Hexarelin - a peptide GH secretagoguewhich stimulates the release of growth hormone (GH)

Hexarelin Profile

Hexarelin (HEX) is a peptide GH secretagogue, structurally similar to GHRP-6,  in the growth factor family which stimulates the release of growth hormone (GH).   It can be used medically to treat GH deficiency.

Background

Although relatively new, Hexarelin is becoming a popular choice as a performance enhancement drug. Hexarelin is currently available from several research companies.

Action

Due to Hexarelin’s ability to increase secretion of natural Growth Hormone, most of its effects are similar to those of synthetic GH, although to a slightly lesser extent.  Effects of its use include:  increase in strength, growth of new muscle fibers, increase in the size of already existing muscle fibers, neural protection, joint rejuvenation, protection and healing.  Also, the GH receptors in adipose (fat) tissue allow for potential fat reduction with Hexarelin use.  The increase of circulating GH through Hexarelin use causes levels of Insulin-Like Growth Factor (IGF-1) to rise in the liver.  IGF-1 is the prime cause of muscle growth in response to GH stimulation.

There is no appetite boost with Hexarelin use (as opposed to GHRP-6’s extreme appetite increase) due to its inability to drastically increase Ghrelin levels that are responsible for added hunger and quicker gastric emptying.

Technical Data

In studies where Hexarelin was injected subcutaneously, Growth Hormone, measured through plasma concentrations, increased significantly and within thirty minutes of injection.  GH levels decreased back to normal around four hours post injection (1).  The GH increase, has been found to be effective up to 2mg/kg, any further increase in dose was found to be ineffective in causing a GH response (2).
Results showed that Hexarelin’s effect on GH stimulation tapered between weeks 4 through 16.  Separating cycles by 4 week off periods, avoided the negative feedback loop and the next cycle of Hexarelin produced the same level of results as the first cycle (3).

User Notes

I used Hexarelin awhile back, at a dose of about 200mcg/day, and found it to be very good for healing my injuries, burning a bit of fat, and helped me gain a bit of muscle.

I also have a couple of friends who are powerlifters, and they were able to use Hexarelin to heal an old Pec injury and train pain free while on it. My bodybuilder friends (yes, not only do I have friends, but some are actually bodybuilders) have said that 400 mcg/day of Hexarelin gave them similar results to low doses of GH (maybe 1-2 iu/day would be a good equivalent).

Overall, Hexarelin is a good all purpose anabolic. Also,  since we know that IGF and GH use produces a shutdown of your endogenous levels of those hormones, Hexarelin also seems very useful for “GH-PCT” or “IGF-PCT”, as it can help restore your natural levels of those hormones after a cycle of them.

References

1. Imbimbo, B.P., et. al Growth hormone-releasing activity of hexarelin in humans. A dose-response study.Eur J Clin Pharmacol. 1994;46(5):421-5.
2. Imbimbo, B.P., et. al Growth hormone-releasing activity of hexarelin in humans. A dose-response study.Eur J Clin Pharmacol. 1994;46(5):421-5.
3. Rahim, A., Shalet, SM Does desensitization to hexarelin occur? Growth Horm IGF Res. 1998 Apr;8 Suppl B:141-3.

Testosterone Boom: Pharma Firms Spread Male Menopause Myth !

The Low Carb Diabetic: Testosterone Boom: Pharma Firms Spread Male Menopause Myth !

"Man, oh man," read the words emblazoned on a white tent set up in the pedestrian zone of the German city of Erfurt. Those who ventured inside received information on a dramatic scientific finding: One in three men over the age of 60 suffers from "testosterone deficiency syndrome." If left untreated, this dastardly condition can cause excess weight, anemia, hot flashes, osteoporosis, lowered sex drive and bad moods.

This same tent will be making appearances through November in Augsburg, Saarbrücken, Hanover and other German cities. Here, men over the age of 40 can have their testosterone level checked at no cost. They can also learn how to counteract testosterone deficiency: either get more exercise, or apply testosterone gel to their skin.

