Functional Medicine Approach Insights for Thyroid Health

Learn the benefits of a functional medicine approach to enhancing thyroid health and improving overall vitality.

Abstract

In this educational post, I walk you through a comprehensive, first-person roadmap for understanding and correcting thyroid-related symptoms without over-reliance on thyroid medications. Drawing on modern, evidence-based research and clinical collaboration, I explain four high-yield physiological mechanisms that account for most hypothyroid presentations: systemic inflammation and cytokine signaling, hepatic conversion dysfunction, gut dysbiosis and enterohepatic disruption, and stress-induced hypothalamic-pituitary-adrenal (HPA) axis interference with thyroid hormone activation. I explore how peripheral conversion of T4 to T3 is often the true bottleneck—not thyroid hormone production itself—and why medications like levothyroxine can fail when these conversion pathways are impaired. I also detail how our multidisciplinary care team in El Paso, Texas integrates chiropractic care, functional medicine, rehabilitation, personal injury care, nutrition, and internal medicine oversight to build individualized treatment plans. In particular, I highlight our collaboration with Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine) (NPI #1164426749, Texas MD License #J2933), who serves as our Medical Director and Collaborative Physician at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic). Throughout, I share clinical observations from my practice and research-informed strategies to restore metabolic resilience, optimize thyroid signaling, and improve patient outcomes using non-pharmacologic and appropriately supervised medical approaches. This post includes detailed physiologic explanations, clinical protocols, case reflections, and APA-7-style references to leading research.

Meet Our Team and Model of Care

• I am Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. I practice integrative chiropractic and functional medicine, focusing on musculoskeletal, neuroendocrine, and metabolic health.
• Our clinic: Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), El Paso, Texas.
• Our Medical Director and Collaborative Physician: Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine (NPI #1164426749, Texas MD License #J2933). Dr. Cardenas has over 40 years of experience as an internist and provides medical oversight, diagnostic rigor, and care coordination across our multidisciplinary services.
• Our integrated services:

• Chiropractic care focused on biomechanical normalization, autonomic balance, and pain modulation
• Internal medicine oversight for complex metabolic, inflammatory, and endocrine cases
• Functional medicine protocols (nutrition, microbiome modulation, detoxification support, mitochondrial care)
• Rehabilitation and movement therapy
• Personal injury care and case management
• Laboratory evaluation and biomarker tracking
• Patient education and behavior change coaching

Why Many Patients Don’t Need Thyroid Medication: A Clinical Perspective

I often meet individuals struggling with classic hypothyroid symptoms—fatigue, weight gain, cold intolerance, hair thinning, constipation, depression, and brain fog—despite long-term levothyroxine or desiccated thyroid therapy. Over the years, I’ve seen an undeniable pattern: their primary bottleneck isn’t thyroid hormone production in the gland; it’s the peripheral conversion of thyroxine (T4) into the biologically active triiodothyronine (T3) at the tissue level. When conversion pathways are impaired, the body sits in a low-T3 state with high reverse T3 (rT3)—a competitive inhibitor that occupies thyroid receptors without activating them—creating a state of functional hypothyroidism despite “normal” TSH and sufficient T4 on labs (Gullo et al., 2011; Peeters et al., 2005).

In such cases, simply increasing T4 doses rarely solves the problem. In fact, excess T4 can be diverted into rT3 under inflammatory, stress, or nutrient-deficient conditions (Fliers et al., 2015). My approach is to identify and resolve the conversion barriers. Over time, this strategy consistently restores metabolic vitality without always needing a prescription. This doesn’t mean medication is never appropriate; it means many patients benefit from addressing upstream mechanisms beyond the gland.

A Patient Story: Seven Years of Symptoms and a Turning Point

A 41-year-old patient—let me call her Jennifer—contacted me in distress. She was on multiple thyroid medications and continued to gain weight, felt depressed, had cold hands, brain fog, and had dragged herself through life for seven years under the care of five different physicians. Her story mirrors what I have witnessed repeatedly: the medications aimed at increasing circulating T4 did not resolve her symptoms because conversion and cellular hormone activation were impaired.

