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The human body has its own built in science lab, careful experimentation can benefit NBE, only "be careful" that it doesn't become a bad science experiment gone wrong and end up hurting yourself, (in other words don't crash the lab). Dodgy

The mechanism of secretion of hormones, their delivery to target cells and purification of metabolic crucial for normal functioning of the endocrine system. Method for production of steroid hormones studied enough, but it is known that these hormones accumulate in those tissues where they are produced.

Thyroid hormones, catecholamines and peptide hormones are packaged into granules are formed from the endoplasmic reticulum. When you combine these vesicles with the cell membrane leads to the release of hormones in the blood.

In many cases, some of the circulating hormones associated with plasma proteins. However, generally speaking, the hormones in physiological concentrations in the dissolved state, and there is no data to indicate any mandatory role of such proteins in the hormonal effects. The reasons for their existence, are unknown. Typically, active apparently free, but are not bound to plasma proteins share of hormone binding in blood plasma, obviously, limits, rather than increases the likelihood of the hormone on target cells.

In some cases, proteins that bind the hormone with high affinity bulk plasma hormones. Examples include thyroxine binding globulin (TBG) and thyroxine prealbumin (TSPA), which binds thyroid hormones, as well as corticosteroid binding globulin (GAC or transkortin), which binds cortisol.

Cholesterol can also be viewed as a hormone, because it is synthesized in the liver, passes from the blood (due, mainly, low-density lipoprotein (LDL)) in peripheral tissues and inhibits its biosynthesis. It may represent an exception to the above generalization: it is completely insoluble steroid and LDL to act as a carrier hormone.

Source: collegiate
Regulation of Hormone Secretion

Sensing and signaling: a biological need is sensed, the endocrine system sends out a signal to a target cell whose action addresses the biological need. Key features of this stimulus response system are:
· receipt of stimulus
· synthesis and secretion of hormone
· delivery of hormone to target cell
· evoking target cell response
· degradation of hormone
This is relevant to the status of the hormone itself, rather than to the type of system that regulates it (neural, endocrine, humoral).

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Oestradiol to sex hormone binding globulin, human serum albumin and other plasma proteins: evidence for non-specific binding of oestradiol to sex hormone binding globulin.

1. The percentage binding of testosterone (T) and oestradiol (E2) to sex hormone binding globulin (SHBG) and human serum albumin (HSA) was determined over a range of SHBG concentrations of 16-250 nmol of dihydrotestosterone (DHT) bound/l. It was found that the binding of both T and E2 to HSA was a function of their binding to SHBG and bore an inverse relationship to it. After removal of both SHBG and HSA from plasma by affinity chromatography a 'residual' binding of about 11% for T and 12% for E2 was still apparent. In addition to the specific high-affinity, low capacity binding of E2 to SHBG, non-specific low-affinity binding of 7-12% was demonstrated after selective denaturation of the specific binding site of the latter. 2. Competition studies indicated that although at the relatively higher levels of SHBG found in the normal female the physiological concentrations of E2, T and DHT need not be taken into account in estimating the unbound fractions of steroids, at the relatively lower levels of SHBG found in normal men and hirsute women, the physiological concentrations of T and DHT are effective in causing statistically significant displacement of E2 from the common, specific binding site on SHBG. 3. A simple computerized technique is described for the determination of fractions of E2 and T respectively, that are unbound to SHBG, unbound to SHBG and HSA, and unbound to all plasma proteins, when the total plasma levels of E2, T, DHT and SHBG are known.
Serum bioavailability of sex steroid hormones.

This chapter has reviewed the factors underlying the transport of testosterone and oestradiol into tissues in vivo. The following points have been emphasized. Albumin-bound testosterone is nearly freely available for transport into brain and liver and is partially available for transport into salivary gland and lymph node; testosterone transport into hair follicles has not been measured thus far. SHBG-bound testosterone is not available for transport into tissues; SHBG-bound oestradiol is available for transport into liver, salivary gland, and lymph node, bug not into brain under normal conditions. The transport of hormone from the circulating plasma protein-bound pool involves tissue-mediated enhanced dissociation of the hormone from the protein without significant exodus of the plasma protein from the microcirculation compartment. The tissue-mediated enhanced dissociation mechanism varies in activity between different organs and is a much more important factor than organ differences in capillary transit times in regulating the amplification of hormone delivery to different tissues. The concentration of free testosterone inside cells in the absence of significant cellular metabolism of the hormone is nearly ten times greater than the concentration of free testosterone in vitro, but is nearly equal to the concentration of free plus albumin-bound hormone. In the presence of active tissue metabolism of hormone, the concentration of cellular free testosterone may be much less than the albumin-bound hormone and may fortuitously approximate the concentration of free testosterone in vitro. This is the situation in salivary gland; the low concentration of testosterone in saliva appears to be due to active salivary metabolism of the hormone, since both free and albumin-bound testosterone are available for transport into salivary gland.

