[Dynseli]

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.

[Lotus]

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


   

[Dynseli]

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.

[Lotus]

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.

   

[Dynseli]

According to https://en.wikipedia.org/wiki/Sex_hormon...g_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 ).

[Lotus]

According to https://en.wikipedia.org/wiki/Sex_hormon...g_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.

[Dynseli]

From Wikipedia, 'Dihydrotestosterone' "The enzyme 5α-reductase synthesizes DHT in the prostate, testes, hair follicles, and adrenal glands" . Women have an equivalent to the prostate, and the ovaries are the female equivalent to the testes.

Aromatase as you say turns testosterone into estrogen. Two different enzyme catalysts turn testosterone into different other hormones. I'm guessing, but 5α-aromatase right?

Because there are two different catalysts that turn testosterone into two different hormones, There could be a chart that shows both processes, but its unlikely for a chart to show it as one process.

A new search for botanicals that lower 5-alpha-reductase (thereby DHT). Pygeum, saw palmetto, green tea, and red reishi, might just be those herbs, but verification is needed.

bound hormones and Dihydro* are different.

[Lotus]

From Wikipedia, 'Dihydrotestosterone' "The enzyme 5α-reductase synthesizes DHT in the prostate, testes, hair follicles, and adrenal glands" . Women have an equivalent to the prostate, and the ovaries are the female equivalent to the testes.

Aromatase as you say turns testosterone into estrogen. Two different enzyme catalysts turn testosterone into different other hormones. I'm guessing, but 5α-aromatase right?

Because there are two different catalysts that turn testosterone into two different hormones, There could be a chart that shows both processes, but its unlikely for a chart to show it as one process.

A new search for botanicals that lower 5-alpha-reductase (thereby DHT). Pygeum, saw palmetto, green tea, and red reishi, might just be those herbs, but verification is needed.

bound hormones and Dihydro* are different.

Gonadotrophins and testicular function

FSH and LH are important regulators of spermatogenesis and steroidogenesis, acting respectively on the Sertoli cells and Leydig cells. They increase intracellular concentrations of free cholesterol and its transport through the mitochondrial membrane by the StAR protein (the regulation of StAR is the rate-limiting step in gonadotrophin-induced steroid synthesis). Here cholesterol is converted into pregnenolone, then in androstenedione, DHEA and testosterone: these androgens bind to an androgen-binding protein (ABP), which carries them in the testicular fluid. Some testosterone is converted to estradiol by Sertoli cell-derived aromatase enzyme.



Leydig cell steroidogenesis is controlled primarily by LH with negative feedback of testosterone on the hypothalamic-pituitary axis. Testosterone and FSH act synergically on the Sertoli cells, that produces inhibin (which has a selective negative feedback action on FSH secretion) and androgen receptors. The small amount of estrogen formed from peripheral aromatization of testosterone can inhibit both FSH and LH secretion.
If testicular androgen production is inhibited by the administration of exogenous androgens then spermatogenesis ceases.

Transport, metabolism and actions of androgens

The 98% of circulating testosterone is bound to albumin or to sex-hormone-binding globulin (SHBG). SHBG is synthesized in the liver and its circulating concentration is increased by estrogen or excess thyroid hormones and decreased by exogenous androgens, glucocorticoids or growth hormone and by hypothyroidism, acromegaly and obesity. In the liver, testosterone is converted to androsterone and etiocholanolone.
In target tissues, testosterone or its reduced form DHT induces release of a heat shock protein, dimerization of two receptors and translocation to the nucleus where the dimer binds to an estrogen-like hormone response element on DNA.
http://flipper.diff.org/app/items/5569


   


On the herbs yes, green tea though is still iffy for lowering DHT.

[Dynseli]

your post about binding affinity to carrier proteins matches up with what is at wikipedia 'SHBG'.

The binding affinity for estrogen wouldn't explain why women have a higher % of more free testosterone. An overall lower level of testosterone could mean lower % of testosterone while having less free testosterone than a male.

"estosterone and estradiol circulate in the bloodstream, bound mostly to SHBG and to a lesser extent serum albumin and corticosteroid-binding globulin (CBG) (AKA transcortin)" wikipedia SHBG

"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." - Lotus; estrogen is responsible for raising SHGB, even though it has lesser affinity for it? SHGB seems to have a minimal impact on women then.

So you see the pattern of estrogen lowering testosterone, prolactin, and progesterone. Prolactin lowering estrogen and testosterone. The 3 hormones, and possibly testosterone (but not DHT) up-regulating the opposing receptors in the breast, making them more sensitive to growth stimulus. The 4 hormones have a seesaw effect, on each other and on the receptors.

We need new threads on binding carrier proteins and reductase.

[Dynseli]

Does anyone think that having pubic, facial, or other body hair is an opportunity to reduce DHT and increase estrogen from testosterone for results?