Thyroid Optimization: What You Should Know About Hormones

Optimize your health by understanding the importance of thyroid health for hormone balance and its effects on your body.

Abstract

I am Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. In this educational post, I share how I evaluate and treat persistent hypothyroid symptoms through a modern, evidence-based lens that centers on tissue-level thyroid signaling, especially free triiodothyronine (free T3). Drawing from my personal journey living without a native thyroid and from thousands of patient encounters at HealthCoach Clinic, I explain the physiology of thyroid hormones, the limitations of thyroid-stimulating hormone (TSH)-only monitoring, and why some patients improve with combination therapy that includes liothyronine (T3) or desiccated thyroid extract. I walk you through deiodinase biology, reverse T3 (rT3) as a metabolic brake, the role of ferritin and micronutrients in T4-to-T3 conversion, and how comprehensive lab strategies guide dosing. I also detail how integrative chiropractic care supports autonomic balance, pain reduction, movement efficiency, and mitochondrial health—key levers that enhance thyroid signaling in real tissues. Throughout, I reference leading research and consensus statements, explain how I time labs and split doses to improve safety and outcomes, and share clinical patterns, protocols, and monitoring strategies that have helped my patients reclaim energy, mood, cognition, and cardiometabolic health.

• About my clinic and ongoing insights:

• • HealthCoach Clinic: healthcoach.clinic/
  • Professional updates: www.linkedin.com/in/dralexjimenez/

My Clinical Mission

Decades ago, a patient’s thyroid function was assessed after thyroid ablation, amid various challenges. Those early experiences shaped my curiosity about how the environment intersects with biology. I also know firsthand what profound hypothyroidism feels like—with TSH levels above 150 mIU/L—including crushing fatigue, cold intolerance, constipation, brain fog, slowed thinking, and a body that seemed to move through molasses. Living through that removed any abstraction from my clinical reasoning.

Today, in my solo chiropractic practice, I care for more than 9,000 patients with thyroid-related conditions. We track outcomes and iterate on protocols. This lived experience continues to push me toward precision, evidence, and whole-person care that actually restores function. By integrating targeted chiropractic adjustments to optimize nervous system function and spinal alignment, I support better endocrine regulation while addressing the full spectrum of thyroid imbalance. Patients often describe not only hypothyroid effects—such as weight gain, low energy, depression, dry skin, hair thinning, muscle weakness, and exercise intolerance—but also the disruptive impact of hyperthyroidism, including unintended weight loss, heat intolerance, anxiety or irritability, rapid heartbeat or palpitations, diarrhea, tremors, restlessness, insomnia, and excessive sweating. This whole-body approach helps move patients beyond normalized labs toward genuine restoration of energy, metabolism, mood, and vitality.

Thyroid Physiology 101: Why T3 Is the Final Common Effector

When patients ask why they still feel hypothyroid despite “normal” labs, I start with the basics.

• The thyroid gland produces mostly thyroxine (T4) and smaller amounts of triiodothyronine (T3).
• T4 is largely a prohormone; its value lies in conversion to T3, the bioactive hormone.
• Inside tissues, deiodinase enzymes control this conversion:

• • D1 (liver, kidney) contributes to circulating T3.
  • D2 (in the brain, pituitary, skeletal muscle, and brown adipose tissue) generates intracellular T3 where it is needed.
  • D3 inactivates T4 and T3, producing reverse T3 (rT3) and T2.

• T3 binds to nuclear thyroid receptors (TR? and TR?), driving gene transcription for oxidative phosphorylation, mitochondrial biogenesis, fatty acid oxidation, glucose uptake, thermogenesis, and Na+/K+-ATPase activity—this is the machinery of energy, heat, and metabolic rate (Silvestri, Santulli, & Morrone, 2014).

Key clinical insight: TSH reflects pituitary sensing and feedback. Because the pituitary is D2-rich, it converts T4 to T3 locally and very efficiently. As a result, the pituitary can feel “euthyroid” while the rest of the body is relatively T3-deficient. This is one reason TSH can be normal or low even when patients have low tissue-level T3 action (Bianco & Kim, 2019; Jonklaas et al., 2014).

In my practice, patients often report classic symptoms—cold intolerance, weight gain, fatigue, constipation, hair thinning, and brain fog—despite a normalized TSH on T4-only therapy. That pattern drives me to look at free hormones and the terrain that supports conversion.

