How To Increase Your Testosterone Levels Naturally | Derek from MPMD
These notes were generated by AI and may contain inaccuracies.
Testosterone supports muscle tissue growth and sustainment, bone health and integrity, insulin sensitivity, neurological health via aromatization to estrogen, erythropoiesis (red blood cell production), intratesticular production critical for fertility. Levels in men are trending downward. Major contributors include pollution and chronic toxic environment inhibiting systems.
Symptoms of low testosterone: reduced libido, harder time losing fat/gaining muscle, bone integrity issues.
Top three supplements for testosterone: zinc, magnesium, vitamin D (not in order).
Derek runs More Plates More Dates YouTube channel on hormones, exercise, training. Featured on Peter Attia's podcast. Runs Marek Health, a preventative health company optimizing hormones.
Testosterone is the primary anabolic hormone for muscle growth/sustainment, bone health/integrity (inhibiting degradation), insulin sensitivity (worsened body composition impairs glucose handling). Supports neurological health via aromatization to estrogen in tissues. In adolescence, 5-alpha reduction to DHT necessary for full maturation and sexual differentiation. Low DHT (genetic or otherwise) leads to inhibited maturation (e.g., intersex cases). Present at 10x concentrations in males vs. females, differentiates sexual identity and male characteristics.
Women produce testosterone at lower levels but it supports cognitive health, cardiovascular support, bone integrity, anabolic activity, muscle tissue (to lower magnitude matching female musculature). Main function: substrate for estrogen production (estradiol, estrone) facilitating female fertility processes.
Females outlive males across mammal species. Testosterone differentiates but speculative trade-offs:
- Larger male infrastructure demands more metabolic resources/hormone production, taxing organ systems (larger humans die quicker).
- Supra-physiological androgens: neurotoxic (dose-dependent), negative cardiac remodeling, dyslipidemia (similar to anabolic steroids but muted as natural testosterone aromatizes protectively).
Host notes: possibly lack of estrogen in men (men aromatize but less than premenopausal women).
Castrati: Boys castrated pre-puberty to preserve angelic singing voices (prevents testosterone/DHT deepening). Last documented within last 100-200 years; recordings on YouTube sound androgynous/youthful.
Consequences:
- Rely on adrenal androgens only (drop in bucket vs. needed levels).
- Insufficient aromatization to estrogen: osteoporosis, incomplete epiphyseal growth plate closure, poor bone development.
- Smaller stature, less muscle/bone (less resource intensive), potentially longer lifespan but dramatically hindered quality of life ("live longer but don't want to").
Total testosterone: Reflects total production in blood (includes bound to proteins).
Free testosterone: 2-3% unbound, readily available for tissues/androgen receptor binding/transcriptional activity.
Binding proteins:
- SHBG (sex hormone binding globulin, liver-produced): ~60%, regulates androgenicity, ensures sex-appropriate hormone delivery (hydrophobic hormones need carriers).
- Albumin: ~38%.
Both total (production capacity, organ/pituitary response) and free (bioavailable) matter.
Optimal testing:
- Early morning (pulsatile secretion: peaks morning, lowest night; ramps during sleep).
- Fasted.
- Avoid biotin/multivitamins (interferes with assays).
- Hydrated (avoids false high hematocrit from dehydration).
- Repeat measures (confirm low/mildly concerning results; single snapshot variable).
Avoid hasty TRT based on one reading (e.g., 495 ng/dL vs. optimal ~1000; clinics may push).
Reference ranges convoluted; don't just target top (e.g., 900+ ng/dL) without symptoms.
- Androgen receptor (AR) content/sensitivity varies: impacts post-binding activity (muscle/bone/neuro support not guaranteed by levels alone).
- Symptoms supersede labs sometimes (e.g., high SHBG → low free T despite high total; AR insensitivity/mutations require higher T).
- Proxies for AR activity: gonadal development assessment (subjective); outlier bloods/symptoms (e.g., natural 1300 ng/dL may signal compensation for poor response via high gonadotropins).
Hypogonadism complicates: primary (testes failure → high LH/FSH to compensate, possible structural defects) vs. secondary (low pituitary output).
Check total/free T + symptoms first.
LH (luteinizing hormone): Pituitary signal to Leydig cells for intratesticular T.
- Primary hypogonadism: high LH/FSH (body overshoots for feedback).
- Age-related: low gonadotropins/response.
Structural: varicocele (varicose veins in testes, twisted like leg varicose veins; ~15% prevalence in males).
Varicocele is on the side of the testes, inhibits thermoregulation, significantly impedes testosterone production locally and fertility. Prevalence: 15% of men. If doing all lifestyle stuff and it's not working, structural defects might be overlooked. First check: capability of testes to respond to signal and if signal is adequate. Primary hypogonadism is structural problem in testes.
