Gut Health and Hormone Balance Treatment

Abstract

I am Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. In this educational post, I guide you through the science and practice of optimizing hormones by treating the gut–liver–hormone axis and reinforcing micronutrient and mitochondrial foundations. I explain how dysbiosis, intestinal permeability, and microbial enzymes like beta-glucuronidase reshape estrogen metabolism and influence conditions such as PCOS, endometriosis, and autoimmunity, and how lipopolysaccharide (LPS) and short-chain fatty acids (SCFAs) affect insulin sensitivity, mood, and inflammation. I translate current research on vitamin D, K2, iodine, selenium, methylated B vitamins, DIM, and shilajit into clinic-ready protocols, and I show where integrative chiropractic care fits by supporting vagal tone, motility, neuromusculoskeletal dynamics, and autonomic balance. You will find practical frameworks, dosing concepts, lab-monitoring advice, and rationale for each intervention, with citations to leading researchers.

---

Why Hormones Are Microbiome-Dependent: The Gut–Liver–Hormone Axis

When I first connected hormone symptoms to gut physiology, I saw a pattern: many “hormone” problems began as microbiome and barrier problems. The gut microbiome—a complex community of bacteria, viruses, fungi, and archaea—regulates digestion, immune tolerance, barrier integrity, and the enterohepatic circulation that clears estrogens. From the earliest studies linking metabolic endotoxemia to insulin resistance, it has become clear that LPS-driven inflammation can disrupt cardiometabolic and reproductive health (Cani et al., 2007).

• When the microbiome is balanced, commensals generate SCFAs (notably butyrate) that nourish colonocytes, tighten junctions, and reduce inflammatory signaling.
• When dysbiosis develops, beta-glucuronidase-producing taxa expand, and LPS permeates, amplifying NF-κB cytokine cascades that alter hormone receptors, hepatic detoxification, and insulin signaling (Fasano, 2012; Slyepchenko et al., 2017).

Clinically, if you manage estrogen symptoms, insulin resistance, or autoimmune patterns, you are managing the microbiome—whether you realize it or not.

---

Dysbiosis and Leaky Gut Explained: Distinct Problems that Reinforce Each Other

Two related but distinct issues commonly coexist:

• Dysbiosis: A shift away from beneficial microbes, with loss of diversity and expansion of pathobionts. Consequences include increased LPS, altered bile acid signaling, and elevated beta-glucuronidase.
• Leaky gut (increased intestinal permeability): Disruption of tight junction proteins (occludin, claudins, ZO-1) allows antigens and endotoxins to enter circulation, thereby increasing systemic inflammation and immune activation (Fasano, 2012).

Why that matters for hormones:

• LPS activates TLR4–NF-κB, increasing TNF-α, IL-1β, and IL-6—cytokines that reduce insulin signaling and alter steroid hormone receptor function (Cani et al., 2007).
• Permeability increases immune load and oxidative stress, thereby consuming methyl donors and glutathione needed for safe phase II detox (methylation, glucuronidation, sulfation) of estrogens.

I screen for these drivers whenever patients report PMS, heavy cycles, PCOS features, endometriosis pain, acne or hair loss, mood changes, fatigue, or autoimmune flares. Correcting the gut often increases the safety and efficacy of hormone therapy.

---

Estrogen Metabolism 101: Enterohepatic Circulation and the Estrobolome

The liver metabolizes estrogens via phase I hydroxylation (CYP1A1, CYP1B1) and phase II conjugation (COMT methylation, glucuronidation, sulfation). Conjugated metabolites pass into bile and should be excreted. In dysbiosis, microbial beta-glucuronidase deconjugates these estrogens, promoting reabsorption and recirculation—the biochemical basis of “estrogen dominance,” even with careful dosing (Plottel & Blaser, 2011).

• 2-hydroxylation generally produces less proliferative metabolites.
• 4- and 16α-hydroxylation yield more proliferative or potentially genotoxic metabolites if methylation and conjugation are suboptimal.

In complex cases or when there is a family history of estrogen-dependent cancers, I consider urinary metabolite testing to map pathways and guide targeted support.

