The Testosterone Trade-Off: Optimizing Anabolism Without the Needle

In an era where male hormonal health is in decline and the temptation of Anabolic-Androgenic Steroids (AAS) is rising, a new review from the Mayo Clinic provides a critical appraisal of “natural” testosterone optimization. The central thesis is that testosterone (T) levels are not merely a product of genetics, but a dynamic readout of energy availability, environmental exposure, and recovery status. The authors argue that before turning to exogenous hormones—which carry severe risks of infertility and cardiovascular strain—athletes and biohackers must first address the “low-hanging fruit” of physiological inhibition.

The review systematically dismantles and validates various “biohacks.” It confirms that energy deficiency (Relative Energy Deficiency in Sport, or REDs) is a primary, often overlooked castration mechanism in natural athletes. It validates sleep not just as rest, but as the active window of T-synthesis, specifically linked to REM cycles. Crucially, it challenges popular recovery modalities; notably, Cold Water Immersion (CWI) is flagged as potentially counterproductive for hypertrophy and testosterone availability immediately post-training.

Furthermore, the paper elevates the conversation around environmental toxins, positioning Endocrine Disrupting Chemicals (EDCs) like bisphenols and phthalates as invisible suppressors of the Hypothalamic-Pituitary-Gonadal (HPG) axis. It also touches on controversial topics, offering cautious support for supplements like Eurycoma longifolia (Tongkat Ali) while debunking the efficacy of most commercial “testosterone boosters”. Ultimately, this is a manifesto for “subtracting interference” (stress, toxins, deficits) rather than just “adding agonists.”

Source:

  • Open Access Paper: Testosterone-Optimizing Strategies in Athletes
  • Institution: Mayo Clinic, USA
  • Journal: Sports Health: A Multidisciplinary Approach, 2026, Feb 2
  • Impact Evaluation: The impact score of this journal is 2.6 (Impact Factor) and 6.4 (CiteScore), therefore this is a Medium impact journal.

Biohacker Analysis

Study Design Specifications

  • Type: Narrative Review (Level 5 Evidence).
  • Subjects: N/A (Review of existing human and animal literature).
  • Methodology: Database search of PubMed for English-language peer-reviewed articles focusing on legal testosterone enhancement.

Lifespan Analysis

  • Relevance: The interventions discussed (e.g., avoiding EDCs, optimizing sleep) are generally aligned with healthspan extension, but the paper offers no direct mortality data.

Mechanistic Deep Dive

The review highlights specific molecular and systemic pathways regulating the HPG axis:

  • HPG Axis Suppression via Energy Stress: The hypothalamus integrates signals of energy availability. Low Energy Availability (LEA) suppresses Gonadotropin-Releasing Hormone (GnRH) pulses, downstreaming to reduced Luteinizing Hormone (LH) and T production. This confirms that caloric restriction (CR), while pro-longevity in some contexts, is anti-anabolic and anti-androgenic if too severe.
  • Aromatase Inhibition & SHBG Modulation:
    • Eurycoma longifolia is highlighted for its ability to inhibit aromatase (preventing T to Estrogen conversion) and dissociate Free Testosterone (FT) from Sex Hormone Binding Globulin (SHBG).
    • Zinc acts as a cofactor for steroidogenic enzymes and antioxidant defense in Leydig cells, essential only in deficiency states.
  • Cortisol Antagonism: High-intensity resistance exercise acutely spikes T, but chronic stress/cortisol competes with T for receptors and inhibits steroidogenesis. Managing the T:Cortisol ratio is cited as a key anabolic lever.
  • Environmental Toxicity: EDCs (plastics, pesticides) mimic estrogens or block androgen receptors (AR), directly disrupting testicular function.
  • Radiofrequency Electromagnetic Radiation (RF-EMR): The paper suggests a mechanism where RF-EMR (e.g., cell phones in pockets) induces oxidative stress (ROS) in testicular tissue, damaging Leydig cells.

Novelty

  • The “Cold” Warning: Unlike general wellness advice that praises cold plunges, this review specifically warns that post-exercise cold water immersion may blunt the acute testosterone response and downstream hypertrophy signaling. This is a critical nuance for biohackers combining resistance training with cryotherapy.
  • Technological Toxicity: It explicitly categorizes RF-EMR (cell phones) and Blue Light/Sleep disruption as endocrine disruptors, moving them from “wellness speculation” to “clinical consideration” for athletes.
  • Dietary Nuance: It differentiates between healthy fats (pro-T) and high-protein/low-carb diets, noting that excessive protein (>3.4 g/kg) with low carbs may actually lower basal testosterone.

Critical Limitations

  • Low Level of Evidence: As a “Level 5” Narrative Review, the conclusions are based on the authors’ selection of studies rather than a systematic, quantitative meta-analysis.
  • Conflicting Data on “Biohacks”: The evidence for Sauna is deemed “unclear” with studies showing neutral or inconsistent effects on T, despite its popularity in longevity circles. Similarly, the link between RF-EMR and human T levels is inconsistent, relying heavily on rodent data.
  • Translational Gaps: Many mechanistic claims (e.g., Eurycoma mechanisms, specific EDC thresholds) are extrapolated from animal models or small, short-term human trials. The clinical impact of these transient hormonal changes on long-term performance or hypertrophy remains unquantified.
  • Female Data Deficit: The authors explicitly admit that most strategies are extrapolated from male physiology, with significantly less data available for female athletes.

