A Few Common Bodybuilding Myths
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.
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