---

PCOS, Endometriosis, and Autoimmunity: What the Microbiome Adds

Recent studies sharpen the microbiome’s role:

• PCOS: Dysbiosis with fewer SCFA producers and higher LPS correlates with insulin resistance, hyperandrogenism, and impaired GLP-1 signaling (Lindheim et al., 2017; Qi et al., 2019). Restoring butyrate producers improves metabolic tone.
• Endometriosis: Altered microbiota, increased permeability, and immune activation correlate with symptom severity. Increased beta-glucuronidase raises estrogen recirculation that can exacerbate lesions and pain (Chen et al., 2017; Jiang et al., 2017).
• Autoimmunity: Barrier dysfunction and loss of tolerogenic species permit pathobiont translocation and molecular mimicry, priming autoimmune activity (Manfredo Vieira et al., 2018).

Clinical translation: Addressing the gut can reduce hormone dosing requirements, expand the therapeutic window, and stabilize mood, sleep, and metabolism.

---

The Simple Question with Big Impact: Are You Pooping Daily?

I ask every patient: “Do you have a daily bowel movement?”

• Estrogen metabolites exit via bile and stool. Constipation increases residence time, giving beta-glucuronidase more opportunity to deconjugate and recirculate estrogens.
• Correcting bowel habits is a core risk-reduction strategy for estrogen-driven conditions.

Practical steps I use:

• Increase hydration and electrolytes.
• Ramp fiber to 25–35 g/day; add PHGG (partially hydrolyzed guar gum) 4–6 g/day for low-bloat prebiotic support.
• Add magnesium glycinate or citrate at night for stool regularity and sleep.
• Encourage postprandial walks and vagal toning (slow exhale breathing, humming).

---

A 3-by-3 Framework for Gut Repair: Remove, Replace, Repair

To keep things doable, I use a 3-by-3 approach:

1. Remove/Reduce Irritants

• Clean up the diet: favor whole foods; limit alcohol, ultra-processed items, added sugars; consider a gluten-light or gluten-free trial for sensitive individuals.
• Medication review: minimize NSAIDs and PPI overuse when clinically safe.
• Stress load: hard-wire breath work, walks, and sleep hygiene.

2. Replace and Restore

• Fiber and prebiotics: 25–35 g/day total fiber; add PHGG for gentle SCFA support.
• Probiotics: multi-strain Lactobacillus and Bifidobacterium blends (e.g., L. rhamnosus GG, B. lactis) for barrier and immune balance.
• Digestive support: bitters and meal hygiene for hypochlorhydria/slow motility; phosphatidylcholine and balanced fats for bile flow.

3. Repair and Rebalance

• Barrier repair: L-glutamine 5 g/day, zinc carnosine, N-acetyl-D-glucosamine, omega-3s as indicated.
• Inflammation control: Berberine for dysbiosis-associated endotoxemia; curcumin and quercetin for NF-κB calming.
• Lifestyle anchors: 150 minutes/week activity; 10-minute post-meal walks; consistent 7–9 hours of sleep.

Why this approach works:

• Prebiotics increase SCFAs, reinforce tight junctions, and support T-regs via HDAC inhibition.
• Probiotics competitively inhibit pathobionts, reduce beta-glucuronidase activity, and enhance mucosal IgA.
• L-glutamine fuels enterocytes and accelerates barrier recovery.
• Berberine improves the microbial balance and activates AMPK to improve insulin sensitivity.

---

Nutrient Foundations for Receptor-Level Hormone Action: D, K2, A, Magnesium, Iodine, Selenium, and Methylation

I frequently see patients with robust serum hormones but poor tissue effects. The missing link is often receptor signaling, cofactors, and membranes.

• Vitamin D3 behaves like a secosteroid hormone that modulates transcription through the VDR. Low vitamin D is associated with all-cause and cardiovascular mortality and can blunt androgen signaling even when total testosterone appears normal (Pilz et al., 2011; Holick, 2017).
• Magnesium is a cofactor for D activation (25- and 1α-hydroxylases); deficiency dampens VDR signaling (Rosanoff et al., 2016).
• Vitamin K2 directs calcium into bone and away from soft tissues by activating matrix Gla protein and osteocalcin; it complements D to protect vessels and build bone (Schurgers & Vermeer, 2000; Beulens et al., 2013).
• Vitamin A supports epithelial integrity, immune balance, and nuclear receptor synergy with vitamin D.