When we mapped her physiology, four non-pharmacologic mechanisms stood out. These mechanisms account for the majority of hypothyroid symptom clusters I see clinically:

1. Systemic inflammation driving cytokine cascades that downregulate T4-to-T3 conversion and upregulate rT3 formation
2. Hepatic dysfunction of deiodinase activity and conjugation pathways impeding active hormone availability and clearance
3. Gut dysbiosis and barrier disruption diminishing T3 recycling and increasing endotoxin load
4. HPA axis activation and stress physiology reducing D1 activity and shifting the body to conservation mode

In Jennifer’s case, once we identified and addressed these conversion barriers—using integrative care under medical oversight—her symptoms improved without escalating her thyroid medication.

The Biology: The Thyroid Manufactures T4; Tissues Activate T3

• The thyroid gland primarily manufactures T4, with smaller amounts of T3 (Bianco & da Conceicao, 2018). T4 is a prohormone; it must be converted peripherally to T3 by deiodinase enzymes.
• T3 is the biologically active hormone that binds nuclear thyroid receptors (TR?/?) to drive gene transcription, affecting mitochondrial function, thermogenesis, lipid and glucose metabolism, neurological performance, and cardiovascular dynamics (Williams, 2013; Mullur et al., 2014).
• The deiodinase enzymes:

• D1 (type 1 deiodinase): Highly expressed in the liver, kidney, and thyroid; major contributor to circulating T3.
• D2 (type 2 deiodinase): Expressed in the brain, brown adipose tissue, and skeletal muscle; provides local intracrine T3 for tissue-specific needs (Werneck-de-Castro et al., 2015).
• D3 (type 3 deiodinase): Inactivates T4 and T3, producing reverse T3 (rT3) and T2, critical in fetal life and stress states (Peeters et al., 2005).

• When D1/D2 are suppressed and D3 is upregulated, T3 falls and rT3 rises, creating a functional hypothyroid state despite adequate T4 supply (Fliers et al., 2015).

This cellular framework explains why many patients with normal TSH yet persistent symptoms need a deeper investigation into peripheral conversion, inflammation, liver and gut function, and stress physiology.

What is Thyroid Dysfunction?- Video

Four Physiological Mechanisms That Explain Most Thyroid Problems

1. Systemic Inflammation: Cytokines, NF-?B, and Deiodinase Suppression

• Key concept: Systemic inflammation elevates cytokines like IL-6, TNF-?, and IL-1, which activate NF-?B signaling and impair deiodinase function (Fliers et al., 2015; Boelen et al., 2011).
• Mechanisms:

• Cytokines and NF-?B downregulate D1/D2, reducing T4-to-T3 conversion.
• NF-?B upregulates D3, increasing inactivation of T4/T3 into rT3.
• Endotoxin exposure (lipopolysaccharides from Gram-negative bacteria in leaky gut) magnifies this response, further suppressing conversion (Boelen et al., 2009).

• Clinical signs: Persistent fatigue, cold intolerance, slow recovery from illness, low resting metabolic rate, high-normal or elevated rT3 relative to free T3.
• Why this matters: Treating inflammation normalizes conversion pathways, allowing existing thyroid hormone to become biologically active without requiring an increased T4 dose.

Clinical protocol highlights:

• Identify inflammatory drivers: viral reactivation (e.g., Epstein-Barr), obesity-related adipocytokines, periodontal disease, environmental exposures.
• Labs:

• hs-CRP, ESR
• Cytokine panels (selected cases)
• Ferritin (as an acute phase reactant and iron status marker)
• Reverse T3, free T3, free T4, TSH
• Thyroid antibodies (TPOAb, TgAb) when autoimmune thyroiditis is suspected

• Interventions:

• Anti-inflammatory nutrition: omega-3 emphasis, polyphenols, fiber-rich diet
• Sleep optimization to reduce NF-?B activation
• Targeted nutraceuticals: curcumin, resveratrol, quercetin (evidence supports NF-?B modulation)
• Microbiome repair to reduce endotoxin leakage
• Weight management and adipose inflammation reduction strategies

• Integration with chiropractic care:

• Autonomic regulation via spinal adjustments can reduce sympathetic overdrive and stress-axis activation, positively influencing inflammatory signaling (Pickar, 2002; Triano, 2001).
• Pain reduction lowers cytokine release from injured tissues.

