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  1. #1
    MuscleChemistry Registered Member Board Certified MD
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    Default Testosterone Gel, Fat Loss, TRT HRT


    By Dan Gwartney, M.D.

    Topical Testosterone for Fat Loss

    Promising Application

    Say testosterone and the immediate image is a horny male in arrested adolescence or a hulking behemoth, hitting a most-muscular pose in a Speedo®. How often does the word "testosterone" elicit the mental image of a six-pack of abs or just cinching the belt a notch tighter?

    Certainly, there has been research showing that testosterone, DHT, and certain anabolic steroids (AAS) may reduce body fat by inhibiting the differentiation (maturation) of fat cells from precursor stem cells, altering the activity of fat uptake/storage/release enzymes, or by increasing energy expenditure (calorie burning) by promoting lean mass gains.1,2

    An interesting study was published in 2005 in the American Journal of Physiology— Endocrinology and Metabolism, investigating the effect of testosterone and/or growth hormone in hypopituitary adult men (male patients who do not secrete sufficient pituitary hormones to stimulate many hormones, such as testosterone and GH/IGF-1).3 These men were subjected to varying treatment protocols, and one finding of interest to nearly every man was that injectable testosterone enanthate increased energy expenditure (calorie burning) and the percentage of calories burned coming from fatty acids also increased.

    So, even a moderately-supraphysiologic dose of testosterone (250 mg, given as a single shot, with effects measured two weeks later), was able to provide significant changes that could promote fat loss. Bear in mind, this effect was seen in men suffering from low testosterone; the effect was increased when low-dose GH was added to the protocol (1.5 units daily prior to bedtime).

    The investigators later questioned whether the effect was due to changes in fatty acid oxidation in the liver, or if peripheral tissue (e.g., skeletal muscle) was stimulated to preferentially shuttle fatty acids to the mitochondria for energy production. While the motivation for their investigation is uncertain, the difference could be substantial for athletes and bodybuilders.

    First, by tipping the balance toward burning fatty acids in the muscle cells, as opposed to glucose and glycogen (a storage form of glucose, the primary metabolic sugar used for energy by human cells), glycogen stores should be maintained to a greater degree and more readily replenished. Second, burning stored fat within the muscle cell improves insulin sensitivity in that muscle.4 Third, the total daily energy expenditure of the liver is fairly static, but the muscle can dramatically increase calorie-burning through voluntary activity or shivering.

    Obviously, athletes would prefer to be able to influence fat-burning by getting better fat-loss effects through greater efforts. Fourth, the body would be marginally protected from hypoglycemia, by protecting sugar stores in active tissue. Low blood sugar stimulates the release of stress hormones that are catabolic (break down muscle and other tissue). It is important to realize that the liver needs to be protected from inappropriately burning stored sugar (glycogen) to prevent stimulating gluconeogenesis, creating sugar from amino acids and fatty acids. So, the ideal finding would be to see an increase in peripheral (muscle) fat burning with minimal change in the liver's metabolism.

    The logical question at this point is, "How do you expose either the muscles or liver to increases in testosterone in an isolated manner?" A study was devised to explore this very question, published in the journal Clinical Endocrinology.5 The design is fairly ingenious, as it takes advantage of something that has long been viewed as a disadvantage for nearly a century.

    The liver has two different blood supplies. It is not an alien with its own heart, but instead gets blood from two distinctly different circulations. Approximately 75 percent of the hepatic (liver) circulation arises from the mesentery (basically, your guts— stomach, intestines, etc.), arriving via the portal artery.6 Blood in the portal circulation is much different from normal arterial blood, because it is poorly oxygenated, having already passed through other tissue, and has extremely high concentrations of nutrients and drugs coming directly from the gastrointestinal system. The remainder comes from the hepatic artery, which branches (indirectly) off the aorta, and is normally oxygenated, with concentrations of drugs and nutrients being consistent with the remainder of the circulation.