Here is the external verification and hierarchy analysis of the claims made in the paper.

Claims & Verification

Claim 1: “Low Energy Availability (LEA) suppresses the HPG axis, lowering testosterone in men (REDs).”

Claim 2: “Post-exercise Cold Water Immersion (CWI) blunts anabolic signaling and testosterone response.”

  • Evidence Level: Level A (Meta-Analysis)
  • Verification: A systematic review with meta-analysis confirms that CWI following resistance exercise attenuates muscular strength gains and hypertrophy. While some acute hormonal data is mixed, the downstream effect on anabolism is negative.

Citation: Throwing cold water on muscle growth: A systematic review with meta‐analysis of the effects of postexercise cold water immersion on resistance training‐induced hypertrophy (2020)

  • Claim 3: “Eurycoma longifolia (Tongkat Ali) significantly increases testosterone in men.”
    • Evidence Level: Level A- (Systematic Review & Meta-Analysis of RCTs)
    • Verification: A 2022 meta-analysis of RCTs supports a significant improvement in total testosterone (SMD = 1.352) in men receiving Eurycoma longifolia, particularly in hypogonadal subgroups.

Citation: Eurycoma longifolia (Jack) Improves Serum Total Testosterone in Men: A Systematic Review and Meta-Analysis of Clinical Trials (2022)

  • Translational Note: While statistically significant, the absolute clinical magnitude in healthy, eugonadal men remains debated.

Claim 4: “Sleep restriction (specifically total sleep deprivation) lowers testosterone.”

Claim 5: “Cell phone radiation (RF-EMR) lowers testosterone and damages sperm.”

Claim 6: “High-protein (>3.4 g/kg), low-carbohydrate diets decrease testosterone.”

  • Evidence Level: Level A (Systematic Review & Meta-Analysis)
  • Verification: A systematic review identified that “very high protein” diets (>3.4 g/kg/day) combined with low carbohydrates are associated with a significant decrease in testosterone (~5.23 nmol/L). Moderate protein intakes (up to ~3 g/kg) do not show this effect.
  • Citation: High-protein diets and testosterone (2022)
  • Note: This is a crucial threshold. Most “high protein” diets fall well below 3.4 g/kg, making this relevant primarily to extreme biohackers/bodybuilders.

Claim 7: “Ashwagandha increases testosterone and DHEA-S.”

Actionable Intelligence

The Translational Protocol: Testosterone Optimization

This protocol synthesizes the review’s findings with external safety and pharmacokinetic data. It prioritizes “Subtraction before Addition” (removing EDCs, cortisol, and sleep deficits) followed by targeted nutraceutical support.

1. Compound: Eurycoma longifolia (Tongkat Ali)

  • Target: Aromatase inhibition, SHBG reduction, Cortisol modulation.
  • Human Equivalent Dose (HED) Calculation:
    • Source Data: Rat NOAEL (No Observed Adverse Effect Level) is established at 1,000 mg/kg for standardized aqueous extract.
    • Math: 1,000 mg/kg multiplied by (6 divided by 37) = 162 mg/kg HED.
    • Human Safety Ceiling (70kg): 162 multiplied by 70 = approx. 11,340 mg.
    • Effective Dose (RCTs): 200–400 mg/day of standardized root extract (e.g., Physta/LJ100).
    • Insight: The massive gap between the effective dose (400 mg) and the theoretical safety ceiling (11 g) suggests a high safety margin for acute toxicity. However, idiosyncratic hepatotoxicity remains a risk.
  • Pharmacokinetics:
    • Bioavailability: Poor (less than 10.5% oral bioavailability).
    • Half-Life: Short (approx. 1–2 hours).
    • Action: Must be taken in divided doses or standardized to high Eurycomanone content (greater than 1.5%) to overcome poor absorption.
  • Safety Profile:
    • Liver Signal: Rare but documented cases of drug-induced liver injury (DILI).
    • Protocol: Cycle 5 days ON / 2 days OFF to mitigate potential hepatic accumulation. Monitor ALT/AST.

2. Compound: Ashwagandha (Withania somnifera)

  • Target: Cortisol reduction (HPG axis disinhibition), DHEA-S upregulation.
  • Dose: 300–600 mg/day (KSM-66 or Sensoril) or 120 mg (Shoden/High-Withanolide).
  • Pharmacokinetics:
    • Newer formulations (35% withanolide glycosides) show significantly superior bioavailability and sustained release compared to generic root powder.
  • Biomarker Verification:
    • Primary: Serum Cortisol (Target: reduction).
    • Secondary: DHEA-S (Target: increase).

