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guy curlingAndrogens are the unquestioned kings for building muscle mass and strength. However, their potency and far-reaching effects throughout the body also have their downsides. Before we begin, readers should be aware that this is not a look at HPTA dysfunction, legality, morality, or any such related issues concerning androgen use. Instead we will focus on visceral adipose tissue (‘roid gut or ‘VAT’), lipid profiles (cholesterol, blood triglycerides), heart disease, and liver toxicity — and why SesaThin™ should be a staple of any androgen cycle (particularly with methylated androgens, which are notoriously more liver-toxic than non-methylated androgens). This situation is even worse if the androgen is non-aromatizing, as estrogen exerts a protective effect on blood lipid profiles (1,2,3).

It is well established in the literature and the real world that heart disease (4,5,6) and abdominal fat accumulation (7,8,9) occurs far more often in males than in females. The reason for this is sex-steroid/hormone testosterone (8,9). And, lest we not forget, synthetic androgens like Trenbolone, 1-Testosterone, et cetera are not only structurally similar, but also activate the same pathways, predominately through their interaction with the androgen receptor, or ‘AR’ (10,11,12,13).

Testosterone, for all its anabolic cash-money-ness, does its damage in several ways—by increasing angiotensin II (14,15,16) and cellular beta adrenergic receptor density (17,18,19), by decreasing 5alpha reductase activity (20,21), and by decreasing 11beta-hydroxysteroid dehydrogenase (11betaHSD) activity (22). These processes work in concert to increase activity of cortisol and the stress axis (20,23,24,25,26,27,28), a process intimately linked with visceral adipose tissue accumulation (26,28,29,30), elevated blood lipids (31,32,33,34), oxidative stress/inflammation (35,36,37), and heart disease (28,38,39,40). And while hopefully your wife or girlfriend (or maybe just the judges at your next Mr. Olympia show) will be willing to shrug off your Test-tummy as ‘kind of cute,’ there’s nothing cute about a self-perpetuating condition that differentiates (re: creates new) fat cells even as it sends your overall health prospects a’-plummeting… pronto. Or, as Larsson and colleagues put it rather tellingly in their 1984 study on abdominal adipose tissue distribution, obesity, and their related health risks, “[Our] results indicate that in middle aged men the distribution of fat deposits may be a better predictor of cardiovascular disease and death than the degree of adiposity” (28). They’re talkin’ VAT gentlemen.

For a full, intricate elaboration on this process, please refer to our article “Ab-Solved Science”, by Par Deus. For the quick, simplified gist, it goes a little something like this. All of the aforementioned dynamics (increased ANGII, increased beta adrenergic receptor density, decreased 5alpha reductase and 11betaHSD activity—coupled with high testosterone/synthetic androgen levels) creates a nasty scenario where cortisol becomes over-active locally in visceral fat depots (and can’t be adequately metabolized/reduced), causing them to perpetually dump their nasty contents into the blood stream to cause oxidative damage and screw over your glucose tolerance. To make matters worse, this very same VAT starts literally spreading itself like a pathogen, setting one up for a host of health-related problems later in life as things keep getting worse and worse until something hits critical.

But have no fear, because this is a new age, and we’ve got one helluva remedy.

SesaThin™, a naturally-occurring, damn-near-miracle sesame lignan, might just be nature’s tailor-made protector against all these problems and pathologies. First and foremost, Sesathin markedly decreases triglyceride (TG) formation and increases TG uptake and fatty acid oxidation (41,42), while decreasing cholesterol levels (43,44). Well, actually, it’s even a little better than that, because Sesathin seems to actually increase HDL cholesterol (the good stuff), while taking your LDL (the bad stuff) out back to the woodshed for a good ‘ole-fashioned ass-whuppin’ (43,44,45). It also just happens to be a potent anti-oxidant and anti-inflammatory (as well as an inhibitor of the metabolism of the anti-oxidant/anti-inflammatory, vitamin E) (46,47,48,49).

In addition to these health benefits, Sesathin’s potent thermogenic and anti-lipogenic properties will stop hormone-induced VAT accumulation dead in its tracks, allowing you to get hyooge, while keeping your gut from ballooning up alongside your massive guns. In other words, for any aesthetically cognizant steroid user who wants to build his or her physique while maintaining (if not improving) definition and/or athletic functionality, Sesathin is like the milk to your highly anabolic and questionably edible ‘goodies’. In fact, it’s not hard to speculate that androgens and Sesathin will be synergistic for improving body composition, since hormones like testosterone are lipolytic in subcutaneous adipose tissue (SAT) and adipogenic in VAT, whereas Sesathin would increase the oxidation of the free-fatty acids liberated from the SAT, and prevent the formation of the VAT. Plus, Sesathin’s potent insulin sensitizing and activation of PPARalpha will only enhance the already-badass repartitioning power of steroids, creating a metabolic scenario where your muscles are getting first dibs on damn-near everything being eaten.

