Your Testosterone Levels — Killing or helping you?

If you haven't gotten your testosterone level, then visit the AndroStat now.
To see what others are saying about the AndroStat, visit this thread.

If you have your testosterone level, here is what it means –

Ready to get in your zone with the AndroSeries?

Just fill out the AndroStat, and get linked to the AndroStacker to start building your AndroSeries stack. Your testosterone level will be automatically filled in, or if you already tested you can link back to the androstat from your email.

We've taken the "testosterone equivalent" values of our AndroSeries products and built them into the AndroStacker program. This allows you to build a stack of AndroSeries products and see the benefits, side-effects and "androgen zone" — so you can make sure you are taking the optimal dose for your custom goals with minimal side-effects.

References:
1. Estrogen and androgen receptors: regulators of fuel homeostasis and emerging targets for diabetes and obesity.
Mauvais-Jarvis F.
Trends Endocrinol Metab. 2011 Jan;22(1):24-33. Epub 2010 Nov 5.

2. Tissue-specific glucocorticoid reactivating enzyme, 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1)–a promising drug target for the treatment of metabolic syndrome.
Masuzaki H, et al.
Curr Drug Targets Immune Endocr Metabol Disord. 2003 Dec;3(4):255-62.

3. Testosterone deficiency and the metabolic syndrome.
Lunenfeld B.
Aging Male. 2007 Jun;10(2):53-6.

4. Gender differences in the cardiovascular effect of sex hormones.
Vitale C, et al
Nat Rev Cardiol. 2009 Aug;6(8):532-42. Epub 2009 Jun 30.

5. The male climacterium: clinical signs and symptoms of a changing endocrine environment.
van den Beld AW, et al.
Prostate Suppl. 2000;10:2-8.

6. Androgens and body fat distribution in men.
Pi-Sunyer FX.
Obes Res. 1993 Jul;1(4):303-5.

7. Androgens and body fat distribution.
Blouin K, et al.
J Steroid Biochem Mol Biol. 2008 Feb;108(3-5):272-80. Epub 2007 Sep 7.

8. Testosterone and regional fat distribution.
Mårin P.
Obes Res. 1995 Nov;3 Suppl 4:609S-612S.

9. Two emerging concepts for elite athletes: the short-term effects of testosterone and cortisol on the neuromuscular system and the dose-response training role of these endogenous hormones.
Crewther BT, et al.
Sports Med. 2011 Feb 1;41(2):103-23. doi: 10.2165/11539170-000000000-00000.

10. Body composition and anthropometry in bodybuilders: regional changes due to nandrolone decanoate administration.
Hartgens F, et al.
Int J Sports Med. 2001 Apr;22(3):235-41.

11. Comparison of the effects of high dose testosterone and 19-nortestosterone to a replacement dose of testosterone on strength and body composition in normal men.
Friedl KE, et al.
J Steroid Biochem Mol Biol. 1991;40(4-6):607-12.

12. Breaking the vicious circle of obesity: the metabolic syndrome and low testosterone by administration of testosterone to a young man with morbid obesity.
Tishova Y, et al.
Arq Bras Endocrinol Metabol. 2009 Nov;53(8):1047-51.

13. Testosterone Threshold Levels and Lean Tissue Mass Targets Needed to Enhance Skeletal Muscle Strength and Function: The HORMA Trial.
Sattler, F et al.
J Gerontol A Biol Sci Med Sci. 2011 Jan;66(1):122-9.

14. Androstenedione does not stimulate muscle protein anabolism in young healthy men.
Rasmussen BB, et al.
J Clin Endocrinol Metab. 2000 Jan;85(1):55-9.

15. Effect of oral androstenedione on serum testosterone and adaptations to resistance training in young men: a randomized controlled trial.
King DS, et al.
JAMA. 1999 Jun 2;281(21):2020-8.

16. Effects of anabolic precursors on serum testosterone concentrations and adaptations to resistance training in young men.
Brown GA, et al.
Int J Sport Nutr Exerc Metab. 2000 Sep;10(3):340-59.

17. Testosterone dose-response relationships in healthy young men.
Bhasin S, et al.
Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1172-81.

18. Comparative pharmacokinetics of testosterone enanthate and testosterone cyclohexanecarboxylate as assessed by serum and salivary testosterone levels in normal men.
Schürmeyer T, et al.
Int J Androl. 1984 Jun;7(3):181-7.

19. Correlates of low testosterone and symptomatic androgen deficiency in a population-based sample.
Hall SA, et al.
J Clin Endocrinol Metab. 2008 Oct;93(10):3870-7. Epub 2008 Jul 29.

20. Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study.
Wu FC, et al.
J Clin Endocrinol Metab. 2008 Jul;93(7):2737-45. Epub 2008 Feb 12.

21. Prevalence of and risk factors for androgen deficiency in middle-aged men in Hong Kong.
Wong SY, et al.
Metabolism. 2006 Nov;55(11):1488-94.

22. Measures of bioavailable serum testosterone and estradiol and their relationships with muscle strength, bone density, and body composition in elderly men.
van den Beld AW, et al.
J Clin Endocrinol Metab. 2000 Sep;85(9):3276-82.

23. Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study.
Wu FC, et al.
J Clin Endocrinol Metab. 2008 Jul;93(7):2737-45. Epub 2008 Feb 12.

24. Correlates of low testosterone and symptomatic androgen deficiency in a population-based sample.
Hall SA, et al.
J Clin Endocrinol Metab. 2008 Oct;93(10):3870-7. Epub 2008 Jul 29.

25. Androgen treatment of abdominally obese men.
Mårin P, et al.
Obes Res. 1993 Jul;1(4):245-51.

26. Testosterone, body composition and aging.
Vermeulen A, et al.
J Endocrinol Invest. 1999;22(5 Suppl):110-6.

27. Effects of testosterone on body composition, bone metabolism and serum lipid profile in middle-aged men: a meta-analysis.
Isidori AM, et al.
Clin Endocrinol (Oxf). 2005 Sep;63(3):280-93.

28. Treatment of 161 men with symptomatic late onset hypogonadism with long-acting parenteral testosterone undecanoate: effects on body composition, lipids, and psychosexual complaints.
Permpongkosol S, et al.
J Sex Med. 2010 Nov;7(11):3765-74. doi: 10.1111/j.1743-6109.2010.01994.x. Epub 2010 Aug 30.

29. Effects of testosterone undecanoate on cardiovascular risk factors and atherosclerosis in middle-aged men with late-onset hypogonadism and metabolic syndrome: results from a 24-month, randomized, double-blind, placebo-controlled study.
Aversa A, et al.
J Sex Med. 2010 Oct;7(10):3495-503. doi: 10.1111/j.1743-6109.2010.01931.x.

