you didn't ask me, but that sounds like a good idea. Possibly avoid it during ovulation, until it is known what that does to LH and FSH. At other times of the cycle, it may take trial and error to find the right ratio. Start off slowly. Add red reishi to counter any DHT that may be produced. If the effects start wearing down, cycle a different hormonal herb, or use massage rather than increase dosage.

you didn't ask me, but that sounds like a good idea. Possibly avoid it during ovulation, until it is known what that does to LH and FSH. At other times of the cycle, it may take trial and error to find the right ratio. Start off slowly. Add red reishi to counter any DHT that may be produced. If the effects start wearing down, cycle a different hormonal herb, or use massage rather than increase dosage.

haha lovely11 HOW COULD I NOT aSK YOU =] ..especially cause your the expert with the cycle !!!!!!!! I was gonna mention it to you too =p on my program page...I was asking about receptors ! wasn't sure if to add in more questions or not !
believe me I have too many nbe questions xD I could ask you =3 lovelly

thank you lovely lovely11 ...red reishi thats the mushroom right? I should get some of that!!! right I don't take my temp but what days you think are the red days and green ..ovulation 14thish day but it different for everybody so maybe day 10-16 are the no T herb days =3
will it might be a good thing to try bubblebra got really good growth!

you didn't ask me, but that sounds like a good idea. Possibly avoid it during ovulation, until it is known what that does to LH and FSH. At other times of the cycle, it may take trial and error to find the right ratio. Start off slowly. Add red reishi to counter any DHT that may be produced. If the effects start wearing down, cycle a different hormonal herb, or use massage rather than increase dosage.

okie I just got your message on my program page thanx

Rocket, you can ask anybody a question on BN, period!.

Estradiol is 100x more potent at the receptor sites then Testosterone. Estrogen and testosterone are secreted in short bursts, pulses which vary from hour to hour and even minute to minute. Hormone release varies between night and day and from one stage of the menstrual cycle to another.

Studies show that T in women helps maintain muscle and bone and contributes to sex drive, or libido. There are also quality-of-life issues. If you give testosterone replacement to testosterone-deficient women, they often say they feel better, but they're not specific as to how.

I'm pretty sure women only produce .03 mg of T daily, however the types of E in men are E2 and E1, so of the 4 types (yes there's 4) it's the same as women. The only way to be sure is a silva test, and I'd make sure you find out what  free T. If anything stopping DHT is still a priority for the girls too.

Good Question!

That is interesting.

Theoretically if there are 2 units of free T. One unit of T is converted into (not necessarily 1 unit of ) Estrogen. The free T that works against progress is negligible, Estrogen:Testosterone 100 to 1 (when you say receptor sites, different receptor sites respond differently) . (As long as the 1 unit of testosterone doesn't become less than 1/100 unit of estrogen) So free T is also necessary for overall function. Free T Might also up-regulate Estrogen receptors. From a study, it said testosterone was negatively Correlated (correlation is not causation) with growth during luteal phase. This sentence is speculation, perhaps it was DHT, or not free T. It could have also been free T, or its indirect effects on DHT or estrogen. Everyone seems to agree that DHT is more inhibiitive than free T. This is a good argument for aromatase, it MIGHT convert free T into estrogen Instead of DHT.

So, I don't know if DHT has an essential function for females. DHT must have a function for males, but the more there is, the more unwanted effects it has for both genders.

I've come across papers that mentioned DH versions of progestogens. I have no idea what they do.

That is interesting.

Theoretically if there are 2 units of free T. One unit of T is converted into (not necessarily 1 unit of ) Estrogen. The free T that works against progress is negligible, Estrogen:Testosterone 100 to 1 (when you say receptor sites, different receptor sites respond differently) . (As long as the 1 unit of testosterone doesn't become less than 1/100 unit of estrogen) So free T is also necessary for overall function. Free T MIGHT also up-regulate Estrogen receptors. From a study, it said testosterone negatively affected growth during luteal phase. This sentence is speculation, perhaps it was DHT, or not free T. It could have also been free T, or its indirect effects on DHT or estrogen. Everyone seems to agree that DHT is more inhibiitive than free T. This is a good argument for aromatase, it MIGHT convert free T into estrogen INSTEAD of DHT.

So, I don't know if DHT has an essential function for females. DHT must have a function for males, but the more there is, the more unwanted effects it has for both genders.

I've come across papers that mentioned DH versions of progestogens. I have no idea what they do.

