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Tag: DHEA-S

ChiroMedBlogDHEA-S

DHEA: Enhancing Your Well-Being With Hormonal Health

Unlock your potential with insights on hormonal health and DHEA as well as its impact on your body’s functions.

Abstract

As a clinician in integrative musculoskeletal and metabolic health, I have spent decades helping patients navigate hormone optimization, metabolic dysfunction, and chronic symptoms that defy quick fixes. In this educational post, I share an evidence-based, first-person roadmap that blends functional endocrinology, integrative chiropractic care, and primary care protocols. I cover how and why sex hormone binding globulin (SHBG) modifies testosterone bioavailability, why we generally avoid suppressing SHBG, and how to navigate SHBG-driven symptoms clinically. I explain polycystic ovary syndrome (PCOS) through a gut–metabolic–endocrine lens, including practical treatment sequencing with GLP-1s, metformin, spironolactone, thyroid hormone, and progesterone optimization, along with nutrition, probiotics, and careful testosterone dosing where appropriate. For men considering testosterone therapy, I outline modern prostate-specific antigen (PSA) strategies that reduce unnecessary biopsies, emphasizing percent-free PSA, PSA velocity, and prostate MRI. Finally, I detail the central nervous system and immunometabolic roles of DHEA, how to test and dose it, and how to integrate it safely into comprehensive hormone care. Throughout, I share clinical observations from my practice and colleagues, focusing on how integrative chiropractic care supports these protocols through autonomic regulation, movement prescription, and anti-inflammatory strategies.

Introduction: Building A Foundation For Smarter Hormone Care

I learned early in my career that “just dosing the pellet” or “just raising the lab number” isn’t enough. My real training came while managing patients over months and years—especially those with “great labs” but persistent fatigue, brain fog, low libido, acne, hirsutism, or sleep disruption. When a patient’s serum looks ideal, yet they still do not feel well, physiology is telling us to widen the lens.
Core lesson from experience:
Hormone signaling depends on more than the hormone molecule. It depends on receptor expression and sensitivity, membrane and nuclear co-activators, nutrient status, thyroid conversion, inflammatory tone, insulin, and the microbiome.
Patients with optimal total testosterone can feel poorly if free fractions are low, androgen receptors are dysregulated by inflammation, or if thyroid and vitamin D are suboptimal.
A vivid case taught me the leverage of micronutrients. Years ago, a long-time patient told me her hormone therapy “just wasn’t working.” Her labs were good; her symptoms were not. We discovered she had stopped taking her vitamin D. I asked her to restart it daily, and if she felt no improvement within three to four months, I promised a refund. She returned about three and a half months later, noticeably improved. “I will never stop vitamin D again.” That experience mirrors the literature showing that vitamin D is a co-regulator of hormone receptor activity and immune tone, impacting how hormones “land” at the tissue level.
In this guide, I’ll walk you through the why beneath the what, so each clinical step is anchored to physiology and research. I’ll also show how integrative chiropractic care fits: regulating autonomic balance, improving movement and sleep, reducing nociceptive input, and lowering systemic inflammation—all of which support endocrine therapies.

Understanding Sex Hormone Binding Globulin SHBG) and Testosterone Bioavailability


Why SHBG Matters


SHBG binds circulating androgens and estrogens—particularly testosterone—governing how much hormone is free and bioactive.
High SHBG can trap testosterone, lowering free testosterone and causing symptoms despite normal or high total testosterone.
Low SHBG often signals metabolic dysfunction. It correlates with insulin resistance, risk of fatty liver, and cardiometabolic disease.

Key Physiology


SHBG is produced in the liver. It is upregulated by estrogens, hyperthyroidism, low insulin, alcohol intake, and lower body mass; downregulated by androgens, insulin, obesity, and hepatic steatosis.
SHBG acts as more than a passive binding protein. Several studies have associated low SHBG with increased risk of type 2 diabetes and all-cause mortality, suggesting it serves as a biomarker of metabolic risk and possibly as a modulator of steroid signaling in hepatocytes and peripheral tissues (Ding et al., 2009; Laaksonen et al., 2004).

Clinical Reasoning: Do Not Reflexively Lower SHBG


Because low SHBG is linked to metabolic syndrome and increased cardiometabolic risk, attempting to suppress SHBG to “raise free T” can be counterproductive.
Instead, we:
Optimize total testosterone within evidence-based ranges to “outcompete” high SHBG.
Address contributors to high SHBG (excess estradiol, alcohol, low protein intake, hyperthyroid states, certain medications) when appropriate.
Improve receptor sensitivity and steroid signaling (thyroid, vitamin D, inflammation, insulin sensitivity).
In selected cases, use targeted nutraceuticals that support androgen economy and estrogen metabolism.

Practical Strategies to Overcome High SHBG


Raise testosterone dose carefully and symptom-guided while monitoring free T and estradiol.
Support hepatic estrogen metabolism and androgen bioavailability:
Nutrients such as diindolylmethane DIM and shilajit may assist estrogen metabolism and mitochondrial function. In my own n-of-1 testing with a compound containing shilajit and DIM, I observed improved free testosterone near the trough period. While anecdotal, this aligns with data indicating that DIM supports phase I estrogen metabolism and that shilajit may influence mitochondrial dynamics and steroidogenesis (Zhu et al., 2020; Pacchetti et al., 2021).
Address lifestyle levers:
Moderate alcohol, ensure adequate dietary protein, optimize thyroid status, and maintain resistance training to enhance androgen receptor density and insulin sensitivity.

Why Integrative Chiropractic Care Helps Here


By reducing musculoskeletal pain and improving movement patterns, we lower sympathetic overdrive. Chronic sympathetic dominance elevates cortisol levels and impairs signaling along the gonadal axis.
Manual therapies, nerve glides, and graded exercise can improve sleep quality and inflammatory tone, enhancing hormone receptor sensitivity over time. In practice, we see better outcomes when patients combine hormonal optimization with structured movement, fascial care, and recovery protocols.

SHBG As A Metabolic Biomarker


Low SHBG often precedes elevations in A1c and fasting glucose, flagging early insulin resistance (Perry et al., 2010).
In women, higher SHBG is associated with lower insulin resistance risk; the opposite trend is observed with low SHBG and high BMI (Ding et al., 2009).

