This is interesting, it's edited with key points that relates to NBE, (always advancing NBE).
Less than 1% of the circulating testosterone is in a free form in males (less that 3% in females). Only when in a free form this hormone can exhibit its properties by connecting to the androgen receptors on the cell walls. Based on a study 14 to 50 per cent of the testosterone is bound to SHBG in males and 37 to 75 in females. It is worth mentioning that SHGB poses very high affinity for binding to testosterone. Therefore, changes in the SHGB levels noticeably influence the level of bioavailable testosterone.
Let’s discuss for a moment what exactly a testosterone bioavailability is. Other than SHGB there are two more testosterone-binding proteins, also called carriers. One of them is albumin. It is a low-affinity binding protein, thus testosterone bound to it is considered “bioavailable”. Albumin binds to testosterone in the range 45 to 85 per cent in men (25 – 65 in women). The third carrier is the cortisol binding globulin, which binds also with low-affinity to less that 1 % of the testosterone in circulation.
The free androgen index (FAI) indicates the amount of bioavailable testosterone. FAI is the sum of the free testosterone and the albumin and cortisol binding globulin. Or it’s the total serum testosterone minus the SHGB-bound testosterone.
It is now clear why we should focus our attention on the properties of SHGB. The levels of this binding protein increase when there is excess estrogen present.
Conversely, SHGB levels drop if the testosterone levels are elevated.
SHGB exhibits higher affinity to testosterone than to estrogen.
Testosterone is an estrogen precursor – it will convert to estrogen under the influence of the enzyme aromatase. Nothing that we don’t know so far. Here is where it gets interesting. Suppose that we have normal testosterone levels and we don’t suffer from any of the health ailments, which influence the SHGB levels. That means that SHGB levels are normal, too.
If more testosterone is converted to estrogen due to abnormal aromatase levels, the SHGB I will increase as well. SHGB, being more readily bound to testosterone, will leave us with excess estrogen levels in the system, which in turn will stimulate increased production of the SHGB protein from the liver. This whole process ultimately amplifies estrogen levels. Estrogen readily binds to the androgen receptors in cells thus leaving less opportunity for the free testosterone. Even more important, estrogen is the messenger molecule that signals the brain to decrease testosterone production.
Another thing of great importance is the fact that over 40 per cent of the SHGB protein circulates unbound in the blood stream in man (over 80 per cent in women), and albumin circulates unbound almost all of the time. Thus increase in the total testosterone levels does not produce any noticeable changes in the free testosterone levels unless there is a significant increase like the one seen after synthetic steroid hormone administration.
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