# Low fruit and vegetable intake in children: a dietary stressor raising renal ammonium and adrenal cortisol secretion

**Authors:** Thomas Remer, Yifan Hua, Jonas Esche, Lijie Shi, Michaela F. Hartmann, Stefan A. Wudy

PMC · DOI: 10.1007/s00424-026-03162-3 · Pflugers Archiv · 2026-03-23

## TL;DR

Low fruit and vegetable intake in children increases cortisol and ammonium excretion, which may harm long-term health.

## Contribution

This study shows that low fruit and vegetable intake in children raises cortisol and ammonium levels, linking dietary acid load to adrenal and renal responses.

## Key findings

- Children with low fruit and vegetable intake had higher urinary free cortisol and ammonium excretion.
- Cortisol metabolites were closely associated with increased ammonium excretion.
- Low potassium intake and reduced aldosterone precursors were observed in children with low fruit and vegetable intake.

## Abstract

Elimination of excess acid loads in metabolic acidosis requires stimulation of ammoniagenesis. Cortisol is critical to increase proximal tubular cells’ ammonia production. We aimed to specifically examine whether children’s low fruit and vegetable (FV) intake, which goes along with an increased dietary acid load, may raise cortisol secretion and whether glucocorticoids relevantly associate with ammonium secretion. Healthy 6–10 years old children (participants of the DONALD study, Dortmund, Germany) with a comparable protein intake and either a low or a high FV-intake were examined in a quasi-experimental design. Urinary 24-h ammonium excretion was analyzed as part of urinary acid-base measurements. Major glucocorticoid metabolites were quantified along with aldosterone precursors in children’s 24-h urine samples by gas chromatography–mass spectrometry to assess adrenal cortisol secretion and aldosterone status. Liquid–chromatography–mass spectrometry was used to quantify urinary free cortisol (UFF) and cortisone. Average FV-intake of children with low compared to high FV-intake was 183 g/d (25th -75th percentile, 129–233 g/d) and 570 g/d (25th -75th percentile, 468–707 g/d), respectively. Both groups’ average protein intake amounted to around 50 g/d. After adjustment for relevant confounders, children with low FV-intake exhibited higher excretion rates of UFF (P = 0.002), cortisone (P = 0.07), potentially bioactive free glucocorticoids (sum of UFF and cortisone) (P = 0.04), 20α-dihydrocortisol (P = 0.02), C21-metabolite sum reflecting cortisol secretion (P = 0.008), and ammonium (P < 0.0001). Concurrently with these children’s lower potassium intake, excretions of the aldosterone precursors tetrahydro-11-dehydrocorticosterone and tetrahydrocorticosterone were reduced (P ≤ 0.02). Urinary ammonium excretion associated closely with UFF (P < 0.0001), cortisone (P < 0.0001), and 20α-dihydrocortisol (P = 0.0003). Our quasi-experimental study indicates the importance of an appropriately high FV-intake in childhood to reduce acid-load-inducible cortisol-increases that are strongly associated with renal ammonium production and may have the potential to adversely affect long-term health.

The online version contains supplementary material available at 10.1007/s00424-026-03162-3.

## Full-text entities

- **Genes:** POMC (proopiomelanocortin) [NCBI Gene 5443] {aka ACTH, CLIP, LPH, MSH, NPP, OBAIRH}, GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, F5 (coagulation factor V) [NCBI Gene 2153] {aka FVL, PCCF, RPRGL1, THPH2, fV}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, IL18 (interleukin 18) [NCBI Gene 3606] {aka IGIF, IL-18, IL-1g, IL1F4}, SERPINA6 (serpin family A member 6) [NCBI Gene 866] {aka CBG}, PRAL (p53 regulation associated lncRNA) [NCBI Gene 109245082] {aka lncRNA-PRAL}, SLC9A3 (solute carrier family 9 member A3) [NCBI Gene 6550] {aka DIAR8, NHE-3, NHE3}
- **Diseases:** cardiometabolism (MESH:D024821), albuminuria (MESH:D000419), renal tubular injury (MESH:D015499), inflammatory (MESH:D007249), Metabolic acidosis (MESH:D000138), detrimental effects on kidney function (MESH:D007674), tubulointerstitial damage (OMIM:162000)
- **Chemicals:** sodium (MESH:D012964), magnesium (MESH:D008274), Tetrahydro-11-dehydrocorticosterone (MESH:C096314), phosphate (MESH:D010710), creatinine (MESH:D003404), flavonoids (MESH:D005419), HCO3- (MESH:D001639), aldosterone (MESH:D000450), Ammonia (MESH:D000641), CO2 (MESH:D002245), 20alpha-dihydrocortisol (MESH:C016499), steroid (MESH:D013256), urea (MESH:D014508), nitrogen (MESH:D009584), glucose (MESH:D005947), citrate (MESH:D019343), GC (MESH:C057580), Cortisol (MESH:D006854), calcium (MESH:D002118), sulfate (MESH:D013431), tetrahydrocortisol (MESH:D013760), NH4 (-), tetrahydrocorticosterone (MESH:C003676), chloride (MESH:D002712), L-lactate (MESH:D019344), acid (MESH:D000143), glutamine (MESH:D005973), cortisone (MESH:D003348), tetrahydrocortisone (MESH:D013761), ammonium (MESH:D064751), potassium (MESH:D011188), oxaloacetate (MESH:D062907), lipids (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13006471/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13006471/full.md

---
Source: https://tomesphere.com/paper/PMC13006471