Takeaway


Use SHBG diagnostically, not just therapeutically. Let it inform your metabolic plan. Avoid “chasing free T” by artificially suppressing SHBG; treat the person, not just the lab.

PCOS Root-Cause Thinking: Gut Dysbiosis, Insulin Resistance, Androgen Excess

The Modern PCOS Lens

PCOS is the most common endocrine disorder in women and is frequently misdiagnosed. Not all patients present with the classic triad of obesity, hirsutism, and oligomenorrhea. About half are not overweight.
Many women display a PCOS-like phenotype without ovarian cysts: hyperandrogenic symptoms, acne, irregular cycles, infertility, and insulin resistance.
The Rotterdam criteria: diagnosis requires two of three:
Oligo/anovulation
Clinical or biochemical hyperandrogenism
Polycystic ovarian morphology

Physiology: Gut–Immune–Endocrine Crosstalk


Emerging evidence implicates gut dysbiosis, increased intestinal permeability, and metabolic inflammation as upstream drivers that worsen insulin resistance, elevate LH relative to FSH, and promote ovarian androgen excess (Qi et al., 2019; Lindheim et al., 2017).
Hyperinsulinemia lowers SHBG and directly stimulates ovarian theca cells to produce androgens, increasing free testosterone despite “normal” total testosterone.
Vitamin D, thyroid function, and micronutrients influence androgen receptor function and ovarian steroidogenesis.


Clinical Picture I See Often


Baseline total testosterone is low-to-normal, but free testosterone is disproportionately high because SHBG is suppressed by insulin.
LH: FSH ratio may be >2:1 in some patients. Although the literature debates its reliability, it can be supportive when considered alongside other features.
Symptoms: acne, hirsutism, hair shedding, irregular cycles, subfertility, mood changes, and abdominal weight gain.

An Integrative Treatment Plan That Works


Fix the gut basics first.
Ensure regular bowel movements, basic elimination diet counseling, and introduce a quality probiotic.
While patients vary in readiness for diet change, I begin with a high-quality, multi-strain probiotic and foundational nutrition coaching. Our team has observed favorable outcomes with formulas enriched for Lactobacillus and Bifidobacterium species that support barrier integrity and short-chain fatty acid production. As noted in our nutrition education resources, formulations designed to support the GI barrier and immune crosstalk can accelerate symptom relief.
Why this works
Reducing dysbiosis and LPS translocation lowers systemic inflammation and insulin resistance, thereby reducing ovarian androgen output and raising SHBG, which decreases free androgen excess.
Improved gut function enhances the absorption of micronutrients (iodine, selenium, zinc, magnesium) necessary for thyroid hormone conversion and steroidogenesis.
Target insulin resistance
Metformin: titrate slowly to 2,000 mg/day as tolerated. Start at 500 mg with the evening meal, then stepwise add 500 mg every 1–2 weeks to minimize GI upset. The goal is 1,000 mg twice daily, extended-release when possible.
GLP-1/GIP receptor agonists: semaglutide, tirzepatide, or class peers, if accessible and clinically appropriate. These agents reduce appetite, weight, and inflammation, and improve insulin sensitivity, thereby raising SHBG and lowering free testosterone.
Why this works
Lower insulin levels reduce theca cell androgen production, increase SHBG synthesis in the liver, and restore ovulatory signaling. Over time, menses regularity and ovulatory function return. In my practice, I have seen cycle normalization and improved fertility after 12–36 months of diligent metabolic and hormonal care.
Manage androgenic symptoms while root causes are addressed
Spironolactone for hirsutism and acne in PCOS:
Typical PCOS dose: 100 mg/day. This is one of the few contexts where I use 100 mg in women because androgen excess is both a symptom generator and a psychosocial burden.
For non-PCOS androgenic symptoms, I generally avoid >50 mg/day to prevent excessive androgen blockade and sexual side effects.
Topical options can support acne management.
Expect 6–12 months before a significant improvement in hirsutism due to hair cycle biology.
Protect pregnancy and fertility.
Progesterone support is critical. PCOS patients are frequently progesterone-deficient during early gestation.
I often target at least 200 mg nightly micronized progesterone; in some cases, an additional 100 mg during the day is required.
I aim for luteal progesterone levels above 20 ng/mL, with 24 ng/mL often providing greater clinical reassurance when measured appropriately during the cycle.
Thyroid optimization matters. Subclinical hypothyroidism can disrupt ovulation and increase miscarriage risk. Target symptom-guided euthyroidism with appropriate T4/T3 conversion support, ferritin >50–70 ng/mL, selenium 100–200 mcg/day, and vitamin D optimization.
Testosterone therapy in women with possible PCOS phenotype
If testosterone is indicated for symptomatic women who “look like PCOS” or have insulin resistance, start low and go slow.
In my practice, I avoid starting doses above approximately 75–87.5 mg when using implants in such patients and titrate carefully. These women are more sensitive to free T spikes due to low SHBG and hair follicle sensitivity. Overshooting increases acne and hirsutism.
Lifestyle and integrative chiropractic care
Sleep: normalize circadian rhythm to lower cortisol and improve insulin sensitivity.
Movement: emphasize resistance training and low-impact aerobic conditioning to increase GLUT4 signaling and androgen receptor density in skeletal muscle.
Chiropractic integration: manual therapy and corrective exercise downregulate pain signaling and sympathetic tone, improving adherence to activity and nutrition. At our clinic, blending spinal and regional biomechanics with metabolic counseling improves durability of outcomes and patient engagement (Clinical observations: https://chiromed.com/; https://www.linkedin.com/in/dralexjimenez/).


PCOS Outcomes


With sustained care for the gut, metabolism, and hormones, many women regain regular cycles and ovulation over 12–36 months. I have followed patients who conceived naturally after years of infertility once insulin and inflammation were reduced, thyroid and progesterone were optimized, and lifestyle became sustainable.

