PAULINA CORREA-BURROWS

Prof. PAULINA CORREA-BURROWS

UNIVERSIDAD DE CHILE
orcid

Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2015 in Journal of Diabetes Research
Verified
Journal Article
Open access
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RBRaquel Burrows
Raquel Burrows
PAULINA CORREA-BURROWSPAULINA CORREA-BURROWS
PAULINA CORREA-BURROWS
MRMarcela Reyes
Marcela Reyes
EBEstela Blanco
Estela Blanco
CAC. Albala
C. Albala
SGS. Gahagan
S. Gahagan
Objective.To determine the optimal cutoff of the homeostasis model assessment-insulin resistance (HOMA-IR) for diagnosis of the metabolic syndrome (MetS) in adolescents and examine whether insulin resistance (IR), determined by this method, was related to genetic, biological, and environmental factors.Methods.In 667 adolescents (16.8 ± 0.3 y), BMI, waist circumference, glucose, insulin, adiponectin, diet, and physical activity were measured. Fat and fat-free mass were assessed by dual-energy X-ray absorptiometry. Family history of type 2 diabetes (FHDM) was reported. We determined the optimal cutoff of HOMA-IR to diagnose MetS (IDF criteria) using ROC analysis. IR was defined as HOMA-IR values above the cutoff. We tested the influence of genetic, biological, and environmental factors on IR using logistic regression analyses.Results.Of the participants, 16% were obese and 9.4 % met criteria for MetS. The optimal cutoff for MetS diagnosis was a HOMA-IR value of 2.6. Based on this value, 16.3% of participants had IR. Adolescents with IR had a significantly higher prevalence of obesity, abdominal obesity, fasting hyperglycemia, and MetS compared to those who were not IR. FHDM, sarcopenia, obesity, and low adiponectin significantly increased the risk of IR.Conclusions.In adolescents, HOMA-IR ≥ 2.6 was associated with greater cardiometabolic risk.

20 May 2015 in Public Health Nutrition
Verified
Journal Article
Open access
RBRaquel Burrows
Raquel Burrows
PAULINA CORREA-BURROWSPAULINA CORREA-BURROWS
PAULINA CORREA-BURROWS
MRMarcela Reyes
Marcela Reyes
EBEstela Blanco
Estela Blanco
CACecilia Albala
Cecilia Albala
SGSheila Gahagan
Sheila Gahagan
Objective: To analyse the prevalence of cardiovascular risk factors in healthy adolescents of low to middle socio-economic status and to study the influence of anthropometric, biological and lifestyle factors on the risk of metabolic syndrome (MetS).Design: Cross-sectional study. BMI, waist circumference, blood pressure, fat and lean mass (by dual-energy X-ray absorptiometry), TAG, HDL-cholesterol, glucose, insulin, homeostatic model assessment–insulin resistance index (HOMA-IR), food intake and physical activity were measured. Cardiovascular risk factors were defined using the International Diabetes Federation criteria and insulin resistance using HOMA-IR ≥2·6. Bivariate and multivariate regressions examined the associations between MetS and anthropometric, biological and lifestyle factors.Setting: Observational cohort study including Chilean adolescents, who were part of a follow-up study beginning in infancy.Subjects: Adolescents aged 16–17 years (n667).Results: In the sample, 16·2 % had obesity and 9·5 % had MetS. Low HDL-cholesterol (69·9 %), abdominal obesity (33·3 %) and fasting hyperglycaemia (8·7 %) were the most prevalent cardiovascular risk factors. In males, obesity (OR=3·7; 95 % CI 1·2, 10·8), insulin resistance (OR=3·0; 95 % CI 1·1, 8·2), physical inactivity (OR=2·9; 95 % CI 1·1, 7·7) and sarcopenia (OR=21·2; 95 % CI 4·2, 107·5) significantly increased the risk of MetS. In females, insulin resistance (OR=4·9; 95 % CI 1·9, 12·6) and sarcopenia (OR=3·6; 95 % CI 1·1, 11·9) were significantly associated with MetS.Conclusions: High prevalences of obesity, abdominal obesity, dyslipidaemia, fasting hyperglycaemia and MetS were found in healthy adolescents. In both sexes, sarcopenia and insulin resistance were important risk factors of MetS. Promotion of active lifestyles at the school level and regulation of the sale of energy-dense foods are needed.

