to none/incomplete primary, secondary or higher education lowered odds of any anthropometric failure (father OR≈0.85, 95% CI: 0.74–0.98; mother OR≈0.76, 95% CI: 0.65–0.89), any anaemia (father OR=0.84, 95% CI: 0.73–0.97; mother OR=0.76, 95% CI: 0.65–0.89), and under-five mortality (father OR=0.62–0.73; mother OR=0.61–0.75 across models).
• Maternal height had a strong protective gradient: increasing categories from <145 cm to ≥160 cm were associated with progressively lower odds of any anthropometric failure (e.g., ≥160 cm vs <145 cm: OR≈0.32, 95% CI: 0.27–0.38) and lower under-five mortality (e.g., 150–154.9 cm vs <145 cm: OR≈0.70–0.71; p<0.01).
• Higher parental BMI was protective for anthropometric failure: compared with BMI <17.00, both fathers’ and mothers’ BMI 18.50–29.99 (and ≥30 for fathers) were associated with substantially lower odds of any anthropometric failure (e.g., mothers 25.00–29.99: OR≈0.52, 95% CI: 0.43–0.63; fathers 25.00–29.99: OR≈0.69, 95% CI: 0.56–0.85). Maternal BMI 18.50–29.99 was also associated with lower odds of child anaemia (e.g., 23.50–24.99: OR=0.74, 95% CI: 0.62–0.90; 25.00–29.99: OR=0.80, 95% CI: 0.67–0.95).
• Maternal tobacco use was linked to higher under-five mortality (Model III OR=1.50, 95% CI: 1.17–1.91).
• Paternal diabetes was associated with higher under-five mortality (Model III OR=1.36, 95% CI: 1.01–1.82).
• Maternal hypertension showed an association with lower odds of any anthropometric failure (Model III OR=0.69, 95% CI: 0.51–0.94), a finding requiring cautious interpretation.
• No consistent associations were observed for parental alcohol use or employment categories across primary outcomes. Complementary analyses (severity strata and mortality timing) generally aligned with primary findings (details in supplements).

The findings demonstrate that a broad set of parental characteristics jointly influence child anthropometric status, anaemia, and survival, addressing the study’s central question. Protective effects of parental education likely operate through improved socioeconomic opportunities, health literacy, and care practices. The associations of higher maternal height and higher parental BMI with lower anthropometric failure align with intergenerational nutrition pathways and prior LMIC evidence, underscoring the importance of maternal early-life nutrition and parental current nutritional status. Lower risks observed among children of fathers aged 30–39 may reflect greater paternal engagement and resources. Elevated under-five mortality associated with maternal tobacco use highlights modifiable behavioural risks amenable to policy (cessation support), while the association of paternal diabetes with child mortality signals potential genetic, environmental, or care-related pathways needing further investigation. Overall, integrating paternal factors alongside maternal ones yields a more comprehensive understanding of determinants of child health in India and informs multi-pronged interventions spanning education, nutrition, and behaviour change.

Early paternal marriage (<18 years) may jeopardize child survival. Parental education is protective against anthropometric failure, anaemia, and under-five mortality. Maternal short stature identifies a higher-risk group, suggesting the value of pre-pregnancy and antenatal nutritional support and targeted child health services for children born to shorter mothers. Maternal tobacco use and paternal diabetes are linked to higher under-five mortality, indicating scope for tobacco cessation programmes targeting women and diabetes detection and control among men. Future work should employ longitudinal cohort designs to clarify causal pathways and mechanisms linking parental characteristics, including NCDs, to child health outcomes.

• Cross-sectional design limits causal inference; associations should not be interpreted as causal effects.
• Parental characteristics were largely self-reported, and child outcomes relied on maternal recall (e.g., age at death), introducing potential recall and social desirability bias.
• Potential measurement error in haemoglobin using HemoCue devices warrants cautious interpretation of anaemia estimates.
• Despite standardized protocols and monitoring for anthropometry and biomarkers (height, weight, Hb, glucose, blood pressure), measurement error cannot be fully excluded.
• Limited ability to explore all mechanistic pathways (e.g., genetic vs environmental) for associations such as paternal diabetes and child mortality.