Meet the Metabolic Conductor: The Thyroid and Mental Health.
When patients tell me, “I feel like I’m moving through molasses,” I listen for patterns—cold hands, fatigue, weight changes, brain fog, low mood, or even anxiety that doesn’t quite fit the story. These aren’t just random symptoms; they can all point to the hypothalamic–pituitary–thyroid (HPT) axis—the metabolic conductor of the body. And if metabolism is the body’s tempo, the mind dances to that rhythm.
Understanding how this axis functions, and how life experiences like stress, trauma, and chronic inflammation reshape it, opens a powerful window into the mind-body connection. Let’s explore how the thyroid affects mental health, how stress and trauma feed back into this axis, how to evaluate thyroid function comprehensively, and how to support it holistically.
The HPT Axis: Your Body’s Metabolic Orchestra
The HPT axis is a three-way conversation between your brain and thyroid gland:
Hypothalamus → TRH. The hypothalamus senses internal cues—light, temperature, energy availability, stress—and releases thyrotropin-releasing hormone (TRH).
Pituitary → TSH. TRH prompts the pituitary gland to produce thyroid-stimulating hormone (TSH), which acts like a messenger to the thyroid.
Thyroid → T4 and T3. TSH signals the thyroid to release mostly T4 (thyroxine) and a smaller amount of T3 (triiodothyronine). But here’s the subtlety: T3 is the active form—the hormone that actually binds to receptors in your cells and regulates metabolism.
Most of your T4 must be converted into T3 in tissues like the liver, gut, and brain. This process depends on enzymes called deiodinases and can also produce reverse T3 (rT3), an inactive form that acts like a brake pedal, slowing metabolism when the body perceives stress or illness (Burman & Gomes-Lima, 2018; Hoermann et al., 2021).
Once T3 enters the cell, it turns on genes that control energy production (mitochondria), temperature, fat and glucose metabolism, and even neural repair. So while TSH tells you what the thermostat is set to, T3 tells you whether the furnace is actually burning.
How Thyroid Hormones Shape Mood and Mind
Thyroid hormones don’t just regulate metabolism—they also profoundly influence brain chemistry. They affect how neurons use oxygen, regulate neurotransmitters like serotonin and dopamine, and even promote neurogenesis (the growth of new brain cells) (Neuropsychiatric Manifestations of Thyroid Diseases, 2023).
When thyroid signaling slows, so does everything else:
Low thyroid function can feel like depression, apathy, slowed thinking, fatigue, and brain fog. Physically, people might notice weight gain, constipation, dry skin, hair loss, or feeling unusually cold (Narrative Review: Hypothyroidism and Depression, 2023).
Over-active thyroid function (hyperthyroidism) often manifests as anxiety, irritability, restlessness, insomnia, and a racing heart—which can easily be mistaken for panic disorder or generalized anxiety (Bode et al., 2023).
Even sub-clinical thyroid dysfunction, where lab results look “normal”, can disrupt mood and cognition. Because every neuron relies on thyroid hormones for optimal function, even small deviations can have large psychological effects (Frontiers in Endocrinology, 2019; van Sloten et al., 2024).
The Mind-Body Feedback Loop: How Stress and Trauma Impact Thyroid Function
The relationship between the thyroid and mental health is bidirectional. Not only does thyroid function affect mood—stress and trauma can suppress thyroid activity.
Chronic stress activates the hypothalamic–pituitary–adrenal (HPA) axis, flooding the body with cortisol and inflammatory signals. Over time, these signals inhibit thyroid function at multiple levels:
Cortisol suppresses TRH and TSH, blunting thyroid signaling (Hoermann et al., 2021; Burman & Gomes-Lima, 2018).
Inflammatory cytokines alter deiodinase activity, leading to less T3 and more rT3—a “protective” downshift sometimes called non-thyroidal illness syndrome (NTIS) or low T3 syndrome (Endotext, 2014; Optimal DX, 2019).
Cells become less responsive to T3, creating a form of thyroid resistance.
In essence, the body slows metabolism to conserve energy under chronic stress—a brilliant survival adaptation in the short term, but harmful when prolonged. This downshift contributes to fatigue, brain fog, and depressive symptoms common in trauma survivors or those under chronic emotional or physiological strain (Amsterdam study on low-grade inflammation & thyroid, 2017).
Even autoimmune thyroid disease, Hashimoto’s thyroiditis or Graves’ disease, is more common among individuals with significant stress histories, suggesting an intersection between immune dysregulation and psychological trauma (Siegmann et al., 2018; Thyroid.org, 2022).
The Functional Medicine Perspective: Evaluating the Full Thyroid Tree
Most conventional thyroid testing only measures TSH, which reflects how hard the pituitary is pushing the thyroid to work. But this tells only part of the story.
A functional medicine approach examines the entire thyroid tree:
TSH: Pituitary signal to the thyroid (the “thermostat”).
Free T4: Circulating inactive hormone available for conversion.
Free T3: Active hormone available to cells (most correlated with how you feel).
Reverse T3 (rT3): Inactive form that blocks T3; elevated in stress or chronic illness (Burman & Gomes-Lima, 2018; Hoermann et al., 2021).
TPO and Tg Antibodies: Immune activity against thyroid tissue (Hashimoto’s).
TRAb/TSI: Antibodies stimulating the thyroid (Graves’ disease).
To interpret these results meaningfully, context matters. Functional practitioners often also assess:
Cortisol rhythms (via saliva or DUTCH testing) to understand stress influence.
Iron, ferritin, zinc, selenium, magnesium, and vitamin D—all essential for thyroid conversion and receptor sensitivity.
