SHBG reducers

[dumanhieu2]

To anyone who has some indepth knowledge into supplements, this question is for you.

It is true that even taking ph's and steroids, there is an upper roof where free test can no longer compete with test bound to shbg (sex hormone binding globulin). This is why some people who juice up lets say 500mg of test a day doesnt get as big as someone who only juices 250mg. shbg is a genetic thing, some people produce more (hardgainers) and some produce less (freaks of nature). Because of this, the amount of exogenous hormones you put into your body doesnt really matter, what matters is the shbg levels. So the perfect anabolic environment would not only be high test levels, but also a low shbg level alongside it.

Alot of hebal medicines have been attributed to lowering the shbg levels, such as avena sativa (wild oats), stinging nettle, catuaba, and tongkat ali.

I have two questions: where and how is shbg produced, and is there anything that has been either proven or widely accepted as being a shbg reducer.

Thank you to those who can give good answers.

[dumanhieu2]

wow, no one really knows, do they?

any mods or people with some good knowledge know where to point me in the right direction?

[RippedUp]

Yes. This was a topic I was interested in as well.

I did an experiment this summer with Avena Sativa - but it was a low grade one (GNC), and the blood test showed that free test was barely affected.

If anyone had already done some research on the external factors that affect SHBG, it would be interesting to hear.


Thanks.

[buddha]

Originally posted by dumanhieu2
I have two questions: where and how is shbg produced, and is there anything that has been either proven or widely accepted as being a shbg reducer.

Thank you to those who can give good answers.

From: http://www.dpcweb.com/medical/reproductive_endocrinology/shbg.html#male

"Sex hormone-binding globulin (SHBG) is a glycoprotein synthesized by the liver. Circulating androgen and estrogen concentrations influence SHBG synthesis. Elevated testosterone, for example, causes SHBG synthesis to decrease, whereas high estrogen stimulates SHBG production. The regulation of SHBG synthesis, combined with SHBG's higher affinity for testosterone, impacts bioavailable testosterone levels.

SHGB binds up to 98 percent of the steroid hormones in the blood including 5a-dihydrotestosterone (DHT), testosterone and androstenediol with particularly high affinity, and estradiol and estrone with slightly lower affinity"

I have also read that approximately 50% of circulating T is bound to SHBG. SHBG is affected by insulin levels, the higher the insulin level, the less SHBG is produced or is circulating, and vice versa.

Tymchuk CN, Tessler SB, Aronson WJ, Barnard RJ.
Effects of diet and exercise on insulin, sex hormone-binding globulin, and prostate-specific antigen.
Nutr Cancer 1998;31(2):127-31
A diet high in fat has been linked to prostate cancer, possibly through an influence on hormones. Sex hormone-binding globulin (SHBG) binds androgens and is regulated in part by insulin. Diet and exercise can modify insulin levels, potentially affecting SHBG and the biologically available levels of androgens. To determine the effects of a low-fat (< 10% of calories), high-fiber diet plus daily exercise on insulin, SHBG, prostate-specific antigen (PSA), and serum lipids, we measured the levels of these factors in the serum of 27 obese men undergoing a three-week diet-and-exercise program. Insulin decreased from 222 +/- 30 to 126 +/- 21 pmol/l (p < 0.01), and SHBG increased from 18 +/- 2 to 25 +/- 3 nmol/l (p < 0.01). Body mass index decreased from 35 +/- 1.9 to 33.4 +/- 1.8 kg/m2 (p < 0.01). PSA levels were normal and did not change significantly, although in a small subset of men (n = 3) with slightly elevated PSA levels (> 2.5 ng/ml) all showed a decrease. The three-week diet-and-exercise intervention decreased insulin and lipid levels while increasing SHBG. The increase in SHBG would result in more testosterone being bound and, therefore, less of the androgen available to act on the prostate. The decrease in insulin might also decrease mitogenic activity in the prostate. The diet-and-exercise regimen did not have a significant impact on normal PSA levels. Although modest, these changes may be protective against the development of prostate cancer.