I often use an ADK formula (D3 with K2 and A) alongside magnesium to safely improve receptor-mediated effects, while monitoring 25(OH)D, calcium, and PTH (Rosen et al., 2012).

Thyroid resilience: iodine and selenium synergy

• Iodine is essential for T4/T3 synthesis, but safe utilization depends on selenium-dependent enzymes (glutathione peroxidases, thioredoxin reductases) to quench the H2O2 generated during iodide organification (Ventura et al., 2017).
• Inadequate selenium increases oxidative stress at the thyroid, raising the risk of autoimmunity when iodine intake rises (Gartner & Gasnier, 2003).
• I pair iodine (200–400 mcg) with selenium (100–200 mcg selenomethionine) and often zinc (10–30 mg), titrated to labs and symptoms (Zimmermann & Boelaert, 2015).

Methylation for estrogen safety

• Methylated B vitamins—methylfolate and methylcobalamin—support COMT-mediated methylation of catechol estrogens, reducing genotoxic stress and stabilizing phase II clearance.

These micronutrients are the bedrock that allows hormones to “dock” and trigger healthy cellular responses.

---

DIM and Estrogen Metabolites: Steering Toward Safer Pathways

Diindolylmethane (DIM) shifts estrogen metabolism toward 2-hydroxylation and away from 16α- and 4-hydroxylation pathways associated with proliferative and genotoxic risk (Zeligs et al., 2006; Reed et al., 2006). Preclinical studies suggest that DIM may also upregulate BRCA1 signaling and promote apoptosis in cancer cell lines (Fan et al., 2009; Li et al., 2010).

How I apply it:

• Women with estrogen-dominant symptoms or unfavorable metabolite profiles: 150–300 mg/day, adjusted to labs and tolerance.
• Men with prostate risk or aromatization-driven symptoms: 300–600 mg/day, personalized.
• I pair DIM with omega-3s, iodine/selenium, and fiber/probiotics to support the entire estrobolome–liver–stool axis.

Rationale: By changing metabolite balance and supporting conjugation, DIM decreases receptor overstimulation and DNA-adduct risk while improving symptom stability.

---

Shilajit for Free Testosterone and Mitochondrial Support

Some patients—particularly young males—present with high total testosterone but low free testosterone and low vitality. Shilajit, a purified, fulvic-acid–rich resin, has randomized data showing increases in total (~31%), free (~51%), and DHT (~37%) over ~90 days at 250 mg twice daily (Pandit et al., 2016). Mechanisms likely include improved mitochondrial function, nutrient transport, and hypothalamic–pituitary–gonadal signaling.

How I use it:

• In those seeking endogenous support without exogenous hormones, I combine shilajit with vitamin D, magnesium, zinc, B12, and iodine/selenium when indicated, then track changes in free T, SHBG, energy, and body composition.

Why this works: Enhancing mitochondrial ATP and cofactor availability raises tissue responsiveness; changes in binding dynamics can increase the bioactive fraction without pushing total testosterone to excessive levels.

---

Vitamin D as a Systemic Modulator: Barrier, Immunity, and Receptors

I routinely optimize vitamin D because it acts at the intersection of immunity, barrier integrity, and endocrine signaling. Observational data tie suboptimal 25(OH)D to higher risks across diseases (Bouillon et al., 2019). Mechanistically, D supports tight junction proteins, cathelicidin, and endocrine receptor sensitivity. Clinically, many patients feel “stuck” until D is restored to an optimal range; I often target 60–80 ng/mL with appropriate monitoring to avoid hypercalcemia (Holick, 2017; Rosen et al., 2012).

---

Integrative Chiropractic Care: The Neuroimmune–Endocrine Interface

As a chiropractor and nurse practitioner, I see daily how autonomic balance, fascial mobility, and pain modulation determine whether patients can absorb nutrients, move consistently, and sleep well—foundations for endocrine success.

• Vagal tone and motility: Gentle spinal and cervical adjustments can influence autonomic balance, improving gut motility, secretory IgA, and anti-inflammatory vagal pathways. Patients with low vagal tone present with constipation, bloating, and poor stress resilience.
• Fascia and diaphragm: Thoracolumbar fascial restrictions and diaphragmatic stiffness impair breathing mechanics and lymphatic flow, promoting sympathetic overdrive. Mobility restores circulation and reduces pain.
• Pain reduction without NSAIDs: Lowering nociception decreases cortisol and protects the mucosa from NSAID-induced permeability.
• Behavioral activation: When pain decreases, patients walk, train, and sleep—activities that increase SCFAs, improve insulin sensitivity, and stabilize mood.

