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.

Pharmacokinetics and Pharmacodynamics of Steroid Esters

Pharmacokinetics and Pharmacodynamics of Steroid Esters in Oil Vehicle:
Effects of Ester, Injection Site, and Injection Volume

Variations in side-chain ester chemistry are important in the pharmacokinetics of androgen esters in oil vehicle. In humans, the very short propionate (three-carbon aliphatic) ester of testosterone has distinctly shorter duration of action than esters with longer (seven- or eight-carbon) side-chains. More subtle changes in side-chain ester structure have proven ineffective in altering human clinical pharmacokinetics, because substitution of a linear aliphatic side-chain of seven carbons (enanthate) with either a saturated, cyclized, seven-carbon aliphatic chain (cyclohexanecarboxylate) or a linear, aliphatic, eight-carbon chain (cypionate) resulted in virtually unchanged kinetics. (2, 4-6, 12, 15)

Testosterone enanthate (TE) or testosterone cypionate (TC), injected intramuscularly, are the most commonly used androgen preparations with terminal half-lifes of 7-12 days. Pharmacokinetic studies indicate that the major limitations of TE and TC include relatively high peak levels and limited duration of T levels within the normal range (approximately 2 weeks), following an injection. Disadvantages of TE and TC highlighted the need for long-acting preparations of T with more stable delivery kinetics. Testosterone undecanoate (TU; 17-hydroxy-4-androsten-3-one undecanoate) is an unsaturated, aliphatic, fatty acid ester of testosterone (T) in 17β-position. In ampules containing 250 mg of the ester in 2 ml of tea seed oil in administration of 500 or 1,000 mg shows a terminal elimination half-life of 18-23 days. (4, 10, 15, 17)

Testosterone
Testosterone

Testosterone Enanthate
Testosterone Enanthate

Testosterone Cypionate
Testosterone Cypionate

Testosterone Undecanoate
Testosterone Undecanoate

Wider variation in ester side-chain chemistry to include greater chain length and/or aromatic ring structures is a more effective determinant of ester pharmacokinetics. Nandrolone hexoxyphenylpropionate ester has far better depot properties, with a prolonged and retarded release profile, compared with the decanoate (aliphatic chain with 10 carbons). Another study indicates the decanoate (aliphatic chain with 10 carbons) ester has better depot properties than a nine-carbon chain including an aromatic ring. Because the vehicle (arachis oil) was unchanged during this latter study and because of the experimental observation that the oil vehicle influences local reaction to the oil injection, as well as androgen ester pharmacology, these conclusions may be extrapolated to other vegetable oil injection vehicles only with caution. (2, 7, 13, 14, 16)

In addition to the chemistry of the side-chain ester, both injection site and volume can systematically influence blood levels after intramuscular injection of esters in an oil vehicle formulation. Injection site may be important because of differences in tissue composition and blood flow. Intramuscular oil-based injections may more accurately be termed intermuscular or intralipomatous. The former reflects the tendency of oil vehicle to distribute along intermuscular fascial planes, whereas the latter depends upon the amount of fat at the injection site (including systematic gender differences) together with needle geometry and anatomy of the injection depot. Intralipomatous deposition of injections with a larger vehicle volume may explain the slower release kinetics of nandrolone decanoate in the gluteal region, as well as the differences from the deltoid site, which has a lower fat content. (1, 13)

Nandrolone

Nandrolone

Nandrolone Decanoate

Nandrolone Decanoate

Nandrolone Phenpropionate (NPP)

Nandrolone Phenpropionate (NPP)

Nandrolone P-Hexoxyphenylpropionate

Nandrolone P-Hexoxyphenylpropionate

There is a rapid and dose-proportional increase in nandrolone serum levels across a dose range after a single intramuscular injection of 50–150 mg nandrolone decanoate in healthy young men with peak serum levels of nandrolone reached 2–3 d after injection. Subsequently, nandrolone levels decreased, but were still measurable 32 d after dosing in approximately half the subjects in the 50-mg group and in all subjects in the 100- and 150-mg groups. The half-life ranged from 7.1 days – 11.8 days. In addition, urinary metabolites 19-NA and/or 19-NE were detectable for up to 6 months after the 100 and 150 mg injection in a significant proportion of subjects. (2)

 Nandrolone Profile

Mean serum concentration profiles for nandrolone after single gluteal muscle injection in 1 ml arachis oil of 50, 100, or 150 mg nandrolone decanoate in healthy men.

