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Updated: May 14, 2025

Assessment of Child Anthropometry in a Large Epidemiologic Study
Published on: February 2, 2017
Relationship Between Parental Obesity, Body Mass Index and High-Sensitivity C-Reactive Protein Levels in Offspring
Luciana Tornquist1, Nathália Quaiatto Félix1, Helen Freitas D'avila1
1Graduate Program in Health Promotion, University of Santa Cruz do Sul, Santa Cruz do Sul, RS, Brazil.
Insights
Children of parents with obesity show higher inflammation markers, like high-sensitivity C-reactive protein (hs-CRP), irrespective of their own body mass index (BMI). Parental obesity directly impacts offspring
Area of Science:
- Pediatrics
- Public Health
- Biochemistry
Background:
- Childhood obesity is linked to systemic inflammation, raising risks for lifelong metabolic and cardiovascular diseases.
- Parental body mass index (BMI) is a key factor influencing offspring's inflammatory health from childhood.
- Understanding the interplay between parental and offspring BMI and inflammation is crucial for early intervention.
Purpose of the Study:
- To investigate how parental BMI moderates the association between offspring BMI and high-sensitivity C-reactive protein (hs-CRP) levels.
- To determine if parental obesity influences inflammatory markers in children independently of their own BMI.
- To analyze the impact of parental obesity on offspring's inflammatory status in a Brazilian population.
Main Methods:
- Cross-sectional study involving 423 children and adolescents in southern Brazil.
- Offspring BMI calculated from measured height/weight; parental BMI from self-report.
- hs-CRP levels measured via high-sensitivity assay; analyzed using multiple linear regression with PROCESS macro.
Main Results:
- A direct linear association was found between offspring BMI and hs-CRP levels.
- Paternal obesity showed a direct relationship with offspring hs-CRP levels.
- An inverse interaction between paternal BMI and offspring BMI indicated that children with lower BMI but obese parents had higher hs-CRP.
Conclusions:
- Children of parents with obesity exhibit elevated inflammation (hs-CRP) regardless of their own BMI.
- Parental obesity is an independent risk factor for increased systemic inflammation in offspring.
- Early life inflammation in children may be influenced by the familial environment, particularly parental weight status.
Abstract:
Childhood obesity has been associated with high levels of systemic inflammation, increasing the risk of metabolic and cardiovascular diseases throughout life. Genetic and environmental factors, such as parental body mass index (BMI), can influence this relationship, impacting the inflammatory health of offspring from childhood. This study investigates the influence of parental BMI on the relationship between BMI and high-sensitivity C-reactive protein (hs-CRP) levels in offspring. A cross-sectional study was conducted with 423 children and adolescents from a municipality in southern Brazil. Offspring BMI was calculated using measured weight and height, while parental BMI was determined from self-reported measurements and classified based on World Health Organization cutoff points. hs-CRP levels were assessed using a high-sensitivity assay. The moderating effect of parental BMI on the relationship between offspring BMI and hs-CRP levels was analyzed through multiple linear regression models using the PROCESS macro extension for SPSS. Results indicated a direct association between offspring BMI and hs-CRP levels across all models, showing that hs-CRP levels increased linearly with BMI in offspring. A direct relationship between paternal obesity and offspring hs-CRP levels was observed, along with a significant inverse interaction between paternal BMI and offspring BMI with hs-CRP levels. Among schoolchildren with lower BMI, those with parents with obesity exhibited higher hs-CRP levels compared to peers with parents classified as eutrophic or overweight. These findings suggest that children of parents with obesity tend to have elevated levels of inflammation, regardless of their own BMI.
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