30. Effects of testosterone supplementation on markers of the metabolic syndrome and inflammation in hypogonadal men with the metabolic syndrome: the double-blinded placebo-controlled Moscow study.
Kalinchenko SY, et al.
Clin Endocrinol (Oxf). 2010 Nov;73(5):602-12. doi: 10.1111/j.1365-2265.2010.03845.x.

31. Dose-dependent effects of testosterone on regional adipose tissue distribution in healthy young men.
Woodhouse LJ, et al.
J Clin Endocrinol Metab. 2004 Feb;89(2):718-26.

32. The erythrocythaemic effects of androgen.
Gardner FH, et al.
Br J Haematol. 1968 Jun;14(6):611-5.

The AndroStat and why it matters

If you haven’t completed the AndroStat questionaire, please check it out here –
http://www.primordialperformance.com/store/androstat/

To see what others are saying about the AndroStat, visit this thread.

What is the AndroStat?

The AndroStat is a questionnaire designed to estimate your average total testosterone level.

It has proven to be exceptionally accurate for predicting the average total testosterone levels in men — being anywhere from 80-100% correlated to lab values for most men.

In fact, we predict that the AndroStat can give a more accurate assessment of your average monthly total testosterone level than a single blood test from the lab.

How can the AndroStat be more accurate than a blood test?

Simply because a blood test is not a true representation of your average monthly or daily testosterone levels. Rather, a single blood test only represents your testosterone level at that very moment.

Research shows that testosterone varies by as much as 25% throughout the day, or possibly even more given physiological or environmental influences. (43,44) For instance, very few individuals enjoy blood tests, and some can become quite anxiety ridden even thinking about blood tests — which can quickly reduce testosterone by causing an immediate surge in stress hormones.

Things that can immediately influence blood testosterone levels include –

  • Stress/anxiety associated with the test itself
  • Quality of sleep from the night before
  • Drug use
  • Exercise
  • Meals

Any of these factors can negatively influence testosterone levels and give a result that is not truly representational of your average daily testosterone levels.

How does the AndroStat estimate total testosterone levels?

The AndroStat calculates total testosterone levels based on data gathered from dozens of studies, including thousands of men. It takes into account a large number of testosterone altering variables including age, body composition, BMI, smoking, exercise, stress, socioeconomic status, etc. The data from the studies was combined in to a mathematical equation that make up the power formula behind the AndroStat. (1-24)

During the development of the AndroStat, we had our AndroSeries v3 product testers (15+) and a number of volunteers complete the questionnaire, and verified the results against their actual blood values for total testosterone. We used this random sampling to verify and calibrate the AndroStat formula for a high degree of accuracy.

Editorial note: Id like to give special credit to Ken Hess, who painstakingly cross examined dozens of research papers to find the strongest correlates for predicting total testosterone levels.

What does the AndroStat have to do with AndroSeries products?

Knowing your testosterone levels helps determine the optimal dose for AndroSeries products.

For instance, men with low androgens (e.g. testosterone) will naturally get more benefit from a lower dose — partly because they are more sensitive to the effects of androgens — and they don’t need as high of a dose to surpass the androgen threshold.

On the other hand, men with higher androgen levels will require a higher dose to see the same dramatic benefits — partly because they are accustomed to the effects of high/normal androgens — and they need a higher dose to surpass the androgen threshold.

NOTE: Many of the immediate effects, like increased sex drive or aggression may not be noticeable to a man with high androgen levels — as these aspects may already be optimized, where further androgens may offer no additional benefit. However, these men can still reap physical benefits from androgen supplementation. These are considered the long-term benefits from androgens.

What is the "androgen threshold"?

The "androgen threshold" is the amount you need to boost your androgen levels in order to see significant improvements in body composition and strength. (25-27)

Research shows that androgen levels (e.g. testosterone) must increase by 1000-1300ng/dl above your current level, to increase lean body mass by 10%, drop total body fat by 10%, and increase strength by 30%. (25-27) This research is based on androgen supplementation for a 16 week period, with no dietary or training intervention. However, research suggests that combining androgens with exercise and dietary intervention can accelerate the achievement of these results. (28-30)

Consider this example subject –

Beginning stats

  • 175lbs with 500ng/dL total testosterone
  • 35lbs body fat (20%)
  • 140lbs lean body mass (80%)

Subject increases his androgen levels to 2700ng/dL (6 softgels of AndroMass for 8 weeks)

Stats after 8 weeks on AndroMass

  • 186lbs with 2700ng/dL Testosterone
  • 32lbs body fat (17%)
  • 154lbs lean body mass (83%)

Therefore, since this subject increased his androgen levels by 2200ng/dL above his natural androgen level the subject was able to reduce his body fat by about 9% and increase his lean body mass by about 10%. These results may be considered normal results from an 8 week cycle of AndroMass combined with resistance training and a lean muscle promoting diet.

I got my AndroStat results, but what do they mean?

Please refer to the Your Testosterone Levels — Killing or helping you? article for interpretation of your testosterone levels.

How much will the AndroSeries products increase my "testosterone"?

AndroSeries products are rated based on "testosterone equivalent" values. This value represents the total combined androgenic, anabolic and estrogenic bio-activity for the 24hr period.

In other words, we have gone through the painstaking effort to calculate the power of each AndroSeries pill relative to its total "testosterone-like" activity.

Here are the "testosterone equivalent" values established for the AndroSeries products –

  • AndroDrive – 217 ng/dL
  • AndroHard – 375 ng/dL
  • AndroLean – 334 ng/dL
  • AndroMass – 450 ng/dL
  • AndroBulk – 450 ng/dL

The reason for using a "testosterone equivalent" value is to give a realistic expectation of results and effects that will be noticed relative to other popular forms of testosterone, such as injectable, topical or oral testosterone. It is important to note; AndroSeries products do not work by increasing testosterone levels alone. Rather, AndroSeries exert most of their effects by converting to other androgens which have similar effects as testosterone — resulting in similar effects on the body. (31-42)

Finally, these values only represent TOTAL combined androgenic, anabolic and estrogenic effects. Remember, each AndroSeries product has a different ratio of androgenic, anabolic and estrogenic effects — as seen here in the AndroSeries Effects Chart.

How do I determine proper dosages for AndroSeries products?

Just fill out the AndroStat, and get linked to the AndroStacker to start building your AndroSeries stack. Your testosterone level is automatically filled in. If you already tested you can link back to the AndroStacker from your email.

Simply click on the items you want to use, and adjust the dosage and cycle length until your desired cycle is created. Click buy. Done!

Need more help. No problem. Just give us a call

Questions?

Talk to a product specialist in Live Chat
Call us – 1-503-841-6702
Email us – info@primordialperformance.com
Or get registered for our free forum

 

 

References –
1. Testosterone deficiency and the metabolic syndrome.
Lunenfeld B.
Aging Male. 2007 Jun;10(2):53-6.