Nandrolone displays so-called flip-flop pharmacokinetics, which means that the ascending phase of the curve represents the disposition of nandrolone and the descending part of the curve represents the rate-limiting process of release of nandrolone decanoate from the muscle into the general circulation. The half-life in the descending phase of the curve is an estimate of the absorption half-life rather than the elimination half-life. (2)

In the following study, 23 healthy men were randomized into four groups receiving a single dose of 100 mg nandrolone esters: nandrolone phenylpropionate in 4 ml arachis oil injected into the gluteal muscle (group 1), nandrolone decanoate in 4 ml arachis oil injected into the gluteal muscle (group 2), nandrolone decanoate in 1 ml arachis oil injected into the gluteal muscle (group 3), or nandrolone decanoate in 1 ml arachis oil injected into the deltoid muscle (group 4). Absolute bioavailability was higher after single-dose injection of 100 mg nandrolone decanoate in 1 ml arachis oil into the gluteal muscle (73%) than in the other three groups (53–56%). (8)

TIME COURSE OF PLASMA NANDROLONE ESTER CONCENTRATIONS

Nandrolone Concentrations

Time course of plasma nandrolone concentrations in 23 healthy men over 32 days after intramuscular injection of 100 mg of nandrolone phenylpropionate in 4 ml of arachis oil vehicle into the gluteal muscle (group 1) () or injection of 100 mg of nandrolone decanoate into the gluteal muscle in 4 ml of arachis oil vehicle (group 2) (?), into the gluteal muscle in 1 ml of arachis oil vehicle (group 3) (•) or into the deltoid muscle in 1 ml of arachis oil vehicle (group 4) (?). Results are expressed as mean and S.E.M., unless the S.E. is smaller than symbol. (8)

Corresponding to the patterns of blood concentrations, pharmacodynamic indices reflecting androgen-induced inhibition of pituitary-testicular function, namely blood testosterone and inhibin concentrations, are also systematically influenced by these factors. Testosterone and inhibin concentrations represent effective markers of endogenous pituitary gonadotropin (LH and FSH, respectively) secretion. This reflects the physiological fact that pituitary LH acts exclusively upon testicular Leydig cells, due to their unique expression of cell surface membrane LH receptors. In healthy men, virtually all circulating testosterone originates from Leydig cells, with an absolute requirement for trophic influence from LH derived from the bloodstream. Similarly, pituitary FSH acts exclusively upon testicular Sertoli cells, which uniquely express FSH receptors on their cell surface membranes, and virtually all circulating immunoreactive inhibin originates from the gonads. As a result, blood levels of these two hormones are useful integrated bioassay indicators of endogenous pituitary gonadotropin secretion, as reflected by the testicular hormonal response to ambient blood LH and FSH levels. These two pharmacodynamic indices show physiologically meaningful distinctions between the esters and the effects of injection site and volume. (8, 9, 11)

TIME COURSE OF PLASMA TESTOSTERONE CONCENTRATIONS AFTER I.M. INJECTION OF 100 MG OF NANDROLONE ESTER

Testosterone Concentrations

Time course of plasma testosterone concentrations in 23 healthy men over 32 days after intramuscular injection of 100 mg of nandrolone phenylpropionate in 4 ml of arachis oil vehicle into the gluteal muscle (group 1) () or injection of 100 mg of nandrolone decanoate into the gluteal muscle in 4 ml of arachis oil vehicle (group 2) (?), into the gluteal muscle in 1 ml of arachis oil vehicle (group 3) (•) or into the deltoid muscle in 1 ml of arachis oil vehicle (group 4) (?). Results expressed as mean and S.E.M., unless the S.E. is smaller than the symbol. (8)

The pharmacodynamic variability in plasma testosterone and inhibin concentrations is accounted for by the variability between esters and the site and volume of injection of the nandrolone injections. The overall kinetics of suppression of testosterone is dominated by the slow negative feedback system, rather than the much faster metabolic clearance of testosterone. This negative feedback is mediated via inhibition of pulsatile gonadotropin-releasing hormone secretion from hypothalamic neurons into the pituitary portal system and then pituitary LH secretion from gonadotropes. This is in stark contrast to a highly potent and specific gonadotropin-releasing hormone antagonist that causes immediate cessation of gonadotropin-releasing hormone action leading to castrate testosterone concentrations within 12 hr, compared with 5 to 10 days with AAS administration. After a single 100 mg injection of NPP, recovery takes 10+ days. After ND, recovery takes 15+ days. It is important to note these are single administrations of 100 mg. HPTA recovery with repeated doses of 200+ mg is long!!!! (3, 8)

