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Curcuma decreases serum hepcidin levels in healthy volunteers: a placebo-controlled, randomized, double-blind,
Fabrice Lainé1,2, Bruno Laviolle1,3, Edouard Bardou-Jacquet2,3
1Inserm, Centre d'investigation Clinique 1414, CHU Rennes, F-35033, Rennes, France.
Insights
Curcuma significantly reduced serum hepcidin levels in healthy volunteers, suggesting its potential for managing inflammation-related iron metabolism disorders. Further studies in patients with chronic inflammation are needed.
Area of Science:
- Biochemistry
- Human Physiology
- Pharmacology
Background:
- Hepcidin regulates iron metabolism by controlling iron release into plasma.
- Inflammation elevates hepcidin via the STAT3 pathway, contributing to anemia of chronic disease.
- Curcumin, found in curcuma, may inhibit hepcidin synthesis by reducing STAT3 activity.
Purpose of the Study:
- To evaluate the effect of curcuma on hepcidin synthesis in humans.
- To assess iron parameters following curcuma administration.
Main Methods:
- A placebo-controlled, randomized, double-blind, cross-over study.
- 18 healthy male volunteers received a single 6g oral dose of curcuma (2% curcumin) or placebo.
- Serum hepcidin and iron parameters were measured up to 48 hours post-dose.
Main Results:
- Curcuma significantly decreased serum hepcidin levels at 6, 8, and 12 hours post-dose compared to placebo.
- A trend towards decreased hepcidin was observed at 24 hours.
- Serum ferritin levels increased significantly at 6 and 8 hours, while other iron parameters remained unaffected.
Conclusions:
- Curcuma administration effectively reduces serum hepcidin levels in humans.
- These findings support curcuma's potential therapeutic use in conditions with hepcidin overproduction, such as chronic inflammation.
- Further research in patient populations is necessary to establish optimal dosage and treatment regimens.
Abstract:
Hepcidin, secreted by hepatocytes, controls iron metabolism by limiting iron egress in plasma. Hepcidin is upregulated during inflammation through the activation of the signal transducer and activator of transcription 3 (STAT3) transduction pathway, which decreases iron bioavailability and may explain the anemia of chronic inflammatory disease. In vitro, it has been shown that curcumin can decrease hepcidin synthesis by decreasing STAT3 activity. We conducted a proof-of-concept study to assess the effect of curcuma on hepcidin synthesis in human. This was a placebo-controlled, randomized, double-blind, cross-over, two-period study performed in 18 healthy male volunteers. Subjects received a single oral dose of 6 g curcuma containing 2% of curcumin or placebo. Serum hepcidin and iron parameters were assessed repeatedly until 48 h after dosing. When compared with a placebo curcuma decreased hepcidin levels significantly at 6 h (-19%, P = 0.004), 8 h (-17%, P = 0.009), and 12 h (-17%, P = 0.007) and tended to decrease hepcidin at 24 h (-15%, P = 0.076). Curcuma also significantly increased serum ferritin levels at 6 and 8 h (+7% for both times, P = 0.018, 0.030, respectively) and had no effects on serum iron, transferrin, and transferrin saturation. This pilot study showed that curcuma decreases serum hepcidin levels in human and supports the idea that curcuma could be useful in treating hepcidin overproduction during inflammatory processes. Confirmatory studies in patients with chronic inflammation are now required to determine the optimal dose and therapeutic scheme of curcuma.
