Type-IIx
Well-known Member
This writing is intended to replace and supersede The Serum IGF-I Test: Its... (version 1.0; Nov 23 2021).
The Serum GH is utterly useless for any purpose we'd be interested in.
The Serum IGF-I test is what's used to determine GH response (Δ IGF-I).
Factors that diminish GH response (↓ Δ IGF-I) include:
1. Negative caloric balance. Dieting, even a slight deficit, modifies GH effects, so as to stimulate predominately energy release (& protein anticatabolism) rather than influx or storage. RhGH, during prolonged subcutaneous administration (in a state of positive energy balance), causes the actions of IGF-I and insulin to prevail 8 - 10 h post-injection.
2. (a) Estrogens. High estrogen levels & especially exogenous estrogens diminish GH response. Whereas aromatizing androgen increases GH response (↑ Δ IGF-I), (b) Trenbolone† (see below) ↓ Δ IGF-I, but at the tissue level, dramatically increases the efficacy of autocrine/paracrine IGF-I activity. Therefore, (c) Sex (women < men in Δ IGF-I).
3. Duration of use (between 4 - 5 mo of continuous rhGH administration, there is a ↓ Δ IGF-I). This is likely due to GH-binding protein (GHBP) dynamics and/or desensitization of downstream elements of the GH receptor (GH-R).
4. Hereditary genetic factors. GHR gene polymorphisms, e.g., GHR phenotype (flfl < fld3 < d3d3). Homozygous d3-GHR carriers showed a more effective short- and long-term response to low rhGH dose with respect to low-density lipoprotein reduction, body composition and blood pressure & a more robust IGF-I increase during short-term follow-up. The prevalence of d3-GHR homozygousity (d3d3) is estimated to be as high as 50% in some populations.
5. Obesity. Higher fat masses decrease GH efficacy. This concern is mostly related to obesity effects on endogenous GH-IGF-I metabolic effects. However, one complication on rhGH treatment of intra-abdominal obesity is that rhGH-induced lipolysis increases circulating FFAs, thus inhibiting GHRH-induced GH secretion. On balance, however, rhGH > no treatment for obesity.
6. Liver dysfunction or disease. Liver-IGF-I-secreting somatotroph activity is diminished by dysfunction or disease. (b) Kidney disease. (c) Diabetes.
7. Age. As usual, there is an age-related decrement in GH response. This may be an evolutionarily conserved mechanism to promote longevity, according to a prevailing theory within epidemiology that posits that winding down IGF-I activity is necessary to stave off diseases of aging, like cancer/neoplasms that depend on cell # as a precondition to mutagenesis and is rooted in observations such as that individuals with larger body sizes tend to die significantly earlier than their smaller age-matched counterparts. This winding down is reflected by GH/IGF-I axis regulation of the adolescent growth spurt where 3.6 IU/day GH secretion is common versus 0.33 IU/day GH secretion being normal for an aged (50 years old, ±) 70 kg man of average build.
Baseline IGF-I measures are critical. If you do not know your base-line, eucaloric (energy in ≥ energy out, stable or increasing body weight) serum IGF-I taken within the last 9 months, you do not have any basis for comparison.
The Purpose of the Serum IGF- Test
IGF-I in serum provides a measure of an individual's GH response not quality/veracity of a rhGH preparation.
Neither the serum IGF-I test nor the serum GH test are advised as a means to determine veracity or quality of an rhGH preparation, as they cannot adequately serve as even a binary test (tell whether or not rhGH has indeed been administered). Instead, analytical laboratory testing using a GC/MS quantitative method is advised for this purpose.
The effects of rhGH on serum IGF-I are nonlinear, and are affected by the user's GHBP and GH receptor density (in fact, there exist relatively common genetic polymorphisms & mutations that cause low response to GH) – the principal determinants in inter-individual variation, as well as body composition (fat mass), age, gender, and health status. It is, indeed, possible that a user has no significant change in serum IGF-I levels in response to rhGH treatment even using supraphysiological reference quality rhGH (e.g., Novo Nordisk). This is rare but not unheard of.
Serum IGF-I levels may increase in response to rhGH markedly over several weeks to months, and decrease somewhat, tending to stabilize around a somewhat narrow range.
GH response (RhGH Dose/Response vis-à-vis Δ IGF-I): the most important data point in your trial of 1
You may view your results if measured under the conditions given, as a measure of your GH response to the product. That is, even if you picked up your 8 IU daily dose of Norditropin from the local pharmacy yourself (so you know it's real) and administered it properly (perhaps you have HIV): if your serum IGF-I levels are insignificantly altered, you are unlikely to see significant benefit from the product (or, indeed, any rhGH preparation). †.
†: Trenbolone. This AAS decreases endogenous GH pulse amplitude & duration, thereby ↓ Δ IGF-I & ↓ IGF-I. It also is potently insulin sensitizing, decreasing blood insulin, IGF-I, & glucose in humans. Trenbolone does more with less. That is, despite the decrement to liver-secreted systemic/circulating IGF-I (↓ IGF-I [liver]), Trenbolone dramatically increases the intramuscular satellite cell responsiveness to autocrine/paracrine IGF-I (IGF-IEa; IGF-IEc, the mechanosensitive isoform [muscle]). These are both increased substantially by rhGH administration & resistance training. Then, Testosterone + Trenbolone + RhGH + Resistance Training are synergistic (greater than additive; 1 + 1 > 2) in their increases to muscle & total body size.
