Testosterone Boosters – It’s Enough to Make You Cry

It’s every where you look, even on billboards. Low testosterone is what’s behind what ails every man older than 30, or so they would make you believe. Regardless of the facts, it’s a booming business and the supplement industry is cashing in.

For quite a while the prohormones fit the bill, although they didn’t really compared to hormonal replacement therapy with testosterone or even the anabolic steroids. However, ever since prohormones were banned several years ago the supplement industry has been looking for substitutes that will enhance testosterone levels and/or provide effects similar to anabolic steroids (or not as long as the story could be told).

Not that the prohormones were anything to talk about as their use often resulted in a triple whammy – they usually had little anabolic/androgenic effects, shut down your own natural production of testosterone, and had all the side effects of real steroids. For more on this have a look at http://www.mauromd.com/det-articles-39-Getting-Off-the-Steroid-Roller-Coaster.php and http://www.mauromd.com/det-articles-57-Boosting-Endogenous-Testosterone-Naturally-with-the-New-TestoBoost-version-IV.php.

But now that the prohormones were illegal the supplement companies had to look elsewhere for the next latest and greatest testosterone booster, regardless of whether or not they boosted testosterone – their marketing machines would take care of that by hyping it all up with their marketing bull**** so that people really “believed” in their products.

So they went for the gusto by pushing plant sterols, dehydroepiandrosterone (DHEA) and/or DHEA metabolites, and other compounds, including fenugreek.

I wrote in detail about the plant sterols over 30 years ago when they were in vogue. In short at that time I wrote that plant sterols, while useful as a raw material that can be chemically changed into biologically active hormones, including testosterone, are not active as androgens in humans, and humans can’t make testosterone from them. In fact many of them have some estrogen effects and are therefore mainly counter productive. Thirty some years later I see no reason to change my views.

That’s not to say that plant sterols are useless because they do have some beneficial effects, for example as antioxidants and in some cases as estrogen replacement therapy to allay menopausal symptoms and as hormonal replacement therapy in post menopausal women.

DHEA and DHEA derivatives, are useful as well under certain circumstances but have no significant anabolic or androgenic activity. However, since it can be legally used in nutritional supplements, they are often misrepresented as useful for increasing testosterone. Often the ingredient isn’t named DHEA but rather it’s chemical names are used as a ruse to make it look more exotic and similar to a prohormones or even an anabolic steroid – for example Androst-5-en-17-one, 3-hydroxy-, (3β)-; Androst-5-en-17-one; 3-β-Hydroxy-5-androsten-17-one; 5-Androstene-3β-ol-17-one; 5-Androsten-3B-ol-17-one. For info on deceptive practices of supplement companies have a look at:

http://www.mauromd.com/det-articles-47-The-Nutritional-Supplement-Industry—Part-1.php

http://www.mauromd.com/det-articles-62-The-Nutritional-Supplement-Industry—Part-2.php

http://www.mauromd.com/det-articles-80-The-Nutritional-Supplement-Industry—Part-3.php

Now there a combinations of compounds that can be useful for increasing testosterone levels, as well as providing an anabolic environment in other ways. Examples of complex formulations that rely on synergistic and additive effects of ingredients are my TestoBoost and GHboost. For info on both see http://www.mauromd.com/det-articles-57-Boosting-Endogenous-Testosterone-Naturally-with-the-New-TestoBoost-version-IV.php and http://www.mauromd.com/det-articles-50-Boosting-Endogenous-Growth-Hormone-Naturally-with-the-New-GHboost-version-IV.php.

Fenugreek

However, many nutritional supplements that are heavily advertised to boost testosterone fall short, often to the point of being counter productive. An example are testosterone boosters containing fenugreek as their main ingredient.

That’s not to say that fenugreek, with its main active compound diosgenin doesn’t have its good points as it may be beneficial in a number of ways. Due to its estrogen-like properties it’s been used to decrease menopausal symptoms and PMS, to induce labor, for breast enlargement and increasing milk production.

With all its possible beneficial effects, mainly in women, it’s never been proven to have testosterone boosting properties. In my experience, it does nothing to significantly boost testosterone and in fact may under some circumstances lower testosterone production.

The hype is all about a few studies that show that fenugreek increases testosterone. Unfortunately these studies were either not published or bankrolled by the manufacturer of the testosterone booster and thus tainted. An independent study in 2009 found that fenugreek did not

So what’s the real story with fenugreek. Does it or doesn’t it raise testosterone levels, provide a significant anabolic effect, or does it want to make you cry?

