A Few Common Bodybuilding Myths - Mind And Muscle

bodybuilder lifting legsby: Karl Hoffman
A Few Common Bodybuilding Myths

Based on my experience of having been either a moderator or administrator on three Anabolic Fitness boards, I’ve put together a collection of what I feel are, for lack of a better term, a few of the most prevalent “bodybuilding myths.” These are topics that are discussed often and at great length, usually accompanied by much misinformation. In some cases “myth” might be an inappropriate term. A better term might be “bodybuilding dogma based on little or no evidence.” Some might even argue that is unfair in some cases, and that these are simply “controversial topics.” These are not myths held by the general public about bodybuilders and drugs, such as “anabolic steroids invariably cause ‘roid rage,’ or anabolic steroids lead to permanent impotence. They are rather what I believe are widespread misconceptions within the bodybuilding community itself about problems encountered and practices employed by the participants themselves.


Estrogen makes a person fat, doesn’t it? Well, women do have a higher body fat content in general than do men, especially in the gluteofemoral (hips and buttocks) region. Is estrogen really the cause of this gender dimorphism in adiposity? Probably not. In fact, there are a wealth of data that implicate estrogen as both an anorectic and antiadipogenic hormone. It is much more likely that progesterone is the culprit in supporting higher levels of gluteofemoral fat in women (1). The model described in (1) has progesterone as the lipogenic hormone. Before menopause, both estrodiol and progesterone are secreted by the ovaries. After menopause, estrone becomes the primary circulating estrogen produced from aromatization of adrenal androgens (primarily the aromatization of androstenedione to estrone by adipose tissue), while progesterone levels drop dramatically since adrenal production of progesterone is minimal.

In premenopausal women, progesterone increases lipoprotein lipase activity, which is greater in the gluteofemoral region, while estrogen suppresses it. Lipoprotein lipase is the body’s primary fat storage enzyme; it is responsible for allowing fats to leave the circulation and enter adipocytes. The progesterone wins out however and before menopause, women tend to have more gluteofemoral fat and less abdominal fat.

Why do women have more gluteofemoral fat while men have more central (abdominal) fat? One popular theory is that women hold fat in the gluteofemoral region where it is far removed from the liver and has fewer fat mobilizing enzymes/more fat retaining enzymes than in men. Men hold fat in the visceral and abdominal subcutaneous region where it is closer to the liver and richer in fat mobilizing enzymes. Proximity to the liver is a factor because the portal circulation connects abdominal fat deposits directly to the liver. Free fatty acids released from abdominal deposits can act directly on the liver to promote gluconeogenesis, providing the body with a ready supply of glucose for “fight or flight” situations.

From an adaptational viewpoint, women’s fat is designed to be stored until needed for lactation and child rearing. Men’s fat on the other hand is designed to be readily mobilized for fight or flight situations during defense and hunting. This theory may be a bit simplistic as well as sexist; but it does make sense to some degree.

Most likely the notion of estrogenic fat originated from the belief that estrogen upregulates alpha 2 receptors in fat cells, retarding lipolysis. This may be just one facet of estrogen’s actions. If one looks at the net result of estrogen’s effects, to quote a leading expert in the field

“Testosterone and GH inhibit LPL and stimulate lipolysis markedly. Oestrogens seem to exert net effects similar to those of testosterone.” (2)

For example, animal studies have shown that testosterone promotes alpha 2 adrenoreceptor mediated antilipolytic activity, just as it promotes beta adrenoreceptor mediated lipolysis.

Interestingly, recent research has even attributed at least part of testosterone’s fat burning properties to its local aromatization to estradiol (3). For instance when testosterone is administered along with an aromatase inhibitor, LPL activity increases, showing that the testosterone itself is devoid of any ability to lower LPL. (4)

There are a number of animal studies where estradiol administration led to significant weight and fat loss. Citing just one, for example:

“The administration of 17 beta-estradiol (500 micrograms/kg, 2 or 4 weeks) to male rats significantly reduced the body weight…Basal lipolysis and adrenaline-induced lipolysis [due to increase in HSL action] were also significantly enhanced in the epididymal adipose tissue from the male rat treated either with 7 mg/kg estradiol 12 h ahead or with 500 micrograms/kg estradiol for 2 weeks. These results indicate that estradiol exerts strong effects on metabolism of the adipose and these effects seems to be mediated through cyclic-AMP.” (5)

This research indicates that in addition to the abovementioned inhibition of LPL, estrogen also stimulates the lipolytic enzyme hormone sensitive lipase.

