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.

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.

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. – (Public, 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.

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.

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.

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.

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.

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.

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

%d bloggers like this: