Deakin University

File(s) under embargo

Is high salt intake inducing obesity via production of cortisol? A novel working hypothesis and pilot study

journal contribution
posted on 2024-03-07, 22:17 authored by Anthony Nowell, Susan TorresSusan Torres, Sarah HallSarah Hall, Michelle KeskeMichelle Keske, David J Torpy, Lewan ParkerLewan Parker, Andrew BetikAndrew Betik, Anne TurnerAnne Turner
Abstract Purpose Evidence is growing that high salt intake is an independent risk factor for obesity, but the mechanisms are unknown. Our novel working hypothesis is that high salt intake drives cortisol production, which in turn, drives obesity. The current study aimed to demonstrate an acute cortisol response following a single high salt meal. Methods Eight participants (age 30.5 ± 9.8 years [mean ± SD], 50% female), consumed high salt (3.82 g; 1529 mg sodium) and low salt (0.02 g; 9 mg sodium) meals in a randomized cross-over design. Results Urinary and salivary cortisol and plasma adrenocorticotropic hormone (ACTH) demonstrated order effects. When high salt was given second, there was a peak above baseline for urinary cortisol (26.3%), salivary cortisol (9.4%) and plasma ACTH (4.1%) followed by a significant decline in each hormone (treatment*time, F[9, 18] = 2.641, p = 0.038, partial η2 = 0.569; treatment*time, F[12, 24] = 2.668, p = 0.020, partial η2 = 0.572; treatment*time, F[12, 24] = 2.580, p = 0.023, partial η2 = 0.563, respectively), but not when high salt was given first (p > 0.05 for all). Conclusion These intriguing findings provide partial support for our hypothesis and support a need for further research to elucidate the role of high salt intake in cortisol production and, in turn, in the aetiology of obesity. Trial registration number ACTRN12623000490673; date of registration 12/05/2023; retrospectively registered.



European Journal of Nutrition










Springer Science and Business Media LLC