If no structural problems, age-related decline not a factor, check upstream pituitary: producing enough LH and FSH. Common in men unsure if they need testosterone: relative proportional inadequate signaling from lifestyle, age decline, toxins, exposures. Opportunity to maximize areas in life to improve output. If sufficient organ function but insufficient output, improve by getting leaner, losing body fat, fixing diet, addressing micronutrient deficiencies, quitting smoking, not drinking, fixing sleep.
SHBG (Sex Hormone Binding Globulin)
SHBG binds testosterone. Questions: what regulates SHBG levels, what regulates how much testosterone escapes binding to exert activity, can dial in on SHBG to solve issues?
DHT (dihydrotestosterone) is primary hormone for full maturity in adolescence; zero DHT from defect in 5-alpha reductase leads to incomplete masculinization (e.g., micropenis). DHT has highest binding affinity for SHBG, then testosterone, then estrogen. Free T vs total T important; also DHT levels (not commonly tested). High SHBG gobbles up more DHT proportionally.
Impact on Females and Oral Contraceptives
Rough in females using combined oral contraceptives (ethinyl estradiol + progestin), cranks SHBG via liver. Suppresses total testosterone 50-60%, free testosterone 70-80% → borderline asexual/castrated. Oral worse than progestin-only IUD (e.g., levonorgestrel). High SHBG (even high-normal) hits DHT hardest; differential between symptomatic or not.
Age: total T declines 1%/year after 30, but SHBG increases faster → free T declines up to 2%/year. Free T is what binds receptors. Dictated by: age, liver health, medications (esp. oral), insulin signaling. Ketogenic/carnivore diets → high SHBG, low free T (despite high total T); need insulin to lower SHBG. Relevant for females too.
Binding Proteins for Other Hormones
Binding proteins for IGF-1, thyroid hormones. Common: normal total but low free hormones (unusable). Especially women: low androgens to start, high SHBG mops up DHT/T → female hypogonadism equivalent, low libido, hard to lose fat/gain muscle, poor bone integrity.
Combined Pill and Lifestyle in Women
Combined oral contraceptives inhibit natural production + lifestyle (sleep, cortisol, fat, obesity). Final blow pushing low drive/quality of life. Not saying avoid all contraceptives; better options exist.
Libido, erection quality (circulatory or hormone), no morning wood, harder to hold/build muscle, losing strength, inhibited recovery, mood dysregulation, irritability. Constellation of symptoms from lifestyle + low T vicious cycle. Genetic/outlier: incomplete puberty (high voice). Average: general symptoms → get tested.
Blood Work Essential
Pre-diabetes, insulin resistance determined by blood work. Vague: quality of life deterioration (erection quality, libido, vigor, muscle/strength, body comp).
Average 1%/year total T decline after 30, but lifestyle modulates/accelerates/slows. Seen 70-year-olds with 900 total T.
Lifestyle/Environmental Factors to Avoid/Minimize
Accelerate T decline, increase SHBG, impair T function:
- Alcohol: direct toxicity to steroidogenesis in testes, impacts sleep → body comp cascade. Dose-dependent; oxidative stress on testes. Spectrum; some tolerate more.
- Smoking: not helpful.
- Fat-deficient diet: hinders hormone production.
- No/low carbs: inhibits free hormone liberation.
- Lack of protein: poor workout recovery, muscle build → worse body comp/hormones.
- Balanced diet, avoid bad food.
- Micronutrients: zinc, magnesium, vitamin D marked impact on production/response. Vitamin D conversion to active form key; deficiency hurts androgen receptor. Multivitamins often inadequate (mag needs 8-10 caps; vit D fat-soluble). Deficiency: 100+ ng/dL drop per micronutrient.
- Obesity: elevates aromatization (T → estrogen/estradiol), negative feedback to HPA axis. Brain signaled by estrogen (not T directly) → 'we're good, stop T'. Obese: half reference range drop.
Weight Loss Effects
Losing visceral/overall fat balances estrogen/T ratio → more T production (needs more T substrate for adequate estrogen signal). Goldilocks zone: 12-15% body fat → dramatic T increase vs obese. Too low (malnourished) starves hormone production.
Excessive Endurance Training
Negative if exceeds recovery capacity. Tolerance varies. Calorie deficit + endurance → malnourishment, hormone deficiency. Natural bodybuilders pre-show: single-digit BF → malnourished, preservation mode, shut down metabolism. Endurance: fuel adequately (5000+ cal/day possible); right macros/micronutrients, or exercise into hypogonadism.
I would caveat not easily.
Training that hard is difficult; kudos to those mentally strong enough.
Excessive endurance training in severe caloric deficit leads women to become amenorrheic, ceasing ovulation. Host's anecdote: in 20s, ran 10 miles/day eating only carrots and hummus (low fat, low protein), got shredded-ish but amenorrheic for months. Had to add calories; body took time to recalibrate.