2. The male climacterium: clinical signs and symptoms of a changing endocrine environment.
van den Beld AW, et al.
Prostate Suppl. 2000;10:2-8.

3. Androgens and body fat distribution in men.
Pi-Sunyer FX.
Obes Res. 1993 Jul;1(4):303-5.

4. Androgens and body fat distribution.
Blouin K, et al.
J Steroid Biochem Mol Biol. 2008 Feb;108(3-5):272-80. Epub 2007 Sep 7.

5. Testosterone and regional fat distribution.
Mårin P.
Obes Res. 1995 Nov;3 Suppl 4:609S-612S.

6. Two emerging concepts for elite athletes: the short-term effects of testosterone and cortisol on the neuromuscular system and the dose-response training role of these endogenous hormones.
Crewther BT, et al.
Sports Med. 2011 Feb 1;41(2):103-23. doi: 10.2165/11539170-000000000-00000.

7. Breaking the vicious circle of obesity: the metabolic syndrome and low testosterone by administration of testosterone to a young man with morbid obesity.
Tishova Y, et al.
Arq Bras Endocrinol Metabol. 2009 Nov;53(8):1047-51.

8. Correlates of low testosterone and symptomatic androgen deficiency in a population-based sample.
Hall SA, et al.
J Clin Endocrinol Metab. 2008 Oct;93(10):3870-7. Epub 2008 Jul 29.

9. Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study.
Wu FC, et al.
J Clin Endocrinol Metab. 2008 Jul;93(7):2737-45. Epub 2008 Feb 12.

10. Prevalence of and risk factors for androgen deficiency in middle-aged men in Hong Kong.
Wong SY, et al.
Metabolism. 2006 Nov;55(11):1488-94.

11. Measures of bioavailable serum testosterone and estradiol and their relationships with muscle strength, bone density, and body composition in elderly men.
van den Beld AW, et al.
J Clin Endocrinol Metab. 2000 Sep;85(9):3276-82.

12. Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study.
Wu FC, et al.
J Clin Endocrinol Metab. 2008 Jul;93(7):2737-45. Epub 2008 Feb 12.

13. Correlates of low testosterone and symptomatic androgen deficiency in a population-based sample.
Hall SA, et al.
J Clin Endocrinol Metab. 2008 Oct;93(10):3870-7. Epub 2008 Jul 29.

14. Androgen treatment of abdominally obese men.
Mårin P, et al.
Obes Res. 1993 Jul;1(4):245-51.

15. Testosterone, body composition and aging.
Vermeulen A, et al.
J Endocrinol Invest. 1999;22(5 Suppl):110-6.

16. Effects of testosterone on body composition, bone metabolism and serum lipid profile in middle-aged men: a meta-analysis.
Isidori AM, et al.
Clin Endocrinol (Oxf). 2005 Sep;63(3):280-93.

17. Treatment of 161 men with symptomatic late onset hypogonadism with long-acting parenteral testosterone undecanoate: effects on body composition, lipids, and psychosexual complaints.
Permpongkosol S, et al.
J Sex Med. 2010 Nov;7(11):3765-74. doi: 10.1111/j.1743-6109.2010.01994.x. Epub 2010 Aug 30.

18. Effects of testosterone undecanoate on cardiovascular risk factors and atherosclerosis in middle-aged men with late-onset hypogonadism and metabolic syndrome: results from a 24-month, randomized, double-blind, placebo-controlled study.
Aversa A, et al.
J Sex Med. 2010 Oct;7(10):3495-503. doi: 10.1111/j.1743-6109.2010.01931.x.

19. Effects of testosterone supplementation on markers of the metabolic syndrome and inflammation in hypogonadal men with the metabolic syndrome: the double-blinded placebo-controlled Moscow study.
Kalinchenko SY, et al.
Clin Endocrinol (Oxf). 2010 Nov;73(5):602-12. doi: 10.1111/j.1365-2265.2010.03845.x.

20. Long term perturbation of endocrine parameters and cholesterol metabolism after discontinued abuse of anabolic androgenic steroids.
Gårevik N, et al.
J Steroid Biochem Mol Biol. 2011 Aug 22. [Epub ahead of print]

21. Effect of long-term testosterone oenanthate administration on male reproductive function: clinical evaluation, serum FSH, LH, testosterone, and seminal fluid analyses in normal men.
Mauss J, et al.
Acta Endocrinol (Copenh). 1975 Feb;78(2):373-84.

22. Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic/anabolic steroids in power athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)

23. The relationship between pubertal gynecomastia, prostate specific antigen, free androgen index, SHBG and sex steroids.
Kilic M, et al.
J Pediatr Endocrinol Metab. 2011;24(1-2):61-7.

24. Anabolic steroids purchased on the Internet as a cause of prolonged hypogonadotropic hypogonadism.
Pirola I, et al.
Fertil Steril. 2010 Nov;94(6):2331.e1-3. Epub 2010 Apr 22.

25. Testosterone dose-response relationships in healthy young men.
Bhasin S, et al.
Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1172-81.

26. Dose-dependent effects of testosterone on regional adipose tissue distribution in healthy young men.
Woodhouse LJ, et al.
J Clin Endocrinol Metab. 2004 Feb;89(2):718-26.

27. Testosterone Threshold Levels and Lean Tissue Mass Targets Needed to Enhance Skeletal Muscle Strength and Function: The HORMA Trial.
Sattler, F et al.
J Gerontol A Biol Sci Med Sci. 2011 Jan;66(1):122-9.

28. Effects of anabolic steroids on the muscle cells of strength-trained athletes.
Kadi F, et al.
Med Sci Sports Exerc 31:1528–1534. (1999)

29. Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy.
Sinha-Hikim I, et al.
Am J Physiol Endocrinol Metab 283:E154–E164 (2002)

30. Comparison of the effects of high dose testosterone and 19-nortestosterone to a replacement dose of testosterone on strength and body composition in normal men.
Friedl KE, et al.
J Steroid Biochem Mol Biol. 1991;40(4-6):607-12.

31. Conversion of androsterone ester to dihydrotestosterone (DHT) — with 10 hour pharmacokinetics
Draws performed by AnyLabTestNow, 714 SW Washington St, Portland, OR 97205 ,  July 2011.
Analysis performed by S.E.D. Medical Laboratories.
(Contact Primordial Performance for full report)

32. In vivo conversion of dehydroisoandrosterone to plasma androstenedione and testosterone in man.
Horton R, et al.
J Clin Endocrinol Metab. 1967 Jan;27(1):79-88.

33. In vitro metabolism of androgens in whole human blood.
Blaquier et al.
Acta Endocrinol (Copenh). 1967 Aug;55(4):697-704. No abstract available.