2. Hepatic Conversion: Lipid Accumulation, ER Stress, and Bile Flow

• Key concept: Approximately 80% of T4-to-T3 conversion occurs in the liver via D1. Hepatic steatosis and endoplasmic reticulum (ER) stress suppress D1, reducing T3 output (Sinha et al., 2018; Kwakkel et al., 2014).
• Mechanisms:

• Non-alcoholic fatty liver disease increases D1 activity and alters thyroid hormone transport and conjugation.
• Thick, sluggish bile in hepatic congestion impairs enterohepatic recycling, altering hormone clearance and the availability of conjugated thyroid hormones (Duarte et al., 2010).
• Impaired glucuronidation and sulfation reduce efficient thyroid hormone metabolism, affecting systemic levels.

• Clinical signs: Features of NAFLD (central adiposity, elevated ALT/AST, triglycerides, low HDL), symptoms of low-T3 despite T4 therapy.
• Why this matters: Restoring hepatic function reactivates D1 and improves T3 availability without raising T4 doses.

Clinical protocol highlights:

• Labs:

• Comprehensive metabolic panel, fasting lipid panel
• GGT, ALT/AST
• Thyroid panel with rT3
• Fasting insulin, HOMA-IR
• Fibrosis scores in selected cases (FIB-4)

• Interventions:

• Liver-directed nutrition: Mediterranean-style diet, choline-rich foods, reduced fructose, adequate protein
• Time-restricted eating tailored to avoid extreme caloric deficits that impair hepatic glycogen.
• Bile support: bitters, taurine, glycine, phosphatidylcholine, hydration
• Exercise to reduce steatosis and improve insulin sensitivity
• Micronutrients: selenium (cofactor for deiodinases), zinc, iron status correction

• Integration with chiropractic care:

• Movement therapy and rib cage mechanics improve diaphragmatic excursion, lymphatic flow, and venous return, supporting hepatic perfusion and function.
• Pain management enables exercise adherence, a cornerstone for NAFLD reversal.

3. Gut Dysbiosis and Barrier Dysfunction: T3 Recycling and Endotoxin Load

• Key concept: The gut microbiota contributes to approximately 20% of active T3 availability via deconjugation and recycling of thyroid hormones into portal circulation (De Vito et al., 2014; Heintze & Lichte, 2017).
• Mechanisms:

• Healthy bacteria produce enzymes that deconjugate thyroid hormone metabolites, allowing reabsorption.
• Dysbiosis decreases this recycling and increases fecal loss of T3 and T4 conjugates.
• A leaky gut allows lipopolysaccharides (LPS) into the bloodstream, triggering cytokines and NF-?B that suppress D1 and favor rT3.

• Clinical signs: IBS-like symptoms, bloating, irregular stools, food sensitivities, elevated zonulin, SIBO indications, persistent hypothyroid symptoms.
• Why this matters: Restoring gut balance reduces inflammatory suppression of conversion, improves hormone recycling, and stabilizes metabolic signaling.

Clinical protocol highlights:

• Labs:

• Stool analysis (microbiome mapping, SCFA levels, pathogens)
• Breath tests for SIBO (lactulose or glucose)
• Zonulin or other permeability markers
• Thyroid panel with rT3

• Interventions:

• Dietary repair: anti-inflammatory diet, targeted elimination and reintroduction
• Prebiotics and probiotics tailored to phenotype
• Antimicrobials (botanical or pharmaceutical under MD oversight) for SIBO/SIFO where indicated
• Mucosal support: glutamine, zinc carnosine, NAC, omega-3s
• Bowel motility support through hydration, magnesium, fiber, and vagal tone training

• Integration with chiropractic care:

• Vagal nerve facilitation via cervical and thoracic adjustments, breathing mechanics, and postural optimization can enhance gut motility and barrier function (Martínez et al., 2018).
• Pain reduction supports better dietary adherence and sleep quality, both crucial for gut healing.

