Hormonal Imbalances Following Concussion and Brain Injury: What to Assess and Why

by | Jul 9, 2025 | Koru Nutrition Blog

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Introduction

Traumatic brain injury (TBI) and concussion, has far-reaching physiological effects beyond immediate cognitive and neurological impairment. One of the most underrecognized yet clinically significant consequences of brain injury is its impact on the endocrine system. The brain, especially the hypothalamus and pituitary gland, plays a central role in regulating hormonal balance. Damage to these areas—commonly referred to as the hypothalamic-pituitary axis (HPA)—can disrupt hormone production, secretion, and regulation, often leading to persistent symptoms that are mistakenly attributed to psychological or structural causes alone.

This article explores the hormonal disturbances that can result from brain injury, the prevalence and mechanisms behind post-traumatic hypopituitarism (PTHP), and provides guidance on which hormones should be assessed in clinical practice.

The Hypothalamic-Pituitary Axis and Brain Injury

The hypothalamus and pituitary gland act as master regulators of the endocrine system. They coordinate the release of multiple hormones critical to metabolism, growth, stress response, mood, sexual function, and fluid balance. TBI can impair these regulatory functions through direct trauma, inflammation, edema, vascular damage, or delayed regeneration of the HPA structures.

Types of Brain Injury That Affect Hormonal Balance

  • Mild TBI (Concussion)
  • Moderate to Severe TBI
  • Repetitive Head Trauma (e.g., athletes, military personnel)

Even mild injuries can lead to significant hormonal disruption, especially if repeated over time (e.g., in contact sports) [1].

Prevalence of Post-Traumatic Hormonal Imbalances

Numerous studies show that hormonal imbalances occur in 15–68% of individuals after TBI, depending on injury severity, timing of testing, and diagnostic criteria [2][3].

  • Acute phase (first 2 weeks post-injury): transient hormonal changes are common.
  • Chronic phase (3 months to several years): permanent dysfunction may persist in up to 25–50% of individuals [4].

A systematic review by Schneider et al. (2007) found that approximately 30% of TBI survivors develop some form of hypopituitarism, with growth hormone deficiency being the most prevalent [2].

Key Hormonal Systems Affected

1. Growth Hormone (GH)

  • Prevalence: 15–20% in moderate/severe TBI, 10% in mild TBI [4].
  • Symptoms: fatigue, reduced muscle mass, poor exercise tolerance, depression, and cognitive dysfunction.
  • Pathophysiology: The somatotropic axis is highly sensitive to injury; the GH-releasing hormone pathway is vulnerable to shear stress.
  • Assessment: Serum IGF-1 is a screening tool, but dynamic stimulation tests (e.g., insulin tolerance test or GHRH-arginine test) are more reliable [5].

2. Adrenocorticotropic Hormone (ACTH) and Cortisol

  • Prevalence: ACTH deficiency is found in up to 10–20% of individuals [6].
  • Symptoms: fatigue, hypotension, nausea, poor stress tolerance, and hyponatremia.
  • Timing: Cortisol levels can be acutely suppressed due to stress or permanently due to HPA axis disruption.
  • Assessment: Morning serum cortisol; if borderline, perform ACTH stimulation test.

Acute cortisol insufficiency can be life-threatening and requires prompt treatment [7].

3. Thyroid Stimulating Hormone (TSH) and Free T4

  • Prevalence: Central hypothyroidism is seen in 5–10% of cases post-TBI [8].
  • Symptoms: fatigue, cold intolerance, weight gain, depression, and bradycardia.
  • Assessment: TSH and free T4 (note that TSH may be inappropriately normal or low in central hypothyroidism).

Thyroid dysfunction may worsen cognitive outcomes and mood, so screening is essential even for mild TBI.

4. Gonadotropins (LH/FSH) and Sex Hormones (Testosterone, Estradiol)

  • Prevalence: Gonadotropin deficiency in up to 20% of men; less frequently studied in women [9].
  • Symptoms in Men: low libido, erectile dysfunction, reduced facial/body hair, and muscle loss.
  • Symptoms in Women: menstrual irregularities, infertility, low libido, and hot flashes.
  • Assessment: LH, FSH, total testosterone (in men), estradiol (in women), and sex hormone-binding globulin (SHBG).

Hormonal imbalance in this axis is associated with depression and reduced quality of life post-injury [10].

5. Prolactin

  • Prevalence: Hyperprolactinemia is occasionally observed.
  • Mechanism: May occur due to pituitary stalk damage or hypothalamic inhibition of dopamine.
  • Symptoms: galactorrhea, infertility, sexual dysfunction.

Testing for prolactin levels is useful in the presence of menstrual or sexual symptoms post-TBI.