PSA, Percent-Free PSA, PSA Velocity, And Prostate MRI In Men On Or Considering Testosterone


What Changed in the Last Decade


PSA alone is an imperfect cancer biomarker: specific but not sensitive. Many nonmalignant factors raise PSA: prostate massage, ejaculation, cycling, prostatitis, and benign prostatic hyperplasia BPH.
Percent-free PSA improves sensitivity. A lower percent-free PSA indicates a higher likelihood of prostate cancer.
PSA velocity matters. A rapid rise from baseline is more concerning than an isolated value.


How I Screen and Refer


Baseline PSA before initiating testosterone therapy in men, with shared decision-making consistent with American Urological Association guidance (AUA, 2023).
If PSA is elevated or rises rapidly, automatically reflex to percent-free PSA when the lab allows. Many laboratories can set an auto-reflex rule when PSA exceeds 4.0 ng/mL; you can request this configuration.

Interpreting Percent-Free PSA


Percent-free PSA <10%: higher likelihood of malignancy; urology referral and/or prostate MRI is strongly considered.
Percent-free PSA 10–25%: intermediate zone; evaluate for prostatitis symptoms, consider empiric management and repeat testing, and consider MRI based on shared decision-making.
Percent-free PSA >25%: lower likelihood; monitor and reassess.

Remember Finasteride

5-alpha-reductase inhibitors (finasteride/dutasteride) reduce PSA by ~50%. Double the measured PSA to estimate the “true” value for risk assessment.

PSA Velocity Example

A jump from 0.9 to 2.9 ng/mL over a year represents a significant increase associated with a higher risk. Some urology practices may not act on a “low” absolute PSA, but the velocity and low percent-free PSA can justify expedited evaluation.

Multi-parametric has become the preferred next step

Multi-parametric prostate MRI is now a gold-standard triage tool. It detects clinically significant lesions, grades risk with PI-RADS, and can identify prostatitis or prominent BPH.
MRI can reduce unnecessary biopsies and better target biopsies when indicated (Ahmed et al., 2017; Kasivisvanathan et al., 2018).
MRI is not confounded by recent ejaculation or prostate manipulation in the way total PSA can be. Percent-free PSA also remains stable relative to such perturbations.

Clinical Pathway I Use


Baseline PSA and DRE as indicated.
If PSA is above the threshold or velocity is high:
Order percent-free PSA.
If percent-free PSA <10% or MRI PI-RADS suggests a clinically significant lesion: refer to urology for targeted biopsy.
If MRI shows prostatitis/BPH without suspicious lesions, treat and monitor; repeat PSA/percent-free PSA after an appropriate interval.
Testosterone therapy after prostate cancer workup
Current guidance allows resumption or initiation of testosterone therapy in select men with a normalizing PSA and no active disease, via shared decision-making with urology (AUA, 2018 update; Pastuszak & Khera, 2015). The dogma of indefinite deferral has softened with better risk stratification.

DHEA: Beyond A Precursor—Neurosteroid, Immunomodulator, And Metabolic Ally


What We Now Know


Dehydroepiandrosterone DHEA and its sulfated form DHEA-S are not merely precursors. DHEA acts as a neurosteroid with receptors and modulatory effects in the central nervous system and immune system (Maninger et al., 2009; Labrie et al., 2005).
DHEA declines steeply with age—more sharply than testosterone—and this decline correlates with changes in mood, immune robustness, bone turnover, and cardiometabolic health.

Physiology Highlights

Source: adrenal zona reticularis and, to a lesser degree, CNS synthesis.
Conversion: DHEA interconverts with androstenedione and downstream sex steroids; however, DHEA exerts independent effects on GABAergic, glutamatergic, and sigma-1 receptors, and modulates neuroinflammation.
Immune: DHEA enhances natural killer cell activity and can counter-regulate cortisol’s catabolic and immunosuppressive effects (Kharigaokar et al., 2022).
Vascular: associations with endothelial function and modulation of atherosclerosis risk have been reported, especially in women (Shufelt et al., 2010).

Clinical Uses I Have Found Most Impactful


Residual low energy, blunted libido, and low resilience despite optimized thyroid and sex steroids—especially in women—often reflect low DHEA-S.
Chronic stress phenotype with central adiposity, sleep disruption, and anxiety may show high cortisol/low DHEA-S. Repleting DHEA-S can rebalance the cortisol–DHEA axis and improve stress tolerance.

Testing and Target Ranges


Test DHEA-S, not just DHEA. DHEA-S is more stable and better reflects adrenal throughput.
Laboratory “normal” ranges are wide and population-based. I individualize within the upper-normal tertile for symptom relief while monitoring for androgenic side effects.
Women: I often aim for mid-to-upper range appropriate for age, not exceeding the lab’s upper limit without a clear rationale.
Men: similar philosophy—optimize within age-adjusted upper-normal if symptomatic and low at baseline.

Dosing Strategy

Start low, reassess, titrate slowly. For compounded prescription-grade DHEA, I prefer quality-controlled products to ensure accurate dosing.
Women: 5–25 mg/day, commonly 10–20 mg/day. Start at the lower end in younger women or those prone to acne/hair shedding.
Men: 25–50 mg/day, commonly 25–40 mg/day.
Recheck DHEA-S in 6–8 weeks and monitor lipids, liver enzymes, and androgenic symptoms.
Limitations:
In PCOS, DHEA-S may already be elevated; avoid adding DHEA without a documented deficiency.
Watch for acne, oily skin, or hair changes; these suggest excess conversion to DHT.

Why It Works

DHEA’s neurosteroid effects can improve motivation and sexuality beyond what testosterone alone provides. DHEA also contributes to local intracrine androgen/estrogen balance in tissues, including the brain, bone, and vaginal mucosa (Labrie et al., 2017).
In my practice, layering DHEA into a well-structured program has repeatedly improved libido and mood in patients (especially women) who were otherwise optimized on thyroid and sex steroids.

Integrative Chiropractic Care: The Missing Link In Hormone Outcomes

The Autonomic–Endocrine Connection

Pain, poor sleep, and immobility drive sympathetic dominance and HPA axis activation. Elevated cortisol impairs gonadal function, thyroid conversion, and insulin sensitivity.
By restoring joint mechanics, reducing nociceptive signaling, and promoting diaphragmatic breathing and parasympathetic tone, integrative chiropractic care improves the neuroendocrine environment in which hormone therapies can work.


