Estrogen is the second factor people often consider. Especially steroid and prohormone users are often plagues with a serious misunderstanding of estrogen and its effects on adiposity. Most are convinced that estrogen increases fat gain or retards fat loss, when in effect the opposite is true. Estrogens, and especially estradiol (E2), is probably a more effective fat loss aid than is testosterone. Although like testosterone, it may have certain anti-lipolytic effects by increasing a2 adrenoreceptors in specific female patterning (harder to lose fat in thighs and butt).
First of all, estradiol also reduces LPL (6), just like testosterone does, so uptake of fatty acids in adipocytes is reduced. Apart from that, its effects can be divided in three categories. Its effect on insulin-related events, its effects on Growth Hormone and its effects on reducing appetite.
Estradiol can cause a reduction in weight, with only a minimal effect in insulin itself (8), but that does not mean it does not alter the body's reaction to insulin. Estradiol lowers insulin receptor number (9), and in very high doses even actual insulin sensitivity (10). It does so in various ways, not in the least by reducing GLUT4 recruitment and translocation in adipocytes (11), which results in less glucose uptake in fat cells.
This will result in a negative energy balance and a greater activation of lipolysis, right where we want it, in the fat tissue. The effect of estradiol on insulin is quite acute, and clearly evident in the fact that short-term modulation drastically reduces glucose appearance (release) and disappearance (uptake) (12), suggesting a dysfunctional glucose transport system.
The second way in which estradiol may increase fat loss, is its effect on growth hormone (13,14). Unlike testosterone, which stimulates the GH/IGF-1 axis, the effect of estrogen may actually be in reducing systemic (liver-derived) IGF-1 (13), which lowers inhibition of Growth Hormone.
In doing so it obviously reduces the anabolic capacity of the body (which is why we don't use estrogen to build muscle) but increases the fat burning capacity since whole-body IGF-1 is reduced, leading to a reduction in adipogenic markers (since IGF-1 and insulin activate the same cascades) and a concurrent increase in Growth Hormone, leading to further decreases in LPL and upregulation of beta-adrenoreceptors (cfr. Part 4). Estradiol may even reduce IGF-1, while increasing IGFBP-3 (15).
This may in effect be the reason why estradiol does not promote growth, since unbound IGFBP-3, which is under normal circumstances the main carrier or IGF-1 in circulation, has been attributed charachteristics that inhibit growth (16). It acts as a pro-apoptotic agent to activate cysteine proteases, much in the same manner that cortisol or TNFalpha would (cfr. Part 4).
This implies that as long as we are seeing an increase in estradiol accompanied by an equal or larger increase in testosterone, we are reaping positive effects, on both fat loss and muscle retention since testerone increases IGF-1, while estradiol prolongs the half-life and effect of the hormone by increasing IGFBP-3 and IGF1-receptor density (20). Without the testosterone increase, it may however increase muscle loss (and potentially increase fat loss further by enhancing apoptosis of fat cells ?).
A third way in which estradiol helps as a fat loss agent is by reducing appetite. It reduces sensations of hunger via modulation of melanin-concentrating hormone. We have discussed the role of orexigenic (hunger inducing) peptides once or twice previously, specifically NPY.
Obviously NPY isn't the only peptide involved. For instance Agouti-related peptide is also involved, as is melanin-concentrating hormone (MCH). When energy intake is restricted, MCH levels sky-rocket, leading to an increased sense of hunger. Estradiol was able to completely abolish this increase in MCH (17), making it a very potent appetite suppressor during low-calorie diets.
Lastly, estradiol increases both the release of arachiconic acid (18) and the actions of cyclo-oxygenase (19) in certain cell types. This results in a quick and effective increase in several prostaglandins, including PGF2 and PGI2, that are related to lower body-fat levels. Because these effects can be highly varying in different cell types it should not automatically assumed that these events do occur, or that they necessarily contribute to fat loss however.
Estradiol can also prevent muscle loss, once again only in the presence of testosterone, by blocking the low affinity glucocorticoid receptors (22), protecting against the effects of cortisol. Testosterone, or another blocker of the high affinity receptors must be present however, otherwise the blocking of the low affinity receptor would not yield very good results.
On a closing note, as with testosterone, the effects of estradiol are not uniformly positive. It has been shown to enhance PPARgamma (20), so modulation of testosterone/estradiol levels should occur in the presence of a PPARgamma blocker for maximal effects on fat loss. And lastly, estrogen increasing products are often omitted during diets for the simple reason that estradiol increases aldosterone (21), a hormone that increases sodium retention, and as a result water retention.
Excess levels of estrogen often lead to water retention and a puffed up look. While this does not affect fat loss one iota, and can be addressed quickly, in only 1 or 2 days, it does make it difficult for the dieter to judge his progress accurately.
From other BB forum.
You know theory and research is one thing, but always for me the most important and awesome is practice and experience!