    Thus, drugs taken orally would be exposed to the liver at higher concentrations than that seen in the peripheral circulation (blood flow to the rest of the body). Also, many drugs, including AAS, are metabolized and inactivated, unless they have been chemically altered to protect against oxidation by the cytochrome P450 complexes, or other metabolizing enzymes.7

    Bodybuilders are thinking at this point, "Well, every AAS is protected against the liver's first pass clearance, so it is bull to think the liver can be exposed to elevated testosterone without affecting the muscles." Think for a moment; testosterone has to be alkylated or esterified to a long-chain fatty acid to survive the liver's enzymatic attacks, or bypass the organ. Unmodified testosterone, or crystalline testosterone, will be able to interact with the liver cells via existing genomic and non-genomic mechanism (the usual receptor-based actions), but will be inactivated and cleared prior to reaching the peripheral circulation.7

    It is a bit more difficult to absolutely avoid the liver, and in fact, it is unlikely that any claim can be made to do so. However, using non-oral testosterone administration, particularly a faster-acting form, one can preferentially expose skeletal muscle, which gets 100 percent of its blood supply through the peripheral circulation to testosterone, versus the liver, which acquires only 25 percent of blood supply that way. There are also some regional differences within the liver, but that exceeds the topic of this article. Nonetheless, a fast-acting peripheral source of testosterone would affect the skeletal muscle, with a slighter effect (based on total organ area under the curve exposure) on the liver. To achieve this, a topical testosterone was used.

    In this study, a group of GH and testosterone-deficient men were provided with either daily treatment of a topical testosterone (5 mg), or incremental (increasing schedules) of oral crystalline testosterone, at daily doses of 10, 20, 40, and 80 mg. The patients were followed and measures of testosterone, IGF-1, resting energy expenditure, fatty acid oxidation, thyroid hormone-binding globulin, and sex-hormone-binding globulin were measured.5

    As would be expected, the transdermal testosterone increased serum testosterone in these hypogonadal men; the oral crystalline testosterone had no effect. Only the 80 mg dose of crystalline testosterone affected the binding globulins (a sign of overexposure of the liver to androgens), reducing both. Serum IGF-1, the secondary growth factor produced by both the liver and skeletal muscle, was unchanged.

    Relative to the point of interest, in this group of men who were not involved in exercise as part of the protocol, resting energy expenditure did not change.5 An increase in resting energy expenditure was reported in the 2005 study, possibly due to the administration of a supraphysiologic dose being administered via a long-acting injectable testosterone ester (250 mg).3 Lean mass changes were not measured, and in the short timespan involved, it is unlikely that the increase in serum testosterone to the normal range caused any significant increase in lean mass.

    However, in this group, who were treated very conservatively, fatty acid oxidation increased significantly (~25 percent) in the group when treated with transdermal testosterone, but not with any dose of the oral crystalline testosterone.

    The authors discussed various routes by which testosterone could increase fatty acid oxidation when affecting peripheral tissues, such as fat and muscle. Androgens, such as testosterone, inhibit the uptake of fat into the fat cell by hindering the actions of an enzyme called lipoprotein lipase (LPL).8 Lipoproteins carry fat through the bloodstream, and LPL cuts away the bound fat, so it can be sucked up by the fat cell.

    Adrenergic stimulation of lipolysis (breaking down stored fat through the actions of epinephrine and related drugs— i.e., clenbuterol, ephedrine) is enhanced by testosterone.9 The net result is that fat cells are less likely to store fat and more likely to release it into the circulation to be used as fuel (calorie-burning for cellular energy). They noted that some of the fat-reducing effects of testosterone may be GH-related as testosterone increases GH secretion, but the IGF-1 concentration was unchanged in the men suffering already from GH-deficiency.5

    An interesting part of the discussion related to a study showing oral estrogens reduce whole-body fatty acid oxidation, due to effects of testosterone on the liver, whereas transdermal estrogens had no effect. The original thought was that oral androgens (testosterone) would have the opposite effect, increasing whole-body or liver fatty acid oxidation. As this was not observed, some might wonder if the testosterone was aromatized in the liver, negating any effect; in fact, there is essentially no aromatase activity in the liver, so that would be a non-issue.

    The conclusion of the study was that transdermal testosterone can increase fatty acid oxidation, and that the effect does not involve changes in the liver's metabolic function; this is in agreement with the prior study showing injectable testosterone had a similar effect on substrate utilization (burning fat versus carbohydrates for energy). Despite the logical hypothesis that the effects of testosterone would be liver-based, the converse of the effects of oral estrogen, this study revealed that the actions of testosterone take place in the peripheral tissues, likely involving the fat cells, skeletal muscle, and likely promoting other changes including neuro-endocrine responses.

    What does this mean for the athlete, bodybuilder, or fitness enthusiast? For a young, healthy, adult male, there may be little benefit, as the dose of transdermal testosterone was that used in conservative hormonal replacement protocols. However, the moderately supraphysiologic injectable administration used in the 2005 study did increase both resting energy expenditure and fatty acid oxidation (fat-burning). For the lifter just passing mid-life who may be experiencing changes in body fat, it may provide incentive to have his serum testosterone profile checked by a qualified health care practitioner.


    1. De Pergola G. The adipose tissue metabolism: role of testosterone and dehydroepiandrosterone. Int J Obes Relat Metab Disord, 2000 Jun;24 Suppl 2:S59-63.

    2. Dieudonne MN, Pecquery R, et al. Opposite effects of androgens and estrogens on adipogenesis in rat preadipocytes: evidence for sex and site-related specificities and possible involvement of insulin-like growth factor 1 receptor and peroxisome proliferator-activated receptor gamma2. Endocrinology, 2000 Feb;141(2):649-56.

    3. Gibney J, Wolthers T, et al. Growth hormone and testosterone interact positively to enhance protein and energy metabolism in hypopituitary men. Am J Physiol Endocrinol Metab, 2005 Aug;289(2):E266-71.

    4. Hegarty BD, Furler SM, et al. The role of intramuscular lipid in insulin resistance. Acta Physiol Scand, 2003 Aug;178(4):373-83.

    5. Birzniece V, Meinhardt UJ, et al. Testosterone stimulates extra-hepatic but not hepatic fat oxidation (Fox): comparison of oral and transdermal testosterone administration in hypopituitary men. Clin Endocrinol (Oxf), 2009 Nov;71(5):715-21.

    6. Baron RL, Oliver JH 3rd. Hepatic perfusion: new perspectives at computed tomography. Rays, 1997 Apr-Jun;22(2):270-94.

    7. Galetin A, Houston JB. Intestinal and hepatic metabolic activity of five cytochrome P450 enzymes: impact on prediction of first-pass metabolism. J Pharmacol Exp Ther, 2006 Sep;318(3):1220-9.

    8. Ramirez ME, McMurry MP, et al. Evidence for sex steroid inhibition of lipoprotein lipase in men: comparison of abdominal and femoral adipose tissue. Metabolism, 1997 Feb;46(2):179-85.

    9. Xu XF, De Pergola G, et al. Testosterone increases lipolysis and the number of beta-adrenoceptors in male rat adipocytes. Endocrinology, 1991 Jan;128(1):379-82.
    All statements from Get_Swole are strictly fictional none of the statements should be taken seriously or literally.

  2. #2
    Presser's Avatar
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    Fuck man its not that it was to long of an article but i had a hard time understanding half of it until i re-read it like 2-3 times to comprehend it,lol, Maybe its me and Im a dummy but alot of that shit went over my head

  3. #3
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    copied to Articles forum
    Author: Ben Presser
    Ph.D. P.E.D. Kinesiology
    Intramuscular Injection Certified

    MuscleChemistry Store

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