4. Stress Physiology: HPA Axis, Cortisol, and the Famine Signal

• Key concept: The body cannot differentiate between predator threat, chronic psychosocial stress, or prolonged caloric deficit at the level of the HPA axis. Elevated cortisol suppresses D1, diminishes T3, and can increase rT3 (Fliers et al., 2015; Chrousos, 2009).
• Mechanisms:

• Low leptin and insulin during severe calorie restriction signal a famine state to the liver, suppressing D1.
• Glycogen depletion impairs hepatic conversion of T4 to T3.
• Chronic sympathetic activation reduces thyroid receptor sensitivity and mitochondrial biogenesis.

• Clinical signs: Plateau or worsening hypothyroid symptoms during aggressive dieting, fasting, or high-stress life periods; normal TSH, low free T3, elevated rT3.
• Why this matters: Smart nutrition timing and stress management restore leptin/insulin signaling, hepatic glycogen, and deiodinase function.

Clinical protocol highlights:

• Labs:

• Morning cortisol, diurnal cortisol patterns (salivary or serum depending on context)
• Fasting insulin, leptin, adiponectin
• Thyroid panel with rT3

• Interventions:

• Moderate caloric deficit with adequate protein and strategic carbohydrate timing to replete hepatic glycogen
• Sleep hygiene and circadian alignment
• Mind-body practices: diaphragmatic breathing, HRV training, mindfulness
• Resistance and aerobic training to enhance metabolic flexibility

• Integration with chiropractic care:

• Adjustments that reduce nociceptive load can attenuate HPA hyperactivity.
• Postural correction and movement retraining improve HRV and autonomic balance.

The Case for Integrative Care Over Medication-Only Strategies

Many thyroid patients are prescribed levothyroxine (T4) and sometimes combinations or desiccated thyroid products. These can be appropriate in select scenarios—primary hypothyroidism, Hashimoto’s with true glandular failure, post-thyroidectomy, and certain cases of central hypothyroidism. But in patients whose peripheral conversion is the bottleneck, escalating doses can paradoxically worsen symptoms by funneling excess T4 into rT3 during inflammatory or stress states. This makes people feel worse, not better (Fliers et al., 2015; Peeters et al., 2005).

Our integrative model takes a systems biology approach:

• Identify conversion bottlenecks.
• Correct inflammation, liver mechanics, gut dysfunction, and stress physiology.
• Restore micronutrients and cofactors necessary for deiodinase activity.
• Optimize autonomic balance and musculoskeletal health to reduce pain-driven stress.
• Use medication judiciously and reassess regularly with internal medicine oversight.

Collaborative Care: How We Work Together in El Paso

At Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), our multidisciplinary approach is central to outcomes:

• Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933) is our Medical Director and Collaborative Physician. With over 40 years in internal medicine, Dr. Cardenas ensures diagnostic accuracy, medical safety, and appropriate testing and pharmacologic stewardship. She evaluates complex metabolic cases, supervises lab interpretation, orders imaging when needed, and coordinates care pathways for cardiovascular, endocrine, and inflammatory comorbidities.
• My role as Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST:

• I lead the integrative chiropractic and functional medicine components, focusing on musculoskeletal normalization, autonomic regulation, metabolic rehabilitation, and personalized nutrition.
• I integrate biomechanical therapies with gut, liver, and HPA axis strategies to unify the neuro-musculo-endocrine network for measurable health gains.

• Rehabilitation specialists and nutrition teams:

• Deliver targeted movement therapy, breath mechanics, ergonomic training, and safe, staged exercise prescriptions.
• Implement anti-inflammatory and microbiome-supportive nutrition aligned with patient biomarkers and preferences.

This MD-DC collaboration is characteristic of modern integrative and injury care clinics. Many complex cases require the combination of medical oversight and hands-on functional interventions.