34. METABOLISM OF ANDROST-4-ENE-3,17-DIONE-4-14C BY RABBIT SKELETAL MUSCLE SUPERNATANT FRACTION. ISOLATION OF 3BETA-HYDROXYANDROST-4-EN-17-ONE-14C AND TESTOSTERONE-14C.
THOMAS et al.
J Biol Chem. 1964 Mar;239:766-72. No abstract available

35. Direct agonist/antagonist functions of dehydroepiandrosterone.
Chen et al.
Endocrinology. 2005 Nov; 146(11):4568-76. Epub 2005 Jun 30

36. Serum androgen bioactivity during 5alpha-dihydrotestosterone treatment in elderly men.
Raivio et al.
J Androl. 2002 Nov-Dec;23(6):919-21.

37. In vitro bioassays for androgens and their diagnostic applications.
Roy et al.
Hum Reprod Update. 2008 Jan-Feb;14(1):73-82. Epub 2007 Dec 4.

38. Determination of androgen bioactivity in human serum samples using a recombinant cell based in vitro bioassay.
Roy et al.
J Steroid Biochem Mol Biol. 2006 Sep; 101(1):68-77. Epub 2006 Aug 8.

39. Circulating bioactive androgens in midlife women.
Chen et al.
J Clin Endocrinol Metab. 2006 Nov;91(11):4387-94. Epub 2006 Aug 29.

40. Partial agonist/antagonist properties of androstenedione and 4-androsten-3beta,17beta-diol.
Chen Fet al.
J Steroid Biochem Mol Biol. 2004 Aug;91(4-5):247-57.

41. Delta-4-androstene-3,17-dione binds androgen receptor, promotes myogenesis in vitro, and increases serum testosterone levels, fat-free mass, and muscle strength in hypogonadal men.
Jasuja R, et al.
J Clin Endocrinol Metab. 2005 Feb;90(2):855-63. Epub 2004 Nov 2.

42. In vivo MRI evaluation of anabolic steroid precursor growth effects in a guinea pig model.
Tang H, et al
Steroids. 2009 Aug;74(8):684-93. Epub 2009 Mar 20.

43. Biological day-to-day variation and daytime changes of testosterone, follitropin, lutropin and oestradiol-17beta in healthy men.
Ahokoski O, et al.
Clin Chem Lab Med. 1998 Jun;36(7):485-91.

44. Mean plasma concentration, metabolic clearance and basal plasma production rates of testosterone in normal young men and women using a constant infusion procedure: effect of time of day and plasma concentration on the metabolic clearance rate of testosterone.
Southren AL, et al.
J Clin Endocrinol Metab. 1967 May;27(5):686-94.

The Delusions & Reality of Hormone Cycling

Are you delusional or realistic about your physique goals?

If I were to ask you point blank what your body fat is what would you tell me face to face?

If I were to show you a picture of someone else's body that is very similar to yours, would you acknowledge it or be in denial?

If you and your significant other see a man walk by twice the musculature that you are and much leaner would you credit him or tell yourself that if you took the same stuff (drugs) he took, you would appear the same?

These are all questions and scenario's that I have witnessed, and reminds me that some people cannot grasp reality. 

Let's start from the beginning…

When you first begin weight training, you are usually clueless and unaware of proper nutrition,rest, training and all the key variables involved in getting results. For the fresh beginner, results will manifest regardless, simply due to the "foreign" stress that is happening to your fresh muscle tissue. Muscle growth, increase in metabolic rate and a better sense of well-being will inevitably happen…..AT FIRST. Once this grace period comes to a plateau (usually a few months) you will need to further educate yourself about proper nutrition and more sound training routines to keep the results soaring.  

Let's investigate a typical hypothetical scenario –

Although everybody gets results in the very early stages of weight training, some people respond ABNORMALLY well to lifting weights and will leave their training partners in the dust! So if both trainees started weight training at the same time, but one surpassed the other by a huge margin, it is very apparent that genetics are crucial in muscle hypertrophy and favorable body composition. The training partners will both accrue more knowledge in regards to nutrition, supplementation, and different training techniques but the genetic superior will always stay way ahead.  As time passes the thought of hormonal assistance is becoming extremely tempting to the genetic inferior.  In fact, he begins his first cycle in hopes to surpass his training partner. He begins to put some weight on (water–>via–>glycogen retention), his strength begins to increase, muscles appear fuller (more 3-dimensional looking) but he still does not look like his training partner?

I mean, he has put on 15-20 lbs. in 4 weeks, and has gotten stronger, but he still is not as impressive as his damn training partner! 

This scenario is so harsh and disheartening for most people to accept that it literally drives them insane. If they don't accept the fact that some peoples genetic makeup responds better to muscle stimuli, food, drugs and all other pertinent aspects of muscle growth- they begin to make assumptions for their short-comings. Perhaps thinking their superior partners are taking some special product behind their backs, taking huge amounts of hormones or all of the above. Let's say that the genetic superior decided to dabble in hormonal assistance, most likely due to other experienced people noticing his potential, telling him how well he'd do in Bodybuilding and what not. 

This is when the genetic elite trainee EXPLODES! His already lean and muscular physique gets even more profound with big & round muscles and low body fat. 

As you can see from this common scenario, it will be obvious right from the beginning who is predisposition to be a lean & muscular elitist among people with mediocre genetics. 

So what can you do about this painful, yet rude awakening fact of life?

Well, first off get your training and nutrition down as best as you can before even CONSIDERING hormonal assistance. How many times have you seen younger "newbies" choose a harsh methylated, designer hormone before considering a high quality protein powder, let alone even looking as if they lift weights to begin with? People want to take short-cuts and assume that hormones are the missing link to them looking like a Greek God. 

Once you stress all variables at your disposal then you may need to turn to hormones for breaking through new grounds. Once you commit to going to the "dark side" of hormonal cycling understand that you will get results, but DO NOT get irate when you don't turn into Mr.Olympia afterwards, 

It is truly sad when someone who fails to grasp reality will cycle steroids and gain a respectable amount of muscle (8-14 lbs.), gains some strength, loses some body fat, yet are pissed off that they did not achieve more? 

For the newbie hormone user or experienced user, you must still continue on with your diligent eating and training regimen that you SHOULD HAVE been doing in the first place. To truly maximize your supra-physiological hormone levels, you must feed the muscle high quality protein, essential fats, and complex carbs every day. Just because you have an athletic friend from Nigeria who can eat candy, potato chips and fast food all day and go to the gym for a half -ass workout and look better than you does NOT mean that you shouldn't do everything in your power to make the most of what you got.

Let's now make a "Pre-Cycle Checklist" for variables that MUST be addressed before committing to a hormone cycle

The Pre-Cycle Checklist – 

1.) I have stressed all avenues of nutrition and found out what suits my body best.

2.) I have stressed all facets of training and found out what suits my body best.

