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.

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.

Exemestane (Aromasin)

Diagram of molecule

Chemical Name(s):

6-methyleneandrosta-1,4-dien-3,17-dione
Chemical Formula: C20H24O2
Molecular Weight: 296
CAS: NA
Q Qatio: NA
Anabolic #: NA
Androgenic #: NA
Oral Bioavailability: Estimated at 15%
AR Binding Affinity: NA
SHBG Binding Affinity: NA
Half Life: 27 hours
Legal Status (US): Prescription only
Average Dose: 10-25mg/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

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

Exemestane is one of the most potent and expensive steroidal aromatase inhibitors currently available on the market. It is available by prescription only. The estrogen inhibition rate for exemestane varies from 85% of estradiol to 95% for estrone.

Exemestane is looked highly upon due to the fact it can be just as effective as Letrozole or Arimidex without causing such a rapid rebound of estrogen, which is a typical problem of non-suicidal aromatase inhibitors.

Exemstane is rarely dosed beyond 25mg/day as this appears to be a high enough dose to suppress estrogen by a significant amount. It can reach maximum estrogen suppression in as little as 7 days. Since it increases testosterone levels, some users may experience androgenic effects.


Related Discussion

The Official Exemestane (Aromasin) Thread
Posted by Eric

References

Anabolic Pharmacology
Seth Roberts (2009)

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

Resveratrol better than Viagra?

Resveratrol Better Than Viagra

October 14th, 2009 – Drugs like Viagra (Sildenafil citrate) and Cialis (Tadalafil) are used to treat erectile dysfunction (ED) by increasing blood flow to the erectile tissue in the penis known as the corpus cavernosum.

These drugs increase blood flow to erectile tissue by inhibiting the phosphodiesterase enzymes (PDE5 & 6), which prolongs the action of cGMP in the smooth muscle tissue, increasing the dilation response from nitric oxide (NO) release. However, inhibition of the phosphodiesterase enzyme system has effects across the entire body and can lead to side-effects including headache, skin flushing, nasal congestion and muscle aches. (1) These are very unwelcome side-effects when trying to stimulate sexual arousal.

New research suggests that resveratrol can also trigger erections by promoting blood flow to the erectile tissue in the penis. (2) This vasodilatory effect appears to occur within minutes of resveratrol exposure, suggesting that supplementation may provide a quick temporary boost in sexual performance. (3)

Evidence suggests that resveratrol does not have the side-effects typically associated with popular ED drugs. Resveratrol improves vasodilation by multiple cellular mechanisms, and does not negatively inhibit the phosphodiesterase enzyme system, which can lead to unwanted side-effects. (3) Whether or not resveratrol is a worthy substitute to powerful prescription drugs such as Viagra and Cialis remains to be determined.

-Eric Potratz
Founder & President


References

1. [Sildenafil (Viagra) in erectile dysfunction. Effective treatment with noteworthy side effects]
C Rolf and E Nieschlag
Dtsch Med Wochenschr, Nov 1998; 123(45): 1356-61.

2. trans-Resveratrol relaxes the corpus cavernosum ex vivo and enhances testosterone levels and sperm quality in vivo.
Shin S, Jeon JH, Park D, Jang MJ, Choi JH, Choi BH, Joo SS, Nahm SS, Kim JC, Kim YB.
Arch Pharm Res. 2008 Jan;31(1):83-7.

2. Resveratrol, a component of red wine, elicits dilation of isolated porcine retinal arterioles: role of nitric oxide and potassium channels.
Nagaoka T, Hein TW, Yoshida A, Kuo L.
Invest Ophthalmol Vis Sci. 2007 Sep;48(9):4232-9.

HCG – Unraveled

Post-Cycle-Therapy is a must upon cessation of steroid use. Many great Post Cycle Therapy protocols have been outlined over the years, and many individuals have had success with following such protocols. Nevertheless, what works can always work better, and I intend to show you the most effective way to recover from AAS. This is especially the case for those that have had a lack of success following popular advice. In this article I will address the misunderstanding and misuse of Human Chorionic Gonadotropin (hCG) and show you the most efficient way to use hCG for the fastest and most complete recovery.