27 January 2023 in Cochrane Database of Systematic Reviews
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Journal Article
Closed access
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LMLucía Méndez-Sánchez
Lucía Méndez-Sánchez
PCPatricia Clark
Patricia Clark
TWTania M Winzenberg
Tania M Winzenberg
PTPeter Tugwell
Peter Tugwell
PAULINA CORREA-BURROWSPAULINA CORREA-BURROWS
PAULINA CORREA-BURROWS
RCRebecca Costello
Rebecca Costello

3 February 2016 in Bulletin of the World Health Organization
Verified
Journal Article
Open access
PAULINA CORREA-BURROWSPAULINA CORREA-BURROWS
PAULINA CORREA-BURROWS
RBRaquel Burrows
Raquel Burrows
EBEstela Blanco
Estela Blanco
MRMarcela Reyes
Marcela Reyes
SGSheila Gahagan
Sheila Gahagan
To explore associations between the nutritional quality of diet at age 16 years and academic performance in students from Santiago, Chile. We assessed the nutritional quality of diet, using a validated food frequency questionnaire, in 395 students aged 16.8 ± 0.5 years. Depending on the amount of saturated fat, fibre, sugar and salt in the foods, diet was categorized as unhealthy, fair or healthy. Academic performance was assessed using high school grade-point average (GPA) and tests for college admission in language and mathematics. Academic results on or above the 75th percentile in our sample were considered good academic performance. We tested associations between nutritional quality of diet and good academic performance using logistic regression models. We considered sociodemographic, educational and body-mass index (BMI) factors as potential confounders. After controlling for potential confounding factors, an unhealthy diet at age 16 years was associated with reduced academic performance. Compared to participants with healthy diets, those with unhealthy diets were significantly less likely to perform well based on language tests (odds ratio, OR: 0.42; 95% confidence interval, CI: 0.18-0.98) mathematics tests (OR: 0.35; 95% CI: 0.15-0.82) or GPA (OR: 0.22; 95% CI: 0.09-0.56). In our sample, excessive consumption of energy-dense, low-fibre, high-fat foods at age 16 years was associated with reduced academic performance.

1 July 2025 in JAMA Network Open
Verified
Journal Article
Open access
PAULINA CORREA-BURROWSPAULINA CORREA-BURROWS
PAULINA CORREA-BURROWS
RBRaquel Burrows
Raquel Burrows
CACecilia Albala
Cecilia Albala
CSCarlos Sepúlveda
Carlos Sepúlveda
FSFelipe Salech
Felipe Salech
CGChristian Gonzalez-Billault
Christian Gonzalez-Billault
Importance: It remains unclear whether obesity accelerates biological aging, potentially leading to early-onset chronic diseases.Objective: To investigate the association between long-term obesity and the expression of biochemical aging markers in younger adults.Design, Setting, and Participants: This multiple-events case-control study, conducted from April 5, 2022, to June 29, 2023, was embedded in the Santiago Longitudinal Study, a prospective Chilean birth cohort of adults aged 28 to 31 years among whom health and nutrition data were collected from September 1992 onward.Exposure: Body mass index (BMI) trajectory across the life course, recorded multiple times since birth. Group 1 had healthy BMI across the life course, group 2 had persistent obesity since adolescence, and group 3 had persistent obesity since childhood.Main Outcomes and Measures: Smoothed BMI trajectories (cubic polynomials) were used to estimate obesity duration. Primary outcomes were DNA methylation–based age and telomere length (TL). Secondary outcomes included levels of aging-related cytokines, growth factors, and adipomyokines.Results: In the sample of 205 adults (mean [SD] age, 28.9 [0.6] years; 100 females [49%]), 89 (43%) were in group 1, 43 (21%) in group 2, and 73 (36%) in group 3. Mean (SD) obesity duration was 12.9 (4.8) years in group 2 and 26.6 (2.3) years in group 3. Long-term obesity was associated with adulthood expression of biomarkers denoting antagonistic and integrative aging hallmarks, including mean (SD) hs-CRP (1.69 [2.1] vs 3.67 vs 4.24 [2.4] mg/L; P < .001; f = 0.57 [95% CI, 0.44-0.70]) and IL-6 (log, 0.69 [0.5] vs 1.03 [0.4] vs 0.99 [0.4]; P < .001; f = 0.53 [95% CI, 0.41-0.62]), as well as FGF-21, IGF-1, IGF-2, apelin, and irisin. Cohen f coefficient indicated a large effect size for the association of long-term obesity with adulthood expression of these markers.Conclusions and Relevance: In this multiple-events case-control study, long-term obesity was associated with the expression of biochemical aging markers in adults aged 28 to 31 years, consistent with epigenetic alterations, telomere attrition, chronic inflammation, impaired nutrient sensing, mitochondrial stress, and compromised intercellular communication. In young adults, chronic health issues may emerge from accelerated biological aging associated with long-term obesity.