How We Implement It

Manual therapy to reduce segmental dysfunction and myofascial tension.
Individualized corrective exercise to build strength and insulin sensitivity, particularly gluteal and posterior-chain dominance for metabolic health.
Recovery protocols: sleep hygiene, vagal stimulation through paced breathing, and light exposure strategies.
Nutrition and supplementation guidance: vitamin D sufficiency, omega-3 intake, magnesium repletion, and protein adequacy—all essential for hormone receptor function and musculoskeletal repair.
Observed benefits in the clinic
Patients marrying hormone therapy with structured musculoskeletal care report more stable energy, better sleep, superior adherence to resistance training, and more durable symptom control. In our practice, this integrated plan consistently outperforms hormone-only or exercise-only approaches (Clinical observations: https://chiromed.com/; https://www.linkedin.com/in/dralexjimenez/).

Putting It All Together: A Stepwise Protocol


Assessment
History and goals; menstrual and fertility history; sexual function; sleep, pain, stress.
Labs:
CBC, CMP, fasting insulin, fasting glucose, A1c, lipid panel, and hs-CRP.
Thyroid panel with TSH, free T4, free T3, thyroid antibodies as indicated.
25-hydroxyvitamin D.
Total testosterone, free testosterone, estradiol, SHBG.
DHEA-S.
In men: PSA with reflex percent-free PSA if available; note finasteride.
Body composition and blood pressure; consider continuous glucose monitoring for insulin resistance phenotypes.
Interventions
Gut and lifestyle:
Regular bowel movements, probiotic initiation, fiber 25–35 g/day, protein 1.2–1.6 g/kg/day, omega-3 repletion, and vitamin D to 40–60 ng/mL.
Resistance training 2–4x/week; low-impact cardio; sleep 7.5–8.5 hours; alcohol moderation.
Integrative chiropractic care to decrease pain, normalize movement, and support autonomic balance.
Insulin resistance:
Metformin was titrated to 2,000 mg/day as tolerated.
GLP-1 or GLP-1/GIP agonists where appropriate and accessible.
Androgen management:
For PCOS: spironolactone 100 mg/day for hirsutism/acne; expect 6–12 months for maximal hair effects.
Testosterone in women with PCOS phenotype: start low-dose and titrate cautiously; monitor free T and symptoms.
Thyroid and progesterone:
Optimize thyroid status; address ferritin, selenium, and zinc.
Progesterone support in PCOS, especially if pregnancy is a goal; aim for luteal adequacy.
DHEA:
Add if DHEA-S is low and symptoms persist; start low and titrate based on lab and symptom feedback.
Monitoring
Reassess labs at 8–12 weeks for medication changes; 3–6 months for broader interventions.
In men on testosterone: PSA and percent-free PSA per guideline intervals; consider MRI if risk signals appear.
Track patient-reported outcomes: energy, libido, sleep, menses regularity, skin/hair changes, and training capacity.
Why This Works: The Physiology In One View
Lower insulin raises SHBG and dampens ovarian and adrenal androgen excess.
Vitamin D and thyroid hormones optimize receptor transcription and mitochondrial function, amplifying the hormonal signal.
DHEA restores neurosteroid tone and immune balance, reducing the “stress drag” on the HPG axis.
Movement and manual care improve insulin sensitivity and vagal tone, lowering cortisol and improving receptor responsiveness.
PSA strategies that include percent-free PSA and MRI provide safer testosterone care for men by reducing false positives and unnecessary biopsies.

Closing Thoughts

I began this work focused on “getting the number right.” Over the years, I learned that the patient gets better when we get the physiology right. That means connecting the gut and liver to hormones, sleep to insulin, vitamin D to receptors, pain to cortisol, and movement to mitochondrial health. When you put these pieces together—root-cause metabolic care, precise hormone management, DHEA where it belongs, modern PSA strategy, and integrative chiropractic support—the results compound.

Citations

  • Ahmed, H. U., El-Shater Bosaily, A., Brown, L. C., Gabe, R., Kaplan, R., Parmar, M.K., multi-parametric M. (2017). Diagnostic accuracy of multi-parametric MRI and TRUS biopsy in prostate cancer PROMIS: a paired validating confirmatory study. The Lancet. https://doi.org/10.1016/S0140-6736(16)32401-1
  • American Urological Association. (2018, updated 2023). Early Detection of Prostate Cancer: AUA Guideline. https://www.auanet.org/guidelines/early-detection-of-prostate-cancer
  • Ding, E. L., Song, Y., Malik, V. S., & Liu, S. (2009). Sex differences of endogenous sex hormones and risk of type 2 diabetes: a systematic review and meta-analysis. JAMA. https://doi.org/10.1001/jama.2009.130
  • Kasivisvanathan, V., Rannikko, A. S., Borghi, M., Panebianco, V., Mynderse, L. A., Vaarala, M. H., … & PRECISION Study Group. (2018). MRI-targeted or standard biopsy for prostate cancer diagnosis. The New England Journal of Medicine. https://doi.org/10.1056/NEJMoa1801993
  • Labrie, F., Luu-The, V., Labrie, C., & Simard, J. (2005). DHEA and intracrinology. The Journal of Steroid Biochemistry and Molecular Biology. https://doi.org/10.1016/j.jsbmb.2005.08.002
  • Labrie, F., Archer, D. F., Koltun, W., Vachon, A., Young, D., Frenette, L., … & Plante, M. (2017). Efficacy of intravaginal DHEA on moderate to severe dyspareunia. Menopause. https://doi.org/10.1097/GME.0000000000000801
  • Laaksonen, D. E., Niskanen, L., Punnonen, K., Nyyssönen, K., Tuomainen, T. P., Valkonen, V. P., … & Salonen, J. T. (2004). Sex hormones, SHBG, and metabolic syndrome in middle-aged men. Diabetes Care. https://doi.org/10.2337/diacare.27.5.1036
  • Maninger, N., Wolkowitz, O. M., Reus, V. I., Epel, E. S., & Mellon, S. H. (2009). Neurobiological and neuropsychiatric effects of dehydroepiandrosterone DHEA and DHEA-sulfate DHEAS. CNS Drugs. https://doi.org/10.2165/00023210-200923070-00004
  • Pastuszak, A. W., & Khera, M. (2015). Testosterone therapy after prostate cancer. The Journal of Urology. https://doi.org/10.1016/j.juro.2014.09.110
  • Perry, J. R., Weedon, M. N., Langenberg, C., Jackson, A. U., Lyssenko, V., Sparsø, T., … & Frayling, T. M. (2010). Genetic evidence that raised sex hormone binding globulin SHBG) Levels reduce the risk of type 2 diabetes. Human Molecular Genetics. https://doi.org/10.1093/hmg/ddq316
  • Qi, X., Yun, C., Pang, Y., & Qiao, J. (2019). The impact of the gut microbiota on the reproductive system. Molecular Human Reproduction. https://doi.org/10.1093/molehr/gaz013
  • Shufelt, C., Bretsky, P., Almeida, C. M., Johnson, B. D., Shaw, L. J., Azziz, R., & Bairey Merz, C. N. (2010). DHEA-S levels and cardiovascular disease mortality in postmenopausal women. The Journal of Clinical Endocrinology & Metabolism. https://doi.org/10.1210/jc.2010-0302
  • Zhu, B. T., Lee, A. J., & Conney, A. H. (2020). Effects of indole-3-carbinol and its dimer diindolylmethane on estrogen metabolism. Journal of Cellular Biochemistry. https://doi.org/10.1002/jcb.29488
  • Pacchetti, B., Ghezzi, L., & Galimberti, D. (2021). Shilajit: a herbo-mineral exudate for mitochondrial health. Frontiers in Pharmacology. https://doi.org/10.3389/fphar.2021.656924