Survival Mode and Reproduction Shutdown
Body shuts down reproduction in survival mode due to insufficient calories: not reproductive/growth mode, but survival.
Men dieting for bodybuilding shows can have hormone profiles more female-like than their girlfriend's in the last week, with testosterone that low. Some may not realize the significant deterioration.
Convinced there's an effect, but magnitude often overhyped.
Low-Hanging Fruit to Avoid
- Don't heat plastic Tupperware; use glass.
- Ensure high-quality air (pollution impairs stress handling, resource allocation).
- Good water quality.
Magnitude negligible vs. obesity, diet, exercise, sleep, lifestyle carcinogens. Address basics first (free/cheap: eat less, gym). Then test baseline bloodwork before tweaks like shower filter.
Mechanisms
Compounds interact with estrogen receptors and androgen receptors, acting as anti-androgens/anti-estrogens by occupying space, competing with endogenous hormones.
Chlorine: maybe effect on T, but more BPA orally (heating plastics, hot beverages in plastic).
True trend downward. Mostly obesity, diet, lifestyle. Environmental factors less favorable but dialing basics eases mind (free/cheap). Baseline blood test, then incremental changes (e.g., chlorine filter); assess gonadotropin output.
Fats: provide substrate (cholesterol backbone for steroid hormones like testosterone, estradiol). Low-fat diets problematic; sufficient fats needed despite no direct dose-response with serum cholesterol.
Carbs: mediate insulin signaling for free androgen balance (IGF-1, T3, estrogens, DHT). Keto can tank free T via low insulin (fails to suppress binding proteins). Not for everyone; measure hormones.
Protein: building blocks.
Deficiency in any expected to impair.
Saturated fats increase endogenous cholesterol.
Descending order of intensity:
- Resistance training (top: muscle/bone building, most impactful).
- HIIT-style.
- Basic movement (least).
Adherence trumps optimal; choose enjoyable sustainable regimen. Calories > everything for versatility (not locked to one diet: Mediterranean, carnivore, vegan). Optimize: energy balance, adequate protein/fat/carbs for exercise intensity.
ZMA (zinc, magnesium, vitamin B6): first T-booster combo; reliable if deficient.
- Zinc: possible via diet.
- Magnesium: hard; choose bioavailable forms (e.g., Rhonda articles).
- Vitamin D: hormone affecting androgen receptor activity, gene transcription.
Facilitate hormone utilization, not just production. Backfill needs, assess bloodwork/symptoms.
Expected Impact if Deficient
Low reference range or hypogonadal: 100-150 ng/dL total T increase (additive; vitamin D/magnesium common deficiencies). Robust in studies but don't overexpect; unmeasured utilization effects.
Boron
Suppresses SHBG (6-12 mg; not typical diet amount). Promising, not guarantee (high to optimal range). Frees total T to free T.
Ashwagandha
Standardized extracts: KSM-66 (5% withanolides), Sensoril (10%). Patented > generic. Sensoril: lower mg dose due to potency.
Indirect via cortisol suppression/stress reduction. 600 mg clinically supported; cumulative effect. +100+ points T for responders (triple digits). Improves sleep, resilience for anxious/stressed. Game-changer for some.
Risks: overdoing causes anhedonia (emotional numbing, black/white world). Cautious if anxious phenotype vs. baseline numb. Literature sound (some company-funded); anecdotal bloodwork supports.
Tongkat Ali
SHBG suppression (main agreed mechanism). Speculative:
- Minor SERM-like (selective estrogen receptor modulator): tissue-selective modulation (e.g., inhibit hypothalamus feedback to boost T; avoid bone inhibition).
- Serum activity.
Tongkat Ali suppresses SHBG to some extent and upregulates steroidogenesis intra-testicularly by locally upregulating steroidogenic acute regulatory protein (StAR), which incorporates cholesterol into the mitochondria for enzymatic cleaving sequences resulting in testosterone production locally. It helps upregulate the enzymatic process that produces testosterone. It works well for individuals with high SHBG levels or potentially higher estrogen levels not fixable via basic lifestyle changes, as metabolism proportions vary. Even with optimal diet and lifestyle, SHBG might be high or a boost needed. It provides 100-200 ng/dL increases depending on standardized extract potency. Look for HPLC-tested for eurycomanone, the active ingredient (spelled Eurycomanone). Avoid vague labels like Tongkat Ali 100:1 or 10:1, as they are meaningless without eurycomanone verification via third-party testing, similar to Ashwagandha.
and what was that ingredient called again? >> Eurycomanone.
