Short Oral Presentation Nutrition Society of Australia 50th Annual Scientific Meeting 2026

Past insights, current evidence and future directions for chestnut-mediated glycaemic control. (147238)

Michael J Houghton 1 2 , Dylan R Peiris 1 , Noha Sulaimani 1 2 3 , Rizliya Visvanathan 1 2 , Luca Nicolotti 4 5 , Barbara R Cardoso 1 2
  1. Nutrition, Dietetics and Food, Monash University, Notting Hill, VIC, Australia
  2. Victorian Heart Institute, Monash University, Clayton, VIC, Australia
  3. Food and Nutrition, King Abdulaziz University, Jeddah, Saudi Arabia
  4. The Australian Wine Research Institute, Adelaide, SA, Australia
  5. Metabolomics Australia, The Australian Wine Research Institute, Adelaide, SA, Australia

Despite its nutritional profile rich in dietary fibre and (poly)phenols, chestnut (Castanea spp.) remains under-researched compared to other tree nuts. Our systematic literature search identified only three human intervention studies evaluating the impact of chestnut on postprandial glycaemia, conducted sporadically over the past century. An initial observation of blunted glucose response in three individuals with diabetes following consumption of 120 g raw chestnuts was published in 1929(1).  The next study followed in 1994, with authors reporting that roasted, but not boiled, chestnuts reduced postprandial glucose response compared with white bread in individuals with type 2 diabetes, although no effects were seen on insulin levels(2). The latest study, published in 2008, demonstrated that a (poly)phenol-rich chestnut skin extract dose-dependently (300-600 mg) suppressed the postprandial glucose response to boiled rice in subjects without diabetes(3). These findings aligned with in vitro evidence demonstrating strong inhibition of α-amylase by the same extract(3).

Building on these historical insights and in vitro evidence, we investigated the postprandial glycaemic and insulinaemic effects of a chestnut flour-enriched bread in a randomised crossover trial of healthy adults (n = 14). Participants consumed isocaloric breads providing 50 g available carbohydrate as either chestnut flour-enriched bread (50% chestnut flour/50% wheat flour) or control bread (100% wheat flour) following an overnight fast. Capillary blood glucose and insulin were measured over 180 min, and incremental areas under the curve (iAUC) were calculated. Total (poly)phenol content in the chestnut and wheat flours and breads was estimated by the Folin-Ciocalteu assay and (poly)phenol profiles were characterised using reverse-phase high-performance liquid chromatography high-resolution Fourier transform mass spectrometry.

Chestnut flour-enriched bread contained notable levels of (+)-catechin, myricetin, and gallic, gentisic, and p-coumaric acids (~480 mg total (poly)phenols vs ~100 mg in the control bread). Chestnut enrichment significantly reduced glucose iAUC by 27% compared to control (p = 0.032, paired t-test). While total insulin exposure (iAUC) was unaffected, inclusion of chestnut significantly advanced the time to peak insulin concentration by ~24 min (p = 0.043, Wilcoxon matched-pairs signed rank test).

Extending a sparse human evidence base spanning more than 90 years, this study demonstrates that partial substitution of wheat flour with chestnut flour in bread significantly attenuates postprandial glycaemia in healthy adults, primarily by suppressing late-phase glucose excursions without increasing insulin demand. These findings likely reflect a combination of effects from the food matrix, dietary fibre, and (poly)phenol-mediated inhibition of carbohydrate digestion, but require further mechanistic validation. Future studies in humans should evaluate varied chestnut preparations within whole-meal contexts, assess potential incretin responses, and conduct longer-term trials in both healthy and metabolically compromised populations to determine the chronic effects of chestnut consumption.

  1. 1. Rosenthal SM & Ziegler EE (1929) Arch Intern Med 44, 344–350
  2. 2. Katsilambros N, Saviolakis A, Philippides P et al. (1994) Nutr Metab Cardiovasc Dis 4, 101-102
  3. 3. Tsujita T, Takaku T, Suzuki T (2008) J Nutr Sci Vitaminol (Tokyo) 54, 82–88