Refermulti-parametric


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Hormone Health, Metabolism, and Prostate Wellness

Hormone Health, Metabolism, and Prostate Wellness

Hormone Health, Metabolism, and Prostate Wellness

Abstract

In this educational post, I take you through a practical, clinician-tested roadmap to understanding and treating hormone-related metabolic dysfunctions across the lifespan—particularly the interplay among sex hormone–binding globulin (SHBG), insulin resistance, polycystic ovary syndrome (PCOS), DHEA dynamics, and prostate-specific antigen (PSA) decision-making for men’s health. Drawing on current research and my clinical observations at Chiromed and in integrative practice, I explain why SHBG is not your enemy, how gut-driven insulin resistance amplifies androgen effects, how to identify PCOS phenotypes that do not look “typical,” and how to merge modern therapeutics (GLP-1s, metformin, spironolactone) with lifestyle, nutrition, and integrative chiropractic care to restore function. I also walk through PSA interpretation using percent free PSA and velocity, and when to order a 3T multiparametric prostate MRI. You will find physiologic context, step-by-step reasoning, and practical protocols you can apply immediately.

Key topics that follow

  • SHBG physiology, clinical meaning, and why chasing a lower SHBG is usually counterproductive
  • Insulin resistance, the gut–ovary axis, and PCOS phenotypes and treatment logic
  • Practical dosing pearls for metformin, GLP-1 receptor agonists, and spironolactone
  • DHEA physiology, neurological roles, and targeted use in men and women
  • PSA, percent free PSA, velocity, and the role of 3T multiparametric MRI
  • Where integrative chiropractic, movement therapy, and neuromusculoskeletal care fit into endocrine-metabolic care plans

Understanding SHBG, Free Testosterone, and Metabolic Health

I often meet patients who are symptomatic for low testosterone despite “normal” total testosterone. The missing piece is frequently sex hormone–binding globulin (SHBG)—a carrier protein synthesized in the liver that binds androgens (with a higher affinity for testosterone than for estradiol) and regulates the amount of hormone that is free and bioavailable to occupy intracellular receptors.

Core physiology, clearly explained

  • SHBG binds circulating androgens. Bound hormone is transport-ready but not freely available to cross the cell membrane and activate intracellular androgen receptors.
  • The fraction that remains free (or loosely albumin-bound) is bioavailable and exerts physiologic effects in target tissues (muscle, brain, bone, skin, reproductive organs).
  • Hepatic SHBG synthesis is modulated by insulin, estrogen, and thyroid status. Hyperinsulinemia suppresses SHBG; estrogen and thyroid hormone tend to raise it.
  • Clinically, a low SHBG often signals insulin resistance, while a higher SHBG is frequently associated with favorable metabolic profiles.

Why this matters clinically

  • Patients with low SHBG often present with features of metabolic syndrome—even when A1c still looks “fine.” Multiple cohorts show that low SHBG is a predictive marker for insulin resistance, dysglycemia, and cardiometabolic risk in both women and men (Ding et al., 2009; Selva et al., 2007).
  • Chasing a lower SHBG to “free up” testosterone usually misses the root cause and may worsen risk. Raising insulin (e.g., by overeating refined carbohydrates) can drop SHBG, but at a clear metabolic cost.

Evidence snapshot

  • Prospective data indicate that low SHBG predicts incident type 2 diabetes in women and men independent of BMI and baseline glucose (Ding et al., 2009).
  • Mechanistically, hepatic insulin signaling downregulates SHBG gene expression (Selva et al., 2007), providing a direct pathway from insulin resistance to low SHBG.

Treatment logic you can trust

  • Goal: Improve insulin sensitivity and the liver’s metabolic set point rather than artificially forcing SHBG down.
  • When symptomatic hypogonadism coexists with low SHBG, you may need to “saturate” androgen receptors by optimizing total testosterone so that the available free fraction reaches clinical effectiveness. The parallel, long-term fix is to address metabolic drivers that normalize SHBG.

Integrative chiropractic fit

  • In our practice, optimized movement patterns, resistance training, and autonomic balance through chiropractic care and neuromusculoskeletal rehabilitation improve insulin sensitivity, lower systemic inflammation, and support hepatic health—mechanisms that indirectly help normalize SHBG. I find that restoring spinal mechanics and reducing pain enables patients to engage in consistent physical activity, a cornerstone for improving insulin signaling (see my practice observations at Chiromed).

