GH Dosing relative to AAS dosage.

[Type-IIx]

What dose are you thinking here?

Do you mean, what are doses of rhGH that induce hyperglycemia & of Tren that pose particular cardiac harms ?

Tren poses these particular (meaning > the average AAS) harms (MR antagonism, corticosteroid derangement) at all doses, almost certainly dose-dependently. So as doses ramp up, so too does risk of a fatal or nonfatal acute coronary event. This risk is multifactorial, and depends on factors like past AAS use history, genetic proclivity (heritable factors), diet (e.g., saturated fat intakes), activity, etc.

RhGH (a term to distinguish it from endogenous GH; but now, also to irritate BiggerP) also directly stimulates insulin resistance within 1 - 2 h, such that doses > replacement (rhGH suppresses GH secretion for ~ 1 day, +/-, with some escape from suppression that differs between individuals) dose-dependently contribute to the risk of hyperglycemia (as doses ramp up, so too does the risk of blood glucose > 130 mg/dL or 7.2 mmol/L after fasting for at least 8 h, defined as fasting hyperglycemia). The consequences of this depends on multiple factors like body fat mass, diet, etc.

 

[Sully1234]

...RhGH (a term to distinguish it from endogenous GH; but now, also to irritate BiggerP)...

Okay that made me spit my coffee lol.

 

[KingOfSushi]

Do you mean, what are doses of rhGH that induce hyperglycemia & of Tren that pose particular cardiac harms ?

Tren poses these particular (meaning > the average AAS) harms (MR antagonism, corticosteroid derangement) at all doses, almost certainly dose-dependently. So as doses ramp up, so too does risk of a fatal or nonfatal acute coronary event. This risk is multifactorial, and depends on factors like past AAS use history, genetic proclivity (heritable factors), diet (e.g., saturated fat intakes), activity, etc.

RhGH (a term to distinguish it from endogenous GH; but now, also to irritate BiggerP) also directly stimulates insulin resistance within 1 - 2 h, such that doses > replacement (rhGH suppresses GH secretion for ~ 1 day, +/-, with some escape from suppression that differs between individuals) dose-dependently contribute to the risk of hyperglycemia (as doses ramp up, so too does the risk of blood glucose > 130 mg/dL or 7.2 mmol/L after fasting for at least 8 h, defined as fasting hyperglycemia). The consequences of this depends on multiple factors like body fat mass, diet, etc.

Sorry, I was referring to what dosing you were thinking of tren to offset some of the hyperglycemia from HGH since ideally we’d want as low as possible because of all the negatives that come alongside tren.

 

[luki7788]

Sorry, I was referring to what dosing you were thinking of tren to offset some of the hyperglycemia from HGH since ideally we’d want as low as possible because of all the negatives that come alongside tren.

instead of trenbolone I recommend harder training more cardio and not doing cheat meals - it will do much better for sensitivity than 300mg tren per week...

 

[pickapeck]

instead of trenbolone I recommend harder training more cardio and not doing cheat meals - it will do much better for sensitivity than 300mg tren per week...

Thank God somebody actually talked about training as a way to manipulate response rather than add another drug.

 

[Type-IIx]

Sorry, I was referring to what dosing you were thinking of tren to offset some of the hyperglycemia from HGH since ideally we’d want as low as possible because of all the negatives that come alongside tren.

You mean at what doses of Tren & rhGH the risk/reward curve is perfectly optimized for you, considering your genetic proclivity to cardiac remodeling & left diastolic dysfunction, insulin sensitivity, dose/response, etc? By Gosh, I do not have an answer for you.

Measure your blood pressure & glucose daily and dose and treat accordingly, limit durations of Tren & rhGH use, measure serum markers like IGF-I, HOMA-IR or QUICKI appropriately, keep saturated fat intakes low & body fat levels low (LISS, diet).

One quantifiable thing you can do is calculate your modified SCORE (10-year risk of fatal cardiovascular disease) by adding a 10-year modifier for long-term (more than 2 cycles in the past 10 years) AAS use using your lipids & blood pressure. You might do this at different times on & off blasts, keep a spreadsheet, derive a regression formula for yourself for this as well as for Apo A/Apo B1.

 

[KingOfSushi]

You mean at what doses of Tren & rhGH the risk/reward curve is perfectly optimized for you, considering your genetic proclivity to cardiac remodeling & left diastolic dysfunction, insulin sensitivity, dose/response, etc? By Gosh, I do not have an answer for you.

Measure your blood pressure & glucose daily and dose and treat accordingly, limit durations of Tren & rhGH use, measure serum markers like IGF-I, HOMA-IR or QUICKI appropriately, keep saturated fat intakes low & body fat levels low (LISS, diet).

One quantifiable thing you can do is calculate your modified SCORE (10-year risk of fatal cardiovascular disease) by adding a 10-year modifier for long-term (more than 2 cycles in the past 10 years) AAS use using your lipids & blood pressure. You might do this at different times on & off blasts, keep a spreadsheet, derive a regression formula for yourself for this as well as for Apo A/Apo B1.

Thanks. I know the question was a bit vague and hard to give any one straight answer, so I appreciate the detail