Tongkat Ali vs. Boron
Boron is a mineral; exact mechanistic differences on SHBG binding unclear. Tongkat Ali works in two ways for bigger impact in men. Boron often in multivitamins but underdosed; stack extra for incremental SHBG decrease. Tongkat Ali more speculative/exotic, last resort after exhausting options (lifestyle perfect, diet dialed, micronutrients accounted, sleep good, no drinking/smoking, total T still inadequate). Reasonable safety profile, efficacious in young healthy men per literature, not just age-related decline. Mechanistically might work similarly in women via SHBG, but no specific study.
Boron potentially a longevity molecule, evidence for improving aging.
Other Supplements: Fenugreek, D-Aspartic Acid, Shilajit
Tribulus, D-aspartic acid, fenugreek largely disproven. Shilajit notable if high quality: enhances organ capacity to respond to hormones by tolerating stress/reactive oxygen species via antioxidant activity, attenuating decrement to performance for more local hormone yield, impactful on intra-testicular antioxidant activity. Requires careful sourcing, speculative/indirect; better ways to manage antioxidants.
Top Supplements for Testosterone
Top three: zinc, magnesium, vitamin D (not in order). Then Tongkat Ali for impact, but boron safer next choice for safety profile. For anxious people, Ashwagandha; cognizant of how it works, possible lower dose/cycling based on response (individual biochemistry varies; studies are protocols, not ideal for everyone).
Host interested in Ashwagandha for stress/cortisol management (complements exercise), potential testosterone boost side effect; plans experiment after bloodwork.
check your blood first, though.
Once you got that blood test, you're going to be like, "Fuck, I shouldn't have taken Ashwagandha cuz now I have no idea what the baseline was."
Cortisol Testing: DUTCH Test Recommended
For cortisol stress response, DUTCH test (salivary) over blood: more indicative than transient serum cortisol snapshot. Salivary provides multiple readings/average curve mapping day vs. single blood draw. Less intrusive (spit in tube multiple times a day).
For men exhausting natural ways (weight loss, lifestyle optimized, total/free T good): clinically low testosterone with symptoms. Obvious scenarios: structural issues unrectifiable by lifestyle (primary hypogonadism ruled out via ultrasound for varicocele, no hot tubs, sleep/micronutrients/calories on point). Rule out pituitary adenoma, structural defects; signaling adequate/supraphysiologic but no response.
Try hCG to stimulate Leydig cells maximally + exogenous FSH; if no response, testes non-functional (primary hypogonadism): on exogenous testosterone (can't fix with clomiphene, hCG, hMG). Not typical outcome; most on TRT via secondary hypogonadism (pituitary inadequate output/response + insufficient amount).
Secondary Hypogonadism and hCG
Testes function suboptimally + low gonadotropin output from lifestyle/diet. Example: Peter (50yo, dialed lifestyle) used hCG (LH mimic) after testes responded to manual signal, replacing hormones as pituitary LH insufficient (age-related decline?). Options: manual backfill signal (hCG) or hormones after exhaustive checks. Worth learning why (due diligence); don't delay if symptomatic/quality of life hurt. hCG middle ground for secondary: distinguishes testicular vs. pituitary issue.
Upstream: Hypothalamus GnRH Axis
Insufficient GnRH output stimulates pituitary LH/FSH cascade; deteriorating signal/response leads to suboptimal testicular response (often age-related).
Work with highly educated medical professional; learn mechanisms to avoid haphazard regimens/shitty clinics committing to lifelong hormones blindly. Identify if natural avenues missed (maintain brain-to-testes signal).
Physiologic replacement alleviates all symptoms. Not exactly like age 20 (metabolism/estrogen response differs). Target: symptom relief (e.g., menopausal therapy eliminates hot flashes, supports bone integrity). Feel better indirectly; relative to deficiency severity (not Superman unless severely deficient). Not shredded in weeks.
Avoid rash decisions on low-normal numbers without symptoms/lifestyle fixes; numbers not everything (genetics, muscle fibers, body fat matter). Natural bodybuilders with 500 ng/dL total T have best physiques; higher T not guarantee.
Controversy on CV risk. TRAVERSE trial (large, placebo-controlled, older hypogonadal men): AndroGel to physiologic restoration (normal range) showed no adverse CV outcomes (promising pre-public data).
Issue: "physiologic restoration" variable (like coffee caffeine). AndroGel to ~400 ng/dL total T ≠ injectable testosterone to 1000 ng/dL + high free T/SHBG drop (infrequent injections). Not all use AndroGel; don't extrapolate to aggressive protocols (erythropoiesis increase, high signaling). Polycythemia expected with more T (increases hematocrit/thickness, stroke/CV risk); ~25% on TRT have thicker blood (not always needing treatment).
More T = more erythropoiesis; if starting hypogonadal, 25% increase not net negative.