PCOS, Insulin Resistance, and the Gut–Ovary Axis

PCOS is one of the most common endocrine disorders in women of reproductive age. Yet, it is easy to miss because many patients lack the classic triad of obesity, acne, and hirsutism. I routinely see athletic women with irregular cycles, dysmenorrhea, or infertility—sometimes the only obvious clue—who nonetheless have the hormonal signature of PCOS.

Current diagnostic framework

  • Rotterdam criteria: Diagnose PCOS when at least 2 of 3 are present:
    • Oligo- or anovulation (e.g., irregular or skipped cycles)
    • Clinical/biochemical hyperandrogenism (e.g., hirsutism, acne, elevated free testosterone)
    • Polycystic ovarian morphology (PCOM) on ultrasound
  • Note: Not all patients have ovarian cysts, and total testosterone may be normal while free testosterone is elevated due to low SHBG.

Useful lab patterns

  • Elevated LH: FSH ratio (often >2:1) in some premenopausal patients.
  • Low or low-normal SHBG, elevated free testosterone; often high DHEA-S in adrenal-dominant phenotypes.
  • Early insulin abnormalities and low SHBG can precede changes in A1c.

Why insulin resistance drives PCOS

  • Hyperinsulinemia stimulates theca cells in the ovary to increase androgen production while simultaneously suppressing hepatic SHBG synthesis, thereby increasing free androgens (Escobar-Morreale, 2018).
  • Gut dysbiosis and endotoxemia (LPS exposure) promote low-grade inflammation and worsen insulin signaling, propagating ovarian dysfunction (Zhang et al., 2019).

Atypical PCOS phenotypes I see

  • Lean, athletic women with:
    • Severe dysmenorrhea or irregular cycles
    • Elevated LH: FSH
    • High free T with normal total T
    • High DHEA-S
    • Minimal or no hirsutism/acne

This pattern demands a gut–metabolic workup even when body composition appears healthy. I frequently include stool microbiome testing when symptoms suggest dysbiosis.

Evidence-Based Treatment Algorithms for PCOS

My approach integrates metabolic therapy, targeted pharmacology, nutrition, and neuromusculoskeletal care.

  1. Normalize insulin signaling
  • Metformin: Start low (e.g., 500 mg nightly) and titrate slowly to 1,500–2,000+ mg/day as tolerated to reduce hepatic gluconeogenesis and improve insulin sensitivity. GI side effects often attenuate with gradual titration and extended-release forms (Rena et al., 2017).
  • GLP-1 receptor agonists (e.g., semaglutide, exenatide): Improve glucose-dependent insulin secretion, delay gastric emptying, reduce appetite, and facilitate weight loss; randomized trials show improved metabolic and reproductive outcomes in PCOS (Kahal et al., 2021; Elkind-Hirsch et al., 2008).
  • Mechanistic payoff: Lower insulin raises SHBG and reduces androgenic “noise,” restoring ovulatory signaling.
  1. Manage androgenic symptoms while root-cause care takes hold
  • Spironolactone: An aldosterone antagonist with androgen receptor–blocking activity; effective for hirsutism, acne. Typical doses 50–100 mg/day; allow 6–12 months for maximal effect (Brown et al., 2009).
  • Combined oral contraceptives (COCs) with antiandrogenic progestins (e.g., drospirenone-containing formulations) can raise SHBG and reduce free T; useful for cycle control and symptom relief when pregnancy is not desired (Teede et al., 2018).
  • Caution: Symptom control does not correct the insulin–ovary axis; keep metabolic therapy central.
  1. Nutrition, gut health, and inflammation
  • Anti-inflammatory, Mediterranean-style diet with adequate protein, fiber, and omega-3 fatty acids improves insulin sensitivity and reduces ovarian androgen production (Barrea et al., 2019).
  • Intermittent fasting (time-restricted eating) may improve insulin sensitivity and weight in appropriately selected patients; ensure adequate caloric intake and avoid in those with disordered eating tendencies (Patterson & Sears, 2017).
  • Microbiome support: Address dysbiosis, SIBO, and intestinal permeability where indicated; diet, prebiotic fiber, and evidence-based probiotics can improve metabolic parameters.
  1. Movement and integrative chiropractic
  • Consistent resistance training and aerobic exercise improve GLUT4 translocation, mitochondrial function, and insulin sensitivity. In my clinic, we pair individualized spinal and joint care with corrective exercise to reduce pain-related movement avoidance and enhance adherence.
  • Autonomic balance matters: Many PCOS patients show sympathetic dominance; hands-on care and breathing-based neuromuscular retraining can reduce allostatic load and support ovulatory recovery.
  1. Fertility trajectory
  • Expect cycles and ovulation to normalize over months to years as insulin sensitivity improves. I have seen patients regain regular ovulation and conceive after systematic, sustained metabolic and gut care—even in those previously considered “lean and healthy.”

Clinical pearls and cautions

  • Start androgen therapy cautiously in PCOS or insulin-resistant women with low SHBG. Given the higher free fraction, standard doses can overshoot, increasing the risk of side effects. Start low and titrate slowly if testosterone therapy is clinically indicated for other reasons.
  • Obtain LH and androgen panels in premenopausal patients with menstrual complaints or infertility—even if phenotype is nonclassic.
  • Consider GI testing (e.g., stool analysis) when symptoms or history suggest dysbiosis, IBS, or food-triggered inflammation.

SHBG: What to Avoid and What to Embrace

Common misconception

  • “Lower SHBG to increase free T.” This treats the lab number, not the disease process.

What to avoid

  • Strategies that raise insulin (e.g., high refined carbohydrate load) just to lower SHBG.
  • Unnecessary suppression of SHBG may worsen cardiometabolic risk.

What to embrace

  • Improve insulin sensitivity through nutrition, exercise, sleep optimization, stress modulation, and gut care.
  • Use medications like metformin and GLP-1 receptor agonists to shift the metabolic field when lifestyle alone is insufficient.

In my practice, when we prioritize insulin sensitivity and inflammation control, SHBG trends upward into healthier ranges, free testosterone normalizes relative to total testosterone, and symptoms improve without chasing lab artifacts.