3.) I have been training diligently for more than 6 months while eating and training consistently.

4.) I understand that genetics play an integral role in nutrition response, training response and hormone response.

5.) I understand that you CANNOT continue gaining 10-15 lbs. each and every cycle.

6.) I understand that there is a "diminishing returns" effect when using higher dosages of hormones and side   effects become prominent.

7.) I understand that to improve upon each cycle I must increase a variable to continue gaining – increase calories or increase weight on lifts or increase dosage of hormone or all of the above.

8.) I understand that SAYING I eat 5000 calories a day is much different than LITERALLY EATING 5000 calories a day.

9.) I understand that SAYING I am 8-9% body fat is much different than LITERALLY being 8-9% body fat with ALL abs fully visible and have very thin skin all over.

10.) I understand and acknowledge all of the above.

If you can understand & oblige to this list, then you are realistic enough and mature enough to engage into hormonal assistance. You must segregate yourself from false perceptions and accept reality. Please do not become discouraged from the information given and use it to your benefit and seek out your underlying potential, just be a realist about it.

I personally have witnessed several competitive Bodybuilders' with average genetics annihilate genetically gifted or "elite" athletes due to impeccable work ethic, adherence to perfect nutrition, and giving everything they had to achieve the end result they sought after. I have noticed a lot of the time, the genetic elite athletes understand that they can do the bare minimum and look better than 95% of everyone else. This awareness makes them LAZY. Can you imagine if that genetically gifted person had the drive, will power, and persistence as the average athlete that is a work horse? It would be a sight to behold. 

I hope everything discussed in this article will "sink in" and let each and every one of you acknowledge the importance of all variables involved in this muscle-building equation. Leave no stone un-turned, and give it everything you got, because for most humans……..building high-quality muscle isn't easy.

Post-Exercise Protein Consumption is Mandatory

In order to gain muscle, you MUST undergo intense resistance training.  In order to gain muscle, you MUST consume protein to re-build muscle tissue.

These two variables work synergistically with each other and to maximize your chances of gaining lean muscle tissue you simply must consume protein alongside a resistance training routine.

The timing of protein ingestion is a highly debatable subject and has been unresolved as to whether precise timing is truly essential for measureable repair/growth opposed to simply consuming enough protein at other times of the day.

A very interesting study was conducted that investigated whether immediate protein consumption or a 2-hour delayed protein consumption had measureable impact on muscle hypertrophy and strength.

13 men with a body mass index (BMI) of 25 ± 1 kg m− 2 (means ± SEM) completed a 12-week resistance training program, training 3 times a week receiving oral protein in liquid form (10 g protein, 7 g carbohydrate, 3 g fat) immediately post workout, OR 2 hours post workout.

Scientists examined muscle hypertrophy by magnetic resonance imaging (MRI) and from muscle biopsies and muscle strength was examined using dynamic and isokinetic strength measurements. They also measured body composition from dual-energy X-ray absorptiometry (DEXA) and food records were recorded over 4 days. 

They also measured insulin response to protein supplementation.  Here are the exciting and convincing results after this experiment was concluded –

  • Cross-sectional area of m. quadriceps femoris (54.6 ± 0.5–58.3 ± 0.5 cm2) and mean fiber area (4047 ± 320–5019 ± 615 μ m2) increased in the P0 group (liquid protein post-exercise group)

  • No significant increase was observed in the 2-hour delayed group

  • Dynamic & isokinetic strength increased by 46% & 15%, respectively (liquid protein post-exercise group)

  • The 2-hour delayed group ONLY improved dynamic strength by 36%

  • No differences in glucose or insulin response were observed between protein intake at 0 and 2 h post-exercise.

 This phenomenal study proves the significance of ingesting a fast acting protein supplement such as; whey protein isolate immediately post-exercise for initiating muscle hypertrophy.

 

References:

1.) B Esmarck,J L Andersen*S Olsen, E A Richter†, M Mizuno, Timing of postexercise protein intake is important for muscle hypertrophy with resistance training in elderly humans. 

August 15, 2001 The Journal of Physiology, 535, 301-311. 

What is the difference between DHEA 1-DHEA 4-DHEA R-DHEA and 7-DHEA?


DHEA
(dehydroepiandrosterone)
(Super-5-DHEA†)
 
Main effects
 
+ Anti-aging (youthful energy)
+ Exercise endurance
+ Recovery
+ Fat loss
+ Muscle sparing (anti-catabolic)
+ Immune system
 
 
Primary metabolite –
 
5-androstenediol (5-AD)
 
Description –
 
DHEA is considered "generic" or regular DHEA. It can technically be called 5-DHEA, since the double bond is located in the 5th position. 
 
DHEA has been popular in the life extension crowd since the 1980’s. It's typically used for its ability to support energy and general wellbeing at a dose of 50-100mg/day. (1-3) More recently, higher doses of DHEA have been used to improve body composition due to DHEA’s mild anabolic and thermogenic effects. (1, 4) This makes DHEA an excellent choice for cutting during a calorie deficient diet, since DHEA has good muscle sparing properties. (1, 17)
 
DHEA converts to testosterone at a rate of about 1%, however it has high conversion to 5-androstenediol, where it gets its mild androgenic and anabolic effects. (5-8) DHEA’s thermogenic properties come from its conversion to 7-oxo-DHEA. (4)
 
Due to DHEA’s mild androgenic effects it rarely produces hair loss or acne. Although DHEA has moderate estrogenic effects, it rarely produces gyno or undesirable estrogenic side effects.(1-3) Some more sedentary users have reported anxiety or sleeplessness with DHEA, which is likely related to the neurosteroid activity in the brain. (3) However, this effect is also reported as “motivational energy” which is a frequently reported benefit of DHEA. 
 
Because of DHEA’s wide range of benefits and its balanced hormonal properties it can easily be used for cutting, or to keep gains lean during a lean mass building cycle.
 

4-DHEA
(4-dehydroepiandrosterone)
(Super-4-DHEA†)
 
Main effects –
 
+ Muscle mass (nitrogen retention)
+ Strength
+ Blood volume (hematopoietic)
+ Recovery
+ IGF-1 & GH
 
 
Primary metabolite –
 
4-androstenediol (4-AD)
 
Description –
 
4-DHEA is a naturally occurring DHEA isomer. It’s structure closely resembles regular DHEA but the double bond in the 4th position dramatically changes its effects.
 
4-DHEA readily converts to 4-androstenediol, rather than 5-androstenediol, boosting its anabolic potency more than 2x over regular DHEA. (6-8, 11) 4-DHEA is also expected to have a higher conversion rate to testosterone compared to regular DHEA. (6, 7) The 4-DHEA also lacks the calorie burning thermogenic properties, therefore offering superior calorie retention for a bulking effect. (4) This increased anabolic potency and reduced thermogenic action will lead to noticeable gains in strength, lean tissue growth, and weight gain. 
 