A cup of green tea a day couldn't hurt:

Chronic green tea consumption decreases body mass, induces aromatase expression, and changes proliferation and apoptosis in adult male rat adipose tissue.

Green tea (GT) and its components have been shown to possess antiobesity properties and the corresponding mechanisms of action are being investigated, given the epidemic proportions of obesity incidence. In the current work, we used 12-mo-old male Wistar rats to test the effect of 6 mo of treatment with GT as the sole drinking beverage (52.8 +/- 6.4 mL/d) on adipose tissue (AT). AT aromatase expression was determined by Western blotting, plasma concentrations of 17beta-estradiol and testosterone were determined by RIA, and adipocyte size determined by measuring diameter in tissue sections. Proliferation and apoptosis were also assessed by Ki67 immunostaining and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling, respectively. Evaluations were made in subcutaneous (sc) AT and visceral (v) AT. Body weight increased over time in both groups (P < 0.001), but the increase was more pronounced in controls (P < 0.001) and food and fluid intake did not influence that effect. At the end of the experiment, aromatase expression increased in the AT (318.5 +/- 60.6% of control in scAT, P < 0.05, and 285.5 +/- 82.9% of control in vAT, P < 0.01). AT of GT-treated rats had a higher percentage of proliferating cells (204.1 +/- 19.5% of control in scAT, P < 0.01, and 246.6 +/- 50.2% of control in vAT, P < 0.01) and smaller adipocytes (78.3 +/- 1.7% of control in scAT, P < 0.001, and 87.9 +/- 3.2% of control in vAT, P < 0.05). GT also increased the number of apoptotic cells in vAT (320.4 +/- 21.9% of control; P < 0.001). These results suggest new mechanisms for GT on body weight and highlight its potential benefit to prevent or treat obesity and the metabolic syndrome.

This study is interesting, and although free estradiol is difficult to determine I wonder how the bioavailability of free E would alter the outcome.

Total estradiol, rather than testosterone levels, predicts osteoporosis in aging men.

To study and establish sex hormone cutoff levels for osteoporosis risk in men over 50 years old.

Case-control study of 216 men > 50 years, 110 with osteoporosis (O) and 106 with normal bone density ©. We measured estradiol (E2), sex hormone binding globulin (SHBG), total testosterone (TT) and albumin. Free testosterone (FT) and bioavailable testosterone (BT) were calculated through Vermeulen's formula.

There was no difference in TT between groups. Relative risks of osteoporosis were 1.89 for E2 < 37 pg/mL (p = 0.02); 1.91 for SHBG > 55 nmol/L (p = 0.019); 2.5 for FT < 7 ng/dL (p = 0.015); 2.7 for BT < 180 ng/dL (p = 0.0003).

In men over 50 years old, TT was not indicative of osteoporosis risk while E2 < 37 ng/mL was. SHBG > 55 nmol/L, FT < 7 ng/dL and BT < 180 ng/dL can represent additional indications for osteoporosis screening in men over 50 years old.

This study indicates that temperature variations fluctuate sex steroids, what's important is that SHBG has a love thing for DHT, (figures). Rolleyes always with the androgens huh? Lol.

The temperature dependence of the binding of 5 alpha-dihydrotestosterone, testosterone and estradiol to the sex hormone globulin (SHBG) of human plasma.

The binding of 5 alpha-dihydrotestosterone (DHT), testosterone and estradiol to the sex hormone binding globulin (SHBG) and albumin in human plasma has been studied at 4, 20 and 37 degrees C using the method of equilibrium partition in an aqueous two-phase system based on dextran, poly(ethylene glycol) and water. The intrinsic association constants for the binding to SHBG and the apparent association constant for the binding to albumin have been determined from Scatchard-type binding plots. The affinity of SHBG for DHT is 1.2-1.3 times higher than that for testosterone and 4 times higher than that for estradiol. The affinity of SHBG for the steroids decreases with increasing temperature. The mean values of the free energy of binding, delta G degree, in the temperature range used are -52.3, -51.7 and -48.9 kJ X mol-1 for the binding of DHT, testosterone and estradiol, respectively, to SHBG. The corresponding values of the enthalpy change, delta H degree, are 73.7, 70.0 and 99.0 J X mol-1 X K-1. These values are discussed in terms of the difference in the structure of the steroids. The affinity of albumin for testosterone and estradiol is almost equal and is lower than that for DHT. The delta G degree for the binding to albumin is about 55% lower than that for the binding to SHBG.