HCG unraveled –

Human Chorionic Gonadotropin (hCG) is a peptide hormone that mimics the action of luteinizing hormone (LH). LH is the hormone that stimulates the testes to increase testosterone levels. (1) More specifically LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone.

When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the testes to stop producing testosterone, which causes rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production. (2-6,19) However, this degeneration can be prevented by a small maintenance dose of hCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that hCG should be used after a cycle, during Post-Cycle-Therapy. Upon reviewing the science and basic endocrinology you will see that a faster and more complete recovery is possible if hCG is ran during a cycle.

Firstly, we must understand the clinical history of hCG to understand its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal testicular sensitivity, the maximum increase of testosterone is seen from a dose of only 250iu, with minimal increases obtained from 500iu or even 5000iu. (2,11) (It appears the testes maximum secretion of testosterone is about 140% above their normal capacity.) (12-18) If you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.

One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity. This is the amount of testosterone your testes can produce from any given level of LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity. If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger natural testosterone production – and this leads to permanently reduced testosterone production. (recovering full testosterone production is a topic for another article)

To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration. (2,9,10) By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%. (2-6)

Note: visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone. (4) This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) So do not judge how “shutdown” you are by testicular size!

The decreased testosterone secretion capacity caused by steroid use was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids. (8) In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size. (7) Another study with men using low dose steroids for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks (6) (INSL3 is an important biomarker for testosterone production potential and sperm production) 20

In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle.

Based on studies with normal men using steroids, 100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG. (2) It is important that low-dose hCG is started before testicular sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start Post-Cycle-Therapy so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)

Based off the above information, an optimal dose of hCG during the cycle would be 250iu every 4 days, or as a less desirable alternative, once a week shot of 500iu. Keep in mind, that the half-life of hCG is 3-4 days, while the half-life of LH is only 1-2 hours. Considering this difference in excretion time, it is best to space each dose of hCG at least 4 days apart for the optimal “peak and valley” replication. However, going more than 7 days between each hCG shot may promote increase the rate of desensitization from lack of LH or hCG stimulation.

If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG “kick starting” dosage by multiplying 40iu x days of LH absence. (ie. 40iu x 60 days = 2400iu HCG dose) Remember, since the testes will be desensitized later in a cycle, you will require a higher dose. Also, the maximum daily dose of hCG should not exceed 5000iu, and 4-7 days must be taken off between each shot. Generally, a higher dose will require a longer off period between each shot. (eg., 2500iu = 7 days between each shot)

Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.

Recap

For preservation of testicular sensitivity, use 250iu every 4 days starting 14 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels. This will initiate a strong LH and FSH surge from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.

In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from “on cycle” to “off cycle” thus avoiding the post cycle crash.

References –

1. Glycoprotein hormones: structure and function.
Pierce JG, Parsons TF 1981
Annu Rev Biochem 50:466-495

2. Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression
Andrea D. Coviello, et al
J. Clin. Endocrinol. Metab., May 2005; 90: 2595 – 2602.

3. Luteinizing hormone on Leydig cell structure and function.
Mendis-Handagama SM
Histol Histopathol 12:869-882 (1997)

4. Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats
SM Mendis-Handagama, et al.
Endocrinology, Dec 1992; 131: 2839.

5. Effect of long term deprivation of luteinizing hormone on Leydig cell volume, Leydig cell number, and steroidogenic capacity of the rat testis.
Keeney DS, et al.
Endocrinology 1988; 123:2906-2915.

6.The Effects of Gonadotropin Suppression and Selective Replacement on Insulin-Like Factor 3 Secretion in Normal Adult Men
Katrine Bay, et al
J. Clin. Endocrinol. Metab., Mar 2006; 91: 1108 – 1111.

7. Successful treatment of anabolic steroid-induced azoospermia with human
chorionic gonadotropin and human menopausal gonadotropin
Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003

8. 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)

9. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate of testosterone cypionate.
Schulte-Beerbuhl M, et al 1980
Fertil Steril 33:201-203

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