Hormones · Melatonin

Gestational diabetes mellitus is associated with higher urinary 6-sulfatoxymelatonin and serum TNF-α levels despite increased consumption of tryptophan-rich foods

In a cross-sectional study of 34 women with GDM and 18 with normal-risk pregnancies, those with GDM reported higher consumption of tryptophan-rich foods (especially milk/dairy and fruits) yet had significantly higher urinary 6-sulfatoxymelatonin (p=0.002) and serum TNF-α levels (p=0.023). Multivariable models confirmed GDM remained associated with higher melatonin metabolite levels, while TNF-α was linked to maternal characteristics and interactions.

1 min readUpdated Jul 11, 20260 RCTsView structured evidence →
Evidence Score32/100
Human RCT☆☆☆☆☆
Meta-analysis☆☆☆☆☆
Mechanism★★★★★
Safety★★★★
Confidencelow

This article is automatically generated from the structured evidence profile behind the claim above. Scores reflect the quality and quantity of available research, not clinical advice.

Gestational diabetes mellitus is associated with higher urinary 6-sulfatoxymelatonin and serum TNF-α levels despite increased consumption of tryptophan-rich foods The current body of evidence comprises 1 study. EvidenceHub rates the overall confidence at 32/100 (low).

The Claim

Gestational diabetes mellitus is associated with higher urinary 6-sulfatoxymelatonin and serum TNF-α levels despite increased consumption of tryptophan-rich foods

This conclusion is most relevant to: Pregnant women (34 with gestational diabetes mellitus, 18 with normal-risk pregnancies).

What the Research Shows

The conclusion draws on 1 linked study. Highlights from the cited literature:

  • Pregnant Women With Gestational Diabetes Mellitus and High Consumption of Tryptophan-Rich Foods Show Increased Levels of 6-Sulfatoxymelatonin in Urine. (Journal of pregnancy, 2026) —

How It Works

The proposed biological pathway:

  • GDM induces metabolic and inflammatory alterations
  • These alterations may influence tryptophan metabolism and melatonin synthesis
  • Higher consumption of tryptophan-rich foods provides substrate for melatonin production
  • Result: Elevated urinary 6-sulfatoxymelatonin and serum TNF-α in GDM group

Who Might Benefit

Evidence fit by population:

  • Pregnant women (34 with gestational diabetes mellitus, 18 with normal-risk pregnancies)

Limitations & Caveats

Important context when interpreting this evidence:

  • Cross-sectional design prevents causal inference
  • Small sample size (n=52 total) limits generalizability
  • Dietary assessment via FFQ may have recall bias

Frequently Asked Questions

What is 6-sulfatoxymelatonin?

It is the primary urinary metabolite of melatonin, used as a biomarker for melatonin production in the body.

Why might GDM increase melatonin levels despite higher tryptophan intake?

GDM is associated with metabolic and inflammatory changes that may alter tryptophan metabolism and melatonin synthesis, potentially leading to higher melatonin metabolite levels even with increased dietary precursor intake.

What was the role of TNF-α in this study?

TNF-α is an inflammatory marker; the study found higher serum levels in GDM women, suggesting an inflammatory component associated with the condition.

Were sleep quality and other confounders adjusted for?

Yes, the generalized linear models adjusted for maternal age, BMI, gestational age, and sleep quality.

References

  1. 1.Coltro DB, de Oliveira Mateus J, de Oliveira Ferreira I, Goettert MI, Costella AP, da Silva GL, Torres ILS, da Silva AA, Laste G. “Pregnant Women With Gestational Diabetes Mellitus and High Consumption of Tryptophan-Rich Foods Show Increased Levels of 6-Sulfatoxymelatonin in Urine..” Journal of pregnancy, 2026. PMID: 42427282 DOI: 10.1155/jp/4762066
Disclaimer: This article is auto-generated from structured research data for educational purposes only and is not medical advice. Evidence scores reflect the quality and quantity of available research, not clinical recommendations. Always consult a healthcare professional before starting any supplement or intervention.