These neurophysiologic effects align with published observations on autonomic modulation and musculoskeletal care (Pickar, 2002; Lehman et al., 2012) and help nutrition and endocrine strategies “stick” in daily life.

For examples of how we operationalize this, see my resources at Chiromed and my professional updates on LinkedIn.

---

A Phased, Clinic-Ready Protocol for Gut and Hormone Optimization

I layer care to build momentum and safety.

Phase 1: Stabilize and Build Trust (Weeks 0–4)

• Ensure daily bowel movements; add PHGG, hydration, and magnesium as needed.
• Start a multi-strain probiotic (Lactobacillus + Bifidobacterium).
• Begin vitamin D3 with K2 and magnesium; consider ADK formulations.
• Introduce walks after meals and fixed sleep schedules.
• Provide chiropractic adjustments and diaphragmatic work to normalize autonomics and reduce pain.
• Baseline labs: CBC, CMP, 25(OH)D, calcium, PTH, thyroid panel (TSH, free T4/T3), thyroid antibodies as needed, ferritin, B12, folate, magnesium, zinc, selenium, CRP, fasting insulin/glucose, lipid profile, estradiol, total and free testosterone, SHBG.

Phase 2: Targeted Gut Repair and Hormone Pathways (Weeks 4–12)

• Add L-glutamine 5 g/day for barrier support when indicated.
• Short berberine course for endotoxemia/dysbiosis; replete with probiotics.
• Add DIM if clinical or metabolite data show proliferative pathways.
• Start a methylated B complex to support COMT and phase II detox.
• Maintain chiropractic care cadence for autonomic and biomechanical resilience.

Phase 3: Personalize, Monitor, and Maintain (Months 3+)

• Reassess symptoms, bowel habits, and targeted labs; titrate to the lowest effective doses.
• Reinforce lifestyle anchors: fiber intake, movement, sleep, and stress practices.
• Schedule periodic tune-ups for the spine, fascia, and breath mechanics to sustain vagal tone and support recovery.

This sequencing respects physiology and behavior: patients feel better first, then commit to more significant changes—resulting in better adherence and durable outcomes.

---

Special Focus: PCOS and Endometriosis

PCOS

• Emphasize insulin sensitization through fiber, postprandial walks, resistance training, and, where appropriate, berberine.
• Reduce LPS: probiotics, polyphenols, and barrier repair to lower endotoxemia.
• Consider inositols for ovulatory support alongside gut therapy.
• Monitor androgenic symptoms as gut protocols progress; improvements often track with better bile acid and SCFA signaling.

Endometriosis

• Reduce beta-glucuronidase pressure via probiotics and fiber to limit estrogen recirculation.
• Calm neuroimmune inflammation with omega-3s, curcumin, and sleep optimization.
• Use gentle movement and manual therapy to address pelvic floor tension and diaphragm mobility; sympathetic downshift reduces pain tone.
• Coordinate with gynecology; gut protocols augment, not replace, indicated care.

---

Case Reflection: High Total Testosterone, Low Vitality

I saw an 18–19-year-old male with low mood, low energy, weight gain, and “low-T” symptoms. His total testosterone was ~900 ng/dL—clearly not low. What we found: very low vitamin D, low B12, and signs of micronutrient insufficiency. I started a robust B-complex, ADK (D3 + K2 + A), iodine paired with selenium, and magnesium. At follow-up, his mother said, “He’s a totally different person.” Energy, mood, and cognition improved, and multiple medications were discontinued. The physiology: hormones were present, but receptor signaling and cellular machinery were underpowered. Restoring micronutrients enabled the hormones to “work.”

In other young men with high total but low free testosterone, I have added shilajit and structured resistance training. Free fractions improved, and vitality followed—without pushing total testosterone into excess.

