Source comparison
CJC-1295 no DAC & Ipamorelin Blood Work Labs Check Before After: Comparison
Primary surrogate marker for GH secretion. More stable than direct GH measurement 300–450 (40–100% elevation from baseline) 500: excessive dosing IGF-1 elevation validates GH axis stimulation. Failure to elevate indicates pr
This comparison does not assign a generated winner or score.
- Primary surrogate marker for GH secretion. More stable than direct GH measurement
- 300–450 (40–100% elevation from baseline)
- <150: non-response or underdosing; >500: excessive dosing
- IGF-1 elevation validates GH axis stimulation. Failure to elevate indicates protocol inefficacy or degraded peptides
- Detects GH-induced insulin resistance
- 85–105 (mild elevation acceptable)
- >110: impaired glucose tolerance
- GH antagonises insulin. Glucose elevation is expected but must remain subclinical
- 90-day average glucose control
- ≥6.0: pre-diabetic range
- Rising HbA1c is the clearest sign of metabolic intolerance. Requires dose reduction or discontinuation
- Central thyroid suppression from chronic GH excess
- 0.8–3.5
- <0.5: central hypothyroidism
- TSH suppression is dose-dependent and reversible. Occurs in 15–20% of long-term users
- Free T3 / Free T4 (pg/mL)
- Confirms thyroid hormone production despite TSH changes
- T3: 2.3–4.2; T4: 0.8–1.8
- Unchanged from baseline
- Low T3/T4 with low TSH: central hypothyroidism
- Free hormone levels distinguish central suppression (T3/T4 normal) from primary thyroid failure (T3/T4 low)
- GH improves lipid metabolism. Worsening lipids suggest dietary or metabolic issues
- Total cholesterol <200, LDL <100, HDL >40, triglycerides <150
- Improved HDL, reduced LDL/triglycerides
- GH typically reduces visceral fat and improves lipid profiles. Worsening lipids are unrelated to peptide use