Can some one tell me the shelf life of un mixed/un opened sealed package of 7 vials of serono Serostim 6mg. The expiration date on the box is 04/02 but I was wondering if it was still potent enough to use since still sealed in box? Any input would be greatly appreciated. Thanks.
The most current research shows t4 is a MUCH better combination with HGH than T3....can anyone elaborate on this?
Hypoglycemia- due to lowered insulin levels.
this statement makes no sense. lowered insulin levels would lead to hyperglycemia as is true with diabetics if they dont take their insulin or antihyperglycemics.
how much is a cycle of hgh?
240-320IUs which will cost you around $480 upwards.
again this is very rough and you should seek out some sources to see what you can obtain.
Just some food for thought here regaring IM vs. SQ GH injections:
Pharmacokinetics and pharmacodynamics of GH: dependence on route and dosage of administration
Full Text Source: Pharmacokinetics and pharmacodynamics of GH: dependence on route and dosage of administration -- Keller et al. 156 (6): 647 -- European Journal of Endocrinology
European Journal of Endocrinology, Vol 156, Issue 6, 647-653
Copyright © 2007 by European Society of Endocrinology
Objective: Pharmacokinetic and pharmacodynamic data after recombinant human GH (rhGH) administration in adults are scarce, but necessary to optimize replacement therapy and to detect doping. We examined pharmacokinetics, pharmacodynamics, and 20 kDa GH after injection of rhGH at different doses and routes of administration.
Design: Open-label crossover study with single boluses of rhGH.
Methods: Healthy trained subjects (10 males, 10 females) received bolus injections of rhGH on three occasions: 0.033 mg/kg s.c., 0.083 mg/kg s.c., and 0.033 mg/kg i.m. Concentrations of 22 and 20 kDa GH, IGF-I, and IGF-binding proteins (IGFBP)-3 were measured repeatedly before and up to 36 h after injection.
Results: Serum GH maximal concentration (Cmax) and area under the time-concentration curve (AUC) were higher after i.m. than s.c. administration of 0.033 mg/kg (Cmax 35.5 and 12.0 µ g/l; AUC 196.2 and 123.8). Cmax and AUC were higher in males than in females (P < 0.01) and pharmacodynamic changes were more pronounced. IGFBP-3 concentrations showed no dose dependency. In response to rhGH administration, 20 kDa GH decreased in females and remained suppressed for 14–18 h (low dose) and 30 h (high dose). In males, 20 kDa GH was undetectable at baseline and throughout the study.
Conclusions: After rhGH administration, pharmacokinetic parameters are mainly influenced by route of administration, whereas pharmacodynamic variables and 20 kDa GH concentrations are determined mainly by gender. These differences need to be considered for therapeutic use and for detection of rhGH doping.
The present data demonstrate that gender, dose and route of administration specifically alter bioavailability of and response to exogenous rhGH in healthy young adults. Pharmacokinetic variables were mainly influenced by the route of administration, whereas pharmacodynamic responses were primarily determined by sex. Furthermore, suppression of the 20 kDa GH isoform after injection of rhGH could be demonstrated only in women; 20 kDa GH levels in males were already low at baseline.
We assessed trained, but not elite level, subjects and highly trained individuals may respond differently to rhGH administration. With no exogenous rhGH, reduced serum IGF-I and IGFBP-3 concentrations have been reported during intense training (18, 19). The dose of rhGH used in this study was supraphysiological, because it can be assumed that illegal use by athletes will be at high doses (20). Physiological rhGH replacement in GH-deficient adults requires approximately one-third to one-fifth of the dose used in this study (21). Despite the high rhGH doses, we observed few of the side effects previously described in adults with GH deficiency (22, 23). However, a high frequency of diarrhea was seen, particularly after administration of the high rhGH dose. We found no explanation in regard to diet or gastrointestinal infections, and speculate that fluid regulation disturbances induced by the high dose could have caused the diarrhea (24).
Cmax and AUC were higher after i.m. than s.c. injection of the identical dose, in accordance with previous reports (25) indicating that serum GH after i.m. injection shows a higher amplitude and shorter duration compared with s.c. injection. Significant differences between males and females were found for GH Cmax and AUC after i.m., but not s.c. injection. Although one could have expected a higher t1/2z after s.c. administration in women, due to the higher s.c. fat (26), t1/2z was not affected by gender, perhaps because the women in the study were trained and lean.