Oh, but it gets better, because in addition to the above, Sesathin also protects another part of the body frequently besieged by steroids: the liver.

Although methylated androgens like Stanazolol (Winstrol) and Oxandrolone (Anavar) have been around for decades, they are certainly a hot topic on the block these days. By carbon-alkylating a steroid (usually at the 17th, 7th, or 1st position, as well as the occasional 2nd or 6th) and protecting the 17b-hydroxy group from being oxidized into a 17keto group, it can be rendered immune to metabolic deactivation, a process which occurs in the liver (13). Unfortunately, this very same alkyl group that makes the steroid orally bioavailable is also responsible for the androgen’s deleteriously taxing effects on the liver, a property known as hepatoxicity (13). Some methylated steroids, like Anavar for instance, are relatively benign. Others, like the infamous 17alpha-methyl-17beta-hydroxy-androst-1-ene-3-one (‘Methyl-1-Test’), are exceedingly, if not dangerously, hepatotoxic (50).

For those of you who do decide to take the plunge however, Sesathin’s got your back, and should be the cornerstone of any true liver-protection stack.

For one, the actives in Sesathin have been shown to potently protect the liver from damage induced by both alcohol (ethanol) and the toxic chemical carbon tetrachloride (51). By providing anti-oxidant activity, improving blood parameters, decreasing nutrient output and one’s hepatic delta5 desaturation index (52), and inhibiting lipid accumulation, Sesathin provides livers with a multi-pronged defense against the types of stress that can arise from the (ab)use of methylated steroids (41,42,48,51).

Need we pitch more?

So, the next time you delve into androgens, don’t forget SesaThin™, your all-in-one on-cycle-therapy provider, compliments of good ole’ Mother Nature and Avant Labs.

References

1. Hong MK, Romm PA, Reagan K, Green CE, Rackley CE. Effects of estrogen replacement therapy on serum lipid values and angiographically defined coronary artery disease in postmenopausal women. Am J Cardiol. 1992 Jan 15;69(3):176-8.

2. de Aloysio D, Gambacciani M, Meschia M, Pansini F, Bacchi Modena A, Bolis PF, Massobrio M, Maiocchi G, Peruzzi E. The effect of menopause on blood lipid and lipoprotein levels. The Icarus Study Group. Atherosclerosis. 1999 Nov 1;147(1):147-53.

3. Abbey M, Owen A, Suzakawa M, Roach P, Nestel PJ. Effects of menopause and hormone replacement therapy on plasma lipids, lipoproteins and LDL-receptor activity. Maturitas. 1999 Dec 15;33(3):259-69.

4. E. Barrett-Connor and T. L. Bush. Estrogen and coronary heart disease in women JAMA, Vol. 265 No. 14, April 10, 1991.

5. Milner KA, Funk M, Richards S, Wilmes RM, Vaccarino V, Krumholz HM. Gender differences in symptom presentation associated with coronary heart disease. Am J Cardiol. 1999 Aug 15;84(4):396-9.

6. Adams KF Jr, Dunlap SH, Sueta CA, Clarke SW, Patterson JH, Blauwet MB, Jensen LR, Tomasko L, Koch G. Relation between gender, etiology and survival in patients with symptomatic heart failure. J Am Coll Cardiol. 1996 Dec;28(7):1781-8.

7. Bjorntorp P. The regulation of adipose tissue distribution in humans. Int J Obes Relat Metab Disord. 1996 Apr;20(4):291-302.

8. A Tchernof, JP Despres, A Dupont, A Belanger, A Nadeau, D Prud’homme, S Moorjani, PJ Lupien and F Labrie Relation of steroid hormones to glucose tolerance and plasma insulin levels in men. Importance of visceral adipose tissue Diabetes Care, Vol 18, Issue 3 292-299, Copyright © 1995

9. Seidell JC, Bjorntorp P, Sjostrom L, Kvist H, Sannerstedt R. Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but negatively with testosterone levels. Metabolism. 1990 Sep;39(9):897-901.

10. J. H. van Roijen, M. P. Ooms, R. F. Weber, A. O. Brinkmann, J. A. Grootegoed and J. T. Vreeburg. Comparison of the response of rat testis and accessory sex organs to treatment with testosterone and the synthetic androgen methyltrienolone (R1881) Journal of Andrology, Vol 18, Issue 1 51-61.

11. Saartok T, Dahlberg E, Gustafsson JA. Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin. Endocrinology. 1984 Jun;114(6):2100-6.