This traveling testosterone counseling service provided by the "German Society for Men and Health" was not born out of a purely charitable impulse -- there is a marketing angle at work here as well. The organization is funded by pharmaceutical company Jenapharm, the leading manufacturer of testosterone gel.

It's one of five companies that sell the male sex hormone, which is rubbed into the skin, and business couldn't be better. This can be seen in the number of prescriptions issued through Germany's statutory health insurance funds. The Scientific Institute of AOK, one of Germany's largest insurers, analyzed this data on behalf of SPIEGEL and found that prescriptions for testosterone gel more than tripled between 2003 and 2011. The most recent statistics show 390,000 daily doses per year. In Germany, a month's supply of the product costs around €60 ($80).

The booming business in testosterone gel provides a prime example of the ways in which pharmaceutical companies exaggerate illnesses to create new markets for their products.

The testosterone trend comes with attendant risks. Used in excess, the male hormone can promote the growth of prostate cancer and increase the risk of heart attacks and strokes. American doctors Lisa Schwartz and Steven Woloshin recently warned in the medical journal JAMA Internal Medicine that this widespread use of testosterone is "a mass, uncontrolled experiment that invites men to expose themselves to the harms of a treatment unlikely to fix problems ... that may be wholly unrelated to testosterone levels."

More on this story here.

1 comment:

Lowcarb team member said...

For many years it has been accepted that women needed to be medicated at every stage of their lives. We are always pre or post something and here is a pill for it all.As we read in another article this seems, at least in the US, to be spreading to children. Men are notoriously difficult to get to the Dr let alone to ask for medication for most things. Some marketing guru has obviously been quite clever in this case. I wonder if it will catch on here? Kath

30 August 2013 17:04

How to Raise Testosterone (hint: orgasm!) | Fat-Burning Man by Abel James: Real Food, Real Results.

Dr. Sara Gottfried: How to Raise Testosterone (hint: orgasm!) | Fat-Burning Man by Abel James: Real Food, Real Results.

Back by popular demand this week is Dr. Sara Gottfried, author of The Hormone Cure. Last time she was on the show we covered how hormones affect women. After receiving a ton of positive feedback, now she’s back with a show for the guys.

Here’s the show.

Podcast: Play in new window | Download

Dianabol (Methandrostenolone) - Wikipedia

Methandrostenolone - Wikipedia, the free encyclopedia

Methandrostenolone (trade names Averbol, Dianabol, Danabol), also known as metandienone (INN) or methandienone, is an orally-effective anabolic steroid originally developed in Germany and released in the US in the early 1960s by Ciba Specialty Chemicals.^[1][2]

Methandrostenolone is a controlled substance in the United States^[3] and Western Europe and remains popular among bodybuilders. An injectable form is sold online from United States based companies.

Methandrostenolone is readily available without a prescription in countries such as Mexico (under the trade name Reforvit-b), and is also being manufactured in Asia and many East European countries.

Contents

• 1 Biophysiology
• 2 Usage
  • 2.1 As a tonic
  • 2.2 Bodybuilding
  • 2.3 Detection of use
• 3 John Bosley Ziegler, M.D.
• 4 Footnotes
• 5 Other references

Biophysiology

Methandrostenolone does not react strongly with the androgen receptor but still exerts its effects through the androgen receptor in vivo.^[4] These include dramatic increases in protein synthesis, glycogenolysis, and muscle strength over a short space of time. In high doses (30 mg or more per day), side effects such as gynecomastia, high blood pressure, acne and male pattern baldness may begin to occur.

The drug causes severe masculinising effects in women even at low doses. In addition, it is metabolized into methylestradiol by aromatase. This means that without the administration of aromatase inhibitors such as anastrozole or aminoglutethimide, estrogenic effects will appear over time in men.

