Taxifolin & Androgen Production: What You Need to Know

observational-study PMID: 29402482

Quick Summary: Research suggests taxifolin, a plant compound, may reduce the production of androgens (like testosterone) in lab settings. This could potentially help with conditions like prostate cancer, but more research is needed.

What The Research Found

Scientists studied how taxifolin affects cells that produce testosterone. They found that taxifolin can significantly reduce the production of testosterone and similar hormones in these cells. This was true even when the cells were stimulated to produce more hormones. The study also showed taxifolin blocked key enzymes needed to make testosterone.

Study Details

Who was studied: Rat cells that produce testosterone (Leydig cells) and human enzymes in a lab setting.

How long: The study was done over a short period, likely hours, in a lab dish.

What they took: The cells were exposed to taxifolin.

What This Means For You

This research is preliminary. It suggests taxifolin might help slow down the production of hormones linked to prostate cancer. However:

It's early: This study was done in a lab, not in people.

Not a cure: Taxifolin is not a proven treatment for any condition.

Talk to your doctor: Always discuss any supplements with your doctor, especially if you have health concerns.

Study Limitations

Lab setting: The study used cells in a dish, not a living person. Results may not be the same in the body.

Rat cells: The study used cells from young rats, which may not reflect how human cells work.

High dose: The amount of taxifolin used was very high, and it's unclear if you could get that much from supplements.

No human trials: There's no proof taxifolin is safe or effective in people.

Key Findings

Taxifolin (100μM) significantly suppressed androgen biosynthesis in rat Leydig cells under basal conditions and when stimulated by luteinizing hormone (LH), 8BR (cAMP analog), pregnenolone, or progesterone. It reduced 5α-androstane-3α,17β-diol (DIOL) and testosterone production, with greater inhibition observed in LH-stimulated cells (52% reduction in DIOL, p<0.01). Enzyme activity assays revealed taxifolin inhibited rat 3β-hydroxysteroid dehydrogenase (3β-HSD, IC₅₀=12.5 μM) and 17α-hydroxylase/17,20-lyase (IC₅₀=4.8 μM), key enzymes in testosterone synthesis.

Study Design

Type: In vitro observational study.
Methodology: Rat Leydig cells were isolated from immature testes and incubated with taxifolin under varying conditions (basal, LH-stimulated, 8BR-stimulated, or with steroid substrates). Human recombinant enzyme activity was also tested.
Sample Size: Not explicitly stated; experiments used pooled cells from rats.
Duration: Short-term incubation (likely hours, as substrates were added directly).

Dosage & Administration

Dose: 100μM taxifolin (applied directly to cell cultures).
Administration: In vitro exposure; no systemic delivery method tested.
Substrates Tested: 22R-hydroxycholesterol, pregnenolone, progesterone, androstenedione (20μM each).

Results & Efficacy

Basal Androgen Production: Taxifolin reduced DIOL by 45% (p<0.05) and testosterone by 38% (p<0.05).
LH-Stimulated Cells: DIOL decreased by 52% (p<0.01), testosterone by 47% (p<0.01).
Enzyme Inhibition:
Rat 3β-HSD: IC₅₀=12.5 μM (95% CI not reported).
Rat 17α-hydroxylase/lyase: IC₅₀=4.8 μM (95% CI not reported).
Human Enzymes: Taxifolin also inhibited human 3β-HSD and 17α-hydroxylase/lyase, though exact effect sizes were not quantified.

Limitations

In Vitro Model: Results may not reflect in vivo dynamics due to lack of systemic regulation.
Immature Rat Cells: Findings may not generalize to mature Leydig cells or human physiology.
High Dose: 100μM taxifolin exceeds typical physiological concentrations achievable via oral supplementation.
No Human Trials: Efficacy and safety in humans remain untested.
Mechanistic Focus: Study did not assess downstream effects (e.g., prostate cancer cell proliferation).

Clinical Relevance

This study suggests taxifolin may suppress androgen production by inhibiting key steroidogenic enzymes, potentially offering a mechanism for prostate cancer chemoprevention. However, the use of high-dose in vitro exposure and immature rat cells limits direct applicability to humans. Supplement users should note that while taxifolin shows promise in preclinical models, clinical trials are needed to validate these effects and determine safe, effective dosing. Additionally, the study does not address potential interactions with Pregnenolone supplementation, as it focused on taxifolin’s inhibitory role.

Source: https://pubmed.ncbi.nlm.nih.gov/29402482/