Well it all depends on several factors. First of all plant estrogens can have paradoxical effects on testosterone levels. That’s because they’re weak estrogens compared to estradiol, the main and most potent endogenous estrogen in both men and women. As weak estrogens what they do is dependant on how much you take in.

Phytoestrogens can function as an estrogen agonist or antagonist. At low levels weak estrogens will bind to the estrogen receptor and displace estradiol thus decreasing estrogen activity in the body. Up to a point this effect of plant estrogens (known as phytoestrogens) can have positive effects on testosterone production by a direct action on the testes, and an indirect action by decreasing the inhibitory effect of estrogen on the hypothalamic-pituitary axis, thus increasing LH, which in turn increases testosterone production in the testicles. Blocking estrogen action is the reason why antiestrogens and aromatase inhibitors (such as Clomid, Nolvadex and Arimidex) are used to increase testosterone production.

The problem, however, is that higher doses of phytoestrogens can increase the overall estrogenic effects in the body and thus decrease testosterone production by the direct and indirect effects on the HPTA (hypothalamic-pituitary-testicular axis).

Note: If you’re lost at this point read up on testosterone production in the article at http://www.mauromd.com/det-articles-39-Getting-Off-the-Steroid-Roller-Coaster.php.

So how much is too much? No one really knows as the studies haven’t been done. However, it’s reasonable to assume that it would depend on many factors, including one’s genetic makeup, epigenetic expression, and the concomitant exposure to environmental estrogens.

What I can tell with some certainty is that in the 1980s, when several bodybuilders and powerlifters that I knew tried using several grams a day of plant sterols they did not see any body composition or strength improvements, and one developed mild symptoms and signs of gynecomastia (breast tissue enlargement in men).

The problem is more complicated today than it was back then. That’s because our exposure to environmental estrogens has increased dramatically. For example BPA

Unfortunately the estrogenic effects of plant sterols acts additively to the estrogenic effects of environmental estrogens so that the two together are more potent inhibitors of the HPTA than either alone.

There’s also the counter productive effects of supplements and foods that increase nitric oxide. It’s been shown that excessive nitric oxide production decreases testosterone production (go to http://www.mauromd.com/det-articles-56-Testosterone-Series—Article-One.php) and many bodybuilders and other athletes use supplements that dramatically increase nitric oxide and thus the use of these supplements likely have an additive effect with phytoestrogens and environmental estrogens on suppressing the HPTA and decreasing endogenous testosterone production. 

As such, it may not take large amounts of phytoestrogens to have counter productive effects on testosterone levels. And this is the folly of testosterone boosters that depend on the phytoestrogens in fenugreek, mainly diosgenin, to increase testosterone. It’s very likely that these supplements either do nothing or worse, decrease testosterone and thus have negative effects on body composition and athletic performance.

For this reason, I didn’t include fenugreek in TestoBoost as there are small but effective amounts of phytoestrogens already in the formulation, in the sense that they won’t cause estrogen overload and thus be counter productive for increasing testosterone.

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Indian J Med Res. 2010 Jun;131:814-9.

In vitro estrogenic activities of fenugreek Trigonella foenum graecum seeds.

Sreeja S, Anju VS, Sreeja S.

Abstract

BACKGROUND & OBJECTIVES:

Trigonella foenum graecum commonly known as fenugreek, has been widely cultivated in Asia, Africa and Mediterranean countries for the edible and medicinal values of its seeds. Earlier reports show that fenugreek seeds provide a mastogenic effect resulting in enhanced breast size. However, very little is known about its estrogenic effect. The present study investigated the effect of chloroform extracts of fenugreek seeds (FCE) in breast cancer cells for its estrogenic effect, and to assess its capacity as an alternative to hormone replacement therapy (HRT).

METHODS:

The effect of FCE on cell proliferation of estrogen receptor (ER) positive breast cancer cells, MCF-7 was studied by MTT assay at a concentration range of 20 to 320 microg/ml. The competitive ER binding assay (HAP assay) was done to find out the ER binding capacity of the extract. Transfection and reporter assay (DLR assay), and RT- PCR with an estrogen responsive gene pS2 were done to find out the transcriptional regulatory activity of FCE.

RESULTS:

FCE stimulated the proliferation of MCF-7 cells, showed binding to ER (IC(50) = 185.6 +/- 32.8 microg/ ml) and acted as an agonist for ER mediated transcription via ERE. It also induced the expression of estrogen responsive gene pS2 in MCF-7 cells.

INTERPRETATION & CONCLUSION:

Our study provided the evidence for estrogenic activities of fenugreek seeds. Further in vitro and in vivo studies could demonstrate its suitability as an alternative to HRT.

