From what i gather you are basically using Insulin to free up test that has binded to the SHBG from the excess Test suspension dosage used? It also acts as an "anti-estrogen" from what i gather too? And how would proviron compare to that of insulin in terms of freeing up test in this case? And in the case of using esterified test, eg test enanthate, how much of it would end up binding to shbg if shot twice weekly at 250mg a time?
I apologize in advance for the dumb questions and if what i interpreted above was wrong but would you care explaining this paragraph in slightly simpler terms for a dumb person like me?
I find this usage of insulin extremely interesting and makes a lot of sense, instead of what mostly others are generally using it for, shuttling carbs pwo and all the weird theories they come up with that make no sense.
Okay first some science geek stuff…
Too much sugar turns off gene that controls the effects of sex steroids
November 10th, 2007
Eating too much fructose and glucose can turn off the gene that regulates the levels of active testosterone and estrogen in the body, shows a new study in mice and human cell cultures that’s published this month in the Journal of Clinical Investigation. This discovery reinforces public health advice to eat complex carbohydrates and avoid sugar=Insulin
Sex hormone-binding globulin (SHBG) is a glycoprotein that binds to sex hormones, specifically testosterone and estradiol. Other steroid hormones such as progesterone, cortisol, and other corticosteroids are bound by transcortin.
SHBG levels appear to be controlled by a delicate balance of enhancing and inhibiting factors. Its level is decreased by high levels of insulin and insulin-like growth factor 1 (IGF-1). Also, high androgen levels decrease SHBG, while high estrogen and thyroxine levels increase it.
There are total, bound and free testosterone plasma levels. Bound testosterone, or any androgen/AAS, is inactive and bound by SHBG (Sex
hormone binding globulin) and has no effect because it cannot merge with receptor sites. Free testosterone is the only active form and accounts for about 1-3% of total testosterone /Androgen plasma levels. So a total testosterone threshold of 100 MG would only provide 1-3 MG, approximately, of free and active testosterone.
Only the free unbound AAS molecules can merge with a receptor-site and
therefore be termed as active. The bondage team that binds hormones are blood proteins called Sex-Hormone-Binding-Globulin (SHGB) and Albumin. Different alterations in chemical structures, either man-made or naturally occurring, are either more or less resistant to binding. This means alterations in an AAS chemical structure could allow it to exist in a greater percentage of unbound/active state. So less could do more.
Testosterone circulates in a bound state at a rate (or percentage) of 98-99% and an unbound state at a rate of 1 -2%. For the curious, 65% is bound by SHBG, and 33% is bound by Albumin, plus or minus 1%.
So the higher the percentage of an AAS circulating in the blood stream in the unbound/active state, the greater the number of potential bindings/mergence with receptor-sites.
Insulin suppressed cortisol release while inhibiting circulatory cortisol activity. It also increased androgen activity and down regulated SHBG. This resulted in an elevated plasma level of free (unbound) testosterone and lower cortisol levels/activity to inhibit androgenic induced protein synthesis. So it obviously required very little endogenous or exogenous testosterone to stimulate anabolism. Insulin is both anabolic and anti-catabolic. We know about insulin's ability to shuttle amino acids and glucose into tissues, unfortunately it also is the main fat storage hormone.(and for this reason I run a no carb high protein calorie diet)
Research has also shown insulin affects storage of only about half of the essential amino acids. But Insulin also reduces SHBG? So when AAS were stacked or layered with Insulin in a protocol there was an existing increase in free testosterone.
Back to Testosterone Enanhate...All drugs have an active-life and a half-life. Knowing a drug's average effective active-life and half-life is important information. An activelife is the entire period of time a parent drug remains active once administered. A drug's half-life is one half of its active-life and the period of time required for half of its administered dosage to disperse and metabolize.
Testosterone Enanthate has an "effective" active-life of about 8 days and a
half-life of about 4 days. Once a 200mg dosage of testosterone enanthate has been administered, it will take about 4 days for 100 mg of the administered dosage to disperse from the injection site and reach peak activity. This is the half-life point.
After the peak activity point/half-life, the second 100 mg disperses over the
following 4 days. The two 4 day periods make up the 8-day "effective" active-life. That explanation would seem idiotic if equal daily dispersal rates actually existed, and it would be nice. Actually, from the point of administration of the 200 mg dosage, the amount of testosterone that is released from the injection site gradually increases until it peaks
at the half-life. After the peak or half-life, the drug is less and less active (less anabolic/less androgenic/less anti-catabolic) until it is completely dispensed and metabolized.
If the goal is a more even dispersal rate, a drug must be administered on a
repeat basis at its average half-life point. This is true regardless of method for drug administration. It also allowed for pre-chosen peaks and dips in a drug's activity for specific-intent, and the ability to structure protocols for specific interests or Action/Reaction Factors.
So breaking it down to a cycle I'll shoot 1ml Testosterone Enhantate ed for 8 day's and layer some insulin in at day 8 where the first shot would have start ramping down the next day the second and so on...I will continue with the insulin for 10 day's on a low carb diet with alot of protein calories.
Yes proviron did also possess the abillity to bind to SHBG at a high rate so also a great SHBG inhibitor.
I hope this will shed some light on your question and help you think out of the box with some logic to take your body to the next level.
.gif "IP Gear")