Some of the most compelling evidence for the antiadipogenic effect of estrogen in both males and females comes from studies of estrogen receptor knockout mice and humans with aromatase deficiency. Both the afflicted humans and the knockout mice exhibit obesity. A detailed look at this topic can be found here:

I also mentioned that estrogen is a potent hunger-suppressing hormone. Research is a bit sketchier here, but the effect is thought to be due to an estrogen-induced inhibition in melanin-concentrating hormone (MCH) signaling (6). MCH is a neuropeptide found in the hypothalamus that is also thought to be involved in leptin’s regulation of appetite. Leptin, an anorectic hormone secreted from the adipose tissue, acts on the specific receptor present on its target neurons in the brain, and suppresses the expression of both MCH and its receptor. So we see that the actions of both estrogen and leptin are at least partly mediated through interactions with MCH.


This notion was dispensed with in Mind & Muscle #10. Here is a brief recap of the relevant findings.

The first study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (7). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Here is a remark about Greer’s classic paper from a later author:

“In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days” (8)

These results have been subsequently verified in several studies (8,9) and a large number of trials where T3 was used to treat obesity. So, contrary to what has been stated in the bodybuilding literature, there is no evidence that long-term thyroid supplementation will somehow damage your thyroid gland.


This is a grossly oversimplified description of the effects of androgens on immunity. The immune system is comprised of two “arms,” so called humor and cellular immunity. Humoral immunity involves the production of antibodies, and is primarily responsible for targeting extracellular pathogens. Cellular, or cell-mediated immunity involves the action of white blood cells including macrophages, neutrophils, and NK (natural killer) cells. These cells mount an attack on invading pathogens and are responsible for the clearance of intracellular pathogens, virus infected cells, and tumor cells. The cell-mediated response is also responsible for the development of inflammation.

Immune cells known as helper T cells, or Th cells, determine which response—humoral or cellular—the body will mount. There are three subsets of Th cells, Th0, Th1 and Th2 cells. The Th1 cells drive the cellular response, whereas Th2 cells control the humoral response. The two Th subsets are mutually inhibitory. Chemicals called cytokines secreted by Th1 cells suppress Th2 cells, and vice versa. The Th0 cells are precursor cells that can give rise to both Th1 and Th2 cells. This process is illustrated schematically here:

Numerous studies have shown that androgens as well as high levels of estrogens such as occur during pregnancy stimulate Th2 cells and hence promote humoral immunity. So in this sense, androgens are immune stimulating. However, as mentioned, the two arms of the immune system inhibit each other, so by virtue of stimulating Th2 cells and humoral immunity, cellular immunity is suppressed. A nice schematic illustration of this process can be found here:

How exactly do androgens stimulate humoral immunity? One idea is that androgens directly stimulate the production of the cytokine interleukin 10, IL-10, by T cells (10). As illustrated in the first link above, when Th2 cells secrete IL-10, this cytokine has a direct suppressive effect on Th1 cells and hence on the cellular immune response.

Probably the most important clinical effect of the suppression of cellular immunity by androgens is the resulting suppression of the inflammatory response. Androgens have been used with varying degrees of success to ameliorate the symptoms of some autoimmune inflammatory diseases like rheumatoid arthritis. Bodybuilders and other athletes commonly remark how certain anabolic steroids, like testosterone and nandrolone, help to alleviate the inflammation associated with injury or overuse.