Administration of androgens such as testosterone and 19-nor-testosterone has been most frequently via depot intramuscular injections of steroid esters dissolved in a vegetable oil vehicle. Intramuscular injections provide sustained androgen release into the circulation and remain the mainstay of androgen replacement therapy. Experimental studies suggest that absorption rates are predicted by the oil/water partition coefficients (or hydrophobicity) and that the oil vehicle is absorbed more slowly than the androgen ester, with gradual release into the extracellular fluid, where esters are rapidly hydrolyzed to liberate biologically active steroid. As the above shows, other factors influence steroid appearance in the bloodstream that include the chemistry of the side-chain ester (hydrophobicity, steric hindrance of hydrolysis, and solubility), as well as injection factors (technique, depth, site, volume, Ph, and osmolarity of the solution).

 1.                  Al-Hindawi MK, James KC, Nicholls PJ. Influence of solvent on the availability of testosterone propionate from oily, intramuscular injections in the rat. J Pharm Pharmacol 1987;39(2):90-5. http://www.ncbi.nlm.nih.gov/pubmed/2882010

2.                  Bagchus WM, Smeets JMW, Verheul HAM, De Jager-Van Der Veen SM, Port A, Geurts TBP. Pharmacokinetic Evaluation of Three Different Intramuscular Doses of Nandrolone Decanoate: Analysis of Serum and Urine Samples in Healthy Men. J Clin Endocrinol Metab 2005;90(5):2624-30. http://jcem.endojournals.org/cgi/content/full/90/5/2624

3.                  Behre HM, Klein B, Steinmeyer E, McGregor GP, Voigt K, Nieschlag E. Effective suppression of luteinizing hormone and testosterone by single doses of the new gonadotropin-releasing hormone antagonist cetrorelix (SB-75) in normal men. J Clin Endocrinol Metab 1992;75(2):393-8. http://www.ncbi.nlm.nih.gov/pubmed/1639941

4.                  Behre HM, Nieschlag E. Testosterone buciclate (20 Aet-1) in hypogonadal men: pharmacokinetics and pharmacodynamics of the new long-acting androgen ester. J Clin Endocrinol Metab 1992;75(5):1204-10. http://www.ncbi.nlm.nih.gov/pubmed/1430080

5.                  Belkien L, Schurmeyer T, Hano R, Gunnarsson PO, Nieschlag E. Pharmacokinetics of 19-nortestosterone esters in normal men. J Steroid Biochem 1985;22(5):623-9. http://www.ncbi.nlm.nih.gov/pubmed/4010287

6.                  Fujioka M, Shinohara Y, Baba S, Irie M, Inoue K. Pharmacokinetic Properties of Testosterone Propionate in Normal Men. J Clin Endocrinol Metab 1986;63(6):1361-4. http://www.ncbi.nlm.nih.gov/pubmed/3782423

7.                  Khankhanian NK, Hammers YA, Kowalski P. Exuberant local tissue reaction to intramuscular injection of nandrolone decanoate (Deca-Durabolin)–a steroid compound in a sesame seed oil base–mimicking soft tissue malignant tumors: a case report and review of the literature. Mil Med 1992;157(12):670-4. http://www.ncbi.nlm.nih.gov/pubmed/1470383

8.                  Minto CF, Howe C, Wishart S, Conway AJ, Handelsman DJ. Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume. J Pharmacol Exp Ther 1997;281(1):93-102. http://jpet.aspetjournals.org/content/281/1/93.full

9.                  Nieschlag E, Cuppers HJ, Wiegelmann W, Wickings EJ. Bioavailability and LH-suppressing effect of different testosterone preparations in normal and hypogonadal men. Horm Res 1976;7(3):138-45. http://www.ncbi.nlm.nih.gov/pubmed/1002121