PDF file of the study is available at http://www.ijmr.org.in/temp/IndianJMedRes1316814-2352162_063201.pdf.

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Fenugreek Extract Supplementation Has No Effect On The Hormonal Profile Of Resitance-Trained Males, Brandon Bushey, Lem W. Taylor, Colin W. Wilborn, Chris Poole, Cliffa A. Foster, Bill Campbell, Richard B. Kreider, Darryn S. Willoughby

International Journal of Exercise Science: Conference Proceedings: Vol. 2: Iss. 1, Article 13. Available at: http://digitalcommons.wku.edu/ijesab/vol2/iss1/13.

Fenugreek is herb that has several purported uses in animal models. Despite no substantiated claims in human research models, fenugreek has been marketed in dietary products as having anabolic potential for resistance trained athletes. PURPOSE: The purpose of this study was to investigate the potential anabolic effects of fenugreek extract supplementation in conjunction with a controlled resistance training program. METHODS: Forty-five resistance trained males were matched by fat free mass and randomly assigned to ingest in a double blind manner capsules containing 500mg of a placebo (PL) (N = 24, 20.1 ± 2.6 yr, 85.5 ±13.4 kg, 177.00 ± 6.1 cm) or fenugreek extract (FE) (N = 21, 21.4 ± 2.95 yr, 89.9 ±18.8 kg, 178.00 ± 6.27 cm). Subjects participated in a supervised 4-day per week periodized resistance-training program for 8 weeks in conjunction with supplementation. Venous blood samples were obtained using standard procedures at baseline (PRE), 4 weeks, and 8-weeks (POST). Serum analyses included cortisol, insulin, leptin, free testosterone, estrogen, and DHT. Statistical analyses utilized a two-way ANOVA with repeated measures for serum hormone responses (p<0.05). RESULTS: A significant interaction (p<0.05) between groups for DHT was observed for PL (PRE: 1187±482; POST: 1258±493 pg/ml) and FE (PRE: 1263±496; POST: 1144±447 pg/ml) indicating that supplementation resulted in significant decrease in DHT levels. Significant differences in DHT responses from supplementation showed a -9.42% change for the FE group accompanied with a 5.98% increase in the PL group. No significant effects for groups or interactions were observed for the anabolic hormones free testosterone and estrogen (p<0.05). Additionally, no significant main effects for groups or time were observed for the metabolic hormones insulin, cortisol, and leptin (p<0.05). CONCLUSIONS: Supplementation of fenugreek extract resulted in a decrease in serum DHT levels in comparison to placebo. However, other anabolic and metabolic hormone analyses were not affected by supplementation. We conclude that in conjunction with structured resistance training, supplementation of fenugreek extract does not appear to affect hormonal status in resistance trained males and shows no anabolic potential as has been purported.

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Toxicol Sci. 2013 Nov 27. [Epub ahead of print]

Co-exposure to Phytoestrogens and Bisphenol A mimic estrogenic effects in an additive manner.

Katchy A, Pinto C, Jonsson P, Nguyen-Vu T, Pandelova M, Riu A, Schramm KW, Samarov D, Gustafsson JA, Bondesson M, Williams C.

Author information

  • Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204-5056, USA.

Abstract

Endocrine-disrupting chemicals (EDC) are abundant in our environment. A number of EDCs, including bisphenol A (BPA) can bind to the estrogen receptors, ERα and ERβ, and may contribute to estrogen-linked diseases such as breast cancer. Early-exposure is of particular concern; many EDCs cross the placenta and infants have measurable levels of e.g. BPA. In addition, infants are frequently fed soy-based formula that contains phytoestrogens. Effects of combined exposure to xeno- and phytoestrogens are poorly studied. Here, we extensively compared to what extent BPA, genistein and an extract of infant soy-based formula (SF) mimic estrogen-induced gene transcription and cell proliferation. We investigated ligand-specific effects on ER activation in HeLa-ERα and ERβ reporter cells; on proliferation, genome-wide gene regulation and non-ER mediated effects in MCF7 breast cancer cells; and how co-exposure influenced these effects. The biological relevance was explored using enrichment analyses of differentially regulated genes and clustering with clinical breast cancer profiles. We demonstrate that co-exposure to BPA and genistein, or SF, results in increased functional and transcriptional estrogenic effects. Using statistical modeling we determine that BPA and phytoestrogens act in an additive manner. The proliferative and transcriptional effects of the tested compounds mimic those of 17β-estradiol, and are abolished by co-treatment with an ER antagonist. Gene expression profiles induced by each compound clustered with poor-prognosis breast cancer, indicating that exposure may adversely affect breast cancer prognosis. This study accentuates that co-exposure to BPA and soy-based phytoestrogens results in additive estrogenic effects, and may contribute to estrogen-linked diseases, including breast cancer.