Many users will combat the estrogenic side effects with Arimidex, Nolvadex or Clomid. In addition, as with other 17α-alkylated steroids, the use of methandrostenolone over extended periods of time can result in liver damage without appropriate care.

The 17α-methylation of the steroid does allow it to pass through the liver with only a small portion of it broken down (hence causing the aforementioned damage to the liver) allowing it to be effective when taken orally. It also has the effect of decreasing the steroid's affinity for sex hormone binding globulin, a protein that de-activates steroid molecules and prevents them from further reactions with the body. As a result, methandrostenolone is significantly more active than an equivalent quantity of testosterone, resulting in rapid growth of muscle tissue. However, the concomitant elevation in estrogen levels - a result of the aromatization of methandrostenolone - results in significant water retention.

This gives the appearance of great gains in mass and strength, which prove to be temporary once the steroid is discontinued and water weight drops. Because of this, it is often used by bodybuilders only at the start of a "steroid cycle", to facilitate rapid strength increases and the appearance of great size, while compounds such as testosterone or nandrolone with long acting esters build up in the body to an appreciable amount capable of supporting anabolic function on their own.

Usage

As a tonic

17α-methandrostenolone confiscated by the DEA in 2008.

In the early 1960s, doctors commonly prescribed a tablet per day for women as a tonic. This use was quickly discontinued upon discovery of the heavily masculinising effects of methandrostenolone.

Bodybuilding

Despite the lack of any known therapeutic applications, the drug remained legal until the early 1990s^{[citation needed]}. The United States Congress added certain kinds of steroids which may or may not include methandrostenolone^{[clarification needed]} to the Controlled Substances Act as an amendment known as the Anabolic Steroid Control Act of 1990^{[citation needed]}. This act placed steroids in the same category as some amphetamines as a "Schedule III" drug and possession of these drugs results in a felony. Contrary to popular belief, steroids were banned by Congress without the support of the FDA, the American Medical Association, the DEA or the National Institute on Drug Abuse^{[citation needed]}. It's used by bodybuilders, and methandrostenolone continues to be used illegally to this day, typically being combined (stacked) with injectable compounds, such as testosterone propionate, enanthate, cypionate as well as other injectable drugs like trenbolone acetate.

Several successful athletes and professional bodybuilders have come forward and admitted long-term methandrostenolone use before the drug was banned, including Arnold Schwarzenegger and Sergio Oliva.^[5][6] Other steroids stacked with methandrostenolone are primarily, if not always, injectable compounds such as testosterone, trenbolone and nandrolone.

Detection of use

Methandrostenolone is subject to extensive hepatic biotransformation by a variety of enzymatic pathways. The primary urinary metabolites are detectable for up to 4 days, and a recently discovered hydroxymethyl metabolite is found in urine for up to 19 days after a single 5 mg oral dose. Several of the metabolites are unique to methandrostenolone. Methods for detection in urine specimens usually involve gas chromatography-mass spectrometry.^[7][8][9]

John Bosley Ziegler, M.D.

See also: Weightlifting at the 1960 Summer Olympics

For a period of time Dr. Ziegler worked at the Ciba Pharmaceutical company, who supplied testosterone for experimental purposes. In the early 1950s his patients included people suffering from burns, as well as the seriously injured or handicapped. In 1954 he administered testosterone, for a period of less than 6 weeks, to several high-level competitive bodybuilders on an experimental basis, but had disappointing results. Dissatisfied and possibly overburdened with patients, he distanced himself from research into performance-enhancing drugs until May 1960, or possibly as early as 1959 (conflicting testimonials).^{[citation needed]}

By the time of the 1960 European Championships in Milan he was understandably suspicious of the Russians - "the Russians are giving their athletes something." Therefore, he asked John Grimek to propose to his chief, Bob Hoffman that steroids be administered to members of the American Olympic team. Mr. Hoffman, however, was cautious and later remarked it was "too close to give to the men who will represent the USA". According to Grimek, "Apparently, he doesn’t think it will do that much good, and may even have detrimental effects , . . .He appears doubtful." Instead, Dianabol was given to two lower level lifters to investigate its effectiveness and safety. After that, Hoffmann retracted his decision and Dianabol was administered to certain Weightlifters on the team.^{[citation needed][10][11]}