10.              Schubert M, Minnemann T, Hubler D, et al. Intramuscular testosterone undecanoate: pharmacokinetic aspects of a novel testosterone formulation during long-term treatment of men with hypogonadism. J Clin Endocrinol Metab 2004;89(11):5429-34. http://www.ncbi.nlm.nih.gov/pubmed/15531493

11.              Schulte-Beerbuhl M, Nieschlag E. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate of testosterone cypionate. Fertil Steril 1980;33(2):201-3. http://www.ncbi.nlm.nih.gov/pubmed/7353699

12.              Schurmeyer T, Nieschlag E. Comparative pharmacokinetics of testosterone enanthate and testosterone cyclohexanecarboxylate as assessed by serum and salivary testosterone levels in normal men. Int J Androl 1984;7(3):181-7. http://www.ncbi.nlm.nih.gov/pubmed/6434435

13.              Tanaka T, Kobayashi H, Okumura K, Muranishi S, Sezaki H. Intramuscular absorption of drugs from oily solutions in the rat. Chem Pharm Bull (Tokyo) 1974;22(6):1275-84. http://www.ncbi.nlm.nih.gov/pubmed/4417722

14.              van der Vies J. Implications of basic pharmacology in the therapy with esters of nandrolone. Acta Endocrinol Suppl (Copenh) 1985;271:38-44. http://www.ncbi.nlm.nih.gov/pubmed/3865480

15.              Weinbauer GF, Partsch C-J, Zitzmann M, Schlatt S, Nieschlag E. Pharmacokinetics and Degree of Aromatization Rather Than Total Dose of Different Preparations Determine the Effects of Testosterone: A Nonhuman Primate Study in Macaca fascicularis. J Androl 2003;24(5):765-74. http://www.andrologyjournal.org/cgi/content/full/24/5/765

16.              Wijnand HP, Bosch AM, Donker CW. Pharmacokinetic parameters of nandrolone (19-nortestosterone) after intramuscular administration of nandrolone decanoate (Deca-Durabolin) to healthy volunteers. Acta Endocrinol Suppl (Copenh) 1985;271:19-30. http://www.ncbi.nlm.nih.gov/pubmed/3865478

17.              Zhang GY, Gu YQ, Wang XH, Cui YG, Bremner WJ. A pharmacokinetic study of injectable testosterone undecanoate in hypogonadal men. J Androl 1998;19(6):761-8. http://www.ncbi.nlm.nih.gov/pubmed/9876028

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Leading the Steroid Revolution

Leading the Steroid Revolution

What makes a steroid revolution?

As a general rule, if you are 100% better at something, you are evolutionary. If you are 1,000% better, you are revolutionary.

Since the mid 90’s, we’ve seen a number of companies bring evolutionary products to the market, including Biotest, Ergopharm, Molecular Nutrition and many others along the way. However, nothing has quite been revolutionary, nor have we seen much development since the major “pro-hormone” ban in 2004.

Technologically our new delivery system is going to be about 10x better than our previous version of Liqua-Vade, making the AndroSeries easily 1,000% better than its predecessors or the nearest competition. This technology allows the specifically chosen natural steroids to be delivered orally at a rate of 75-85% — with biological effects calculated down to the milligram – so we can predict the exact effects relative to actual injectable steroids.

But the fuel behind the fire is more than just technology – there is ideology.


Steroids for the Heart, Mind & Muscle

Our definition of a “steroid” is a hormone that is naturally produced by the body. We aren’t talking about synthetic chemically modified steroids – like the toxic methylated steroids that are almost single handedly responsible for creating the negative stigma around the word “steroid”. We are talking about natural steroids, and don’t forget, testosterone is a steroid.

Now forget the media’s spin of the word “steroid” and consider ours –

Steroids for the Heart, Mind and Muscle

The phrase could be taken literally if you like. However, our definition is more abstract. We chose to define it with timeless human attributes –

Heart = Honorable, warm and spirited.
Mind = Logical, purposeful and dignified
Muscle = Rugged, independent and powerful

To us, this is the true definition of a Testosterone fueled man – which anyone can willfully become.

But let me make something very clear.

We aren’t saying that steroids will give you these qualities. No, that would be obscene. We only hope that the statement will inspire you to fulfill these qualities – as a moral reminder, each time you face a challenge, opportunity or reward.


Steroids saving America

Vice President Joe Biden testifying before congress on steroids, a qyote from the movie Bigger, Stronger, Faster: “There is something un-American about this.”  What America has this man been residing in?


