Hormone Replacement Therapy (HRT)

Evidence-Based Hormonal Optimization for Regeneration, Metabolism, and Healthy Aging

Hormone Replacement Therapy (HRT) is a medical approach designed to restore key hormones to physiological levels when endogenous production declines due to aging, pituitary dysfunction, or endocrine disease. When appropriately prescribed and medically supervised, HRT improves quality of life, metabolic health, tissue regeneration, cognitive function, immune balance, and overall vitality.

At Dr. Alan Inman’s clinic, hormone replacement is practiced as precision, evidence-based medicine, guided by laboratory-confirmed deficiencies, individualized protocols, and continuous monitoring. This approach is fundamentally different from supraphysiologic or non-medical hormone use.

This page summarizes the scientific and clinical evidence supporting Growth Hormone (GH) Replacement Therapy and Testosterone Replacement Therapy (TRT).

Growth Hormone Replacement Therapy (GH / hGH / rhGH)

GH as the Body’s Global Regenerative Hormone

Growth Hormone is widely recognized as the body’s primary anabolic and regenerative hormone. High-quality physiological reviews consistently demonstrate that GH:

  • Stimulates growth and repair in nearly all tissues and organs
  • Acts through endocrine, paracrine, and autocrine pathways
  • Regulates protein synthesis, lipid metabolism, and carbohydrate utilization
  • Plays a central role in wound healing, muscle repair, bone remodeling, and connective tissue regeneration

Devesa et al. (2016) emphasize that GH receptors are expressed in practically all tissues, explaining its systemic regenerative capacity.

Skin, Collagen, and Tissue Regeneration

Human clinical trials confirm that in GH-deficient adults, GH replacement produces true structural remodeling of the skin, not merely cosmetic effects.

  • A randomized placebo-controlled trial demonstrated that GH significantly increases type I collagen synthesis and measurable skin thickness, confirming real dermal collagen deposition (Kann et al., 1996).
  • Experimental studies show that GH protects dermal fibroblasts and keratinocytes from UVB-induced damage and increases gene expression of collagen, elastin, and IGF-1 (Taghizadeh et al., 2024).
  • In a human-skin wound model, local recombinant GH doubled healing speed and produced thicker, better-organized regenerated skin (Cristóbal et al., 2019).

Clinical interpretation:
Physiologic GH replacement supports healthier, thicker, more resilient skin through genuine extracellular matrix regeneration.

Cognitive Function, Memory, and Psychological Well-Being

Adult GH deficiency is consistently associated with impairments in memory, attention, and mood.

  • A meta-analysis of 13 studies confirmed that GH deficiency leads to measurable cognitive deficits and that GH replacement significantly improves memory and attention (Falleti et al., 2006).
  • Randomized trials show normalization of memory after one year of GH therapy in adults with childhood-onset GHD (Deijen et al., 1998).
  • Long-term follow-up studies demonstrate sustained improvements in mood, anxiety reduction, and vigor during GH treatment (Arwert et al., 2005).

Immune System and Thymus Function

GH plays a direct role in immune regulation:

  • The thymus is a GH target organ, expressing GH receptors and responding to GH with increased thymocyte proliferation and cytokine secretion (Savino et al., 2002).
  • Reviews show that age-related GH decline contributes to thymic involution, while GH administration partially reverses thymic atrophy (Taub & Murphy, 2010).
  • In adults with GH deficiency, withdrawal of GH leads to reduced thymic T-cell output, indicating that GH replacement supports immune competence (Morrhaye et al., 2009).

Metabolism, Muscle Mass, and Fat Loss

GH has strong lipolytic and anabolic effects, particularly in GH-deficient adults:

  • Randomized controlled trials demonstrate significant reductions in visceral fat, inflammatory markers, and cardiovascular risk factors (Beauregard et al., 2008).
  • Long-acting GH increases lean body mass and skeletal muscle while reducing fat mass (Johannsson et al., 2020).
  • Long-term GH replacement improves BMI, waist circumference, lipid profile, and hepatic steatosis (Scarano et al., 2021).

Bone Density and Musculoskeletal Health

Meta-analyses and randomized trials show that GH replacement:

  • Increases lumbar spine and femoral neck bone mineral density
  • Improves bone turnover markers
  • Supports cartilage, muscle, and connective tissue repair

(Barake et al., 2014; Sneppen et al., 2002).