It’s never been completely clear to me exactly how this notion originated. As far as I can tell it was part of the dubious Class I/Class II theory of steroid action that was spawned on anabolic boards and now generally considered meritless. But many people still seem to believe that oral anabolic steroids such as methandrostenelone (Dianabol) and stanozolol (Winstrol) act directly on the liver to stimulate the production of insulin like growth factor (IGF-1) independently of any increase in growth hormone production. As most readers are aware, normally the pituitary gland secretes growth hormone (GH), and the GH then acts on the liver to stimulate the production of IGF-1. In fact, some “experts” have claimed that it is essential to include an oral steroid in any cycle for this reason.

Some oral androgens have been shown to increase IGF-1 levels, but these same drugs also elevate GH levels. So any increase in circulating liver-derived IGF-1 is almost certainly due to an increase in GH. There is not much research in this area to fall back on, but oxandrolone (10) and methandrostenolone (12) have both been shown to elevate GH in humans. Interestingly, when methandrostenolone was administered to rats whose pituitary glands had been removed, it demonstrated no anabolic effects, suggesting that GH secretion is important to the growth promoting effects of Dianabol (13).

Also, as was demonstrated in (14) and a number of other studies, plain old testosterone increases both GH and IGF-1 production. Perhaps most importantly, testosterone has been shown to stimulate the production of IGF-1 directly in muscle tissue, where it acts in an autocrine manner to stimulate growth (15). Locally produced IGF-1 is believed to play a more important role in muscle growth than does liver-derived IGF-1. So this renders moot the argument that it is necessary to incorporate an oral steroid in a cycle in order to elevate hepatic IGF-1 levels.


Or is it upregulate? It seems there are two schools of thought on this, with the answer probably lying somewhere in between. Short-term in vitro and in vivo studies generally show that androgens upregulate the androgen receptor (AR) in skeletal muscle. For example, in humans given 15 mg of oxandrolone daily for 5 days, the skeletal muscle AR density nearly doubled (15). When exposed to testosterone in vitro, skeletal muscle AR expression increased significantly (16).

In longer-term studies the picture is somewhat different. One study looked at AR expression in androgen treated sedentary rats vs nontreated exercised rats over 8 weeks. To quote from the abstract:

Results show that contractile muscular activity always increased the quantity of receptors whereas the steroid treatment decreased it. Thus for EDL (extensorum digitorum longus) and SOL (soleus) of control trained rats the quantity of receptors was 0.78 and 0.82 fmol/mg protein, respectively, compared to 0.23 and 0.43 fmol/mg protein for sedentary testosterone-treated rats. (17)

In long term studies in humans we get yet a different picture. In work conducted by Sheffield-Moore et. al., (18) older men were supplemented with testosterone so as to bring their testosterone levels into the mid-to-high physiological range. Androgen receptor expression had more than doubled after one month of treatment, yet by 6 months had returned to baseline. This pattern suggested to the authors that cycling androgen replacement much as bodybuilders cycle AAS might be a viable strategy:

This pattern of AR expression raises the possibility that cycling of testosterone administration could produce effects on skeletal muscle analogous to continuous administration. Such a paradigm would be beneficial by administering significantly less testosterone for similar anabolic outcomes, thus minimizing the possibility of side effects.

So despite the passion with which advocates of either AR upregulation or downregulation defend their positions, the research is equivocal. Would exercise combined with AAS maintain increased AR expression, or would the addition of exercise serve to offset the AAS induced AR downregulation observed in the study by Bricout et al? These are just a couple of questions that require further research, and could lead to answers on why exercise combined with AAS use is so much more productive than simply using steroids alone when it comes to building muscle mass.


Before delving into this subject, I’d like to say first and foremost, that in users of anabolic/androgenic steroids (AAS) the first step in combating the development of gynecomastia, or male breast enlargement, is to eliminate the causative agent: the anabolic steroid. Drug-induced gynecomastia almost invariably resolves on its own when a person quits taking the drugs responsible for it, if caught before permanent fibrosis develops. Unfortunately, most AAS users don’t want to employ this simple approach, for obvious reasons, so the foregoing will all be under the assumption that a person wants to prevent or treat gyno and still continue steroid use.

In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia, in lieu of more traditional drugs like tamoxifen.