Footnotes

1. ^ Yesalis CE, Anderson WA, Buckley WE, Wright JE (1990). "Incidence of the nonmedical use of anabolic-androgenic steroids". NIDA Res. Monogr. 102: 97–112. PMID 2079979.
2. ^ Fair JD (1993). "Isometrics or Steroids? Exploring New Frontiers Of Strength in the Early 1960s". Journal of Sport History 20 (1): 1–24.
3. ^ Drug Enforcement Administration. Controlled Substances, Alphabetical Order.
4. ^ Roselli CE (May 1998). "The effect of anabolic-androgenic steroids on aromatase activity and androgen receptor binding in the rat preoptic area". Brain Res. 792 (2): 271–6. doi:10.1016/S0006-8993(98)00148-6. PMID 9593936.
5. ^ Steve Theunissen: Arnold & Steroids: Truth Revealed 2002
6. ^ "Interview with Sergio Oliva". Fitnessprat.no. 2010-10-18. Retrieved 2012-02-13.
7. ^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 952-954.
8. ^ Schänzer W, Geyer H, Fusshöller G, Halatcheva N, Kohler M, Parr MK, Guddat S, Thomas A, Thevis M. Mass spectrometric identification and characterization of a new long-term metabolite of metandienone in human urine. Rapid Commun. Mass Spectrom. 20: 2252-8, 2006.
9. ^ Fragkaki AG, Angelis YS, Tsantili-Kakoulidou A, Koupparis M, Georgakopoulos C. Schemes of metabolic patterns of anabolic androgenic steroids for the estimation of metabolites of designer steroids in human urine. J. Steroid Biochem. Mol. Biol. 115: 44-61, 2009.
10. ^ "The Ultimate Strength Exercise 1, Bill Starr" (PDF). Retrieved 2012-02-13.
11. ^ "The Ultimate Strength Exercise 2, Bill Starr" (PDF). Retrieved 2012-02-13.

Other references

• Wilder EM (October 1962). "Death due to Liver Failure Following the Use of Methandrostenolone". Can Med Assoc J 87 (14): 768–9. PMC 1849648. PMID 14000685.
• Foss GL (April 1960). "Some Experiences with a New Anabolic Steroid (Methandrostenolone)". Br Med J 1 (5182): 1300–5. doi:10.1136/bmj.1.5182.1300. PMC 1967563. PMID 13824087.
• Zingg W (October 1965). "The Effect of Methandrostenolone on Nitrogen Excretion Following Open-Heart Surgery". Can Med Assoc J 93 (15): 816–7. PMC 1928923. PMID 5318132.

Dangerous hormonal effects of paleo & low-carb diets - Andrew Kim Blog:

Andrew Kim Blog: An examination of popular "diets" -- avoid them all

Some of the dietary practices that are currently promoted have the inconvenience of producing some of the effects that these practices are being undertaken to check in the first place—namely cortisol and estrogen. 

If any person were so persuaded to do so, he or she should bear in mind that a deficiency of calories, carbohydrate, salt, calcium, and excessive amounts of histamine, choline, and prostaglandins are some of the factors that activate both cortisol and estrogen. 

I’ve written about stress and the reasons for keeping it as low as possible.  Refer back to those for context for this post.  But briefly, the stress hormones—cortisol, adrenalin, noradrenalin, growth hormone, glucagon, and some others—are all catabolic and estrogenic.  When they persist in the blood too long or excessively, irreversible degenerative processes are set in motion that affect all aspects and all levels of the body.