Cardiovascular Health and Mortality Risk

Untreated adult GH deficiency is associated with increased cardiovascular morbidity and mortality.

  • GH replacement improves lipid profile, inflammation, and insulin sensitivity (Gazzaruso et al., 2014).
  • Meta-analyses show improved cardiac structure and function with GH therapy (Maison et al., 2003).
  • Long-term data suggest GH replacement contributes to normalization of mortality risk compared to untreated GHD populations (van Bunderen & Olsson, 2023).

Sleep Quality and Biological Aging

GH replacement improves sleep architecture in GH-deficient patients, normalizing slow-wave sleep and circadian regulation (Morselli et al., 2013).

Mechanistic studies demonstrate that the GH–IGF-1 axis regulates telomerase activity and cellular lifespan. While human trials confirming telomere elongation are lacking, the biological plausibility is well established (Bayne et al., 2005).

Testosterone Replacement Therapy (TRT)

Energy, Vitality, and Quality of Life

Large randomized trials demonstrate that restoring testosterone to physiological levels in hypogonadal men results in:

  • Increased energy, motivation, and vitality
  • Improved mood and well-being
  • Better overall quality of life

(Snyder et al., 2016; Almehmadi et al., 2016).

Mood, Depression, and Cognition

  • A meta-analysis of 27 randomized trials showed that TRT significantly reduces depressive symptoms, especially in hypogonadal men and treatment-resistant depression (Walther et al., 2019).
  • TRT also improves cognitive performance when baseline impairment exists (Jung et al., 2016).

Body Composition, Metabolism, and Diabetes

Long-term TRT leads to:

  • Increased lean muscle mass
  • Sustained fat loss and waist circumference reduction
  • Improved insulin sensitivity, glucose control, and lipid profile

(Yassin & Doros, 2013; Francomano et al., 2014; Cai et al., 2014).

Libido, Sexual Function, and Vascular Health

TRT reliably improves libido, sexual desire, sexual activity, and satisfaction. Mechanistic studies show testosterone facilitates erectile function via nitric oxide and cGMP pathways (Becker et al., 2000).

Nervous System, Immune Modulation, and Sleep

Testosterone supports myelin repair, neuroprotection, and anti-inflammatory immune signaling. TRT often improves sleep quality, though careful monitoring is required in patients at risk for sleep apnea.

Overall Clinical Summary

When prescribed for documented hormonal deficiencies, physiologic Hormone Replacement Therapy:

  • Restores systemic regeneration and tissue repair
  • Improves cognition, mood, and sleep
  • Enhances immune balance and metabolic health
  • Reduces visceral fat and cardiovascular risk
  • Improves sexual health and quality of life

All therapies are designed to restore normal physiology, not exceed it, and are delivered under strict medical supervision.

Selected Medical References (MLA)

  1. Beauregard, C., et al. J Clin Endocrinol Metab, 2008. DOI: 10.1210/jc.2007-2371
  2. Deijen, J.B., et al. Psychoneuroendocrinology, 1998. DOI: 10.1016/S0306-4530(97)00092-9
  3. Falleti, M.G., et al. Psychoneuroendocrinology, 2006. DOI: 10.1016/j.psyneuen.2006.01.004
  4. Barake, M., et al. J Clin Endocrinol Metab, 2014. DOI: 10.1210/jc.2013-3832
  5. Savino, W., et al. Scandinavian Journal of Immunology, 2002. DOI: 10.1046/j.1365-3083.2002.01077.x
  6. Taub, D.D., Murphy, W.J. Curr Opin Pharmacol, 2010. DOI: 10.1016/j.coph.2010.04.015
  7. Morselli, L.L., et al. Eur J Endocrinol, 2013. DOI: 10.1530/EJE-12-1037
  8. Kann, P., et al. Exp Clin Endocrinol Diabetes, 1996. DOI: 10.1055/s-0029-1211462
  9. Cristóbal, L., et al. Int J Mol Sci, 2019. DOI: 10.3390/ijms20174157
  10. Taghizadeh, B., et al. J Photochem Photobiol B, 2024. DOI: 10.1016/j.jphotobiol.2024.112961
  11. Snyder, P.J., et al. N Engl J Med, 2016. DOI: 10.1056/NEJMoa1506119
  12. Walther, A., et al. JAMA Psychiatry, 2019. DOI: 10.1001/jamapsychiatry.2018.2734