In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF-1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.

Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (19). Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (20). However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted.

According to research cited in (20), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels:

The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.

So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.

GH and IGF-1 are considered critical to the proliferation of mammary tissue. An excellent review of the role played by these hormones, as well as a general overview of gynecomastia can be found here:

Since elevated GH and IGF-1 are considered important to the anabolic effect of AAS, it would be impractical and counterproductive to attempt to prevent gynecomastia by blocking GH/IGF.

Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF-1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia (21). In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach.

DHT gel (Andractim) or a generic knockoff might help as well. DHT is thought to act as an aromatase inhibitor (23) and perhaps compete directly with estrogen for binding at the estrogen receptor (24). DHT has been used in several case reports and controlled trials to successfully treat gynecomastia. So perhaps a viable strategy would be to combine DHT gel with tamoxifen. I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to succesfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best.

Undoubtedly, due to space limitations, I have left out a number of what are surely many readers’ pet myths. Perhaps in a future issue we can address more of these myths and questionable notions. Feedback is always welcome, and if readers wish to submit their ideas for myths that need to be examined in the future, please feel free to contact Mind & Muscle with your ideas.


(1) Price TM, O’Brien SN, Welter BH, George R, Anandjiwala J, Kilgore M. Am J Obstet Gynecol 1998 Jan;178(1 Pt 1):101-7

(2) Bjorntorp P. Hum Reprod 1997 Oct;12 Suppl 1:21-5

(3) Ramirez ME, McMurry MP, Wiebke GA, Felten KJ, Ren K, Meikle AW, Iverius PH Metabolism 1997 Feb;46(2):179-85

(4) Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD. Metabolism 1993 Apr;42(4):446-50

(5) Tomita T, Yonekura I, Okada T, Hayashi E
Horm Metab Res 1984 Oct;16(10):525-8

(6) Mystkowski P, Seeley RJ, Hahn TM, Baskin DG, Havel PJ, Matsumoto AM, Wilkinson CW, Peacock-Kinzig K, Blake KA, Schwartz MW. J Neurosci 2000 Nov 15;20(22):8637-42

(7) Greer,M. N Engl J Med 244:385, 1951

(8) Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH. N Engl J Med 1975 Oct 2;293(14):681-4

(9) Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN J Clin Endocrinol Metab 1975 Jul;41(1):70-80

(10) Liva SM, Voskuhl RR J Immunol 2001 Aug 15;167(4):2060-7

(11) Ulloa-Aguirre A, Blizzard RM, Garcia-Rubi E, Rogol AD, Link K, Christie CM, Johnson ML, Veldhuis J Clin Endocrinol Metab 1990 Oct;71(4):846-54

(12) Hochman IH, Laron Z Horm Metab Res 1970 Sep;2(5):260-4
(13) Steinetz BG, Giannina T, Butler M, Popick F
Endocrinology 1972 May;90(5):1396-8

(14) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

(15) Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR,
Ferrando AA
J Clin Endocrinol Metab 1999 Aug;84(8):2705-11

(16) Doumit ME, Cook DR, Merkel RA..Endocrinology 1996 Apr;137(4):1385-94

(17) Bricout VA, Germain PS, Serrurier BD, Guezennec CY.Cell Mol Biol (Noisy-le-grand) 1994 May;40(3):291-4

(18) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7

(19) Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F
Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72

(20) Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607

(21) Grunberg SM, Weiss MH, Spitz IM, Ahmadi J, Sadun A, Russell CA, Lucci L, Stevenson LL J Neurosurg 1991 Jun;74(6):861-6

(22) Nomura K, Suzuki H, Saji M, Horiba N, Ujihara M, Tsushima T, Demura H, Shizume K
J Clin Endocrinol Metab 1988 Jan;66(1):230-2

(23) Perel E, Stolee KH, Kharlip L, Blackstein ME, Killinger DW
J Clin Endocrinol Metab 1984 Mar;58(3):467-72

(24) Casey RW, Wilson JD.
J Clin Invest 1984 Dec;74(6):2272-8

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