I find this interesting, The total estradiol production rate in the human male has been estimated to be 35-45 μg (0.130-0.165 μmol) per day, of which approximately 20% is directly produced by the testes [13,14]. Roughly 60% of circulating estradiol is derived from direct testicular secretion or from conversion of testicular androgens. The remaining fraction is derived from peripheral conversion of adrenal androgens [15].

To get an accurate assessment of your testosterone levels, you need to have two measurements. One measures the combined level of bound testosterone and free testosterone (the active kind that matters in terms of what symptoms you're experiencing) in your blood, while the other measures only the testosterone that's bound to proteins. By subtracting the second number from the first, you'll find your level of free testosterone. Because free testosterone can bind protein in a test tube, and bound testosterone can be displaced, the resulting number will be, at best, a close approximation.
Michael Roizen, MD

Bound testosterone must be SHBG. Bound estrogen and testosterone must bind to proteins in the blood steam instead of breast protein receptors. DHT must be different than SHBG. SHBG seems inactive, and DHT seems potent. SHBG might be good for inhibiting free T from converting into DHT.

"

Roughly 60% of circulating estradiol is derived from direct testicular secretion or from conversion of testicular androgens. The remaining fraction is derived from peripheral conversion of adrenal androgens [15].

"

Testicular or ovaries by different amounts.

Bound testosterone must be SHBG. Bound estrogen and testosterone must bind to proteins in the blood steam instead of breast protein receptors. DHT must be different than SHBG. SHBG seems inactive, and DHT seems potent. SHBG might be good for inhibiting free T from converting into DHT.

"

Roughly 60% of circulating estradiol is derived from direct testicular secretion or from conversion of testicular androgens. The remaining fraction is derived from peripheral conversion of adrenal androgens [15].

"

Testicular or ovaries by different amounts.

So what is Free Testosterone?



Free T is testosterone that is present within the bloodstream or not bound (locked) to a chemical called albumin. But it's also the functional T, If we were to breakdown testosterone say like how we know estrogen is, i.e.. E1, E2, E3,

Generally,

FT-Free T is about 2% (this is the functional T)

BT-Bound T or 98%
-which is 38% albumin (bloodstream)
-SHBG is 60% (sex-hormone-binding-globulin)

This is complicated, however I'd like find an illustration where 5-ar and aromatase are expressed at the same time and to which pathway it takes within a cell receptor site.

According to https://en.wikipedia.org/wiki/Sex_hormone-binding_globulin SHBG binds to estrogen and testosterone. IGF-1 and prolactin reduce SHBG. SHBG levels that are too low cause problems. SHBG has higher binding affinity for DHT than Testosterone, and lesser affinity for estrogens. Estrogens raise SHBG.

https://en.wikipedia.org/wiki/Transcortin Transcortin binds to progesterone. (transcortin is the equivalent to SHBG)

https://en.wikipedia.org/wiki/Dihydroprogesterone At least two forms of Dihydroprogesterone
5α-Dihydroprogesterone is an agonist to PR. 20α-Dihydroprogesterone is created by the corpus luteum and placenta ( http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?q=all&cid=8956#ec ).

According to https://en.wikipedia.org/wiki/Sex_hormone-binding_globulin SHBG binds to estrogen and testosterone. IGF-1 and prolactin reduce SHBG. SHBG levels that are too low cause problems. SHBG has higher binding affinity for DHT than Testosterone, and lesser affinity for estrogens. Estrogens raise SHBG.

https://en.wikipedia.org/wiki/Transcortin Transcortin binds to progesterone. (transcortin is the equivalent to SHBG)

https://en.wikipedia.org/wiki/Dihydroprogesterone At least two forms of Dihydroprogesterone
5α-Dihydroprogesterone is an agonist to PR. 20α-Dihydroprogesterone is created by the corpus luteum and placenta ( http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?q=all&cid=8956#ec ).

Funny you should mention SHBG,

Associations of sex-hormone-binding globulin (SHBG) with non-SHBG-bound levels of testosterone and estradiol in independently living men.
http://www.ncbi.nlm.nih.gov/pubmed/15509641

Therefore, we conclude that in eugonadal men, higher SHBG levels are associated with lower levels of non-SHBG-E2 but slightly higher levels of non-SHBG-T. This means that SHBG cannot be regarded as an estrogen amplifier in eugonadal men.

I'm still checking on this one though, see post:

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.