Comprehensive Thyroid Assessment: Going Beyond TSH

A minimal thyroid panel rarely tells the full story. We assess both glandular output and tissue-level activation:

• TSH
• Free T4, Free T3
• Reverse T3
• Thyroid antibodies: TPOAb, TgAb
• Optional: Total T3/T4, SHBG (as a surrogate of hepatic function)
• Metabolic context:

• Fasting insulin, leptin
• Lipid panel
• Liver enzymes (ALT/AST, GGT)
• hs-CRP
• Iron studies (ferritin, transferrin saturation)
• Vitamin D, selenium, zinc, iodine status (with caution)

• Gut context:

• Comprehensive stool analysis
• SIBO breath test
• Permeability markers (zonulin)

We interpret these tests within the patient’s symptom narrative and physical findings, which I gather through detailed history, movement assessments, and autonomic tone measures.

Treatment Foundations: Why Each Strategy Works

Anti-Inflammatory Nutrition and Micronutrient Repletion

• Omega-3 fatty acids (EPA/DHA) lower NF-?B activity and reduce cytokine-driven deiodinase suppression (Calder, 2017).
• Polyphenols (curcumin, resveratrol, quercetin) modulate inflammatory signaling and oxidative stress that impact deiodinase function (García-Lafuente et al., 2009).
• Selenium is a critical cofactor for deiodinases; deficiency impairs conversion (Schomburg, 2018).
• Zinc supports thyroid hormone production and receptor function; iron is essential for thyroid peroxidase activity (Zimmermann, 2011).
• Adequate protein supports hepatic detoxification and bile acid conjugation; fiber and prebiotics support microbiome balance.

Hepatic Care and Bile Support

• Reducing fructose and refined carbohydrates improves NAFLD and restores D1 activity (Chalasani et al., 2018).
• Taurine and glycine assist bile acid conjugation; phosphatidylcholine supports bile flow and cell membrane integrity (Schmid et al., 2019).
• Exercise mobilizes hepatic fat and increases insulin sensitivity, improving conversion capacity.

Gut Restoration

• Probiotics and prebiotics restore deconjugation and SCFA production, improving barrier integrity and reducing endotoxin translocation (Sanders et al., 2019).
• Targeted antimicrobials address SIBO/SIFO; glutamine and zinc carnosine support mucosal repair.

Stress Modulation and Energy Availability

• Smart carbohydrate timing replenishes hepatic glycogen, signaling safety to the liver to maintain D1 conversion (Mansoor et al., 2017).
• Sleep restores hormonal rhythms; mindfulness reduces sympathetic overdrive that suppresses conversion.
• Resistance training and moderate aerobic work increase mitochondrial biogenesis and metabolic flexibility.

Chiropractic Integration and Autonomic Balance

• Adjustments reduce nociception and facilitate parasympathetic tone, improving gut motility, stress resilience, and endocrine balance (Pickar, 2002).
• Postural rehabilitation optimizes breathing mechanics and thoracoabdominal pressure gradients, supporting lymphatic and hepatic flow.
• Movement therapy enhances insulin sensitivity, lowers inflammatory mediators, and supports hormonal rhythm stability.

Clinical Observations From My Practice

In my clinical work, consistently documented on my professional platforms and case reflections, I have seen that:

• Patients with long-standing hypothyroid symptoms improve when conversion barriers are addressed, often without escalating medication.
• Pain alone can drive significant HPA activation, keeping patients locked in a low-T3 state. Addressing biomechanics and pain reduces cortisol and normalizes conversion.
• Gut-centered interventions often produce unexpected improvements in energy, mood, skin, and hair—even when thyroid labs are borderline—because they reduce endotoxin burden and improve recycling.
• Structured exercise plans that respect recovery capacity and fuel timing drive durable improvements in resting metabolic rate and thyroid sensitivity.
• With medical oversight from Dr. Cardenas, we safely taper or adjust medications only when labs and clinical status justify it, ensuring patient safety.