Next up, Controlling and uncovering cortisol (in-depth). Smile

Following this paragraph below one could expect how elevated cortisol could make for a bad day in relation to NBE.
Quote:Cortisol can exert it’s effects on peripheral tissue. Once in circulation, cortisol is typically bound to a specific glucocorticoid-binding alpha2-globulin called transcortin. About 75% of cortisol is bound to transcortin, 15-20% bound less tightly to albumin, and 5% of circulating cortisol is unbound. This is an important factor to take into consideration when measuring cortisol levels. The 24-hour urinary excretion of unmetabolized cortisol is one of the best ways to accurately gauge cortisol levels. This helps take into account bound and free cortisol. Exogenous cortisol has a half-life of about 70-90 minutes. Cortisol can be converted to it’s 11-keto analogue cortisone (you know, the stuff you take when you have some bad swelling or inflammation).

Vitamin C – This vitamin, mainly known for it’s anti-oxidant properties, may also have some anti-cortisol effects. A study done by Stone entitled “Effects of Vitamin C on cortisol and the Testosterone: cortisol ratio” showed a decrease in cortisol levels in 17 junior elite weight lifters. This study also showed that the individuals taking Vitamin C (an extra gram a day) improved their testosterone: cortisol ratio by over 20%. This type of decrease in cortisol can lead to increased muscle and connective tissue hypertrophy and enhanced recovery from training. Since Vitamin C also decreases your chances of suffering from a cold or flu infection by 30% (14) and may aid in collagen synthesis, it would be wise to take some extra vitamin C when involved in an intense weight training program.

CORTISOL and Muscle Breakdown
Why Take Vitamin C?

10) Inflammation. There is gathering evidence that Vitamin C may improve inflammation, particularly in at risk men. One prominent example was a 2009 study showed that CRP (C-Reactive Protein) can be reduced by 25% in men (and women) with at risk levles > 1.0 mg/L. [14] What is remarkable is that this was achieved with a mere gram per day, which is a fairly low intake by "Linus Pauling" standards.

Vitamin C - My Current Dosage and Strategy

My (the author) strategy is to take 3 500 mg doses of Ester-C or one of the equivalent supplements. And I will take more if I feel as if I might be getting sick. And I always take Vitamin C with no fat in my stomach. Of course, this is no problem for me as I almost always consume a Low Fat Diet anyway.

NOTE: Regular Vitamin C is acidic and can be hard on the stomach: you may want to consider the Ester-C (500 mg) , which is neutralized, if you do decide to take it.
How Does Vitamin C Affect the Hormone Cortisol?

Ascorbic acid, more commonly known as vitamin C, is a water-soluble vitamin that humans need to ingest on a regular basis. Unlike most animals, humans cannot make their own vitamin C. To the general public, it is probably one of the more familiar vitamins but many people may be unaware of the ways it is used by the body and its effect on the hormone cortisol.

Vitamin C
Vitamin C has a wide array of functions. The Linus Pauling Institute reports that this vitamin is needed for the body to create the collagen which is part of blood vessels, tendons, muscles, bones and skin. Vitamin C is an antioxidant which helps to protect against "free radicals" -- atoms, ions or molecules thought to be involved in degeneration and disease; it affects the digestion of cholesterol, and is involved in the synthesis of norepinephrine, a chemical in the brain.

Cortisol is a steroid hormone secreted by the adrenal glands in response to stress or when the level of cortisol in the blood is low. The body uses cortisol to increase blood sugar. Cortisol also aids in the metabolism of fat, protein and carbohydrates, and can decrease bone formation. It prevents the release of inflammatory substances, and is used medically to treat Addison's disease, rheumatoid arthritis and allergies.

Current Research
Elevated cortisol levels are a factor in suppressing the immune system, and research is being conducted to determine if vitamin C supplementation can boost immune system function by reducing cortisol levels. At the Dalhousie University in Nova Scotia, researchers have studied the effect of vitamin C supplementation on human subjects subjected to exercise-heat stress. The authors state: "Prolonged physical exertion and environmental heat stress may elicit postexercise depression of immune cell function, increasing upper respiratory tract infection (URTI) susceptibility." They found that vitamin C was more effective than a placebo in reducing cortisol levels. A study in Germany measured the response of human subjects to stress testing -- public speaking and mental arithmetic -- using both vitamin C and a placebo. This study found that vitamin C supplementation decreased measures of stress and that the subjects' elevated cortisol levels recovered more quickly. In a study reported in the October 2001 "International Journal of Sports Medicine," marathoners who received vitamin C supplements showed decreased cortisol levels.

Considerations and Warnings
While vitamin C and cortisol do interact, the research implications are still unclear. The Linus Pauling institute -- although Pauling himself recommended very high doses of vitamin C -- states that adult men and women should consume at least 400 mg of vitamin C daily. This is the equivalent of ten servings or five cups of fruits and vegetables, so the Institute suggests supplemental vitamin C in two separate 250 mg doses, taken morning and evening. It is unwise to self-medicate with vitamin C or any other supplement for a specific condition, and if you have questions or concerns, you should discuss them with your health care professional.


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