First and foremost, a deficiency of glucose—in the cell and blood—potently activates the stress metabolism, operating centrally by way of the hypothalamic-pituitary-adrenal axis.  At the same time, the stress metabolism decreases the output of thyroid hormones: Indeed, it’s been repeatedly observed that thyroid hormone output and adrenal cortex activity share an inverse relationship.

Glucagon and growth hormone are increasingly secreted by the pancreas and pituitary gland in response to a deficiency of glucose. (Overexertion, exposure to cold, trauma, and emotional arousal also stimulate the secretion of these hormones, reinforcing the designation of these hormones as “stress hormones.”)  These hormones liberate free fatty acids, which do not simply stimulate fatty acid oxidation, but also stick to proteins, diffuse in and out of cells, disrupt the structure of cellular water and their associated proteins, and activate inflammatory pathways in fat, white blood cells, etc.

The catecholamines, adrenalin and noradrenaline, can temporarily elevate glucose levels, but they also inhibit the secretion of insulin, promoting the wasteful conversion of amino acids to glucose and glucose to lactic acid.  Lactic acid increases the acidity near the cells that produce it, and this local decrease in pH favors the protonated form of acids, including free fatty acids, in which form they are more likely to enter cells from the blood, potentiating their toxicity.  Keeping these stress hormones as low as possible permits the efficient oxidative metabolism of glucose.

Some stressed people quickly respond by shifting their “autonomic nervous system” away from sympathetic dominance and more toward parasympathetic dominance, of which choline is the grandee transmitter.  Choline acutely stimulates the secretion of insulin, aggravating hypoglycemia, thereby contributing to the exaggerated swings in blood glucose levels.

Recently, I was asked a question on Facebook about agents for diarrhea, and I remembered offhand that anti-histamines, as a side effect, are also anti-cholinergic, which decrease gastrointestinal motility and secretion so as to help with diarrhea.

The so-called first generation anti-histamines, notably diphenhydramine or Benadryl, can be supportive in times of stress by buffering against hypoglycemia—both by blocking choline, which, once again, stimulates insulin secretion, and histamine, thereby activating uncoupling proteins in the pancreas.  Because pantothenic acid (vitamin B5) and riboflavin (vitamin B2) are needed by insulin-degrading enzyme (or insulinase) to break down insulin, a deficiency of pantothenic acid or riboflavin could therefore cause insulin to persist in the blood, aggravating hypoglycemia, too.

Parenthetically, in haste, I forgot to mention the role of anti-histamines in acne in my previous post.  It turns out that histamine receptors are expressed in keratinocytes and that topically applied diphenhydramine reduces stratum corneum lipids and the production of squalene by sebocytes in culture.¹

A high protein diet, as in the Paleo diet, leads to a persistent elevation of the stress hormones, mainly glucagon, adrenalin, and cortisol.  The resulting free amino acids (namely tryptophan, phenylalanine, tyrosine, and leucine) and free fatty acids, inhibit the uptake of T₃ into cells and into the central nervous system by way of the blood brain barrier.² Diets such as these are promoted to be anti-inflammatory and beneficial for metabolism and weight loss, but nothing could be more wrong; they are proinflammatory and anti-metabolic in every sense.

People talk about sugar as if it is a drug, affecting the brain in a way that cocaine does.  Be that as it may, consider for a moment that practically all body changes are made known to the hypothalamus and the hypothalamus governs much of the endocrine system and immune system, in which many (real) functional disorders are thought to originate.  But these functional disorders are really problems of the hypothalamus, rather than problems of the immune system, endocrine system, or whatever.  Know also that there exists a connection between the cerebral cortex and the hypothalamus, and this connection underlies the physiological effects of psychological stress, such as mental conflict.  What has been the effect of telling people to avoid certain foods like sugar and to fight their natural cravings for such?  Or of telling people that they have (imaginary) disorders with no basis in anything?