---

Safety, Lab Monitoring, and Personalization

• Monitor: 25(OH)D, calcium, PTH for vitamin D repletion; thyroid panel and antibodies for iodine–selenium strategies; ferritin, B12, folate, magnesium, zinc, selenium, CRP for micronutrient and inflammatory status; sex hormones including free testosterone and SHBG.
• Adjust doses to labs and symptoms. If vitamin D stays low despite oral dosing, assess bile flow, fat absorption, and adherence; consider supervised loading.
• Cautions:
  • Vitamin A: avoid hypervitaminosis; use caution in pregnancy.
  • Iodine: go slowly with autonomous nodules or hyperthyroidism; collaborate with endocrinology.
  • Zinc: long-term high dosing can lower copper; keep the balance.
  • DIM and shilajit: use third-party-tested products; personalize the dose.
  • Berberine: short targeted courses; watch for GI sensitivity and drug interactions.

---

How Integrative Chiropractic Care Complements Endocrine and Gut Strategies

Mechanistically, chiropractic-informed care bridges biochemistry and behavior:

• Reduces nociception and sympathetic overdrive, lowering cortisol drag on thyroid conversion and gonadal axes (Lehman et al., 2012).
• Improves respiratory mechanics and fascial glide, supporting lymphatic flow, nutrient delivery, and waste clearance.
• Enhances vagal tone, supporting motility, secretory IgA, and peristalsis—foundations for microbiome stability.
• Facilitates movement prescriptions (resistance training, mobility, aerobic intervals) that reduce aromatase activity, improve insulin sensitivity, and raise androgen receptor density.

In my practice, patients combining endocrine protocols with spinal–fascial optimization report better sleep, steadier energy, more predictable lab trajectories, and lower required doses—an elegant synergy of systems biology and hands-on care. Explore our integrative approach at Chiromed and my professional notes on LinkedIn.

---

Why Each Technique Matters: Systems Biology Rationale

• Fiber/PHGG: Feeds SCFA producers, tightens junctions, and supports GLP-1 signaling.
• Probiotics: Reduce beta-glucuronidase, improve barrier integrity, and temper endotoxemia.
• L-glutamine: Primary fuel for enterocytes; accelerates epithelial repair.
• Berberine: Reshapes the gut microbiota, lowers LPS levels, and activates AMPK to improve insulin sensitivity.
• DIM: Steers estrogen toward 2-hydroxylation, lowering proliferative load.
• Methylated B vitamins: Enable COMT activity and conjugation; reduce genotoxicity of catechol estrogens.
• Vitamin D + K2 + A + Mg: Align receptor signaling and calcium kinetics; protect vessels and bone.
• Iodine + selenium: Support thyroid synthesis while detoxifying H2O2 to prevent autoimmune escalation.
• Shilajit: Enhances endogenous androgens via mitochondrial and HPG-axis support.
• Chiropractic care: Normalizes autonomic function, reduces pain, and supports movement habits that sustain microbiome and endocrine gains.

Each intervention nudges a different lever; together, they realign the system.

---

Clinical Observations from Practice

Across patient cohorts at my clinic, we see reproducible patterns:

• Resolving constipation reduces PMS and “estrogen rollercoaster” symptoms within weeks.
• Regular adjustments correlate with improved sleep and stress tolerance, enabling consistent training and meal timing that benefit the microbiome.
• Vitamin D optimization often coincides with improved mood, less joint pain, and better responses to both gut and hormone protocols.

These observations are consistent with the mechanistic and clinical literature, reinforcing the rationale for why foundational steps deliver outsized results. For more, visit Chiromed and my LinkedIn updates.