6. Antidiuretic Hormone (ADH) and Sodium Balance

  • Disorders:
    • Diabetes Insipidus (DI) – deficiency of ADH
    • Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) – excess ADH
  • Symptoms: Polyuria, polydipsia, dehydration (DI); hyponatremia, fluid retention (SIADH).
  • Assessment: Serum sodium, urine osmolality, plasma osmolality, ADH levels.

These imbalances often occur in the acute phase and can be life-threatening if unrecognized [11].

7. Insulin and glucose metabolism

Following a traumatic brain injury (TBI), including mild forms such as concussions, significant alterations in insulin regulation and glucose metabolism can occur, contributing to both acute and chronic neurological and metabolic consequences. The brain plays a critical role in regulating systemic metabolism, and damage to regions such as the hypothalamus or pituitary gland can disrupt insulin sensitivity and secretion.

Studies have shown that after a TBI, patients may develop insulin resistance, even in the absence of pre-existing metabolic disease. This insulin resistance is thought to arise from neuroinflammation, oxidative stress, and impaired neuronal insulin signaling pathways (15,16).

Prevalence of insulin resistance and dysregulated glucose metabolism: Research indicates that up to 50% of moderate-to-severe TBI patients develop some form of glucose metabolism disturbance, including hyperglycemia or insulin resistance in the acute phase post-injury (17). Moreover, even in cases of mild TBI or concussion, subtle but persistent changes in insulin function have been observed, particularly in individuals with repetitive head injuries, such as athletes.

Long term impact: These changes are associated with increased risk for long-term cognitive decline and neurodegenerative diseases like Alzheimer’s, which are themselves linked to insulin resistance in the brain (18).

Timing of Hormonal Assessment

  • Acute phase (first 2–4 weeks): Focus on cortisol and ADH abnormalities.
  • Subacute phase (1–3 months): GH, TSH, gonadal hormones should begin to normalize or demonstrate deficiency.
  • Chronic phase (>3 months): Full endocrine workup recommended, especially in symptomatic patients.

Repeat testing is important, as some deficiencies are transient while others develop over time [12].

Clinical Symptoms That May Indicate Hormonal Dysfunction

Because symptoms of hormonal deficiency can overlap with post-concussive syndrome (e.g., fatigue, poor concentration, mood swings), clinicians must maintain a high index of suspicion. Red flags include:

  • Persistent fatigue and malaise unresponsive to rest
  • Sexual dysfunction or amenorrhea
  • Weight gain or loss with no lifestyle explanation
  • Depression or anxiety that worsens over time
  • Cold intolerance, dry skin, or hair thinning
  • Hypoglycemia or hypotension

Populations at Higher Risk

  • Moderate to severe TBI patients
  • Individuals with skull fractures, especially basilar
  • Those requiring neurosurgery or ICU admission
  • Patients with repetitive mild TBIs (e.g., athletes, veterans)
  • Children and adolescents (disruption of growth and puberty)

Athletes with repeated concussions may develop chronic traumatic encephalopathy (CTE), which also involves hormonal changes, particularly low testosterone and GH deficiency [13].

Recommended Hormonal Panel After TBI/Concussion

  Hormone   Test   When to Assess
  Cortisol  8am serum cortisol ± ACTH stimulation   Acute and chronic
  GH axis   IGF-1, GHRH-arginine test   Chronic (>3 months)
  Thyroid   TSH, Free T4   Subacute and chronic
  Gonadal   LH, FSH, Testosterone/Estradiol   Subacute and chronic
  Prolactin   Serum prolactin   If symptoms suggest
  ADH   Sodium, osmolality, ADH   Acute phase, if symptomatic
  Insulin   Insulin, glucose fasting, HBA1C   Chronic

 

Treatment and Follow-Up

Hormone replacement, nutraceuticals (herbs, supplements, glandulars), diet and lifestyle can significantly improve quality of life and neurocognitive recovery in TBI individuals. Individualized therapy is guided by deficiency severity, patient symptoms, and comorbidities. Referral to an Endocrinologist or Naturopath Doctor is essential for proper diagnosis and dynamic testing.

  • GH replacement improves energy, mood, cognition, and body composition [14].
  • Cortisol therapy may be life-saving in adrenal insufficiency.
  • Thyroid and sex hormone replacement alleviates fatigue, mood issues, and sexual dysfunction.
  • Glandulars, herbs and nutrient supplementation can help to balance hormones
  • Nutrition and Lifestyle strategies can help to mitigate issues

Conclusion

Brain injury—even mild concussion—can disrupt multiple hormonal pathways, contributing to prolonged or unexplained symptoms. The hypothalamic-pituitary axis is especially vulnerable, and damage may lead to deficiencies in growth hormone, cortisol, thyroid hormones, gonadal hormones, insulin, prolactin, and antidiuretic hormone. Timely endocrine evaluation is critical for optimal management. In patients with persistent symptoms post-concussion, hormonal assessment should be part of the routine workup to prevent misdiagnosis and to enhance recovery outcomes.