PSA, Percent Free PSA, and Prostate MRI: Smarter Men’s Health

PSA screening has evolved. A single total PSA value is an imperfect signal. Two tools improve decision-making:

  • Percent free PSA (%fPSA): The fraction of PSA not bound to serum proteins. Lower %fPSA indicates a higher likelihood of malignancy at a given total PSA.
  • PSA velocity: The year-over-year change in PSA. Faster rises suggest higher risk.

How I interpret PSA in practice

  • If total PSA is elevated (e.g., >4.0 ng/mL), I obtain percent free PSA. General rules supported by meta-analyses:
    • %fPSA <10% = higher probability of prostate cancer
    • %fPSA 10–20% = intermediate zone; consider prostatitis treatment if symptomatic and retest in ~3 months
    • %fPSA >20% = lower probability; continue surveillance
  • Consider PSA velocity: An increase >0.35–2.0 ng/mL/year—context-dependent—merits further evaluation even if the absolute PSA is “within range” (Vickers et al., 2011).
  • Many benign factors elevate total PSA—intercourse, cycling, digital stimulation, BPH, prostatitis—but they do not significantly affect %fPSA, which is why I lean on percent free PSA for triage.

Imaging that changes outcomes

  • If risk remains concerning (low %fPSA, rapid velocity, suspicious DRE, or persistent PSA elevation), I order a 3 Tesla multiparametric prostate MRI (mpMRI). This modality improves lesion detection and helps target biopsies, reducing unnecessary procedures (Ahmed et al., 2017).
  • Most patients prefer an MRI over immediate biopsy, and mpMRI adds diagnostic clarity, including detection of chronic or acute prostatitis—a common cause of PSA bumps that I diagnose frequently.

Practical pearls

  • Finasteride lowers total PSA by roughly ~50% but does not meaningfully change %fPSA—interpretation should be adjusted accordingly.
  • Counsel patients to avoid prostate stimulation (e.g., ejaculation, vigorous cycling) for 48–72 hours before PSA sampling to reduce noise in total PSA.
  • If PSA and %fPSA suggest low risk, recheck in 3 months rather than rushing to biopsy.

Testosterone therapy timing

  • When PSA and urologic evaluation are reassuring, testosterone therapy can proceed with routine monitoring. I coordinate closely with urology, recognizing that practice styles vary.

DHEA Physiology, Brain Receptors, and When to Treat

Dehydroepiandrosterone (DHEA) and its sulfated form, DHEA-S, are produced primarily by the adrenal cortex and function as both endocrine prohormones and neurosteroids, with receptors and actions in the brain. Levels peak in the 20s and decline steadily with age. In both sexes, suboptimal DHEA can present as low vitality, depressed mood, impaired stress tolerance, and reduced sexual function—even when testosterone looks “good.”

Why DHEA matters

  • Neurosteroid action: DHEA modulates GABAergic and glutamatergic tone, supporting mood, cognition, and arousal (Maninger et al., 2009).
  • Peripheral conversion: DHEA can be converted to androgens and estrogens via tissue-specific enzymes; in women, a portion is converted to DHT in peripheral tissues, contributing to libido and sexual response.
  • Immunometabolic effects: DHEA has anti-inflammatory properties and may influence endothelial function and bone metabolism.

Clinical patterns I see

  • Women with adequate total and free testosterone who remain symptomatic for low libido or anorgasmia sometimes have low DHEA-S in the double digits. Carefully titrated DHEA supplementation often improves sexual function and overall well-being.
  • In men and women with persistent fatigue and low mood despite thyroid/hormone optimization, DHEA can be the missing link.

Dosing logic

  • I typically optimize thyroid and sex hormones first; DHEA often rises when metabolic stress decreases.
  • If DHEA-S remains suboptimal:
    • Women: 5–10 mg/day compounded DHEA; reassess at ~6 weeks
    • Men: 20 mg/day compounded DHEA; reassess at ~6 weeks
    • Over-the-counter options vary in potency; when used, I start around 25 mg/day with close follow-up.
  • Monitor for androgenic side effects, especially in PCOS (who often already have high DHEA-S); avoid in hyperandrogenic phenotypes.

Evidence notes

  • Studies link low DHEA-S to reduced well-being, depression, and sexual dysfunction, with improvements seen in targeted supplementation cohorts (Arlt et al., 1999; Wierman et al., 2014). Age-associated decline is robust and correlates with multiple health outcomes.

Why Integrative Chiropractic Care Belongs in Endocrine-Metabolic Programs

The neuromusculoskeletal system interfaces with the endocrine and immune systems through shared inflammatory and autonomic pathways. Here is how integrative chiropractic care fits, based on observations from my clinic and the scientific literature:

Mechanistic bridges

  • Inflammation: Chronic pain amplifies IL-6 and TNF-α signaling, worsening insulin resistance. By reducing nociceptive drive and improving joint mechanics, manual therapies can lower inflammatory load and facilitate activity.
  • Autonomic balance: Spinal and rib mechanics influence sympathetic/parasympathetic tone. Improved thoracic mobility and diaphragmatic function promote vagal activity, which supports glycemic control and gut motility—both key to the gut–ovary axis.
  • Movement competency: Targeted strength and mobility programs enhance GLUT4 activity in skeletal muscle, thereby improving insulin sensitivity and supporting healthy SHBG levels.

In practice at Chiromed

  • We build individualized plans that synchronize:
    • Spinal and extremity joint care to enable pain-free training
    • Progressive resistance training emphasizing posterior chain and hip mechanics
    • Aerobic conditioning at sustainable intensities
    • Breathing retraining and sleep hygiene to normalize cortisol rhythms
  • This approach improves adherence to metabolic prescriptions, enabling the nutrition and pharmacology to “land” in real life.

Search-optimized section title Practical Protocols and Case-Style Reasoning

Putting it all together, here is how I apply the logic in daily care.

When SHBG is low, and symptoms suggest androgen deficiency

  • Evaluate metabolic health: fasting insulin, lipids, liver enzymes, hs-CRP, A1c.
  • Address insulin resistance first-line with nutrition, exercise, sleep, and stress management; consider metformin and/or GLP-1 RAs.
  • If symptoms persist, carefully optimize testosterone with awareness that low SHBG increases free fraction—start low, titrate to symptom relief and physiologic targets.

