Hair cortisol concentrations measuring chronic stress show no meaningful association with most cardiac structures or functions among middle-aged adults, according to a cross-sectional observational study published October 7 in Heart. Led by Simon Söderholm of Linköping University in Linköping, Sweden, the research examined 3,005 participants aged 50 to 64 years from an imaging-based cohort, Medscape reported.
Scalp Hair Cortisol Levels and Heart Phenotypes
Researchers measured cortisol concentrations in the proximal portions of participants’ scalp hair to capture cumulative stress exposure over several months. The cohort had a mean age of 56.9 years, and 64% of the participants were women. Investigators evaluated 19 individual echocardiographic measures and grouped them statistically into three broad functional phenotypes: structural and volumetric remodeling, cardiac output and flow, and diastolic function and myocardial mechanics. These categories accounted for 45.5% of the total variation across the measured metrics. Statistical models were adjusted for age, sex, body mass index, smoking history, alcohol intake, and physical activity levels.
Left Atrial Volume Findings in Adjusted Analyses
The analysis revealed no meaningful link between hair cortisol concentrations and the three primary heart phenotypes derived from echocardiographic assessments. Most of the 19 individual echocardiographic metrics displayed negligible effects and lacked a clear relationship with the stress biomarker. However, adjusted models showed that each one-unit higher log10-transformed concentration of hair cortisol correlated with a 0.178 standard deviation higher left atrial end-systolic volume index. This amounted to a predicted difference of 0.734 mL/m² across the interquartile range of hair cortisol levels. Sensitivity analyses confirmed these findings, showing no consistent evidence of interactions influenced by sex.
Alternative Physiological Pathways for Cardiovascular Risk
Although elevated hair cortisol has been linked to increased cardiovascular disease risk in prior literature, the current findings do not support a direct relationship with echocardiographic measurements of cardiac structure or function in this demographic. The authors noted that any effects of chronic stress on heart disease risk might be mediated through alternative physiological pathways rather than direct changes to cardiac dimensions or pumping mechanics. Study limitations included the cross-sectional design, which precluded determining cause and effect, alongside reliance on self-reported data for smoking, alcohol consumption, and physical activity. Participants were generally healthy middle-aged adults, restricting the generalizability of the results to older populations or individuals with pre-existing heart disease.
Funding and Financial Disclosures
Three authors reported serving as fellows or associated clinical fellows of the Wallenberg Centre for Molecular Medicine and received funding from the Knut and Alice Wallenberg Foundation. Additional financial support for the research was provided by Dr P Håkanssons Foundation. The hair cortisol laboratory analysis received grants from Swedish AFA Insurance and the County Council of Östergötland. The authors declared no competing financial interests.
Frequently Asked Questions About Hair Cortisol and Cardiac Health
How was chronic stress measured in the study?
Researchers measured cortisol concentrations in the proximal sections of participants’ scalp hair. This method reflects cumulative cortisol exposure over several months, offering a reliable biomarker for chronic stress compared to single blood or saliva samples.
What demographic groups were included in the Swedish cohort?
The study evaluated 3,005 participants aged 50 to 64 years from an imaging-based cohort in Sweden. The mean age of the participants was 56.9 years, and 64% of the cohort identified as women.
Did the study prove that hair cortisol causes changes to the left atrium?
No, the study was observational and cross-sectional, meaning it could not establish cause and effect. While adjusted analyses found a minor association with left atrial end-systolic volume index, the design only demonstrates correlation rather than direct causation.
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