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Indian J Exp Biol. 1992 May;30(5):367-70.

Diosgenin–a growth stimulator of mammary gland of ovariectomized mouse.

Aradhana, Rao AR, Kale RK.

Abstract

Estrogenic action of diosgenin on the mammary epithelium of ovariectomized (OVX) mouse has been reported. Diosgenin when administered (sc) at the dose levels of 20 and 40 mg/kg body weight for a period of 15 days stimulated the growth of mammary epithelium. This was indicated by the increase in DNA content, increase in number of ducts and appearance of terminal endbuds. There was a significant increase in the mammary development scores in the presence of diosgenin. Concomitant treatment of estrogen and diosgenin showed augmentation of estrogenic effect of diosgenin especially at the higher dose level (40 mg/kg body wt). Diosgenin showed a lack of progesterogenic action as was apparent from the absence of alveolar development even in the presence of exogenous estrogen.

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J Endocrinol. 2011 Jun 8. [Epub ahead of print]

Differential control of steroidogenesis by nitric oxide and its adaptation with hypoxia.

Ducsay C, Myers D.

Source

C Ducsay, Center for Perinatal Biology, Loma Linda University, Loma Linda, 92354, United States.

Abstract

Nitric oxide (NO) plays a role in a wide range of physiological processes. Aside from its widely studied function in the regulation of vascular function, NO has been shown to impact steroidogenesis in a number of different tissues. The goal of this review is to explore the effects of NO on steroid production and further, to discern its source(s) and mechanism of action. Attention will be given to the regulation of NO synthases in specific endocrine tissues including ovaries, testes and adrenal glands. The effects of hypoxia on generation of NO and subsequent effects on steroid biosynthesis will also be examined. Finally, a potential model for the interaction of hypoxia on NO synthesis and steroid production is proposed.

Full paper at http://joe.endocrinology-journals.org/content/early/2011/06/15/JOE-11-0034.full.pdf.

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Toxicol Appl Pharmacol. 2000 Dec 15;169(3):222-30.

Decreased steroid hormone synthesis from inorganic nitrite and nitrate: studies in vitro and in vivo.

Panesar NS, Chan KW.

Department of Chemical Pathology, The Chinese University of Hong Kong, Shatin, New Territories, SAR China. nspanesar@cuhk.edu.hk

Abstract

Nitrites and nitrates are consumed nonchalantly in diet. Organic nitrates are also used as vasodilators in angina pectoris, but the therapy is associated with tolerance whose mechanism remains elusive. Previously, we found inorganic nitrate inhibited steroidogenesis in vitro. Because adrenocorticoids regulate water and electrolyte metabolism, tolerance may ensue from steroid deficiency. We have studied the effects of nitrite and nitrate on in vitro synthesis and in vivo blood levels of steroid hormones. In vitro, nitrite was more potent than nitrate in inhibiting human chorionic gonadotropin (hCG)-stimulated androgen synthesis by Mouse Leydig Tumor cells. At concentrations above 42 mM, nitrite completely inhibited androgen synthesis, and, unlike nitrate, the inhibition was irreversible by increasing hCG concentration. The cAMP production remained intact but reduced with both ions. The nitric oxide (NO) scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxy-3-oxide (c-PTIO) significantly increased hCG- or cAMP-stimulated androgen synthesis in all buffers, suggesting that NO is a chemical species directly involved in the nitrite/nitrate-induced inhibition. This is further supported by c-PTIO countering the inhibitory action of methylene blue on androgen synthesis. Rats given distilled water containing 50 mg/L NaNO(2) or NaNO(3) for 4 weeks drank significantly less daily. At the end, their blood corticosterone and testosterone levels were significantly decreased. The adrenocortical histology showed bigger lipid droplets, which are pathogonomic of impaired steroidogenesis. Nitrite and nitrate are metabolized to NO, which binds heme in cytochrome P450 enzymes, thereby inhibiting steroidogenesis. Therapeutic nitrates likewise may decrease adrenal (and gonadal) steroidogenesis. Cortisol deficiency would impair water excretion causing volume expansion, and aldosterone deficiency would cause sodium loss and raised renin. Paradoxically, volume expansion without sodium retention and raised renin has all been reported in tolerance.

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