3. Behavioral “Subtraction” Protocol

  • Cold Water Immersion (CWI):
    • Action: PROHIBITED within 4–6 hours post-hypertrophy training. CWI blunts acute anabolic signaling (p70S6K) and satellite cell activity.
  • Sleep:
    • Action: 8+ hours. REM sleep is the primary window for LH pulsatility.

Feasibility & ROI

  • Sourcing:
    • Eurycoma: High risk of adulteration. Must source patented extracts (LJ100, Physta) to ensure eurycomanone content.
    • Ashwagandha: Widely available, low cost.
  • Cost vs. Effect:
    • Eurycoma: Approx. $30–50/month. ROI: Moderate (Variable responder rate).
    • Ashwagandha: Approx. $15/month. ROI: High (Reliable cortisol reduction).
    • Total Protocol: Approx. $65/month.

The Strategic FAQ

1. “You cite a mouse NOAEL of 1,000 mg/kg for Tongkat Ali, but aren’t there reports of liver failure in humans?” Answer: Yes. While the calculated safety ceiling is high, idiosyncratic Drug-Induced Liver Injury (DILI) has been reported in humans. This is likely due to contamination (heavy metals/sildenafil in grey-market products) or individual metabolic variants, rather than intrinsic dose-dependent toxicity of the root itself. You must use a third-party tested source and monitor liver enzymes (ALT/AST).

2. “I’m taking Metformin for longevity. Does this protocol conflict?” Answer: CONFLICT. Metformin significantly lowers total and free testosterone in men. The mechanism is independent of glucose control. If your primary goal is anabolism/T-optimization, Metformin is counter-productive. You are pressing the gas (Tongkat) and the brake (Metformin) simultaneously.

3. “Can I stack this with Rapamycin?” Answer: Likely safe. Rapamycin can induce glucose intolerance (insulin resistance), which Ashwagandha helps mitigate via insulin-sensitizing pathways. There is no direct pharmacokinetic clash (CYP3A4 inhibition by Tongkat is weak/negligible).

4. “Does Tongkat Ali actually raise Testosterone, or just ‘Free’ Testosterone?” Answer: Primarily Free Testosterone. The mechanism is largely displacing T from SHBG and inhibiting aromatization to estrogen. Do not expect a supraphysiological surge in Total T comparable to TRT; expect a functional improvement in bioavailable androgen status.

5. “I use a sauna and cold plunge daily. What is the optimal timing?” Answer: Sauna: Post-workout is fine (and potentially boosting). Cold Plunge: Never post-resistance training. Move CWI to rest days or pre-workout to avoid blunting the inflammatory signals required for hypertrophy and hormonal adaptation.

6. “Will Ashwagandha make me lethargic?” Answer: Possible. It is a GABA-mimetic and can be sedating (“Somnifera” means sleep-inducing). If you experience anhedonia or lethargy, switch dosing to evening only or cycle off.

Image of GABA receptor complex

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7. “How do I verify this is working without a blood test?” Answer: You can’t. Subjective “libido” is a poor proxy for serum testosterone. You need to test Free Testosterone and SHBG at baseline and Week 8.

8. “Is 17-alpha Estradiol compatible with this stack?” Answer: Proceed with caution. Both 17-alpha estradiol and Ashwagandha/Tongkat are metabolized by the liver. While 17-aE is non-feminizing, adding multiple hepatic loads (plus potential “dirty” supplements) increases DILI risk.

9. “What is the ‘Ferrari’ version of this protocol?” Answer: Swap generic extracts for Liposomal delivery systems or specific high-yield extracts (e.g., 10% Eurycomanone, 35% Withanolides). Couple with hCG monotherapy (clinical prescription required) rather than herbal secretagogues for guaranteed LH pulsing.

10. “Why not just take TRT?” Answer: TRT induces testicular atrophy and infertility (azoospermia) by shutting down the HPG axis feedback loop. This protocol preserves and optimizes your endogenous production. If you want fertility and testicular volume, this is the path; if you want guaranteed supraphysiological numbers regardless of biology, TRT is the path.

Interaction Check: Longevity Stack

Compound Interaction Verification Status
Metformin Antagonistic. Metformin lowers serum Testosterone in men. Major Conflict
Rapamycin Synergistic. Ashwagandha may buffer Rapa-induced glucose intolerance. Safe
SGLT2 Inhibitors Additive. Potential hypoglycemia risk if combined with Ashwagandha. Monitor Glucose
17-alpha Estradiol Hepatic Load. Theoretical risk of cumulative liver stress. Monitor Liver
PDE5 Inhibitors Additive. Vasodilation stacking; watch for hypotension. Safe (usually)

Hopefully they also mentioned obesity as a driver of low testosterone. I think there are recent studies that show that anti obesity meds can have a normalizing effect Anti-obesity medications can normalize testosterone levels in men | Endocrine Society

I don’t know why ai suggests hcg when it’s worried about shutting down the hpg axis. Hcg shuts down endogenous LH production over time.

These recommendations probably apply to someone with secondary hypogonadism, but will not work for someone with primary hypogonadism.