4-DHEA will have mild estrogen conversion that can be easily balanced with a non-aromatizing steroid like androsterone or 1-DHEA. Overall gains will be similar to the original “4-AD” banned in the 2004 Steroid Control Act.
 
As with the other DHEA isomers, 4-DHEA is naturally occurring and non-toxic. (9) Side-effects such as oily skin or reduced fertility are considered mild and temporary. The most notable side-effect would be suppression of natural testosterone production, which makes PCT necessary after a cycle. Overall 4-DHEA is a very safe and effective lean muscle building agent.
 
The only downfall to 4-DHEA is its high cost due to the high dose that is required to see significant muscle building effects.
†:The “Super” (ex., "Super-5-DHEA") signifies a fatty ester attachment to the steroid molecule to assist in bioavailability.

1-DHEA
(1-dehydroepiandrosterone)
(Super-1-DHEA†)
 
Main effects –
 
+ Muscle mass (nitrogen retention)
+ Strength
+ Hardening
+ Bloat reduction
+ Recovery
 
 
Primary metabolite –
 
1-androstenediol (1-AD)
 
Description –
 
1-DHEA is a naturally occurring DHEA isomer which cannot convert to testosterone or estrogen — but instead converts to the non-estrogenic 1-testosterone. (10)
 
The total conversion to 1-testosterone is probably less than 2%. (6,7) However, 1-DHEA gets most of its effects from conversion to 1-androstenediol, which has potent muscle building and hardening effects in and of itself. (8, 11, 12) 1-androstenediol was sold as “1-AD” prior to the 2004 Steroid Control Act, and was known for producing rapid gains in lean mass with zero water retention or bloat.
 
1-DHEA does not convert to estrogen nor does it activate the estrogen receptor like DHEA is known to do. (13) It could be referred to as “dry DHEA”. Because of this, it will stack well with other estrogenic steroids such as 4-DHEA to produce† clean gains in muscle tissue.
 
As with the other DHEA isomers, 1-DHEA is naturally occurring and non-toxic. (14) Side-effects such as oily skin, reduced fertility or increased hair shedding are considered mild and temporary. The most notable side-effect would be suppression of natural testosterone production, which makes PCT necessary after a cycle. This makes 1-DHEA a very safe, legal and effective lean muscle building agent. Some users have reported lethargy with 1-DHEA. This seems to be less severe when balanced with DHEA or 4-DHEA which tend to have an anti-lethargic effect.

7-oxo-DHEA
(7-oxo-dehydroepiandrosterone)
(Super-7-DHEA†)
 
Main effects –
 
+ Fat loss
+ Weight loss
+ Muscle sparing (anti-catabolic)
+ Immune supporting
 
 
Primary metabolite –
 
Androstenetriol (AET)
 
Description –
 
7-oxo-DHEA is a naturally occurring metabolite of DHEA. It’s well known for its weight loss effect due to its strong thermogenic action. (4, 15, 16)
 
The strong thermogenic effect from 7-oxo-DHEA come from its ability to increase two thermogenic enzymes, which increases the body’s ability to burn off calories as heat. (4) Although DHEA shares a similar effect, 7-oxo-DHEA is about 2.5x more active than DHEA. (4) Human studies have shown that 7-oxo-DHEA can increase weight loss, with a majority of weight loss being actual fat tissue. (15-16) Aside from the thermogenic action, 7-oxo-DHEA also appears to be an aromatase inhibitor, which can reduce estrogen levels. 
 
Because of the modification in the 7th position, 7-oxo-DHEA cannot convert to testosterone or estrogen, nor does it have any androgenic or anabolic effects. (15) Because of this, it does not produce side-effects such as hair loss, acne or prostate inflammation. It also blocks the catabolic effect of cortisol, which helps to retain muscle during a low calorie diet.
 
Side-effects of 7-oxo-DHEA may include anxiety or sleeplessness similar to regular DHEA due to the neuro-stimulating effect. However, this is generally mild, and seems to only occur in some users. Overall 7-oxo-DHEA is very tolerable and safe at the typical 100-200mg/day dose. (15, 16)
 
While 7-oxo-DHEA can be useful for a cutting or weight loss protocol, it would not be wise to use during a bulking or mass building cycle. Its tendency to increase the metabolism and rate of calorie burning will make it difficult to build additional muscle mass. (4)
 
†:The “Super” (ex., "Super-5-DHEA") signifies a fatty ester attachment to the steroid molecule to assist in bioavailability.

R-DHEA
(androsterone)
(Super-R-DHEA†)
 
Main effects –
 
+ Strength 
+ Hardening
+ Bloat reduction
+ Recovery
+ Anti-estrogen
+ Sex drive
+ Aggression 
 
 
Primary metabolite –
 
Androstanediol (5-AA)
 
Description –
 
R-DHEA is known as “Reduced DHEA” because it is a 5a-reduced metabolite of DHEA. It’s more commonly referred to as androsterone.
 
This naturally occurring hormone cannot convert to testosterone, but instead converts to the dihydrotestosterone (DHT). (10, 18) Similar to testosterone, DHT is responsible for masculine traits such as aggression, sex drive, and physical strength. (19,20) However, because DHT cannot convert to estrogen, it also helps reduce fat storage and water retention, making it an excellent steroid for increasing muscular hardness and vascularity. 
 
R-DHEA will stack well with 5-DHEA or 4-DHEA as it will help reduce water retention from under the skin, thus creating a “dry” and hard appearance. R-DHEA also has moderate anabolic properties thus allowing it to help enhance lean muscle gains. (21)
 
Strength gains will also be noticeable with R-DHEA due to its strong androgenic effect which will activate the central nervous system and increase muscular power. (20) This will increase explosive power with minimal bodyweight increase. The increased aggression is typically a welcomed benefit, which manifests as increased confidence and an “alpha male” feeling in sexual and social activities. 
 
The strong androgenic action from R-DHEA will also help support libido and erection hardness. (20) This makes R-DHEA useful to help counter the sexually suppressive effects from other steroids. The powerful androgenic effect will also block estrogenic effects, and help prevent (and reverse) gyno. (22, 23)
 
Side-effects from R-DHEA will be limited to androgenic side-effects such as oily skin, acne, and increased hair shedding if the user is prone. These side effects are mild and temporary for most users.
 
 
†:The “Super” (ex., "Super-5-DHEA") signifies a fatty ester attachment to the steroid molecule to assist in bioavailability.
References –
 
1. DHEA treatment for HIV patients: Effects on mood, androgenic and anabolic parameters. 
Rabkin, J., et al. 
Psychoneuro endocrinology. R. 25, 53-68. 2000
 
2. Activation of immune function by dehydroepiandrosterone (DHEA) in age- advanced men. 
Khorram O, et al.
J Gerontol 1997; 52A:M1- M7.
 
3. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age.
Morales AJ, et al
J Clin Endocrinol Metab. 1994 Jun;78(6):1360-7. Erratum in: J Clin Endocrinol Metab 1995 Sep;80(9):2799.
 
4. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone.
LARDY H, et al. 
Proc Natl Acad Sci USA 92: 6617-6619, 1995.
 
5. Dehydroepiandrosterone: kinetics of metabolism in normal men and women.
Bird CE et al.
J Clin Endocrinol Metab. 1978 Oct;47(4):818-22.
 
6. In vivo conversion of dehydroisoandrosterone to plasma androstenedione and testosterone in man.
Horton R, et al.
J Clin Endocrinol Metab. 1967 Jan;27(1):79-88.
 
7. In vitro metabolism of androgens in whole human blood.
Blaquier et al.
Acta Endocrinol (Copenh). 1967 Aug;55(4):697-704. No abstract available.
 
8. Androgens and anabolic agents
Julius A. Vida
Chemistry and pharmacology (1969) 
 
9. METABOLISM OF ANDROST-4-ENE-3,17-DIONE-4-14C BY RABBIT SKELETAL MUSCLE SUPERNATANT FRACTION. ISOLATION OF 3BETA-HYDROXYANDROST-4-EN-17-ONE-14C AND TESTOSTERONE-14C.
THOMAS et al.
J Biol Chem. 1964 Mar;239:766-72
 
10. Seized designer supplement named “1-Androsterone” identification as 3b-hydroxy-5a-androst-1-en-17-one and its urinary elimination.
Maria K et al.,
Steroids. 2011 Feb 16.
 
11. Circulating bioactive androgens in midlife women.
Chen et al.
J Clin Endocrinol Metab. 2006 Nov;91(11):4387-94. Epub 2006 Aug 29.
 
12. Partial agonist/antagonist properties of androstenedione and 4-androsten-3beta,17beta-diol.
Chen Fet al.
J Steroid Biochem Mol Biol. 2004 Aug;91(4-5):247-57.
 
13. Direct agonist/antagonist functions of dehydroepiandrosterone.
Chen et al.
Endocrinology. 2005 Nov; 146(11):4568-76. Epub 2005 Jun 30
 
14. Testosterone metabolism revisited: discovery of new metabolites.
Pozo, et al.
Anal Bioanal Chem. 2010 Oct;398(4):1759-70. 
 
15. A randomized, double blind, placebo controlled study of 3 – acetyl – 7 – oxo – dehydroepiandrosterone in healthy overweight adults. 
Kalman, D., et al. 
(2000). Curr. Ther. Res. 61, 435-442.
 
16. The effect of 7 – keto Naturalean on weight loss: A randomized, double blind placebo controlled trial. Zenk, J., et al. 
(2002). Curr. Ther. Res. 63, 263-272.
 
17. Antiglucocorticoid function of androstenetriol. Psychoneuroendocrinology 
Loria RM. Et al.
1997;22 Suppl 1:S103-8.
 
18. Physiological Changes in Dehydroepiandrosterone Are Not Reflected by Serum Levels of Active Androgens and Estrogens But of Their Metabolites: Intracrinology
Fernand Labrie, et al.
J Clin Endocrinol Metab. 1997 Aug;82(8):2403-9
 
19. Evaluation of androgen antagonism of estrogen effect by dihydrotestosterone.
Hung TT, et al. 
J Steroid Biochem. 1983 Oct;19(4):1513-20.
 
20. The effects of transdermal dihydrotestosterone in the aging male: a prospective, randomized, double blind study.
Kunelius P, et al.
J Clin Endocrinol Metab. 2002 Apr;87(4):1467-72.
 
21. Comparative activities of compounds of the androsterone-testosterone series.
Deanesly R, et al.
Biochem J. 1936 Feb;30(2):291-303.
 
22. Treatment of persistent pubertal gynecomastia with dihydrotestosterone heptanoate.
Eberle AJ, et al
J Pediatr. 1986 Jul;109(1):144-9.
 
23. Successful percutaneous dihydrotestosterone treatment of gynecomastia occurring during highly active antiretroviral therapy: four cases and a review of the literature.
Benveniste O et al.
Clin Infect Dis. 2001 Sep 15;33(6):891-3. 

Anti-inflammatory Benefits of Androstenetriol (5-androstene-3 beta-7 beta-17 beta-triol, beta AET)


Androstene-3 beta-7 beta-17 beta-triol (AET) represents a key naturally occurring 7-hydroxy dehydroepiandrosterone (DHEA) metabolite. Produced from the adrenal gland, DHEA and its sulfate are the major circulating adrenal steroids in humans. Serum levels peak in young adults, but then steadily decline with age, falling over 80% by age 70. DHEA serves as a precursor of male and female sex hormones. (1, 3, 5, 6)


DHEA demonstrates a plethora of anti-aging properties in rodents, including anti-inflammatory, anti-obesity, anti-diabetic, immune enhancing activities, and opposes certain activities of endogenous glucocorticoids (GC). As the literature grew, DHEA became widely used as an anti-aging, anti-stress dietary supplement. Despite these well-documented activities in animal models, DHEA supplementation in humans has yielded inconclusive results and the value of DHEA replacement in humans is controversial. Such widely different outcomes in rodents and humans have been referred to as ‘the DHEA conundrum’. Moreover, the potential therapeutic use of DHEA is limited by its side effects due to its conversion to sex hormones.


One possibility to explain these discrepancies is that a metabolite(s) of DHEA, rather than DHEA itself, may be necessary for its full action in human physiology. DHEA undergoes extensive conversion and derivatization to multiple products by phase 1 reactions involving the cytochrome P450 system, and studies have shown that these phase 1 products can be more potent than parental DHEA. Phase 1 reactions frequently decline in elderly subjects, and since such subjects have been the major participants in human DHEA treatment studies, it is possible that biologically active metabolites of DHEA were not produced in adequate amounts in previous human studies. It is also possible that qualitative changes in DHEA metabolism between rodents and humans will account for these differences.


DHEA oxidation via the action of the enzyme CYP7B leads to the 7-hydroxy derivatives of C-19 steroids, which are collectively present in low nanomolar concentrations in human circulation and are not readily metabolized to potent androgens or estrogens. Many of the functions initially attributed to DHEA from observations in rodents are now thought to be properties of these oxygenated metabolites, particularly AET.