Senator Joe Biden once said steroids are “un-American”.

What America was he talking about?

Steroids are the sovereign juice that fueled the formation of America. If it wasn’t for the testosterone pulsing through the veins of the Patriots, the American Revolution never would have happened. It’s testosterone that fuels the hard working blue collar American – it fuels us during a time of recession and difficult times – and fuels us to get back up again.

If anything, this nation is currently a little short on steroids. We are in a time where testosterone levels have continued to decline each and every decade — while depression, sexual impotence and obesity related diseases continue to increase.

Are steroids going to save us?

They already are.

Obesity, diabetes, impotence, depression, and muscle wasting diseases — all being treated with steroids. (1-4)

Perhaps the slogan “Steroids for the Heart, Mind and Muscle” was a literal statement after all – Or perhaps it’s something bigger – Perhaps it’s the beginning of a steroid revolution.

References –

1. 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.

2. A new oral testosterone undecanoate formulation.
Köhn FM, et al
World J Urol. 2003 Nov;21(5):311-5. Epub 2003 Oct 25

3. Therapeutic effects of nandrolone and testosterone in adult male HIV patients with AIDS wasting syndrome (AWS): a randomized, double-blind, placebo-controlled trial.
Sardar P, et al.
HIV Clin Trials. 2010 Jul-Aug;11(4):220-9

4. 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.

Methylepitiostanol (Epistane)

Diagram of molecule

Chemical Name(s):

2a,3a-epithio-17a-methyl-etioallocholan-17b-ol
2a,3a-epithio-17a-methyl-5a-androstan-17b-ol
Chemical Formula: C20H30OS
Molecular Weight: 320.5
CAS: NA
Q Qatio: 12
Anabolic #: 1,100
Androgenic #: 91
Oral Bioavailability: Estimated at 40%
AR Binding Affinity: NA
SHBG Binding Affinity: NA
Half Life: ~6 hours
Legal Status (US): Not listed as a controlled substance
Average Dose:
40-50mg/day standalone
10-20mg/day when stacked
Average Cycle Length: 4-6 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

Methylepitiostanol is a methylated version of the steroid Epitiostanol. It is readily active and does not require conversion. Under the influence of heat methylepitiostanol readily breaks down to 17a-Methyl-androstan-2-en-17b-ol (DMT), a now illegal anabolic steroid.

It does not aromatize, however it is possible that methylepitiostanol may offset estrogen and testosterone from SHBG thus increase the risk of gyno for certain individuals with high SHBG levels. Gyno symptoms from this compound may also be a result of this compounds inability to form a potent androgen such as DHT (to antagonize the effects of estrogen). However, in other cases methylepitiostanol can be used to prevent or reduce gynecomastia from an estrogenic steroid by acting as an aromatase inhibitor to keep estrogen down.

It is a DHT derivative with a fairly moderate androgenic value so the chances of hair loss may be increased in certain sensitive users. Swelling of the prostate may also become an issue. The powerful estrogen suppressing action of this steroid and its 17aa stucture will cause it to negatively influence the cholesterol profile by lowering HDL and increasing LDL. It has also been reported to cause stiff joints, possibly related to its suppressive effect on estrogen levels.

Anecdotal reports of appetite suppression and general fatigue would lead one to believe that the liver stress from this 17aa compound is rather severe. For this reason it is recommended to use a liver protecting supplement prior to and during the use of this steroid.

Methylepitiostanol has a strong anabolic action that will lead to quick gains in lean muscle mass and strength with very little bloat. The gains will appear with minimal fat gain and increased vascularity.

Because methylepitiostanol can negatively affect joint comfort it is recommended to be stacked with an aromatizing or progestational compound. However, it is not recommended to stack this steroid with another 17aa oral.