References:

• Thyroid Hormone and Mitochondrial Function (Silvestri et al., 2014)
• Biochemistry, Physiology, and Pathophysiology of Thyroid Hormone Action (Bianco & Kim, 2019)
• Guidelines for the Treatment of Hypothyroidism (Jonklaas et al., 2014)

Why TSH Alone Often Fails: The Pituitary Island Effect

TSH is a great starting point — but it has limits once treatment begins.

• TSH is extremely effective at detecting brand-new thyroid problems.
• Once you’re already on thyroid medication, however, TSH can be misleading. The pituitary gland (the source of TSH) is protected by very high levels of the D2 enzyme, so it can still make plenty of active T3 locally even when the rest of your body is short on it (Peeters, 2017; Fliers, Boelen, & Wiersinga, 2011).
• Adding external T4 can actually make things worse elsewhere in the body: it often slows the helpful D1 and D2 enzymes and ramps up D3, which turns more T4 into the inactive reverse T3 (rT3). That rT3 sits on the receptors like a brake pedal without ever pressing “go” (Endocrine Practice, 2018).

What this means for you:
A “good” or normal TSH on paper does **not** guarantee that your heart, muscles, brain, and brown fat are getting enough active T3. If you still have symptoms, I look beyond TSH and check free T3, free T4, and the full context to get the real picture.

References:

• Non-thyroidal illness syndrome (Fliers et al., 2011)
• Thyroid hormones and aging (Peeters, 2017)
• Role of reverse T3 in thyroid physiology and illness (Endocrine Practice, 2018)

Reverse T3: Understanding the Metabolic Brake

Reverse T3 (rT3) is an isomer that binds thyroid receptors without activating them. Under conditions of inflammation, illness, caloric restriction, high cortisol, or nutrient deficits, D3 rises, leading to more rT3. In the acute setting, that energy-conserving response can be adaptive. Chronic, it mimics hypothyroidism at the tissue level.

• Signals that drive rT3 up: chronic stress, sleep disruption, infection, iron deficiency, and poorly controlled insulin resistance.
• Clinical pattern: normal TSH, normal or high-normal free T4, low free T3, and elevated rT3—with robust hypothyroid symptoms.

When I see this, I correct the terrain—iron, selenium, zinc, vitamin D, sleep, inflammation, insulin resistance—then consider T3-inclusive therapy if symptoms persist (Grozinsky-Glasberg, Fraser, & Nahshoni, 2009; Wiersinga, 2014).

References:

• Thyroxine-triiodothyronine combination therapy versus thyroxine monotherapy (Grozinsky-Glasberg et al., 2009)
• Paradigm shifts in thyroid hormone replacement therapies (Wiersinga, 2014)
• Role of reverse T3 in thyroid physiology and illness (Endocrine Practice, 2018)

The T4-to-T3 Conversion Bottleneck: Deiodinases, Nutrients, and Inflammation

Conversion depends on healthy D1/D2 activity, which, in turn, depends on micronutrients and a low-inflammatory milieu.

• Selenium supports deiodinase activity and may reduce thyroid peroxidase antibody levels (Ventura, Melo, & Carrilho, 2017).
• Iron/ferritin is crucial. Low ferritin levels impair conversion, and iron deficiency reduces mitochondrial ATP production—compounding fatigue (de Jongh et al., 2016; Zimmermann & Hurrell, 2007).
• Zinc supports receptor integrity and TSH biology.
• Vitamin D supports immune balance and musculoskeletal function.

My clinical rule: if ferritin is low, correct it first. Many patients feel better once ferritin rises into functional ranges (often >50–70 ng/mL, individualized). I also time iron away from thyroid medication by at least 4 hours to avoid interference with absorption.

References:

• Endocrine and metabolic effects of low iron status (de Jongh et al., 2016)
• Nutritional iron deficiency (Zimmermann & Hurrell, 2007)
• Selenium and thyroid disease (Ventura et al., 2017)

Levothyroxine vs Combination Therapy vs Desiccated Thyroid: Who Benefits and Why

Many patients do well on levothyroxine (T4) alone, particularly when conversion is intact. A meaningful subset remains symptomatic, with low or low-normal free T3 and signs of rT3 dominance. For them, I consider:

• Combination therapy (T4+T3): Allows precise titration of liothyronine. I often start with 2.5–5 mcg once or twice daily and reassess in 4–6 weeks, watching HR, BP, symptoms, and free hormone levels (Jonklaas et al., 2014; Jonklaas et al., 2021).
• Desiccated thyroid extract (DTE): Offers a fixed T4:T3 ratio that some patients prefer and respond to; I frequently split doses to smooth T3 peaks (Hoang et al., 2013).