A decrease in ATP generation tends to reinforce itself, in part, by inhibiting the uptake of thyroxin, T₄, into cells, which is an energy dependent process.  In the liver, free fatty acids inhibit the uptake of T₄ and this is, I think, the major cause of the deficiency of T₃ in diabetes and low-carbohydrate and Palo dieters, as much of the conversion of T₄ to T₃ (about 60 percent) occurs in the liver.

As to the brain, when the energy charge decreases, neurons become hyperexciteble.  The inability to generate adequate amounts of ATP keeps neurons partially depolarized, which, by allowing calcium to flow into the cell from the blood in droves, increases the neuron’s likelihood of becoming “excited” upon stimulation.   And, the inability to regulate the uptake of calcium into pre-synaptic nerve terminals leads to the inappropriate release of transmitters, which are then available to act on, and to stimulate, their target cells excessively.  Epilepsy, seizure, psychosis are some neurological conditions affected negatively by a deficiency of energy, for which pharmaceutical companies have taken advantage of and developed drugs that target said conditions somewhat rationally.

In the heart, a deficiency of ATP depresses left ventricular functioning, as there is less energy available for robust contractions and complete relaxations.  The impaired contraction also increases the ventricular blood volume so as to impose an increase in pressure on the left side of the heart.   Less blood is pumped for every beat of the heart as a result (reduced stroke volume).  Moreover, the increased resistance to flow in the blood vessels due to the deficiency of energy (or oxygen) adds further to the stress on the heart.  Anything that increases the oxidative metabolism of glucose (of which there are some agents currently in the pipeline) appears to increase the heart’s viability and the chances of survival in patients with heart failure and arrhythmia. 

The addition of magnesium, by sparing ATP, and fructose (or sucrose), by decreasing the cell’s redox potential and by stimulating respiration, can quickly reverse these pathological cellular events.  More generally, a deficiency of energy, acidosis, and hypoxia can be corrected with some supportive care that includes some of the B vitamins, insulin, bicarbonate, and sugar.  Estrogen could apparently aggravate all these problems by interfering with oxygen use.

Persistent hyperglycemia and hypertension are two prominent signs that a person is operating on high levels of stress hormones, due to cortisol and aldosterone, respectively.   An increased susceptibility to infections, gastric ulcers, and eventually, diabetes and cardiovascular disease are others.

Avoiding starvation, high protein, low-carbohydrate, and salt-restricted diets keep the aromatase enzyme, aldosterone, and cortisol in check. (Seems obvious, right?) Prostaglandins and histamine are activators of cyclic AMP-dependent protein kinase and thus aromatase, so NSAIDs and diphenhydramine can help to balance excess estrogen levels.

Hydroxylated flavones—apigenin, chrysin, and quercetin—inhibit the final rate-limiting step in cortisol synthesis, cytochrome P450 1B1.³ However, quercetin is known to induce the aromatase enzyme, while apigenin, as well as naringenin, inhibit the aromatase enzyme.  I mention aromatase here to point out the fact that aromatase is activated by stress, like cortisol, aldosterone, glucagon, etc., are.  Finding fruits and vegetables that contain the desirable balance of these flavonoids has been thus far elusive.

There is some indirect evidence that caffeine has anti-estrogenic effects and the organic acids in coffee inhibit the regeneration of cortisol in tissues.⁴ In men, cortisol increases the expression of aromatase and estrogen, and estrogen, in turn, activates the enzyme that regenerates cortisol—the same enzyme that is inhibited by coffee.

I have to go, but I will delve into some of the even more annoying ideas that are bandied about as fact on the Internet.  For now, suffice it to say that if you read about or try a diet the goes against your base instincts (believe it or not, even telling you to eat despite not being hungry), run the other way while waving your hands in the air and screaming.


References

1.       Pelle, E. et al. Identification of histamine receptors and reduction of squalene levels by an antihistamine in sebocytes. The Journal of investigative dermatology 128, 1280–5 (2008).