Common Clones:

Epistane by Innovative Body Enhancement (IBE)
Havoc by Primaforce
Havoc by Recomp Performance Nutrition (RPN)
Epi-MAX by Anabolic Formulations
M14-E by Purus Labs
Methyl-E by Engineered Sports Technology (EST)
E-Max by Juggernaut Nutrition
E-Stane by Competitive Edge Labs (CEL)
Hemaguno by Spectra Force Research
Hemapolin by Starmark Labs
Epi-Mass by Armour Nutrition
Epidrol by Genera Labs
Methyl Freak by Rockhard Formulations
Epistrong by Mrsupps


Related Discussion

The Official Methylepitiostanol (Epistane) Thread
Posted by Eric

References

“2{alpha},3{alpha}-Epithio-5{alpha}-androstan-17ß-yl 1-Methoxycyclopentyl Ether in the Treatment of Advanced Breast Cancer —A Preliminary Clinical Trial”

SOICHI KUMAOKA, M.D., OSAMU TAKATANI, M.D., MINORU YOSHIDA, M.D., SHIGETO MIURA, M.D., TETSUTO TAKAO, M.D., YÜJI HAMANAKA, M.D., MASARU IZUO, M.D. and TADAKAZU OKADA, M.D.
Japanese Journal of Clinical Oncology 4:65-68 (1974)

“Inhibited growth in vivo of a mouse pregnancy-dependent mammary tumor (TPDMT-4) by an antiestrogen, 2alpha, 3alpha-epithio-5alpha-androstan-17beta-ol (10275-S).”
Matsuzawa A, Yamamoto T.Cancer Res. 1976 May;36(5):1598-606.

“Antitumor Effect of Two Oral Steroids, Mepitiostane and Fluoxymesterone, on a Pregnancy-dependent Mouse Mammary Tumor (TPDMT-4)1”
Akio Matsuzawa and Tadashi Yamamoto
Cancer Research 37, 4408-4415, December 1, 1977

Lipoprotein Lipase Important for Fat Burning

Lipoprotein lipase important for fat burningJanuary 7th, 2010 – Lipoprotein lipase (LPL) is an enzyme that breaks apart fat (triglycerides) into their fatty acid components for transport and use inside cells.

An increase in lipoprotein lipase activity means an increase in the flow of fatty acids into the cell.  An increase in LPL activity in muscle cells means they will use more fat and less sugar for energy, which is a good thing if you are trying to stay lean.  An increase in LPL activity in fat cells, however, will mean increased fat stores.  There are many factors involved in the regulation of LPL activity, but two big contributors are the hormones insulin and testosterone.

Insulin increases LPL activity in fat cells, while decreasing LPL activity in muscle cells.  (1) Anything that drives up insulin (mainly dietary carbohydrates) will increase the flow of fatty acids into fat cells for storage and cause muscle cells to burn sugar instead of fat.

Testosterone also has a regulatory effect on LPL activity in muscle. Lipoprotein lipase activity in the fat cells of the abdominal region is greater in men than in women, and reduced testosterone levels only increases activity.  Keeping testosterone levels high, however, works to reduce LPL activity in the male abdominal fat cells thus discouraging fat storage in this area. (2)

References –

1. Lipoprotein lipase regulation by insulin and glucocorticoid in subcutaneous and omental adipose tissues of obese women and men.

Fried SK, Russell CD, Grauso NL, Brolin RE.

J Clin Invest. 1993 Nov;92(5):2191-8

2. Good Calories Bad Calories

Gary Taubes

Alfred A Knopf 2007 Pages 397-399

Sunlight Increases Testosterone Production

Sunlight Increases Testosterone

October 14th, 2009 – Interested in boosting your testosterone levels? Try Sunlight.

Research shows that testosterone levels are highest in men during the summer months of June though July. (1) In a study involving men between the ages of 19-30, researchers found that only 1 hour of sunlight exposure stimulated luteinizing hormone (LH) production by 69.5% (2) luteinizing hormone is the primary hormone that signals the testes to increase testosterone production.

Sunlight exposure is also the main source of vitamin D production in the body, and low vitamin D levels are a good indicator of insufficient sunlight exposure. Therefore, testing for vitamin D can be an excellent way to ensure you are getting enough sunlight for optimal testosterone levels.

The take home message – Get outside as much as possible!

-Eric Potratz
Founder & President


References

1. Variation in Levels of Serum Inhibin B, Testosterone, Estradiol, Luteinizing Hormone, Follicle-Stimulating Hormone, and Sex Hormone-Binding Globulin in Monthly Samples from Healthy Men during a 17-Month Period: Possible Effects of Seasons
Anna-Maria Andersson, et al
J. Clin. Endocrinol. Metab., Feb 2003; 88: 932 – 937.

2. Luteinizing hormone following light exposure in healthy young men
IY Yoon, et al.
Neurosci Lett, April 24, 2003; 341(1): 25-8

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