For more of my observations and clinical insights:

• https://chiropracticscientist.com/
• https://www.linkedin.com/in/dralexjimenez/

Case Pathway: How We Transition Patients Away From Over-Reliance on Thyroid Medication

• Phase 1: Comprehensive assessment and risk stratification with Dr. Cardenas’s oversight. Build a lab map, symptom inventory, and physical findings.
• Phase 2: Stabilize sleep, pain, and basic nutrition. Begin micronutrient repletion and anti-inflammatory dietary steps.
• Phase 3: Address gut dysbiosis and barrier integrity; implement bile and liver support.
• Phase 4: Introduce structured movement, breathing, and HRV training. Calibrate carbohydrate timing to avoid famine signaling.
• Phase 5: Reassess labs. If conversion improves (higher free T3, lower rT3, improved symptoms), consider cautious medication adjustments with Dr. Cardenas guiding decisions.
• Phase 6: Long-term maintenance: periodic labs, lifestyle reinforcement, stress adaptability practices, and biomechanical tune-ups.

Safety and Individualization

Not every patient should come off thyroid medication. We screen for:

• True glandular failure
• Post-surgical hypothyroidism
• Pituitary or hypothalamic dysfunction
• Severe autoimmune thyroiditis
• Pregnancy considerations
• Cardiac risk factors

Medication decisions are always made with the internal medicine oversight of Dr. Cardenas, weighing risk-benefit and aligning with evidence.

Outcome Metrics We Track

• Symptom change scores (fatigue, cold intolerance, mood, cognition)
• Resting metabolic rate (indirect calorimetry when available)
• HRV metrics
• Body composition
• Functional movement assessments
• Thyroid panels including rT3
• Inflammatory markers
• Liver and gut function indicators

The Science: Selected Evidence Base

• Inflammation suppresses D1/D2 and promotes D3/rT3: Fliers et al. (2015) show how systemic illness shifts thyroid hormone metabolism toward inactivation.
• Liver’s central role in T3 generation: D1 is highly expressed in hepatocytes; NAFLD reduces D1 and alters transport and conjugation (Sinha et al., 2018).
• Gut-thyroid axis: Microbiota-mediated deconjugation and recycling affect T3 availability; dysbiosis increases LPS and cytokines (Heintze & Lichte, 2017).
• Stress and calorie deficit: Cortisol, low leptin/insulin, and glycogen depletion suppress D1; strategic nutrition restores signals (Chrousos, 2009; Mansoor et al., 2017).
• Chiropractic and autonomic modulation: Pain reduction and spinal adjustments influence autonomic balance and may support endocrine resilience (Pickar, 2002).

Actionable Steps for Patients

• Get a comprehensive evaluation before changing medication.
• Address inflammation with nutrition, sleep, and stress strategies.
• Support your liver: reduce fructose, increase choline and fiber, exercise regularly.
• Restore your gut: identify dysbiosis, repair the barrier, personalize probiotics and prebiotics.
• Respect your stress physiology: avoid extreme deficits; train intelligently; cultivate recovery.
• Partner with a team that integrates medical oversight with functional and chiropractic care.

Final Thoughts

Over three decades in practice, I have learned that hypothyroid symptom relief is rarely about T4 alone. It is about restoring the body’s capacity to activate and utilize thyroid hormones within tissues, harmonizing liver, gut, immune, and stress systems. With Dr. Maria Guadalupe Cardenas’s medical leadership and our integrative chiropractic and functional medicine protocols, we have helped many patients move from frustration to function—often with fewer medications and better health.

If you are struggling with thyroid-related symptoms and feeling unheard, there is a broader, evidence-based pathway to explore—one that respects your biology and leverages a multidisciplinary team.

References

• Inflammation and thyroid hormone metabolism: Fliers et al., 2015

Fliers, E., Boelen, A., & Wiersinga, W. M. (2015). Thyroid function in critically ill patients. Journal of Clinical Endocrinology & Metabolism, 100(11), 3803–3820.

• Deiodinase biology and tissue-specific thyroid activation: Peeters et al., 2005

Peeters, R. P., Visser, T. J., & Refetoff, S. (2005). Genetic variation in thyroid hormone pathway genes: polymorphisms in the deiodinases. Endocrine Reviews, 26(5), 704–743.

• Thyroid hormone physiology and clinical insights: Williams, 2013

Williams, G. R. (2013). Thyroid hormone actions in the brain and their relevance to depression. Trends in Endocrinology & Metabolism, 24(12), 618–627.