The increase in IGF-I was positively correlated to baseline concentration, and was not affected by route of administration. Compared to IGFBP-3, the increase in serum IGF-I was faster and more pronounced, consistent with previous publications indicating that the ratio of IGF-I/IGFBP-3 increases immediately after rhGH injection (27). The increase in IGFBP-3 was delayed, not clearly dose dependent and did not return to baseline during the observation period, confirming that IGF-I is a more sensitive marker of GH action in trained adults than IGFBP-3.
The increase in IGF-I, but not the increase in IGFBP-3, shows a marked sexual dimorphism. Integrated IGF-I release after rhGH injection was significantly higher in males than females, whereas Tmax and Cmax did not differ between sexes. IGF-I and IGFBP3 response is higher in males at low dose. However, it might be the case that the high dose of rhGH being a stronger stimulus also evokes a higher response in females. The difference between sexes is of course most likely due to the influence of estrogens, as all females were on oral contraceptives. No clear difference was seen in IGF-I response but the study was not specifically designed to investigate the impact of estrogens. It has been proposed that use of oral estrogens interferes with hepatic IGF-I production, but women not using estrogen supplementation also exhibit a lower IGF-I response than males (1). Studies in animals indicate that complex mechanisms, including modification of hepatic GH receptor expression, lead to the sexual dimorphism in the somatotropic axis (28). In contrast to serum GH concentrations, IGF-I and IGFBP-3 concentrations did not return to pre-treatment levels within the observation period, supporting the idea of use of these markers to detect doping with rhGH (13, 27, 29).
The existing studies on the relationship between 22 kDa and 20 kDa isoforms suggest that the secretion is a part of constant percentage of total GH. Therefore, the lower 20 kDa level and the long-term suppression in males seem to be a consequence of the lower total GH concentration. The 20 kDa GH isoform was also suppressed in females after administration of rhGH, consistent with a negative feedback of exogenous rhGH on pituitary GH secretion; the duration of suppression was dose dependent and re-occurrence of 20 kDa in the circulation was seen 26–28 h after low-dose rhGH and 34 h after high dose rhGH. The prolonged changes provide further evidence that the GH isoform pattern can be used to detect the administration of rhGH in females. With the assay method used in this study, 20 kDa GH levels in males were almost undetectable, making it impossible to demonstrate further suppression. Thus, more sensitive assays to quantify the amount of 20 kDa GH are necessary.
In summary, our data show that in healthy trained adults, responsiveness to rhGH administration is regulated by a variety of factors. Pharmacokinetic parameters are mainly influenced by the route of administration, with higher GH Cmax and AUC after i.m. injection, while pharmacodynamic parameters are mainly determined by gender. These differences need to be considered when decisions are made regarding therapeutic dosing with rhGH. Changes in the molecular isoforms in circulation after injection of rhGH show that in females, measurement of 20 kDa GH could be a useful parameter to detect rhGH doping in athletes.
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should a 18 or 19 year old consider growth hormones and IGF instead of steroids?
I do not recomend use but i agree to a point on the above. I think GH is more effective than IGF-1 no matter who you are. its all about dose, food and routine. I think IGF is good for long long runs. I think GH would "show" sooner. Now i say i think because my testing for those 2 wont begin until summer. I hope to report back good infor though.
Thanks for the info, 2 question's, i have just got the Serono, Saizen Gh, how much is in that bottle when mixed up, also i am using a 100 cc insluin gauge, what is the best dosage for a new guy on gh??
I just cant work out how much i should be taking, ie the whole bottle everyday or part of it??
I am 5'3" 144lbs at about 13 to 14% bf right now. Would taking 2iu per day for 60 days/ standalone do anything? I don't want to use too much with it because of previous issues with gyno. I had surgery and had it removed, but the Dr said he left a little bit of each gland so my nipples wouldn't fall off. Anyway, I have a bottle of Havoc, which is supposed to be very mild. Would that be worth using while on GH? Thanks in advance.
Do i still need to take T3 even if my GH dosage will be 6iu/day along with insulin ?
Does these 6iu of GH still lowers endogenous thyroid hormone in the body ?
Is there any scale on the dosage of GH which requires T3 intake ? Maybe over 8 - 10iu ?
Thanks for any advice.
Yes definitely! You still have high test levels and you aren't finished growing. You can really benefit. I started at 40 and got gains in size, decrease in body fat, more energy, better mood and yes after 2 years people think I've been juicing when they see me. It is slow, but steady.
There are many different online sources that claim to sell HGH, if permitted, can anyone tell me which ones are legit?