Starting from hypogonadal levels, which is why many begin TRT, a 25% bump in hematocrit might be needed for adequate oxygen carrying capacity to fuel the body. It's not net bad or good; it depends on the individual. Symptom relief can occur at 450 total T for some, or 800 for others. Even at 800, it's high normal on reference ranges, so not inherently bad. Androgens drive erythropoiesis in a dose-dependent manner, induce cardiac remodeling if pushed too hard (not necessarily within physiologic limits), and dyslipidemia becomes more concerning at higher levels, varying by administration method and frequency.
Infrequent dosing like once-weekly shots differs from daily pulsatile cream or subcutaneous micro-injections, which bleed out the effect more evenly. No direct data says replacing to 800 total T is dangerous or safe; extrapolate from TRAVERSE trial and graded dose-response studies. For those wanting high normal for optimal vitality, weigh risks: monitor hematology panel for unsustainable hematocrit (may need phlebotomies), energy levels, etc. Requires understanding interplay, rigorous doctor, blood work monitoring.
TRAVERSE trial isn't a get-out-of-jail-free card. Different administration impacts outcomes; unlikely on AndroGel at low dose to hit 420 ng/dL. Dyslipidemia, increased blood viscosity, SHBG suppression (elevates androgenic signaling beyond physiologic with infrequent injections). Most are transiently supra-physiological (e.g., peaks at 1200-1500 total T, high free T) with once- or twice-weekly injections, not mimicking daily production.
Ideal Protocols Mimic Daily Testicular Output
Ideal is replacing daily testicular output: scrotal cream twice daily or daily subcutaneous micro-injections. Many prefer one-and-done weekly shots. Pharma setups like Xyosted (pre-loaded testosterone enanthate auto-injector pens) force infrequent high doses.
25% of men hit supra-physiological levels due to injection protocols. Cream drawbacks: adherence (lifelong, twice-daily scrotal application inconvenient, especially traveling; quick hypogonadal drop if missed), stroke risk, cardiovascular disease. Many favor adherence/sustainability over optimal, accepting risk profile.
Other Risk Profile Elements
Prostate: Androgen saturation model – from hypogonadal to eugonadal (~300+ ng/dL), stimulates prostate growth/PSA rise positively, but beyond that, no dose-dependent increase (bodybuilders on thousands mg/week don't have exploding prostates). Monitor PSA trends longitudinally with age; no spawning cancer from scratch if healthy. Hypogonadal likely means small prostate initially; normalization isn't bad.
Testosterone maximizes male secondary characteristics: extra estrogen/DHT management needed to avoid acne, hair loss, gynecomastia (excessive local aromatization), scalp hair loss, excessive body/facial hair, voice deepening (noticeable if low T baseline pushed to high normal). Sleep apnea exacerbated by neck/muscle size increases contributing to airway obstruction.
If physiologically replacing, many risks moot. Pushing to 'optimal' increases sleep apnea risk; recommend baseline sleep study (home devices measure apnea episodes/hour) before/after TRT to track changes.
Supra-Physiological Peaks from Infrequent Injections
Trough-day blood work (lowest levels) for long-ester like cypionate/enanthate (once/twice weekly). Peaks hit 1300-1500 total T, disproportionate free T/DHT (SHBG suppression), more aromatization, acute erythropoiesis beyond physiologic, then crash. Europe: testosterone undecanoate or Sustanon every few weeks – stratosphere peaks to hypogonadal crashes (rollercoaster like amplified female cycles, aggression/irritability).
For low risk profile (benefits without bodybuilding supra levels): frequent subq better than weekly IM to avoid peaks.
High Normal Tolerable if Youth Levels and Monitored
If high normal matches what body handled in youth, done responsibly (monitor biomarkers, lean/healthy diet/lifestyle), low oversight after dialing in – likely fine, not zero risk. Hypogonadal far worse (cardiotoxic, neurotoxic, QoL tanked). Benefits outweigh risks if responsible; monitor biomarkers key.
Best Administration Methods
Avoid pellets. AndroGel suboptimal for males (female different). Scrotal cream via compounding pharmacies: ideal absorption/pharmacokinetics mimicking natural pulsatile secretion, local conversion (5α-reduction in skin), physiologic levels, favorable outcomes. Drawbacks: adherence, transference risks (kids/pets; cases of accidental masculinization).
Injections: predictable; modulate via ester (cypionate half-life 8-10 days), subq into fat (vs IM) bleeds effect more stably. Every other day subq very stable, frequent dosing adherence feasible.
Oral testosterone undecanoate (lymphatic absorption: Tlando, Jatenzo, Kyzatrex): swallowable, non-hepatotoxic (unlike old 17α-alkylated orals), mid-high replacement, symptom relief, sustainable but expensive/newer.
Nasal (e.g., Natesto): erythropoiesis-free, acute/on-demand (unsustainable multiple daily for men; novelty fades).
Injections/creams most common. Choose sustainable adherence for safety/symptom relief. Injections sterile/logistically easier (no hand cleanliness/transference worries). Three viable: scrotal cream, IM/subq injection, oral (more data needed). Frequent subq minimizes supra peaks vs weekly IM.