Evidence shows mixed group-level outcomes for combination therapy; however, randomized trials and meta-analyses consistently reveal subsets who prefer and benefit from T3-inclusive regimens. Genetic variability in DIO2 may partly explain why some individuals thrive on combination therapy (Panicker et al., 2009; Biondi & Wartofsky, 2014).

References:

• Guidelines for the Treatment of Hypothyroidism (Jonklaas et al., 2014)
• Thyroid Hormone Therapy: ATA Position Statements (Jonklaas et al., 2021)
• Desiccated thyroid extract compared with levothyroxine (Hoang et al., 2013)
• DIO2 polymorphisms and response to levothyroxine therapy (Panicker et al., 2009)
• Combination treatment with T4 and T3: Toward personalized replacement therapy (Biondi & Wartofsky, 2014)

Lab Strategy That Matches Physiology: What I Order and When I Draw

I do not rely on TSH alone when patients are symptomatic. My core labs include:

• TSH, free T4, free T3
• Reverse T3 when conversion problems are suspected
• TPO and thyroglobulin antibodies
• Ferritin/iron studies, CBC
• Vitamin D, selenium, zinc, magnesium, B12/folate
• Lipid panel, fasting insulin, HbA1c
• hs-CRP or other inflammatory markers
• SHBG and, when indicated, sex hormone panels

To improve reproducibility, I standardize lab timing:

• For patients on T3-containing regimens or DTE, I schedule labs 5–6 hours after the morning dose. This window avoids the sharp 1–2-hour post-dose T3 peak and better reflects the functional state throughout the day.
• I document the time of the last dose on the lab requisition and in the EMR and reschedule if timing is off.

Why this matters: Understanding T3 kinetics prevents misinterpretation and reduces the risk of over- or under-treatment based on an arbitrary peak or trough (Jonklaas et al., 2014; Bianco & Kim, 2019).

References:

• Guidelines for the Treatment of Hypothyroidism (Jonklaas et al., 2014)
• Biochemistry, Physiology, and Pathophysiology of Thyroid Hormone Action (Bianco & Kim, 2019)

Dosing Principles: Why I Split T3 and How I Reduce Side Effects

Liothyronine (T3) has a brisk serum peak. To reduce palpitations, jitteriness, and afternoon crashes, I commonly use split dosing (BID or TID) and calibrate dosing timing to the patient’s energy curve.

• Start low: 2.5–5 mcg once daily, then split to morning and early afternoon if tolerated.
• For DTE, I often use a larger morning dose with a smaller early-afternoon dose to smooth peaks.
• I ask: “When is your fastest heartbeat?” Wearables like the Apple Watch help confirm if peaks occur about two hours post-dose. If so, I divide or redistribute dosing to blunt the peak.

This approach balances receptor activation and autonomic comfort while maintaining steady tissue exposure. I coordinate closely with cardiology for patients with a history of arrhythmia and titrate slowly, with HR/BP/ECG monitoring as needed (Jonklaas et al., 2014; Wiersinga, 2014).

References:

• Guidelines for the Treatment of Hypothyroidism (Jonklaas et al., 2014)
• Paradigm shifts in thyroid hormone replacement therapies (Wiersinga, 2014)

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Thyroid Dysfunction-Video

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Hashimoto’s Thyroiditis: Autoimmunity, Conversion, and Practical Supports

Patients with Hashimoto’s often need more than gland replacement because chronic inflammation alters deiodinase activity and can create tissue-level thyroid hormone resistance.

What I do:

• Stabilize dosing with split T3 to smooth energy and cognition.
• Replete selenium (often 200 mcg/day as clinically appropriate), zinc, vitamin D, and correct iron deficiency—the quartet that most often unlocks conversion.
• Use an anti-inflammatory nutrition template; many patients benefit from a gluten-free diet
• Address gut integrity and sleep, and reduce stressors that drive rT3.

This comprehensive approach reduces inflammatory impedance and supports consistent T3 signaling at tissues (Ventura et al., 2017; de Jongh et al., 2016).

References:

• Selenium and thyroid disease (Ventura et al., 2017)
• Endocrine and metabolic effects of low iron status (de Jongh et al., 2016)

Iodine: Requirements, Risks, and Clinical Nuance

Iodine is essential for thyroid hormone synthesis. Both deficiency and excess can cause dysfunction. In Hashimoto’s, abrupt high-dose iodine can provoke flares, especially if selenium is low.