If you or you client is interested in completing hormonal testing please reach out to Koru Nutrition for a free discovery call or book in with one of our naturopath doctors.

Or, if you or your client was involved in a motor vehicle accident, then please complete our online referral form so we can complete the OCF-18.

References

 

  1. Zgaljardic DJ, et al. (2008). “Neuroendocrine dysfunction after traumatic brain injury: an update on diagnosis and treatment.” Current Opinion in Endocrinology, Diabetes and Obesity, 15(4):301-307. doi:10.1097/MED.0b013e3283064a4f
  2. Schneider HJ, et al. (2007). “Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review.” JAMA, 298(12):1429–1438. doi:10.1001/jama.298.12.1429
  3. Klose M, et al. (2007). “Prevalence and predictive factors of post-traumatic hypopituitarism.” Clinical Endocrinology, 67(2):193–201. doi:10.1111/j.1365-2265.2007.02873.x
  4. Aimaretti G, et al. (2005). “Hormonal deficiencies after traumatic brain injury in humans.” Horm Res, 64(6):293–299. doi:10.1159/000088786
  5. Tanriverdi F, et al. (2010). “Pituitary dysfunction after traumatic brain injury: a clinical and pathophysiological approach.” Endocrine Reviews, 31(2): 244–277. doi:10.1210/er.2009-0008
  6. Bondanelli M, et al. (2004). “Hypopituitarism after traumatic brain injury.” European Journal of Endocrinology, 152(5):679–691. doi:10.1530/eje.0.1520679
  7. Agha A, et al. (2005). “The natural history of post-traumatic hypopituitarism: implications for assessment and treatment.” American Journal of Medicine, 118(12):1416.e1–1416.e7. doi:10.1016/j.amjmed.2005.01.073
  8. Schneider M, et al. (2013). “Endocrine dysfunction following TBI: a review.” Journal of Neurotrauma, 30(11):1017–1030. doi:10.1089/neu.2012.2602
  9. Urban RJ, et al. (2005). “Hypogonadism after TBI.” Journal of Neurotrauma, 22(11):1141–1147. doi:10.1089/neu.2005.22.1141
  10. Wagner AK, et al. (2010). “Biopsychosocial correlates of hypopituitarism after traumatic brain injury.” Brain Injury, 24(3): 297–305. doi:10.3109/02699050903421119
  11. Kristof RA, et al. (2009). “Acute changes of the hypothalamic–pituitary–adrenal axis after traumatic brain injury.” European Journal of Endocrinology, 160(1):137–143. doi:10.1530/EJE-08-0612
  12. Krahulik D, et al. (2010). “Dynamic changes in hormonal levels in acute phase of TBI.” J Neurosurg Sci, 54(3):77–83.
  13. Kelly DF, et al. (2000). “Neuroendocrine dysfunction after traumatic brain injury: a critical review.” Neurosurgery, 47(6):1343–1352. doi:10.1097/00006123-200012000-00003
  14. High WM, et al. (2010). “Effect of growth hormone replacement therapy on cognition after traumatic brain injury.” Journal of Neurotrauma, 27(9): 1687–1695. doi:10.1089/neu.2010.1312
  15. Bhowmick, S., D’Mello, V., Ponery, N., & Chatterjee, S. (2018). Brain insulin resistance and its link to cognitive dysfunction: Potential implications in traumatic brain injury. Neuropharmacology, 136(Pt B), 190–197. https://doi.org/10.1016/j.neuropharm.2017.11.009
  16. Jalloh, I., Helmy, A., Shannon, R. J., Gallagher, C. N., Menon, D. K., & Hutchinson, P. J. (2015). Lactate uptake by the injured human brain: Evidence from an arterio-venous gradient and cerebral microdialysis study. Journal of Neurotrauma, 32(9), 689–699. https://doi.org/10.1089/neu.2014.3675
  17. Wagner, A. K., Sokunbi, O. F., Ren, D., Chen, X., Li, Y., & Conley, Y. P. (2017). Controlled cortical impact injury influences insulin signaling pathway gene expression in the brain. Journal of Neurotrauma, 34(5), 1041–1049. https://doi.org/10.1089/neu.2015.4272
  18. De Felice, F. G., & Ferreira, S. T. (2014). Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease. Diabetes, 63(7), 2262–2272. https://doi.org/10.2337/db13-1954
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