Jim, not everyone uses "the net" as a reference.
My roommates started using gh in the late 90s and I bought my first kits of Humatrope in 2002. Back then no one did gh serum tests. IGF tests were all we had and most guys were using pharma gh until Jintropin came on the scene. The way you and many others talk about generics now is EXACTLY how some argued that Jins were garbage and the Chinese could not produce legit 191aa. IGF test was the only weapon we had at the time to test any growth we used. If not for those tests I would have never tried Jins.
I've personally never gone above 4ius of pharma gh but my roommate and several coworkers who were competitive BBers at the time cruised in the 6-8 iu range. Several of the bloods I saw had IGFs in the 600 range and higher.
Check out this study. Figure 1, bottom chart shows mens IGF levels on 9.5ius well over 750.
http://press.endocrine.org/doi/full/10.1210/jcem.85.11.6964
Am I reading it wrong?
Best post on this thread in quite a while. Thank you.
From the study:
"The aim of the present study was to assess the impact of GH administration in supraphysiological doses on the circulating levels of IGF-I and related variables in healthy adults of both sexes. Collection of such data is relevant in view of the ongoing interest in the use of exogenous GH for unlicensed indications in general and GH abuse by athletes in particular (12).
The main findings include 1) IGF-I is the most sensitive marker of GH exposure; 2) the GH-induced increase in IGFBP-3 and ALS is markedly lower compared with that in IGF-I; 3) IGFBP-2 responds very little to GH; and 4) a marked gender difference exists, with men being more responsive to exogenous GH administration.
The large sample size and the randomized design, including two different doses, strengthens the validity of the observations, but the study population, on the other hand, covered a narrow age range of young, healthy, and physically fit individuals. Extrapolations to older people or patients should therefore be made with caution.
At baseline no gender differences were recorded, apart from higher ALS levels among women. Comparable levels of IGF-I, IGFBP-3, and IGFBP-2 between healthy adult males and females has previously been reported (6, 13), but gender differences in IGF-I levels have been observed in particular age groups (14). Females may exhibit slightly higher IGF-I levels than males at puberty and in early adulthood, whereas the opposite has been reported in middle-aged adults (9, 15). In adult hypopituitary patients with documented GH deficiency IGF-I levels are consistently higher in men than in women (9, 16). Our observation of higher ALS levels in women has been reported recently (17), but is in contrast with a previous report in which no gender differences were observed in any age group (7).
The pattern among males was characterized by high and almost identical increments in IGF-I after the two GH doses. In women, the IGF-I response was lower, but a distinct dose responsiveness was observed. Thus, the lower GH dose group apparently reached the top of the dose-response curve in males, but not in females. It is evident that the present study involved the high end of the dose-response curve, but there is evidence from the literature that a gender difference in GH sensitivity also exists with lower GH doses. The relative GH resistance in women has been described by Ghigo
et al. (18), who reported that the minimum exogenous GH dose needed to elicit an IGF-I response in normal subjects is higher in women than in men. Both spontaneous and stimulated GH levels are elevated in women compared with men (16, 19, 20), which has been causally linked to differences in estradiol levels. It is, however, unresolved whether the stimulatory effect of estradiol on GH release involves a central stimulation or a negative feedback linkage to peripheral reduction of IGF-I production. In favor of the latter hypothesis, several studies have shown that administration of exogenous estradiol lowers serum IGF-I levels concomitantly with amplification of endogenous GH release (21). It has, on the other hand, recently been reported that both GH release and serum IGF-I levels increase during the periovulatory phase in normal young women, which coincides with elevated endogenous estradiol levels (22). Alternatively, it could be hypothesized that androgens play a permissive role for GH-stimulated IGF-I production. This could explain the suppression of IGF-I production in postmenopausal women during exogenous estradiol administration, which is likely to inhibit endogenous androgen secretion, and it may also account for the low IGF-I levels in hypopituitary females. This theory is supported by Erfurth
et al. (23), who found a significant correlation between free testosterone and IGF-I levels. Recently, Span
et al. (24) reported that estrogen replacement in GH-deficient women significantly increased GH requirements, and androgen substitution in GH-deficient men increased GH sensitivity. Regardless of the physiological mechanisms the present study demonstrates that women, relative to men, are resistant to GH in terms of IGF-I generation. A similar gender difference has recently been shown regarding the acute lipolytic response to a physiological GH bolus (25). These observations in healthy adults are in accordance with the idea that the GH dose requirements in hypopituitary adults are higher in female patients, as judged by serum IGF-I levels as well as changes in body composition (19). In both sexes GH discontinuation was followed by an abrupt decline in total IGF-I levels.
The elevations in IGFBP-3 and ALS were far less pronounced than those in IGF-I, and again, the response was lower in women than in men. Ghigo
et al. (18) reported that IGFBP-3 levels were less increased than IGF-I levels after GH exposure.
It has previously been shown that the circulating total IGF-I/IGFBP-3 ratio is elevated in active acromegaly (13) and after GH administration in both GH-deficient adults (26) and healthy controls (18). Accordingly, we also recorded a significantly increased IGF-I/IGFBP-3 ratio in the present study, which prevailed even 2 weeks after cessation of GH administration.
Serum IGFBP-2 concentrations did not consistently change during GH administration, which contrasts with at least one previous study in which GH administration suppressed circulating IGFBP-2 levels (27). Juul
et al. reported decreased IGFBP-2 levels in acromegalic patients (13), and Jørgensen
et al. (5) observed suppressed IGFBP-2 levels in active acromegaly, which became normalized after successful surgery, whereas Clemmons
et al. (28) reported normal IGFBP-2 levels in active acromegaly and moderately elevated levels in hypopituitary adults.
Our study clearly demonstrated that IGF-I is superior to IGFBP-2, IGFBP-3, and ALS regarding the ability to identify exposure to supraphysiological doses of exogenous GH in healthy subjects. Using the upper 4 sd level of IGF-I in the GH-untreated state as an arbitrary cut-off limit, 86% of men were identified while receiving the high GH dose, and the IGF-I level was not completely returned to baseline 14 days after termination of GH administration. As previously mentioned, this percentage was significantly lower in women. As a mean to detect GH abuse in athletes, a single measurement of IGF-I in serum is probably not sufficiently robust, at least not in females. Whether measurements of other GH-dependent growth markers, alone or in combination with IGF-I, will prove more efficacious must await further analysis."