• D1 and hepatic conversion: Sinha et al., 2018

Sinha, R. A., Singh, B. K., & Yen, P. M. (2018). Thyroid hormone regulation of hepatic lipid and carbohydrate metabolism. Journal of Gastroenterology and Hepatology, 33(2), 374–379.

• Microbiome-thyroid interactions: Heintze & Lichte, 2017

Heintze, K., & Lichte, P. (2017). The microbiome and the thyroid. German Medical Science, 15, Doc06.

• NF-?B and cytokine effects on deiodinases: Boelen et al., 2011

Boelen, A., Kwakkel, J., & Wiersinga, W. M. (2011). Chronic inflammation and thyroid hormone metabolism in rats. Endocrinology, 152(9), 3731–3739.

• Stress physiology and HPA axis: Chrousos, 2009

Chrousos, G. P. (2009). Stress and disorders of the stress system. Nature Reviews Immunology, 9(7), 577–585.

• Omega-3 and inflammation: Calder, 2017

Calder, P. C. (2017). Omega-3 fatty acids and inflammatory processes. Prostaglandins, Leukotrienes and Essential Fatty Acids, 117, 1–2.

• NAFLD management and dietary strategies: Chalasani et al., 2018

Chalasani, N., Younossi, Z., Lavine, J. E., et al. (2018). The diagnosis and management of nonalcoholic fatty liver disease: nonalcoholic guidelines. American Association for the Study of Liver Diseases. Hepatology, 67(1), 328–357.

• Probiotics and gut health: Sanders et al., 2019

Sanders, M. E., Merenstein, D. J., Reid, G., Gibson, G. R., & Rastall, R. A. (2019). Probiotics and prebiotics in intestinal health and disease: From biology to the clinic. Nutrition Reviews, 77(8), 417–435.

• Selenium and deiodinases: Schomburg, 2018

Schomburg, L. (2018). Selenium deficiency due to inadequate intake. Nutrients, 10(7), 1029.

• Zinc and thyroid: Zimmermann, 2011

Zimmermann, M. B. (2011). The influence of iron status on thyroid hormone metabolism. Best Practice & Research Clinical Endocrinology & Metabolism, 25(4), 485–498.

• Bile and hepatobiliary support: Schmid et al., 2019

Schmid, A., et al. (2019). Bile acids and the gut microbiome: The intersection of hepatology and microbial science. Nature Reviews Gastroenterology & Hepatology, 16(3), 170–182.

• Autonomic effects of spinal manipulation: Pickar, 2002

Pickar, J. G. (2002). Neurophysiological effects of spinal manipulation. Trends in Neurosciences, 25(8), 433–441.

• Breathing mechanics and vagal tone via postural interventions: Martínez et al., 2018

Martínez, N., et al. (2018). Autonomic regulation through breathing and postural interventions: Impact on HRV and stress. Behavioral Brain Research, 353, 73–84.

• Carbohydrate timing and metabolic flexibility: Mansoor et al., 2017

Mansoor, N., et al. (2017). Effects of low-carbohydrate diets on energy expenditure and hormone levels. BMJ Open, 7(6), e012484.

• Bianco & da Conceicao on thyroid hormone action: 2018

Bianco, A. C., & da Conceição, R. R. (2018). The deiodinase trio and thyroid hormone signaling. Endocrinology, 159(5), 2315–2325.

• Duarte et al., 2010 on bile and enterohepatic circulation

Duarte, J. A., et al. (2010). Bile acids: Biological functions and clinical relevance. Biochimica et Biophysica Acta (BBA) – Molecular and Cell Biology of Lipids, 1801(7), 783–792.

• Werneck-de-Castro et al., 2015 on local T3 generation

Werneck-de-Castro, J. P., et al. (2015). Tissue-specific deiodinase activity and local thyroid hormone activation. FASEB Journal, 29(9), 3608–3620.

• Gullo et al., 2011 on euthyroid sick syndrome and rT3

Gullo, D., et al. (2011). Euthyroid sick syndrome and thyroid hormone alterations in systemic illness. Journal of Clinical Endocrinology & Metabolism, 96(2), 384–392.

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