Belanger A, Locong A, Noel C, Cusan L, Dupont A, Prevost J, Caron S, Sevigny J.
Influence of diet on plasma steroids and sex hormone-binding globulin levels in adult men.
J Steroid Biochem 1989 Jun;32(6):829-33
Several experimental studies have suggested that diet can alter the production and metabolism of steroids in men. The purpose of this study was to determine the levels of unconjugated steroids and steroid glucuronides as well as sex hormone-binding globulin (SHBG) among normal adult men who were either omnivorous or vegetarians. The participants were white volunteers ranging from 25-35 years of age and the blood samples were taken between 0900 h and 1000 h and between 1600 h and 1700 h for two consecutive days. No significant statistical change was found in plasma dehydroepiandrosterone, dehydroepiandrosterone sulfate, testosterone, dihydrotestosterone and estradiol levels. Vegetarian group showed a higher levels of sex hormone-binding globulin (SHBG) while the free androgen index (FAI; calculated by the ratio testosterone/SHBG) was lower in this group. Although the concentrations of androsterone glucuronide were higher in vegetarian group, the vegetarians had a 25-50% lower level of androstane-3 alpha, 17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide. Our data further indicate that both, androstane-3 alpha,17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide concentrations are significantly correlated with SHBG levels and with the FAI values. The increases in androstane-3 alpha,17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide levels in the omnivorous group are probably a consequence of the elevation of the FAI. Our data suggest that in a vegetarian group, less testosterone is available for androgenic action.

Metabolism. 1990 Sep;39(9):967-70. Related Articles, Links
Regulation of sex hormone-binding globulin production by growth factors.
Plymate SR, Hoop RC, Jones RE, Matej LA.
Department of Clinical Investigation, Madigan Army Medical Center, Tacoma, WA 98431-5454.

Sex hormone-binding globulin (SHBG) is a glycoprotein whose production has been demonstrated to be regulated by both sex steroids, as well as by thyroid hormone and peptide hormones such as insulin. However, none of these regulatory factors would explain the marked decrease in serum SHBG seen throughout the prepubertal and pubertal time period in both boys and girls. Furthermore, current in vitro data show that both androgens and estrogens can stimulate SHBG production by the human hepatoblastoma cell line Hep G2; yet, in vivo androgens appear to suppress SHBG levels, while estrogens are associated with elevated levels. This study was undertaken to determine possible mechanisms to explain this phenomenon. Hep G2 cell cultures were incubated with insulin-like growth factor I (IGF-I), epidermal growth factor (EGF), transforming growth factor alpha (TGF-alpha), or dehydroepiandrosterone (DHEA). Significant decreases in the level of SHBG in the culture medium relative to control cultures occurred for each of the growth factors (P less than .01), whereas an increase in SHBG levels was observed in the medium of DHEA-treated cells. When cells were coincubated with IGF-I and thyroxine (T4), which alone stimulates SHBG production both in vivo and in vitro, the SHBG response to T4 was blunted. These results suggest that growth factors, as well as insulin, may be important determinants in SHBG production.

[jhov]

Bump to Buddha's post. The link in the post at the bottom is what I was referencing at the time when I saw buddha's post:
http://www.dpcweb.com/documents/news&views/spring00/techreports/zb170-b.pdf

1. SHBG is synthesized in the liver and its concentrations can be influenced by estrogen, thyroid hormone excess, exogenous androgens, growth hormone, acromegally and obesity.

2. From what I understand elevated test levels causes SHBG synthesis to decrease while elevated estrogen levels causes synthesis to increase. It has a very high binding affinity to DHT and test and a low affinity to estradiol. It effectively raises estrogen levels RELATIVE TO TEST/DHT it could be said. (SEE LINK)

3. The only thing I can think of with regards to your question would be something with low affinity to SHBG, non/low estrogenic. If I am not mistaken Trenabolone suites both criteria. 19 nor products and 17methylated compounds also come to mind but I am far from sure about those and hopefully someone else can answer in that regard as I have not researched them extensively and am speaking of the top of my head on that aspect!
peace
J

[Big Cat]

Reducing SHBG specifically has absolutely no effect. When SHBG goes up, its generally as a result of a rise in testosterone, and subsequent increases in estradiol. This binds the excess testosterone, prolonging its half-life, spreading the dose out. Sort of an automatic time-release effect.

Likewise, when you reduce SHBG, free test levels will not be affected for longer than a few minutes tops, as this increases test excretion. So total testosterone is lowered and free testosterone remains the same. SHBG manipulation has not proven a valid way of increasing gains.

With testosterone a ceiling is reached. In mice, 1 mg/kg/day showed to be just as potent as 10 mg/kg/day. This may in part be because of the SHBG, although no significant increases at all were noticed, which makes it unlikely that it is the only factor in this ceiling. Especially since we know test to be dose responsive up to 600 mg/week, and the 1 mg/kg/day would correspond to 800-1200 mg in most people.

At the point this ceiling is reached the best answer is therefor to administer products less prone to binding by SHBG, rather than adressing SHBG. As jhov also pointed out, two structures that are particularly resistant to SHBG are 17-alpha-alkylations and 19-Nor structures. Norethandrolone (Nilevar) for instance possesses both. Of course in the interest of maintaining SHBG levels a concomittant increase in estrogen is not desired, therefor trenbolone may be more suited. Its not liver toxic, its a more potent androgen and it works synergistically and non-redundantly with testosterone to lower cortisol.