2.       Hennemann, G. et al. Plasma membrane transport of thyroid hormones and its role in thyroid hormone metabolism and bioavailability. Endocrine reviews 22, 451–76 (2001).

3.       Cheng, L.-C. & Li, L.-A. Flavonoids exhibit diverse effects on CYP11B1 expression and cortisol synthesis. Toxicology and applied pharmacology 258, 343–50 (2012).

4.       Atanasov, A. G. et al. Coffee inhibits the reactivation of glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1: a glucocorticoid connection in the anti-diabetic action of coffee? FEBS letters 580, 4081–5 (2006).

80 Year Old Bodybuilder Jim Arrington - at Muscle Beach Competition 9/3/12

Published on 4 Sep 2012

80 Year Old Bodybuilder Jim Arrington was competing at the Muscle Beach Labor Day Competition 9/03/12.

• mryorkielover 2 weeks ago

  Jim admits to taking testosterone. But keep in mind, just because you take testosterone, your body doesn't automatically grow muscles like that. Jim has been working out his whole life since he was in his early teens. Jim looks like that because of hard work, clean diet, and clean living.

  · in reply to ChudFapper (Show the comment)
• 
  ChudFapper 2 weeks ago

  Actually, there is no way in hell any of those are natural. It's basically physically impossible to look like that at that age, without testosterone supplements.
  It's become a fairly common thing, and is actually legal. Men's testosterone start to decline with age, and it's become a trend for men in the 50s and 60s to start supplementing with testosterone to get back to their natural levels. It's actually healthy and almost works like a fountain of youth.

  · in reply to Yashas Redd (Show the comment)

Dr. Jeff Life - The Benefits of Optimizing Your Hormones, with Randy Alv...

SHBG: The Master Regulator for Testosterone and Estrogen

Do You Know Your Sex Hormone Status? By Zach White

Life Extension® has long emphasized the importance of maintaining a balanced and robust sex hormone profile as a core anti-aging strategy.

Hundreds of published studies link improper testosterone and estrogen balance (in men and women) with the onset of age-related pathologies such as coronary artery disease, stroke, osteoporosis, and bone fracture.1-5

But in order for you to optimize your sex hormone status, precise and accurate measurement is of paramount importance.

In this article you will learn of a critical blood marker of hormonal balance called sex hormone-binding globulin or SHBG. Newly published studies reveal that the interaction of SHBG with testosterone and estrogen affects overall hormonal balance—yet very few doctors test for it.

As you will read, sex hormone imbalances precipitated by SHBG abnormalities are associated with multiple diseases of aging in both sexes. These include cardiovascular disease (especially in women), cancer, type 2 diabetes, metabolic syndrome, and sleep apnea.6-10

SHBG: The Master Regulator for Testosterone and Estrogen

SHBG is a protein produced primarily in the liver, although the testes, uterus, brain, and placenta also synthesize it. It serves as a transport carrier, shuttling estrogen and testosterone to sex hormone receptors throughout your body.11,12 SHBG also safeguards these vital hormones from degrading too rapidly and prevents their clearance from the body.

It thus acts as the master regulator of your sex hormone levels, maintaining the delicate balance between estrogen and testosterone critical to overall health in aging humans.

New evidence further indicates that the SHBG molecule itself plays another key role in the body: conveying essential signals to the heart, the brain, and adipose (fat) tissue that ensure their optimal function.13 There’s even a special SHBG receptor molecule on cell surfaces that functions much like the ubiquitous vitamin D receptor protein, helping cells communicate with one another.14,15 In other words, SHBG itself functions much like a hormone.

Knowing your SHBG levels, along with testoste-rone and estrogen, thus gives you and your doctor a more precise picture of your overall health—and enables you to take preventive measures against life-threatening conditions for which you may be at greater risk.

Aging Humans and Increasing SHBG: An Overlooked Threat

As you age, SHBG levels may steadily rise, even though your production of sex hormones continues to decline.8,16 The result? SHGB binds to what few sex hormones you have remaining and reduces their bioavailability to cells in your body.