12. JA Kemppainen, MV Lane, M Sar and EM Wilson. Androgen receptor phosphorylation, turnover, nuclear transport, and transcriptional activation. Specificity for steroids and antihormone. J. Biol. Chem., Vol. 267, Issue 2, 968-974, 01, 1992

13. Vida J. Androgens & Anabolic Agents: Chemistry & Pharmacology (New York & London: 1969), pp. 1-4; 33-34, 75-77.

14. Bachmann J, Feldmer M, Ganten U, Stock G, Ganten D. Sexual dimorphism of blood pressure: possible role of the renin-angiotensin system. J Steroid Biochem Mol Biol. 1991;40(4-6):511-5.

15. Okuyama A, Nonomura N, Koh E, Kondoh N, Takeyama M, Nakamura M, Namiki M, Fujioka H, Matsumoto K, Matsuda M. Induction of renin-angiotensin system in human testis in vivo. Arch Androl. 1988;21(1):29-35.

16. K Naruse, M Naruse, K Obana, R Demura, H Demura, T Inagami and K Shizume Renin in the rat pituitary coexists with angiotensin II and depends on testosterone Endocrinology, Vol 118, 2470-2476

17. Xu XF, De Pergola G, Bjorntorp P. Testosterone increases lipolysis and the number of beta-adrenoceptors in male rat adipocytes. Endocrinology 1991 Jan;128(1):379-82.

18. Collins S, Quarmby VE, French FS, Lefkowitz RJ, Caron MG. Regulation of the beta 2-adrenergic receptor and its mRNA in the rat ventral prostate by testosterone. FEBS Lett. 1988 Jun 6;233(1):173-6.

19. Petrovic SL, McDonald JK, Snyder GD, McCann SM. Testosterone control of brain and anterior pituitary beta-adrenergic receptors. Life Sci. 1984 Jun 11;34(24):2399-406.

20. Russell DW, Wilson JD. Steroid 5 alpha-reductase: two genes/two enzymes. Annu Rev Biochem. 1994;63:25-61.

21. Shalender B. Role of 5-alpha Reductase in Testosterone Action. Grant Number: 7R01HD043348-03, BU Medical Center: NICHD: ongoing.

22. SC Low, SN Assaad, V Rajan, KE Chapman, CR Edwards, and Seckl JR . Regulation of 11 beta-hydroxysteroid dehydrogenase by sex steroids in vivo: further evidence for the existence of a second dehydrogenase in rat kidney. Journal of Endocrinology 1993, Vol 139, Issue 1, 27-35

23. Ames R et al. Prolonged Infusions of Angiotensin II and Norepinephrine and Blood Pressure, Electrolyte Balance, and Aldosterone and Cortisol Secretion in Normal Man and in Cirrhosis with Ascites. J Clin Invest. 1965 July; 44(7): 1171–1186.

24. Laragh JH et al. Hypotensive agents and pressor substances. The effect of epinephrine, norepinephrine, angiotensin II, and others on the secretory rate of aldosterone in man. JAMA 1960 Sep 17;174:234–240.

25. Katz JR et al. An in vivo study of the cortisol–cortisone shuttle in subcutaneous abdominal adipose tissue. Clinical Endocrinology January 1999, vol. 50, no. 1, pp. 63-68(6)

26. Rosmond R and Björntorp P. Occupational Status, Cortisol Secretory Pattern, and Visceral Obesity in Middle-aged Men. Obesity Research 8:445-450 (2000)

27. Björntorp, P, Holm, G, Rosmond, R. (1999) The pathogenesis of the metabolic syndrome Ailhaud, G Guy-Grand, B eds. Progress in Obesity Research: 8 ,555-565

28. Larsson B, Svardsudd K, Welin L, Wilhelmsen L, Bjorntorp P, Tibblin G. Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow up of participants in the study of men born in 1913. Br Med J (Clin Res Ed). 1984 May 12;288(6428):1401-4.

29. Rosmond, R, Dallman, MF, Björntorp, P. (1998) Stress-related cortisol secretion in men: relationships with abdominal obesity and endocrine, metabolic and hemodynamic abnormalities J Clin Endocrinol Metab. 83,1853-1859

30. Rosmond, R, Lapidus, L, Mårin, P, Björntorp, P. (1996) Mental distress, obesity and body fat distribution in middle-aged men Obes Res 4,245-252

31. Grundy SM Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome. Am J Cardiol. 1998 Feb 26;81(4A):18B-25B.

32. Solini A et al. Protein Metabolism in Human Obesity: Relationship with Glucose and Lipid Metabolism and with Visceral Adipose Tissue. The Journal of Clinical Endocrinology & Metabolism 1997 Vol. 82, No. 8 2552-2558

33. Björntorp P et al. Visceral Obesity and Diabetes. Drugs, 1999, vol. 58, no. Supplement 1, pp. 13-18(6)

34. Kreisberg RA. Diabetic dyslipidemia. Am J Cardiol. 1998 Dec 17;82(12A):67U-73U; discussion 85U-86U.

35. Suematsu et al. The Inflammatory Aspect of the Microcirculation in Hypertension: Oxidative Stress, Leukocytes/Endothelial Interaction, Apoptosis. Microcirculation, Vol. 9:4, 2002, 259-276.