Detailed Notes: Chunk 6 - TRT Protocols, Fertility, and Monitoring
For individuals concerned about risk, such as those with family history of cardiovascular disease or stroke, injecting twice a week or three times every other day lowers potential side effects. Fertility is another consideration for men wanting to reproduce.
A rule of thumb: the closer dosing is to natural production from healthy testes, the less impact on unintended consequences from hormone spikes. Natural testosterone pulses multiple times daily; more frequent micro-dosing stabilizes levels, avoiding supra-physiological spikes. Daily administration preferred; cream twice daily, injections every day or every other day with diminishing returns beyond. Bleeding out doses works.
Exogenous testosterone crushes fertility significantly, if not entirely. Intratesticular testosterone mediates spermatogenesis. Bodybuilders on huge steroid doses sometimes cause accidental pregnancies despite expected infertility; unknown epigenetic effects. Do not rely on it for contraception.
Even baseline TRT inhibits fertility to low or azoospermic levels by shutting down brain signaling.
HPG Axis Mechanism
- Hypothalamus releases GnRH (gonadotropin-releasing hormone).
- Pituitary produces gonadotropins: LH (luteinizing hormone) and FSH (follicle-stimulating hormone).
- LH stimulates Leydig cells in testes to produce intratesticular testosterone.
- FSH supports Sertoli cells for spermatogenesis (women have theca cells).
Exogenous testosterone signals brain: "enough hormones," suppressing GnRH, then LH/FSH. No signaling leads to testes atrophy.
Replicate natural signaling with hCG (mimics LH) + recombinant FSH to maintain testes size, function, sperm production. Retains fertility or super-physiological levels. Adjust exogenous testosterone dose due to extra endogenous production; account for local aromatization differences.
hCG (from pregnant women's urine) can cause high estrogen; speculation on long-term effects (not bioidentical LH, human chorionic gonadotropin). No known epigenetic issues in babies from hCG+FSH. Cost-prohibitive: recombinant FSH expensive, hCG costly atop TRT.
Many accept atrophy for affordability, then intensive restoration later (hCG/FSH blasts). Easier to maintain than restore; atrophied testes may not fully recover volume, sperm quality/capacity.
Expect fertility to go down the toilet without adjunct protocol, but it's possible to sustain.
Misinformation led many bodybuilders to unnecessary atrophy.
Suppression of gonadotropins within days of starting injections. Atrophy over weeks to months, variable by individual; activity halts immediately.
Treat TRT seriously, as lifelong commitment; not for experimentation, especially non-hypogonadal men chasing muscle gains.
Essential Baseline and Ongoing Panels
- Hematology: RBC count, hematocrit, hemoglobin.
- Metabolic parameters: Insulin sensitivity (fasting insulin, HbA1c), progress metrics (muscle mass benefits).
- CMP: Kidney function via cystatin C, eGFR, SDMA (symmetric dimethylarginine, kidney marker proxy for inulin clearance), ADMA (asymmetric dimethylarginine, vasodilation/cardiovascular).
- Avoid creatinine-based eGFR (skewed by muscle mass, creatine intake).
- Lipid panel: Baseline HDL (suppressed dose-dependently).
- SHBG/binding proteins: Suppressed by exogenous androgens, dose-dependent (bodybuilders single digits).
- Testosterone assays:
- Total testosterone: LC-MS/MS (gold standard; avoid immunoassay, inaccurate at low levels).
- Free testosterone: Equilibrium dialysis or ultrafiltration (not calculated).
- Estradiol: LC-MS.
- Gonadotropins: LH/FSH should be suppressed to bottom (confirms adequate replacement; elevated suggests inhibition issues).
- Other: PSA, liver markers, clotting (factor V Leiden), Lp(a) (suppressed by androgens), thyroid (TSH, free T4/T3), IGF-1.
Comprehensive baseline essential; starting without obscures changes.
Not just total/free T; monitor health benefits like insulin sensitivity.
Reference Range and Testing
LabCorp: 15-70 ng/dL (roughly 1/10th men's). Low T harder to define near zero; requires sensitive LC-MS assays.
Consider contraceptives suppressing T. Symptoms similar to men.
Lifestyle First
Same as men: micronutrients, adequate calories (avoid starvation/amenorrhea), normal menstrual cycle.
TRT Candidates
Off-label in US (no FDA-approved; Australia has it). Use male formulations (e.g., pea-sized AndroGel on arm) under oversight.
Oral contraceptives suppress to hypo territory; assess if suitable.
Hyperandrogenic women may need suppression (anti-androgens for hirsutism).
Irreversible sides terrifying: voice deepening destroys quality of life for women (unlike men).
For women, irreversible voice deepening can be quality-of-life destroying and cannot be fixed. Cutting-edge doctors may overshoot with aggressive protocols aiming for 200 ng/dL total testosterone, which is too high.
Derek shares anecdote: A respected doctor had a cookie-cutter aggressive protocol that caused his mom's voice to change dramatically within days. They stopped it immediately, and it partially self-regulated, but it could have led to permanent virilization in weeks.
Advice: Be hyper-aware even with knowledgeable doctors. Download a vetted app that monitors voice tone, inflection, deepness in real-time objectively, as daily micro-changes are unnoticed subjectively.
Changes like hair loss, facial hair are insidious but quick; women may overlook due to feeling great on protocol. Lower doses can provide same symptom relief.
"You got to be careful if you're a woman like replacing test especially cuz it's uh there are a lot of doctors that like especially the ones have cookie cutter protocols that are like you know everyone should get to a total te of you know 200 to 300"
Women's testosterone range is narrow; even sensitive tests may be inaccurate, leading to unnecessary TRT (off-label, no FDA approval for women). Feels like wild west.
Nuanced Approach to Women's Testosterone
Testosterone decline in menopause slower than estrogen/progesterone plummet; much mediated by adrenal synthesis and peripheral conversion, not all ovarian. Varies by genetics; some fine with just estrogen/progesterone.
No cookie-cutter protocols. Educate yourself before starting off-label therapy; know ideal protocol. Find responsible doctor; do due diligence.
Podcasts help educate.
Alternative: If adrenal insufficiency or low DHEA, supplement DHEA (women's total T: 15-70 ng/dL; significant chunk from DHEA conversion). Use DHEAS as proxy biomarker.
DHEA restores T suppressed by combined oral contraceptives (e.g., from 70 to 30 ng/dL, back to 70).
DHEA dosing: 25-50 mg per studies; start lower. Treat as androgen (acne, side effects possible). Women respond favorably when warranted.
Testosterone doses tiny (cream/gel blip). Know target reference range, symptom relief; consult trusted community sources, multiple opinions, avoid cowboy docs.
Hair loss from androgenic alopecia (DHT-mediated miniaturization of follicles).
Despite advanced tech (AI, ApoB crushing for ASCVD), hair loss unexplained beyond DHT inhibition.
Myths: Viral articles (UCLA rodents, sulforaphane, broccoli sprouts on head) don't work; Reddit experiments fail.
Mechanism: Tissue-specific 5-alpha reductase high in scalp skin converts testosterone to DHT (highest local concentration except prostate, scrotum). Causes miniaturization.
Fringe cases: Nutrient deficiencies, hypothyroidism; usually pattern hair loss.
If delayed, fibrosis makes recovery impossible (no regrowth until hair cloning). Preventative/proactive like ASCVD; cumulative like arterial plaque.
"Why is it that when your DHT levels are at their highest, when you're young, you have no hair loss, but then when you're old, you have hair loss? It's like the same reason that you've been stacking plaque in your arteries since you were like a teenager. Like, it's cumulative."
Downstream: TGF-beta, Wnt pathway; follicle starves, anagen phase shortens, apoptosis, fibrosis.
Transplanted follicles from resistant areas (e.g., back) don't miniaturize in bald zones.
Susceptibility: Genetics; rare to keep full hair at 50+ (outlier: host's dad full thick white hair).
Inheritance: Thought mom's dad, but not always.
Proactive Hair Loss Prevention
Weigh risk-reward of DHT inhibition; earlier intervention = milder protocol. Higher hormones amplify scalp androgen load (5AR density highest there).
Basis of drugs: 5-alpha reductase gene mutation (pseudohermaphrodites): normal T, low DHT → no temporal recession, poor secondary sex characteristics.
Testosterone also affects but less; early 5AR inhibition sufficient.
Won't notice until 25%+ loss; 70-100k follicles; 10-30k loss visible.
Literature: Finasteride, dutasteride side effects similar to placebo in large studies (media overblown; minority devastated).
Assess risk: Low-androgen baseline + hair loss = higher side effect risk vs. vital high-androgen.
Some impact inevitable (e.g., nitric oxide, erections, fertility via intratesticular DHT/spermatogenesis); studies show low prevalence.
Dutasteride (near-full DHT inhibition) similar profile to finasteride (60-70%, type 1/2 inhibition; dutasteride all 3).
ROI: Read studies; individual response varies (like Tylenol).
Most effective: DHT inhibition. High-dose dutasteride nearly prevents loss.
Tailor: Susceptibility dictates; add topical anti-androgens, topical 5AR.
Minoxidil, pumpkin seed oil, saw palmetto don't inhibit miniaturization.
Women: PCOS quick; rare androgenic vs. alopecia areata, Hashimoto's, deficiencies.
Evidence: Men lose hair aging vs. women; even biohackers bald without DHT drugs.