Blood sugar and lipid panels, as thyroid dysfunction often alters both.
Inflammation markers like CRP.
Gut health, since the microbiome and intestinal permeability directly affect hormone metabolism and immune balance.
A typical conventional panel might miss sub-clinical issues like poor conversion of T4 to T3, autoimmunity, or stress-induced thyroid suppression, all of which can profoundly impact mood and cognition.
Supporting the Thyroid Holistically
Restoring thyroid health isn’t just about medication—it’s about re-establishing metabolic safety and coherence across body and mind.
1. Regulate the Stress Response
The first step in thyroid healing is addressing the nervous system state. Practices that lower chronic sympathetic tone—therapy, breathwork, mindfulness, somatic experiencing, and safe relationships—reduce cortisol and inflammation, which allows T3 conversion to recover naturally.
2. Restore Circadian Rhythm
The thyroid follows circadian cues. Morning sunlight, consistent sleep/wake times, and reduced evening light exposure support hypothalamic rhythm and steady TRH/TSH signaling.
3. Optimize Nutrition
The thyroid depends on specific micronutrients:
Selenium: critical for T4→T3 conversion and antibody reduction.
Zinc: supports receptor sensitivity.
Iron: needed for thyroid peroxidase activity.
Magnesium and vitamin D: modulate immune function and hormone signaling.
Adequate protein: provides tyrosine, the amino acid backbone of thyroid hormones.
Caloric restriction and over-exercise can actually suppress T3, while balanced meals and moderate exercise promote metabolic resilience.
4. Address Gut and Immune Health
Up to 70% of the immune system resides in the gut. Dysbiosis, constipation or gluten sensitivity can perpetuate autoimmune thyroiditis. Supporting gut integrity and microbial diversity improves both immune tolerance and hormone metabolism.
5. Reduce Inflammation
An anti-inflammatory, whole-food diet rich in omega-3s, colorful plants, and fiber supports immune balance. For Hashimoto’s, research suggests selenium and myo-inositol may lower antibody levels and TSH.
6. Medication and Integrative Approaches
When overt hypothyroidism is present, thyroid hormone replacement (usually levothyroxine) is essential and often transformative. For those with persistent symptoms despite therapy, combination T4/T3 treatment or low-dose T3 augmentation can be considered—particularly in cases of treatment-resistant depression under clinical guidance.
Bringing It All Together
Thyroid function sits at the crossroads of metabolism, immunity, and emotion. When it falters, it’s rarely just a glandular problem, it’s a story of energy, safety, and adaptation.
So if you’ve been feeling chronically tired, foggy, or emotionally flat, it’s worth asking: Has my thyroid been fully evaluated?
And if you’re a clinician, it’s worth remembering: each lab is a story about safety, energy, and communication between systems.
When we listen to the thyroid as part of that larger story, we don’t just restore metabolism, we restore meaning.
References
Bode, H., Ivens, B., Bschor, T., Schwarzer, G., Henssler, J., & Baethge, C. (2023). Hyperthyroidism and clinical depression: A systematic review and meta-analysis. Frontiers in Psychiatry, 14, Article 11345. https://doi.org/10.3389/fpsyt.2023.11345
Burman, K. D., & Gomes-Lima, C. (2018). Reverse T3 or perverse T3? Still puzzling after 40 years. Cleveland Clinic Journal of Medicine, 85(6), 450–456. https://doi.org/10.3949/ccjm.85a.17079
Endotext. (2014). The non-thyroidal illness syndrome. In L. De Groot et al. (Eds.), Endotext (Internet). MDText.com, Inc. https://www.ncbi.nlm.nih.gov/books/NBK285570/
Gavrila, A. (2022, April). Association of hypothyroidism with depression may depend on the severity of thyroid disease and age. Thyroid News & Views, 15(4), 3–4. https://www.thyroid.org/patient-thyroid-information/ct-for-patients/april-2022/vol-15-issue-4-p-3-4/
Hoermann, R., Midgley, J. E. M., Larisch, R., Dietrich, J. W., & Hoermann, R. (2021). Physiological role and use of thyroid hormone metabolites. Frontiers in Endocrinology, 12, Article 842450. https://doi.org/10.3389/fendo.2021.842450
Neuropsychiatric manifestations of thyroid diseases. (2023). Frontiers in Psychiatry, 14, Article 10837. https://doi.org/10.3389/fpsyt.2023.10837
Optimal DX. (2019, June 15). Free T3 : Reverse T3 ratio. https://www.optimaldx.com/blog/free-t3-reverse-t3-ratio
Siegmann, E.-M., Müller, H. H. O., Luecke, C., Philipsen, A., Kornhuber, J., & Grömer, T. W. (2018). Association of depression and anxiety disorders with autoimmune thyroiditis: A systematic review and meta-analysis. JAMA Psychiatry, 75(6), 577–584. https://doi.org/10.1001/jamapsychiatry.2017.4402
Van Sloten, T. T., Kok, A., Groenewegen, K. A., Hoenderdos, J., Visser, T., & Eikelenboom, M. (2024). The association between depressive and thyroid function indicators stratified by age and gender — Cross-sectional analysis among 12,502 adults. Frontiers in Endocrinology, 15, Article 1454744. https://doi.org/10.3389/fendo.2024.1454744
Zhou, Y., Xiong, J., Yu, C., Huang, Z., & Zhu, C. (2021). Comparison of thyroid hormone levels between patients with major depressive disorder and healthy controls: A cross-sectional study. Frontiers in Psychiatry, 12, Article 750749. https://doi.org/10.3389/fpsyt.2021.750749