36. Chung et al. Molecular inflammation hypothesis of aging based on the anti-aging mechanism of calorie restriction. Microscopy Research & Technique, Vol. 59:4, 2002, 264 – 272

37. Reckelhoff et al. Role of oxidative stress in angiotensin-induced hypertension. Am J Physiol Regul Integr Comp Physiol 284: R893-R912, 2003

38. Yudkin JS, Kumari M, Humphries SE, Mohamed-Ali V. Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis. 2000 Feb;148(2):209-14.

39. Singal PK, Khaper N, Palace V, Kumar D. The role of oxidative stress in the genesis of heart disease. Cardiovasc Res. 1998 Dec;40(3):426-32.

40. Stoney CM, Davis MC, Matthews KA. Sex differences in physiological responses to stress and in coronary heart disease: a causal link? Psychophysiology. 1987 Mar;24(2):127-31.

41. Ashakumary L, Rouyer I, Takahashi Y, Ide T, Fukuda N, Aoyama T, Hashimoto T, Mizugaki M, Sugano M. Sesamin, a sesame lignan, is a potent inducer of hepatic fatty acid oxidation in the rat. Metabolism. 1999 Oct;48(10):1303-13.

42. Ide T, Ashakumary L, Takahashi Y, Kushiro M, Fukuda N, Sugano M. Sesamin, a sesame lignan, decreases fatty acid synthesis in rat liver accompanying the down-regulation of sterol regulatory element binding protein-1. Biochim Biophys Acta. 2001 Nov 30;1534(1):1-13.

43. Hirose N et al. Inhibition of cholesterol absorption and synthesis in rats by sesamin. Journal of Lipid Research 1991, Vol 32, 629-638.

44. Nakabayashi A, Kitagawa Y, Suwa Y, Akimoto K, Asami S, Shimizu S, Hirose N, Sugano M, Yamada H. alpha-Tocopherol enhances the hypocholesterolemic action of sesamin in rats. Int J Vitam Nutr Res. 1995;65(3):162-8.

45. Ogawa H, Sasagawa S, Murakami T, Yoshizumi H. Sesame lignans modulate cholesterol metabolism in the stroke-prone spontaneously hypertensive rat. Clin Exp Pharmacol Physiol Suppl. 1995 Dec;22(1):S310-2.

46. Fukuda Y, Nagata T, Osawa T, Namiki M. Contribution of lignan analogues to antioxidative activity of refined unroasted sesame oil. J Am Oil Chem Soc 1986;63:1027–31.

47. Utsunomiya T et al. Effects of sesamin-supplemented dietary fat emulsions on the ex vivo production of lipopolysaccharide-induced prostanoids and tumor necrosis factor alpha in rats. American Journal of Clinical Nutrition 2000, Vol. 72, No. 3, 804-808

48. Sugano M, Akimoto K. Sesamin: a multifunctional gift from nature. J Chin Nutr Soc 1993;18:1–11.

49. Hemalatha S, Raghunath M, Ghafoorunissa. Dietary sesame oils inhibits iron-induced oxidative stress in rats [corrected] Br J Nutr. 2004 Oct;92(4):581-7.

50. Although a lack of literature exists on the exact hepatoxicity of many more recent methylated androgens, clinical blood-work from numerous users of these compounds have shown post-cycle liver enzyme values (AST/ALT) to be elevated far above and beyond levels that would be deemed medically safe or healthy.

51. Akimoto K, Kitagawa Y, Akamatsu T, Hirose N, Sugano M, Shimizu S, Yamada H. Protective effects of sesamin against liver damage caused by alcohol or carbon tetrachloride in rodents. Ann Nutr Metab. 1993;37(4):218-24.

52. Umeda-Sawada R, Fujiwara Y, Abe H, Seyama Y. Effects of sesamin and capsaicin on the mRNA expressions of delta6 and delta5 desaturases in rat primary cultured hepatocytes. J Nutr Sci Vitaminol (Tokyo). 2003 Dec;49(6):442-6.

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