With elevated SHBG in the blood, too much testosterone may be sequestered and thus functionally unavailable to healthy tissues. Because testing for SHBG is largely overlooked, many older men (and their doctors) may be led to believe through standard testing that they have “normal” total testosterone levels—but since most of it may be bound to elevated levels of SHBG, in actuality they may be testosterone deficient.16

Why? Testosterone, like all steroid hormones, is derived from cholesterol, a fat molecule.16 Fats don’t dissolve in water, so the amount of testosterone floating freely in your bloodstream is small (about 0.5-2% of the total amount).16,17 Most of the circulating testosterone in your blood is either bound to the protein albumin or to SHBG.18-20

It is the combination of free and albumin-bound testosterone that ultimately determines your bio-available testosterone status.16,21-24

As a result of imprecise testosterone measurement, aging men may experience signs of feminization as their increased SHBG binds testosterone, preventing testosterone from exerting its effects and leaving estrogen’s physiological impact on the male physiology unchecked.16 These may include gynecomastia (the development of fatty breast tissue in men), diminished libido and poor sexual performance, cognitive decline, and chronic fatigue.

Combating Metabolic Syndrome

While excess SHBG creates problems with sex hormone balance, having SHBG levels that are too low is associated with other disorders. Nowhere is the impact of low SHBG so profound as in the cluster of conditions known as the metabolic syndrome, which encompasses obesity, insulin resistance, lipid abnormalities, and chronic high blood pressure.9

In men, low total testosterone and low SHBG are predictors for a higher incidence of metabolic syndrome and many of its components.9,25-29
 
In late postmenopausal women, low SHBG and high estrogen levels correlate with the inflammatory state associated with metabolic syndrome.30 SHBG abnormalities have also been linked to an increased risk of acne, infertility, polycystic ovary syndrome, and uterine cancer in overweight women.6,31-33

The high insulin levels found in people stricken with metabolic syndrome have also been shown to suppress SHBG, creating a vicious cycle of abnormal SHBG activity.34,35

The good news is that testosterone supplementation for men, and bioidentical hormone replacement for women, may safely and effectively reverse many of these adverse, age-related metabolic changes.36,37 Obtaining accurate measurement of sex hormone levels through SHBG blood testing thus enables you and your doctor to prevent or combat common medical disorders.

Low SHBG Is a Key Marker of Cardiovascular Disease

SHBG levels have an important relationship with nearly every biomarker of cardiovascular disease, from C-reactive protein (CRP) to arterial calcification.38,39 Low SHBG is also associated with elevated triglycerides and low-density lipoprotein (LDL).40

Calcification of blood vessels, an early finding in cardiovascular disease, is also associated with lower SHBG levels, especially in women.10,38 Low SHBG in women is associated with higher levels of C-reactive protein (CRP), an important marker of inflammation and cardiovascular risk.39 In men, low SHBG indicated an increased risk of death from cardiovascular disease.35 In both men and women, low SHBG levels are strongly correlated with obesity.41

SHBG, alone and in the context of specific sex hormone levels, thus constitutes an integral predictor of a major chronic age-related condition. Some experts are now recommending SHBG measurements as another means of evaluating cardiovascular and metabolic risk.42

What You Need to Know: Sex Hormone-Binding Globulin

Optimal sex hormone status, including a healthy balance of testosterone and estrogen, is a core component of any anti-aging strategy. New scientific evidence has revealed the crucial importance to hormone balance of a widely overlooked active protein called sex hormone-binding globulin or SHBG. SHBG is an important regulator of your testosterone and estrogen levels, responsible for distributing sex hormones throughout your body—yet few doctors test for it. SHBG abnormalities are associated with multiple killer diseases of aging in both sexes, including cardiovascular disease (especially in women), cancer, type 2 diabetes, metabolic syndrome, sleep apnea, and osteoporosis.