My approach:

• Assess baseline status and antibodies.
• In autoimmune patients, start conservatively and ensure selenium repletion to reduce intrathyroidal oxidative stress.
• Educate that transient TSH changes may reflect NIS and transporter upregulation during repletion, rather than necessarily indicating worsening hypothyroidism (Zimmermann & Boelaert, 2015; Leung, Pearce, & Braverman, 2012).

References:

• Iodine deficiency and thyroid disorders (Zimmermann & Boelaert, 2015)
• Iodine nutrition in pregnancy and lactation (Leung et al., 2012)

Integrative Chiropractic Care: Aligning Autonomics, Movement, and Mitochondria

Thyroid hormones act throughout the body, but patients experience their effects locally—through muscle tone, joint kinematics, fascial glide, pain thresholds, and autonomic balance. Hypothyroidism often presents with myofascial stiffness, tendinopathy, reduced collagen turnover, and slowed nerve conduction. These issues magnify fatigue and limit training capacity.

How integrative chiropractic care helps:

• Autonomic regulation: Targeted spinal and soft-tissue interventions, breathwork, and HRV-guided recovery increase vagal tone and reduce sympathetic overdrive—physiologic states that favor D1/D2 activity and better T4-to-T3 conversion (Oakley et al., 2018).
• Pain reduction and neuroinflammation: Reducing nociceptive drive lowers cytokines that otherwise drive up D3 and rT3, improving T3 availability in tissues.
• Movement therapeutics: Progressive resistance training and zone 2 cardio increase mitochondrial biogenesis and GLUT4 expression—contexts where T3 signaling is most effective.
• Sleep optimization: You cannot overdose on a broken sleep architecture. Gentle manual therapy and sleep coaching improve slow-wave sleep and endocrine resilience (Irwin, 2015).

In my clinic, patients who pair well-titrated thyroid therapy with chiropractic adjustments, mobility work, and graded strength and aerobic progression consistently report faster improvements in energy, thermoregulation, and exercise tolerance than medication alone.

References:

• Autonomic Modulation Through Manual Therapy (Oakley et al., 2018)
• Sleep and the Endocrine System (Irwin, 2015)

Cardiometabolic and Cognitive Links: Why Free T3 Tracks Outcomes

Across cardiology and critical care, low free T3 correlates with worse outcomes, while TSH and free T4 often do not in treated patients.

• The heart is T3-dependent: T3 regulates myosin heavy chain isoforms, SERCA2a, and endothelial function. Low T3 depresses ejection fraction and lusitropy and impairs vascular remodeling (Iervasi & Pingitore, 2013; Pingitore & Iervasi, 2016).
• In critical illness and ARDS, low T3 on admission predicts mortality and ventilator dependence (Fliers et al., 2011).
• In cognition and mood, low T3 associates with faster progression from mild cognitive impairment and can blunt antidepressant response; adjunctive T3 can potentiate recovery in selected depression cases (Joffe & Singer, 2020).

Clinically, when I address low free T3—by optimizing conversion and terrain, and adding T3 judiciously as needed—patients often demonstrate better exercise tolerance, HRV, mood, and cognitive performance.

References:

• Thyroid hormones and cardiovascular system (Iervasi & Pingitore, 2013)
• Triiodothyronine and the cardiovascular system (Pingitore & Iervasi, 2016)
• Non-thyroidal illness syndrome (Fliers et al., 2011)
• Liothyronine augmentation in depression (Joffe & Singer, 2020)

Practical Protocol: How I Evaluate, Treat, and Monitor

I use a clear, step-by-step plan that addresses the whole picture — not just the thyroid hormone numbers. Here’s how it works in plain language:

Phase 1: Stabilize and Clarify

• – Confirm the exact diagnosis and screen for autoimmune Hashimoto’s or central hypothyroidism (a problem higher up in the brain).
• – Order the full set of labs (see the Lab Strategy section).
• – Review your sleep, stress levels, current medications (such as amiodarone or steroids), extreme dieting, and any environmental factors that could be playing a role.

Phase 2: Optimize Replacement

• Carefully adjust and titrate levothyroxine (T4) to the right dose for you.
• If symptoms continue and free T3 is low or low-normal (or reverse T3 is high), we trial a combination of T4 + T3 or desiccated thyroid (DTE). I monitor heart rate and blood pressure closely and always time labs 5–6 hours after the morning dose for accurate results.

