Effect of Peptide Therapy on IGF-1 Levels

Growth Hormone-Based Peptide Therapy

Growth hormone is a potent stimulator of systemic IGF-1 levels and has been shown to increase lean body mass in underweight patients with COPD participating in pulmonary rehabilitation programs 1
Growth hormone and IGF-1 appear to be physiological modulators of myocardial structure and function, with GH activating cardiac cell growth and inducing physiological ventricular remodeling 2
Growth hormone administration to patients with GH deficiency is associated with increased wall thickness and normalization of cardiac performance through IGF-1 mediated mechanisms 2
Studies are ongoing to investigate the efficacy and safety of growth hormone-releasing factors to improve body composition and functional capacity, which work by stimulating endogenous IGF-1 production 1
Anabolic steroids may improve outcomes through stimulation of protein synthesis either directly or indirectly by interaction with the IGF-1 system 1
Low-dose anabolic steroids increase fat-free mass through mechanisms that include modulation of the IGF-1 system and regulation of the myostatin gene 1

Recombinant human IGF-1 (rhIGF-1) administration directly increases IGF-1 levels and bone formation markers in adolescents and adults with anorexia nervosa 3, 4
In one RCT in adult women with anorexia nervosa, rhIGF-1 combined with oral estrogen led to a 2.8% significant increase in bone mineral density compared to controls 3, 4
IGF-1 is a bone trophic factor secreted by the liver in response to growth hormone and is also produced locally in an autocrine manner by target tissues such as bone 3, 4

Oral estrogen peptides suppress hepatic IGF-1 production through first-pass liver metabolism, which upregulates synthesis of IGF-1 binding proteins (IGFBP-1) that further reduce IGF-1 bioavailability 3, 4
The suppressive effects of oral estrogen on hepatic IGF-1 production have been implicated in the lack of efficacy of oral estrogen in improving bone mineral density in energy-deficient states 3, 4
This suppression is particularly problematic in amenorrhoeic athletes who already have low endogenous IGF-1 concentrations 3, 4

Growth hormone therapy is expensive and has been associated with undesirable side effects including salt and water retention and impairment in glucose metabolism 1
Chronic excess of GH and IGF-1 secretion in acromegaly results in biventricular cardiac hypertrophy and can progress to dilated cardiomyopathy with impaired systolic and diastolic performance 2
Transdermal estradiol circumvents hepatic first-pass metabolism and therefore does not suppress IGF-1 production like oral estrogen, making it potentially superior for maintaining bone health 3, 4

Growth hormone is a peptide hormone secreted by the pituitary that directly stimulates hepatic production of insulin-like growth factor-1 (IGF-1), with the American College of Physicians recommending its use in certain clinical scenarios 5
Growth hormone administration increases serum IGF-1 levels and has been shown to increase lean body mass in clinical studies, though strength improvements are less consistent, according to the American Journal of Respiratory and Critical Care Medicine 5

In chronic kidney disease, supraphysiological doses of recombinant human GH can overcome GH insensitivity by stimulating IGF-1 synthesis and normalizing somatomedin bioactivity, as recommended by the National Kidney Foundation 6

Platelet-Derived Growth Factor-BB (PDGF-BB) demonstrates synergistic effects with IGF-1 on mitogenesis of periodontal and bone precursor cells, though it does not directly increase systemic IGF-1 levels, according to the American Academy of Periodontology 7
Early clinical trials combined rhPDGF-BB (150 μg/mL) with IGF-1 for periodontal regeneration, demonstrating enhanced bone formation, with a strength of evidence rated as moderate by the Periodontology 2000 journal 7