So nothing is contrary - to sum up
Thus far, with what has been presented, nothing appears to be contrary to the points I was attempting to make. In fact, they have only validated them. They are:
1. It has been shown that, "in the presence of IGF-1 proliferation stops and those new "cells" are tasked... which means they will no longer proliferate".
Translation - IGF is capable of overriding proliferation. Thus if so, it would be unwise to dose IGF prior to proliferation occurrence.
2. MGF has been shown capable of either proliferation or differentiation. Agreed. "Therefore we want MGF to behave as MGF and not as IGF-1 and do so in autocrine fashion."
How can this be achieved? As Anthony Roberts suggested in the link I provided in another thread, admin MGF Post WO. This would also appear, at least on the surface to coincide - "in the environment where your body creates & utilizes MGF...that is post-weightlifting."
3. MGF and IGF behavior also appears to be governed via the presence or absence of particular compounds, i.e. "Insulin-like growth factor-I can induce proliferation in some environments in the presence of some compounds. In other environments and in the absence of those compounds it promotes differentiation."
Is there anything else that has been shown here that reflects contrary to any of the above assertions? I'm partially beginning to wonder if we are actually saying much of the same thing, with the exception of what I see as a differrent intepretation of Dats statement involving "or IGF-1 masquerading as (pretending to be) peg-MGF". If he is saying what you imply, then there must be a reason contrary to the other suggested protocol provided earlier.
Hopefully we can conclude this and perhaps agree to disagree. Though I'm not exactly sure what we are disagreeing about.
Thus far, with what has been presented, nothing appears to be contrary to the points I was attempting to make. In fact, they have only validated them. They are:
1. It has been shown that, "in the presence of IGF-1 proliferation stops and those new "cells" are tasked... which means they will no longer proliferate".
Translation - IGF is capable of overriding proliferation. Thus if so, it would be unwise to dose IGF prior to proliferation occurrence.
2. MGF has been shown capable of either proliferation or differentiation. Agreed. "Therefore we want MGF to behave as MGF and not as IGF-1 and do so in autocrine fashion."
How can this be achieved? As Anthony Roberts suggested in the link I provided in another thread, admin MGF Post WO. This would also appear, at least on the surface to coincide - "in the environment where your body creates & utilizes MGF...that is post-weightlifting."
3. MGF and IGF behavior also appears to be governed via the presence or absence of particular compounds, i.e. "Insulin-like growth factor-I can induce proliferation in some environments in the presence of some compounds. In other environments and in the absence of those compounds it promotes differentiation."
Is there anything else that has been shown here that reflects contrary to any of the above assertions? I'm partially beginning to wonder if we are actually saying much of the same thing, with the exception of what I see as a differrent intepretation of Dats statement involving "or IGF-1 masquerading as (pretending to be) peg-MGF". If he is saying what you imply, then there must be a reason contrary to the other suggested protocol provided earlier.
Hopefully we can conclude this and perhaps agree to disagree. Though I'm not exactly sure what we are disagreeing about.
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