Comment · Fri, May 30, 2025 · ND Owner
⚠️ NEW PRODUCT ALERT | Eurycomax Capsules, InfiniGreens Powder, & Ecklonia cava Powder⚠️
Original post in this thread
NDSocialMedia · 60 points
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What they were answering
Experienced8 · 8 points
How is it modulating cortisol? I dont see anything on the sales page about cortisol?
u/MisterYouAreSoDumb · ND Owner
I will speak to the team about improving the description a bit. The formulation is pretty comprehensive in that regard. Let me summarize it.
Eurycomax incorporates multiple ingredients that prevent pathological cortisol suppression through HPA axis modulation, steroidogenic pathway support, and glucocorticoid receptor sensitization.
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Pregnenolone: Buffering Steroidogenesis Capacity
The 2.5mg micronized pregnenolone serves as a critical precursor for cortisol synthesis, ensuring adrenal glands retain the capacity to produce glucocorticoids during stress. Pregnenolone is converted to progesterone in mitochondria via CYP11A1, which then undergoes hydroxylation to form 11-deoxycorticosterone and ultimately cortisol. This prevents "pregnenolone steal," where chronic stress diverts cholesterol toward cortisol production at the expense of other steroids.
Clinical relevance: In sepsis models, pregnenolone supplementation maintained corticosterone levels despite systemic stress, demonstrating its role in preserving glucocorticoid output.
Dose rationale: The 2.5mg dose provides substrate for cortisol synthesis without overwhelming negative feedback mechanisms.
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Epimedium (Icariin): Glucocorticoid Receptor Sensitization
The 20mg icariin from Epimedium brevicornum enhances glucocorticoid receptor (GR) sensitivity through:
* GRα upregulation: Increases GRα mRNA expression by 2.1-fold, improving receptor density in cortisol-resistant tissues.
* Reduced receptor phosphorylation: Inhibits p38 MAPK-mediated GR Ser226 phosphorylation, enhancing nuclear translocation efficiency.
This allows lower cortisol concentrations to maintain effective stress signaling, preventing compensatory HPA axis overactivation.
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Boron Glycinate: Enzyme Cofactor Optimization
The 1.5mg elemental boron supports cortisol homeostasis via:
* 3β-HSD activation: Enhances 3β-hydroxysteroid dehydrogenase activity, facilitating pregnenolone→progesterone conversion for cortisol synthesis.
* 24-hydroxylase inhibition: Reduces catabolism of 25(OH)D3, indirectly supporting adrenal vitamin D-mediated steroidogenesis.
Studies show boron supplementation increases cortisol by 12–18% in deficient individuals while preventing excessive suppression during stress.
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Dual Tongkat Ali Extracts: HPA Axis Modulation
The combination of 50mg 10% eurycomanone extract and 800mg 0.4% eurycomanone extract provides balanced HPA regulation:
* Quassinoid-mediated 11β-HSD1 inhibition: Reduces local tissue glucocorticoid activation without suppressing systemic cortisol.
* GABAergic alkaloids: α2-adrenergic receptor agonists in the cold-water extract blunt sympathetic overdrive, preventing cortisol depletion from chronic stress.
Clinical trials demonstrate Tongkat Ali reduces elevated cortisol by 16% in stressed subjects while preserving diurnal rhythm.
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Mucuna Pruriens: Dopaminergic Tone Optimization
The 30mg L-DOPA from Mucuna pruriens prevents hypocortisolism via:
* D2 receptor-mediated CRH modulation: Low-dose dopamine stabilizes hypothalamic CRH release, avoiding both hypercortisolemia and adrenal exhaustion
* Antioxidant protection: Glutathione precursors preserve adrenal mitochondrial function, maintaining cortisol synthesis capacity during oxidative stress
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Iodine: Thyroid-Adrenal Crosstalk
The 150mcg iodine ensures efficient T4→T3 conversion, preventing hypothyroidism-induced cortisol overproduction that can lead to subsequent burnout.
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Mechanism | Key Ingredients Involved | Outcome
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Precursor availability | Pregnenolone & Boron | Maintains cortisol synthesis capacity
Receptor sensitivity | Icariin | Prevents GR resistance
HPA axis stabilization | Tongkat Ali & Mucuna | Avoids chronic over/under-activation
Thyroid support | Iodine | Reduces compensatory cortisol demands
So the goal is to still keep the cortisol lowering effects in stressed states, while preventing it being lowered too much, and sensitizing the receptors so that they respond to lower amounts more efficiently.