---

References

• Bouillon, R., Marcocci, C., Carmeliet, G., Bikle, D., White, J. H., Dawson-Hughes, B., Lips, P., Munns, C. F., Lazaretti-Castro, M., Giustina, A., & Bilezikian, J. (2019). Skeletal and extraskeletal actions of vitamin D: Current evidence and outstanding questions. Endocrine Reviews, 40(4), 1109–1151.
• Cani, P. D., Amar, J., Iglesias, M. A., Poggi, M., Knauf, C., Bastelica, D., Neyrinck, A. M., Fava, F., Tuohy, K. M., Chabo, C., et al. (2007). Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes, 56(7), 1761–1772.
• Chen, C., Song, X., Wei, W., & Zhong, H. (2017). The role of the gut microbiota in the pathogenesis of endometriosis. Digestive Diseases and Sciences, 62(9), 2345–2355.
• Fasano, A. (2012). Leaky gut and autoimmune diseases. Clinical Reviews in Allergy & Immunology, 42(1), 71–78.
• Holick, M. F. (2017). The vitamin D deficiency pandemic: Approaches for diagnosis, treatment and prevention. Reviews in Endocrine and Metabolic Disorders, 18, 153–165.
• Jiang, I., Desailloud, R., & Rousset, B. (2017). Gut microbiota and endometriosis: A bidirectional relationship. Best Practice & Research Clinical Endocrinology & Metabolism, 31(4), 613–621.
• Lindheim, L., Bashir, M., Münzker, J., Trummer, C., Zachhuber, V., Pieber, T. R., Gorkiewicz, G., Höfner, G., Jesner, R., & Obermayer-Pietsch, B. (2017). The gut microbiome: A key player in the pathophysiology of PCOS. Endocrine, 58(3), 467–479.
• Manfredo Vieira, S., Hiltensperger, M., Kumar, V., Zegarra-Ruiz, D., Dehner, C., Khan, N., Costa, F. R. C., Tiniakou, E., Greiling, T. M. S., Ruff, W. E., & Kriegel, M. A. (2018). Translocation of a gut pathobiont drives autoimmunity in the presence of other triggers. Science, 359(6380), 1156–1161.
• Pandit, S., et al. (2016). Clinical evaluation of purified shilajit in healthy volunteers: Effects on testosterone and gonadotropic hormones. Andrologia, 48(5), 570–575.
• Pilz, S., et al. (2011). Vitamin D and mortality in older men and women. Clinical Endocrinology, 75(3), 341–347.
• Plottel, C. S., & Blaser, M. J. (2011). Microbiome and malignancy. Nature Reviews Cancer, 11(11), 782–792.
• Reed, G. A., et al. (2006). Single-dose pharmacokinetics and tolerability of absorption-enhanced 3,3′-diindolylmethane. Cancer Epidemiology, Biomarkers & Prevention, 15(12), 2477–2481.
• Rosen, C. J., et al. (2012). Calcium and vitamin D supplementation revisited. Journal of Bone and Mineral Research, 27(2), 223–230.
• Rosanoff, A., Weaver, C. M., & Rude, R. K. (2016). Suboptimal magnesium status in the United States: Are the health consequences underestimated? Nutrition Reviews, 74(3), 169–182.
• Schurgers, L. J., & Vermeer, C. (2000). Determination of gamma-carboxyglutamic acid residues in proteins by HPLC. Thrombosis and Haemostasis, 84(6), 958–962.
• Beulens, J. W., et al. (2013). Vitamin K intake and all-cause mortality in The Netherlands. Journal of Nutrition, 143(6), 1029–1035.
• Fan, S., et al. (2009). BRCA1 and BRCA2 as primary targets for chemoprevention of breast cancer. Journal of Cellular Biochemistry, 106(1), 24–32.
• Li, Y., et al. (2010). Indole-3-carbinol and DIM in cancer prevention and therapy. Anti-Cancer Agents in Medicinal Chemistry, 10(9), 727–731.
• Qi, X., Yun, C., Pang, Y., & Qiao, J. (2019). The impact of the gut microbiota on the cardiovascular system and obesity. Frontiers in Microbiology, 10, 2155.
• Slyepchenko, A., et al. (2017). Tryptophan catabolites, inflammation, and the gut–brain axis in depression. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 80, 1–19.
• Calder, P. C. (2015). Marine omega-3 fatty acids and inflammatory processes: Effects, mechanisms and clinical relevance. Biochimica et Biophysica Acta, 1851(4), 469–484.
• Gartner, R., & Gasnier, B. C. (2003). Selenium in the treatment of autoimmune thyroiditis. BioFactors, 19(3–4), 145–152.
• Ventura, M., et al. (2017). Selenium and thyroid disease: From pathophysiology to clinical evidence. Acta Clinica Belgica, 72(5), 326–333.
• Zimmermann, M. B., & Boelaert, K. (2015). Iodine deficiency and thyroid disorders. The Lancet Diabetes & Endocrinology, 3(4), 286–295.
• Pickar, J. G. (2002). Neurophysiological effects of spinal manipulation. The Spine Journal, 2(5), 357–371.
• Lehman, G. J., et al. (2012). The role of spinal manipulation in modulating pain and autonomic function. Journal of Manipulative and Physiological Therapeutics, 35(8), 611–623.