 

Molecular Structure of Androstenetriol


AET possesses some of the anti-inflammatory and GC-opposing activities that have been attributed to DHEA, but with greater apparent potency. Studies with AET demonstrate it markedly up regulates host immune response, prevents immune suppression, modulates inflammation and improves survival after lethal infections by pathogens and lethal radiation. (1, 3, 5, 6)


AET has been shown to be protective against traumatic shock. Traumatic shock activates the hypothalamic-pituitary-adrenal axis (HPA) to mediate a cascade of defensive mechanisms that often include overwhelming inflammatory response and immunosuppression, which may lead to multiple organ failure. In a relevant traumatic hemorrhagic shock rodent model that applies to both combat and civilian sectors, AET provided a significant protective effect and improved survival. In a murine thermal injury model that includes glucocorticoid-induced osteopenia, AET significantly preserved bone mineral content, restored whole body bone mineral content and bone growth, suggesting reversal of GC-mediated adverse effects.


Since AET is a naturally occurring compound there is no patent protection leaving the door wide open for AET analogue research. Harbor BioSciences, Inc. – http://www.harborbiosciences.com/ (Public, OTC:HRBR – http://www.google.com/finance?q=OTC:HRBR ) is exploring a synthetic derivative of AET for the treatment of diseases with underlying chronic inflammation. HRBR has developed 17alpha-Ethynyl-5-androsten-3beta, 7beta, 17beta-triol (HE3286), a synthetic derivative AET. (1, 2, 4, 7)


Within the past two years, animal model studies of HE3286 successfully demonstrate the treatment of lung inflammation without immune suppression, the reduction of established disease of rheumatoid arthritis, and both glucose-lowering and cholesterol-lowering effects. Harbor BioSciences most ambitious project to date is their recently released data regarding that plasma levels of AET positively correlate with BMI in healthy men and women.(1) These observations suggest a compensatory role for AET in preventing the development of metabolic syndrome and obesity. The AET structural core may provide the basis for novel pharmaceuticals to treat this disease, HE3286. Stay tuned.



1. Auci DL, Ahlem CN, Kennedy MR, Page TM, Reading CL, Frincke JM. A Potential Role for 5-Androstene-3[beta],7[beta],17[beta]-triol in Obesity and Metabolic Syndrome. Obesity. http://www.nature.com/oby/journal/vaop/ncurrent/abs/oby2010204a.html


2. Conrad D, Wang A, Pieters R, et al. HE3286, an oral synthetic steroid, treats lung inflammation in mice without immune suppression. Journal of Inflammation 2010;7(1):52. http://www.journal-inflammation.com/content/7/1/52


3. Loria RM. Antiglucocorticoid function of androstenetriol. Psychoneuroendocrinology 1997;22 Suppl 1:S103-8.


4. Lu M, Patsouris D, Li P, et al. A new antidiabetic compound attenuates inflammation and insulin resistance in Zucker diabetic fatty rats. American Journal of Physiology – Endocrinology And Metabolism 2010;298(5):E1036-E48. http://ajpendo.physiology.org/content/298/5/E1036.full


5. Malik AK, Khaldoyanidi S, Auci DL, et al. 5-androstene-3?,7?,17?-triol (?-AET) Slows Thermal Injury Induced Osteopenia in Mice: Relation to Aging and Osteoporosis. PLoS ONE;5(10):e13566. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0013566


6. Marcu AC, Paccione KE, Barbee RW, et al. Androstenetriol Immunomodulation Improves Survival in a Severe Trauma Hemorrhage Shock Model. The Journal of Trauma 2007;63(3):662-9.


7. Offner H, Firestein GS, Boyle DL, et al. An Orally Bioavailable Synthetic Analog of an Active Dehydroepiandrosterone Metabolite Reduces Established Disease in Rodent Models of Rheumatoid Arthritis. Journal of Pharmacology and Experimental Therapeutics 2009;329(3):1100-9. http://jpet.aspetjournals.org/content/329/3/1100.full


8. Stiles AR, McDonald JG, Bauman DR, Russell DW. CYP7B1: One Cytochrome P450, Two Human Genetic Diseases, and Multiple Physiological Functions. Journal of Biological Chemistry 2009;284(42):28485-9.

Androstenetrione (6-OXO)

Diagram of molecule

Chemical Name(s):

4-androsten-3,6,17-trione
3,6,17-androstenetrione
androst-4-ene-3,6,17-trione
6-ketoandrostenedione
Chemical Formula: C19H24O3
Molecular Weight: 300
CAS: NA
Q Qatio: NA
Anabolic #: NA
Androgenic #: NA
Oral Bioavailability: Estimated at 4%
AR Binding Affinity: NA
SHBG Binding Affinity: NA
Half Life: 3-6 hours
Legal Status (US): Not listed as a controlled substance
Average Dose: 300-600mg/day
Average Cycle Length: 4-8 weeks
Stimulator
Inhibitor

-5
-4
-3
-2
-1

0
1
2
3
4
5

Muscle Gain

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Strength Gain

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Fat Gain (negative indicates fat loss)

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Water Retention (extra-cellular bloat)

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Aggression

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Libido

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Acne

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Hair Loss

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Prostate Enlargement

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Liver Toxicity

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Lethargy

[]
-5
-4
-3
-2
-1

0
1
2
3
4
5

Characteristics

6-OXO is a steroidal aromatase inhibitor, known as a suicidal inhibitor because it permanently binds to the aromatase enzyme.

It is used for its anti-estrogen and testosterone boosting effects.

There is debate about whether or not 6-oxo actually lowers estrogen or increases testosterone. Several human studies have shown an increase in estrone levels following 6-oxo supplementation. However, one of the primary metabolites of 6-oxo is 6-oxoestrone which may have given a false positive for elevated estrone levels. The human study also concluded that 6-oxo raised testosterone levels, however it is possible that 6-oxotestosterone (which is another metabolite of 6-oxo) gave a false positive for the testosterone level as well.

Another interesting element to these articles is that despite the supposed increase in testosterone (enough to cause significant improvements in body composition if given via injection) no improvements where found for fat free mass (FFM) or strength. Therefore, 6-oxo is either a weak AI that doesn’t really inhibit estrogen at the recommended dose and simply converts to metabolites which give false readings, or it actually does increase testosterone, while the 6-oxo metabolites antagonize the androgen receptor enough to block any anabolic effect from testosterone.

Either way, no ergonomic or real world benefit could be found after 6-oxo supplementation.

Its also worth mentioning that 6-oxo should never be used post cycle, as its steroidial effects would likely interfere with recovery of natural testosterone production.


Related Discussion

The Official Androstenetrione (6-OXO) Thread
Posted by Eric

References

Immunological interference of the synthetic aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD) and its metabolite(s) in the radioimmunoassay for testosterone.

MD Donaldson and MG Forest
Steroids, Dec 1980; 36(6): 717-21

Testosterone dose-response relationships in healthy young men
Shalender Bhasin, et al.
Am J Physiol Endocrinol Metab, Dec 2001; 281: E1172 – E1181.

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