Phase 3: Correct the Terrain

• Bring iron (ferritin) up to healthy levels, and remind you to separate it from thyroid meds by at least 4 hours to ensure proper absorption.
• Make sure selenium, zinc, and vitamin D are at optimal levels.
• Support gut health and follow an anti-inflammatory, nutrient-rich diet.

Phase 4: Movement and Autonomic Reset

• Build a strong foundation with steady zone 2 cardio and progressive strength training.
• Add integrative chiropractic care, breathwork, and heart-rate-variability (HRV) training to lower pain and calm overactive” fight-or-flight” nervous system signals.

Phase 5: Neuroendocrine Cohesion

• Fix sleep issues (screen for apnea and use CBT-I strategies when needed) and address stress patterns that drive up reverse T3.
• In the right patients, we also optimize sex hormone levels to help rebuild muscle and boost energy production within cells.

Phase 6: Monitor and Iterate

• Re-check symptoms, vital signs, HRV, and labs every 4–12 weeks (depending on how things are changing).
• Adjust doses slowly and thoughtfully, aiming for free T3 in the mid-to-upper normal range — while keeping your heart rate, blood pressure, and other signs stable and free of any over-treatment effects.

Why this works
We restore the raw materials your body needs, improve the conversion of T4 to active T3, reduce the metabolic “brake” (reverse T3), and balance your nervous system and movement. That removes the hidden obstacles, so the thyroid medication can finally reach your tissues and work as it’s supposed to.

Clinical Observations from HealthCoach Clinic

Here are some of the common roadblocks and how we clear them

• • People who have lived with hypothyroidism for years often develop a strong habit of avoiding movement because pain and fatigue make everything feel harder. Starting early with gentle hands-on therapy (manual therapy) and simple mobility exercises helps lower those barriers and gets the body reconditioned much faster.
  • Many patients who still feel unwell on T4-only medication (levothyroxine) have low free T3 and/or high reverse T3 (rT3). Adding a modest amount of T3 — given in split doses at the right times — frequently unlocks real improvement.
  • Fixing iron deficiency is one of the biggest issues we have. Bringing ferritin levels up to a healthy range often leads to better hair growth, improved mood, more energy, and stronger conversion of T4 into active T3.
  • In properly screened patients, optimizing androgen (testosterone) levels helps the body build muscle protein more effectively and makes it easier to stick with exercise. This finally allows the full metabolic benefits of thyroid treatment to shine through.
  • For patients who have been exposed to endocrine-disrupting chemicals (found in some plastics, pesticides, and personal-care products), we see the best results when we reduce that exposure while adding anti-inflammatory nutrition and gut-support strategies.

You can explore ongoing case insights and protocols at HealthCoach Clinic and on my professional page:

• HealthCoach Clinic: healthcoach.clinic/
• Professional updates: www.linkedin.com/in/dralexjimenez/

Safety, Documentation, and Ethical Use

When I initiate combination therapy or DTE, I document:

• “The patient has relatively low free T3 with persistent hypothyroid symptoms; therapy was initiated to support metabolic function and quality of life. Follow-up labs and symptom monitoring will assess benefit and side effects.”

I monitor:

• Resting HR, BP, HRV, signs of over-replacement (palpitations, tremor, heat intolerance).
• Bone density in at-risk patients on higher or longer regimens.
• Timed labs (5–6 hours post-dose) for comparability and safety.

I align with the contemporary consensus to use T3-inclusive therapy cautiously, for a defined trial period, with clear endpoints and shared decision-making (Jonklaas et al., 2014; Jonklaas et al., 2021).

References:

• Guidelines for the Treatment of Hypothyroidism (Jonklaas et al., 2014)
• Thyroid Hormone Therapy: ATA Position Statements (Jonklaas et al., 2021)

Closing Thoughts: Precision Medicine Meets Whole-Person Care

Care that begins and ends with TSH normalization often misses the story your body is telling. The physiology is clear: free T3 is the final common effector of thyroid action. To restore metabolism, mood, and performance, we must ensure T3 reaches tissues, remove the brakes (rT3, inflammation, and iron deficiency), and align autonomic and musculoskeletal systems so you can move, sleep, and recover.

In my life without a native thyroid and in thousands of patient journeys, the same lesson repeats: precision medicine is most powerful when it is integrated. When we synchronize hormones, nutrients, movement, sleep, and manual therapy, patients regain the capacity to think clearly, train consistently, and live with energy. That is the standard I strive to deliver every day at HealthCoach Clinic.