When PCOS is likely, but the phenotype is atypical

  • Order LH, FSH, total and free T, SHBG, DHEA-S, fasting insulin/glucose, and consider stool testing.
  • Begin metabolic therapy plus symptom-directed therapy (spironolactone or COCs if appropriate and pregnancy not desired).
  • Integrate resistance training and chiropractic-guided movement plans to accelerate insulin sensitivity and ovulatory recovery.

When initiating or adjusting DHEA

  • Confirm suboptimal DHEA-S and symptom alignment (low mood, libido, vitality).
  • Start low, reassess in 6–8 weeks, and monitor for androgenic side effects.
  • Avoid in hyperandrogenic PCOS unless clearly indicated and monitored.

When PSA is elevated or changing fast

  • Obtain percent free PSA and calculate velocity.
  • If %fPSA <10% or velocity is concerning, proceed to 3T mpMRI; if prostatitis is suspected, treat and retest.
  • Collaborate with urology based on mpMRI and clinical findings; delay testosterone changes until evaluation clarifies risk.

Why We Use Each Technique: The Physiology Behind the Protocols

  • Metformin: Reduces hepatic gluconeogenesis and improves peripheral insulin sensitivity via AMPK activation; lowers insulin, allowing SHBG to normalize and free T to calm down.
  • GLP-1 receptor agonists: Enhance glucose-dependent insulin secretion, reduce appetite, and reduce systemic inflammation; improved ovulatory function reported in PCOS.
  • Spironolactone: Direct androgen receptor blockade plus inhibition of 5α-reductase at higher doses; symptom relief while metabolic causes are corrected.
  • DHEA: Restores neurosteroid tone and supports sexual function with selective peripheral conversion; used when clinically and biochemically indicated.
  • Integrative chiropractic and movement: Improves neuromechanics and reduces pain, enabling training volume and intensity that improve insulin sensitivity; enhances autonomic balance affecting gut and endocrine axes.

Final Takeaways for Patients and Providers

  • Think metabolically first: Low SHBG is often a metabolic distress signal, not a target to suppress.
  • PCOS can be lean and subtle: Free T, LH: FSH, and DHEA-S mapping, plus gut assessment, can catch atypical cases.
  • Combine symptom control and root-cause therapy: Use spironolactone or COCs for hirsutism/acne while you restore insulin sensitivity and gut health.
  • Use smarter PSA strategies: Percent free PSA and PSA velocity reduce unnecessary biopsies and guide timely imaging with 3T mpMRI.
  • Integrate care: When manual therapy, structured exercise, and metabolic medicine are aligned, recovery timelines shorten and outcomes improve.

References

Ahmed, H. U., El-Shater Bosaily, A., Brown, L. C., Gabe, R., Kaplan, R., Parmar, M. K., … Emberton, M. (2017). Diagnostic accuracy of multi-parametric MRI and TRUS biopsy in prostate cancer (PROMIS): a paired validating confirmatory study. The Lancet, 389(10071), 815–822.

Arlt, W., Callies, F., van Vlijmen, J. C. M., Koehler, I., Reincke, M., Bidlingmaier, M., … Allolio, B. (1999). Dehydroepiandrosterone replacement in women with adrenal insufficiency. New England Journal of Medicine, 341(14), 1013–1020.

Barrea, L., Marzullo, P., Muscogiuri, G., Di Somma, C., De Alteriis, G., Colao, A., & Savastano, S. (2019). Nutritional aspects of PCOS: an update. Advances in Nutrition, 10(2), 270–292.

Brown, J., Farquhar, C., Lee, O., Toomath, R., & Jepson, R. (2009). Spironolactone versus placebo or in combination with steroids for hirsutism and/or acne. Cochrane Database of Systematic Reviews, (2), CD000194.

Ding, E. L., Song, Y., Manson, J. E., Hunter, D. J., Lee, C.-C., Rifai, N., … Liu, S. (2009). Sex hormone–binding globulin and risk of type 2 diabetes in women and men. JAMA, 301(17), 1777–1786.

Elkind-Hirsch, K., Marrioneaux, O., Bhushan, M., Vernor, D., & Bhushan, R. (2008). Comparison of single and combined treatment with exenatide and metformin on menstrual cyclicity in obese polycystic ovary syndrome. Journal of Clinical Endocrinology & Metabolism, 93(7), 2670–2678.

Escobar-Morreale, H. F. (2018). Polycystic ovary syndrome: definition, aetiology, diagnosis and treatment. Human Reproduction Update, 24(6), 671–698.

Kahal, H., Aburima, A., Ungvari, T., Rigby, A. S., Coady, A. M., Vince, R. V., & Kilpatrick, E. S. (2021). The effect of GLP-1 receptor agonists on cardiovascular risk factors in women with PCOS. Endocrine, 71, 199–206.

Maninger, N., Wolkowitz, O. M., Reus, V. I., Epel, E. S., & Mellon, S. H. (2009). Neurobiological and neuropsychiatric effects of DHEA and DHEA-S. Psychoneuroendocrinology, 34(3), 273–286.

Patterson, R. E., & Sears, D. D. (2017). Metabolic effects of intermittent fasting. Annual Review of Nutrition, 37, 371–393.

Rena, G., Hardie, D. G., & Pearson, E. R. (2017). The mechanisms of action of metformin. Nature Reviews Molecular Cell Biology, 19(1), 31–44.

Selva, D. M., Hogeveen, K. N., Innis, S. M., & Hammond, G. L. (2007). Monosaccharide-induced lipogenesis regulates the human hepatic sex hormone–binding globulin gene. Journal of Clinical Investigation, 117(12), 3979–3987.

Teede, H. J., Misso, M. L., Costello, M. F., Dokras, A., Laven, J., Moran, L., … International PCOS Network. (2018). Recommendations from the international evidence-based guideline for the assessment and management of PCOS. Human Reproduction, 33(9), 1602–1618.

Vickers, A. J., Savage, C., O’Brien, M. F., Lilja, H. (2011). Systematic review of pretreatment prostate-specific antigen velocity and doubling time as predictors for prostate cancer. Journal of Clinical Oncology, 29(33), 447–453.