The capacity to which you address hair loss is dictated by genetics, androgen load in the scalp, and free androgenic signaling. Risk profile is based on individual tolerance and interpretation of scientific literature.
Adjunctive Treatments like Ketoconazole Shampoo
Once miniaturization potential is attenuated through androgen-related activity in the scalp, adjuncts like ketoconazole shampoo provide additive protection. It's a mild anti-androgen, equivalent to 2% minoxidil in hair growth results via a different mechanism—significant for an over-the-counter shampoo. It attenuates dandruff and seborrheic dermatitis, improves scalp environment (especially with fungal overgrowth), acts as a mild 5-alpha reductase inhibitor and topical anti-androgen. Good shampoo without finasteride or dutasteride risk profile. Typically insufficient alone unless mildly prone; layer with pharmaceutical 5-alpha reductase inhibition.
Minoxidil as FDA-Approved Growth Stimulant
Minoxidil works reliably but hit-or-miss based on enzymatic conversion to minoxidil sulfate in the scalp via sulfotransferase enzyme. Inadequate activity leads to non-responders despite full dose. Issues include unhealthy scalp environment, unclean scalp, insufficient dose, or formulation. Proper high-dose use limits by enzymatic pathway.
Upregulating Sulfotransferase: Tretinoin and Microneedling
- Compound minoxidil with tretinoin to upregulate sulfotransferase for better conversion.
- Microneedling dramatically turns non-responders into responders or multiplies results via improved absorption and upregulated enzyme activity through micro-damage. Studies show regrowth even from scalp burns recruiting growth factors.
Originally Loniten, an oral blood pressure drug (potassium channel opener) causing hypertrichosis, fainting, low blood pressure, water retention. Repurposed topically, avoids most systemic effects. Oral version risky: liver sulfotransferase causes pericardial effusion, water retention, electrolyte dysregulation, arrhythmias, chest pains. Dermatologists prescribe low-dose oral haphazardly. Topical is benign, over-the-counter (Amazon, Costco), similar benefits but requires adherence.
Escalation for Topical Minoxidil Efficacy
Elevate with tretinoin-compounded minoxidil or microneedling. Start topical minoxidil; if no response, add weekly microneedling (0.6mm depth now sufficient vs. old 1.5mm drawing blood; quicker recovery, less cosmetic issue). Newer literature supports 0.6mm efficacy.
No extra drugs; quick scalp recovery. Potential downstream issues unknown but data positive. Used on face for skin effects too. Dermatologist studies combine with stem cell growth factors for hair regrowth via better absorption.
Microneedling + Minoxidil Synergy
Majority benefit from ensuring absorption; microneedling alone vs. minoxidil alone inferior to combo (4x results in studies). Ensures drug reaches target.
Neurological via neurotransmitter imbalance, allopregnanolone inhibition (implicated in postpartum depression; brexanolone restores it). GABAergic/anxiolytic signaling disruption; severity varies.
Post-Finasteride Syndrome (PFS) and Nocebo Effect
Post-finasteride syndrome real but post-dutasteride syndrome rare (media-driven). Significant nocebo effect: reading side effects convinces users of issues. Genes/SNPs (e.g., via 23andMe) predict placebo/nocebo susceptibility.
"You can actually nocebo yourself into real side effects by believing you have them."
Growth stimulant only; does nothing to attenuate DHT-induced miniaturization. Ketoconazole mild but insufficient; need finasteride, dutasteride, or topical anti-androgens. Cosmetic offset via growth, but eventual net loss if no anti-androgen. Delays visual loss; transplants/transplants bide time. Complete bypass requires scalp-level anti-androgen effect (mild exaggeration: like turning scalp female).
On dutasteride for years: no detriment to cognition, sexual function. Respected anti-aging/longevity figures use it. Used for BPH up to 2.5mg daily with low minor side effects; decade-plus follow-ups exist.
Speculation on Longevity Benefits
DHT most androgenic hormone; inhibiting it may increase longevity (decreases stimulation). No muscle benefit in adults (studies: dutasteride + supra testosterone no impact on strength/hypertrophy). On TRT (800 total T, high-normal free T), dutasteride may counter excitotoxicity/cardiotoxicity via increased local estradiol (15-20%; vasoprotective, antioxidant). Speculative; anti-aging studies on finasteride/dutasteride exist. Interesting for TRT + blockers on life expectancy/CVD.
Individual decision; side effects real. Balding depression may outweigh risks for some. Do not follow podcast advice for hormone-modulating drugs; respect them.
Podcast Wrap-Up
Hours-long discussion (8 hours, first back-to-back double pod). Thanks to Derek.
Follow Derek:
- YouTube/Podcast: More Plates More Dates
- Healthcare: Marek Health (marekhealth.com; @marekhealth social)
- Twitter: @DerekFitness
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