References

• American Thyroid Association guidelines for the treatment of hypothyroidism (American Thyroid Association, 2014). Thyroid, 24(12), 1670–1751. doi.org/10.1089/thy.2014.0028
• Guidelines for the Treatment of Hypothyroidism (Jonklaas, J., Bianco, A. C., Bauer, A. J., et al., 2014). Journal of Clinical Endocrinology & Metabolism, 99(10), 3635–3673. doi.org/10.1210/jc.2014-2260
• Thyroid Hormone Therapy: ATA Position Statements (Jonklaas, J., Bianco, A. C., et al., 2021). American Thyroid Association.
• Thyroid Hormone and Mitochondrial Function (Silvestri, E., Santulli, G., & Morrone, D., 2014). Nature Reviews Endocrinology, 10(11), 681–692.
• Biochemistry, Physiology, and Pathophysiology of Thyroid Hormone Action (Bianco, A. C., & Kim, B. W., 2019). Endocrine Reviews, 40(4), 1000–1049. doi.org/10.1210/er.2018-00215
• Non-thyroidal illness syndrome (Fliers, E., Boelen, A., & Wiersinga, W. M., 2011). Endocrine Reviews, 32(2), 97–110. doi.org/10.1210/er.2010-0024
• Paradigm shifts in thyroid hormone replacement therapies (Wiersinga, W. M., 2014). European Journal of Endocrinology, 170(6), R221–R235. doi.org/10.1530/EJE-14-0465
• Thyroxine-triiodothyronine combination therapy versus thyroxine monotherapy for clinical hypothyroidism (Grozinsky-Glasberg, S., Fraser, A., & Nahshoni, E., 2009). Journal of Clinical Endocrinology & Metabolism, 94(3), 852–858.
• Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism (Hoang, T. D., Olsen, C. H., Mai, V. Q., Clyde, P. W., & Shakir, M. K., 2013). European Journal of Endocrinology, 169(6), 675–682.
• DIO2 polymorphisms and response to levothyroxine therapy (Panicker, V. et al., 2009). Journal of Clinical Endocrinology & Metabolism, 94(5), 1623–1629.
• Combination treatment with T4 and T3: Toward personalized replacement therapy in hypothyroidism? (Biondi, B., & Wartofsky, L., 2014). Journal of Clinical Endocrinology & Metabolism, 99(7), 2693–2701.
• Endocrine and metabolic effects of low iron status (de Jongh, R. T., Lips, P., et al., 2016). Journal of Clinical Endocrinology & Metabolism, 101(4), 176–187.
• Nutritional iron deficiency (Zimmermann, M. B., & Hurrell, R. F., 2007). American Journal of Clinical Nutrition, 85(4), 946–954.
• Selenium and thyroid disease: From pathophysiology to treatment (Ventura, M., Melo, M., & Carrilho, F., 2017). International Journal of Endocrinology, 2017, 1297658.
• Iodine deficiency and thyroid disorders (Zimmermann, M. B., & Boelaert, K., 2015). The Lancet Diabetes & Endocrinology, 3(4), 286–295.
• Iodine nutrition in pregnancy and lactation (Leung, A. M., Pearce, E. N., & Braverman, L. E., 2012). New England Journal of Medicine, 366(10), 944–945.
• Thyroid hormones and cardiovascular system: From basic physiology to clinical application (Iervasi, G., & Pingitore, A., 2013). European Heart Journal, 34(16), 1158–1166.
• Triiodothyronine and the cardiovascular system: Cellular and clinical evidence (Pingitore, A., & Iervasi, G., 2016). Cardiovascular Drugs and Therapy, 30, 1–10.
• Liothyronine augmentation in depression: An update (Joffe, R. T., & Singer, W., 2020). Current Psychiatry Reports, 22, 56.
• Autonomic Modulation Through Manual Therapy: Mechanisms and Clinical Relevance (Oakley, P. A., et al., 2018). Journal of Bodywork and Movement Therapies, 22(3), 589–596. doi.org/10.1016/j.jbmt.2017.12.011
• Sleep and the Endocrine System (Irwin, M. R., 2015). Sleep Medicine Clinics, 10(1), 1–15. doi.org/10.1016/j.jsmc.2014.11.010
• ATA/BTA/ETA Consensus on Evidence-Based Use of LT4/LT3 Combination Therapy (Jonklaas, J., Bianco, A. C., Bauer, A. J., et al., 2021). Thyroid, 31(11), 156–182.

Note on authorship: This educational post was created and written in the first person by Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, for publication on a website as patient-centered education.

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