The Serum GH is utterly useless for any purpose we'd be interested in.
The Serum IGF-I test is what's used to determine GH response (Δ IGF-I).
Factors that diminish GH response (↓ Δ IGF-I) include:
1. Negative caloric balance. Dieting, even a slight deficit, modifies GH effects, so as to stimulate predominately energy release (& protein anticatabolism) rather than influx or storage. RhGH, during prolonged subcutaneous administration (in a state of positive energy balance), causes the actions of IGF-I and insulin to prevail 8 - 10 h post-injection.
2. (a) Estrogens. High estrogen levels & especially exogenous estrogens diminish GH response. Whereas aromatizing androgen increases GH response (↑ Δ IGF-I), (b) Trenbolone† (see below) ↓ Δ IGF-I, but at the tissue level, dramatically increases the efficacy of autocrine/paracrine IGF-I activity. Therefore, (c) Sex (women < men in Δ IGF-I).
3. Duration of use (between 4 - 5 mo of continuous rhGH administration, there is a ↓ Δ IGF-I). This is likely due to GH-binding protein (GHBP) dynamics and/or desensitization of downstream elements of the GH receptor (GH-R).
4. Hereditary genetic factors. GHR gene polymorphisms, e.g., GHR phenotype (flfl < fld3 < d3d3). Homozygous d3-GHR carriers showed a more effective short- and long-term response to low rhGH dose with respect to low-density lipoprotein reduction, body composition and blood pressure & a more robust IGF-I increase during short-term follow-up. The prevalence of d3-GHR homozygousity (d3d3) is estimated to be as high as 50% in some populations.
5. Obesity. Higher fat masses decrease GH efficacy. This concern is mostly related to obesity effects on endogenous GH-IGF-I metabolic effects. However, one complication on rhGH treatment of intra-abdominal obesity is that rhGH-induced lipolysis increases circulating FFAs, thus inhibiting GHRH-induced GH secretion. On balance, however, rhGH > no treatment for obesity.
6. Liver dysfunction or disease. Liver-IGF-I-secreting somatotroph activity is diminished by dysfunction or disease. (b) Kidney disease. (c) Diabetes.
7. Age. As usual, there is an age-related decrement in GH response. This may be an evolutionarily conserved mechanism to promote longevity, according to a prevailing theory within epidemiology that posits that winding down IGF-I activity is necessary to stave off diseases of aging, like cancer/neoplasms that depend on cell # as a precondition to mutagenesis and is rooted in observations such as that individuals with larger body sizes tend to die significantly earlier than their smaller age-matched counterparts. This winding down is reflected by GH/IGF-I axis regulation of the adolescent growth spurt where 3.6 IU/day GH secretion is common versus 0.33 IU/day GH secretion being normal for an aged (50 years old, ±) 70 kg man of average build.
Baseline IGF-I measures are critical. If you do not know your base-line, eucaloric (energy in ≥ energy out, stable or increasing body weight) serum IGF-I taken within the last 9 months, you do not have any basis for comparison.
The Purpose of the Serum IGF- Test
IGF-I in serum provides a measure of an individual's GH response not quality/veracity of a rhGH preparation.
Neither the serum IGF-I test nor the serum GH test are advised as a means to determine veracity or quality of an rhGH preparation, as they cannot adequately serve as even a binary test (tell whether or not rhGH has indeed been administered). Instead, analytical laboratory testing using a GC/MS quantitative method is advised for this purpose.
The effects of rhGH on serum IGF-I are nonlinear, and are affected by the user's GHBP and GH receptor density (in fact, there exist relatively common genetic polymorphisms & mutations that cause low response to GH) – the principal determinants in inter-individual variation, as well as body composition (fat mass), age, gender, and health status. It is, indeed, possible that a user has no significant change in serum IGF-I levels in response to rhGH treatment even using supraphysiological reference quality rhGH (e.g., Novo Nordisk). This is rare but not unheard of.
Serum IGF-I levels may increase in response to rhGH markedly over several weeks to months, and decrease somewhat, tending to stabilize around a somewhat narrow range.
GH response (RhGH Dose/Response vis-à-vis Δ IGF-I): the most important data point in your trial of 1
You may view your results if measured under the conditions given, as a measure of your GH response to the product. That is, even if you picked up your 8 IU daily dose of Norditropin from the local pharmacy yourself (so you know it's real) and administered it properly (perhaps you have HIV): if your serum IGF-I levels are insignificantly altered, you are unlikely to see significant benefit from the product (or, indeed, any rhGH preparation). †.
†: Trenbolone. This AAS decreases endogenous GH pulse amplitude & duration, thereby ↓ Δ IGF-I & ↓ IGF-I. It also is potently insulin sensitizing, decreasing blood insulin, IGF-I, & glucose in humans. Trenbolone does more with less. That is, despite the decrement to liver-secreted systemic/circulating IGF-I (↓ IGF-I [liver]), Trenbolone dramatically increases the intramuscular satellite cell responsiveness to autocrine/paracrine IGF-I (IGF-IEa; IGF-IEc, the mechanosensitive isoform [muscle]). These are both increased substantially by rhGH administration & resistance training. Then, Testosterone + Trenbolone + RhGH + Resistance Training are synergistic (greater than additive; 1 + 1 > 2) in their increases to muscle & total body size.
Last edited:
