Estrogen and Fat: A review and new avenues

It has been commonly assumed that estrogen plays at least some role in the retention of body fat in males, particularly when attempting to lean out severely (i.e., contest prep). Indeed, Mr. Don Alessi has made the claim that by assessing one’s fat retentive areas one can determine if their fat profile is more associated with estrogenic fat or insulin resistence. For quite some time, fat topography, and more specifically adipose tissue endocrinology has been a pursuit of mine to determine just how much and to what extent certain areas of fat on the body are related to various endocrinological nuances or disturbances.

As such, I wanted to throw out what appears to be the latest reserach on estrogen and fat, and see if anecdotally, there are different reports.

Estrogenic fat areas are commonly assummed (perhaps incorrectly) to be such areas as behind the tricep, around the lower back, and around the navel (in males). In addition, it is well known that gynecomastia is directly estrogen related. This common assumption has lead to the use of anti-e’s and anti-aromatase formulas following cycles and during diet phases to allow for the prevention or reduction of what is believed to be estrogenic fat.

Ken Stark was the first to point out a study that seemingly showed that treatment of male-female transexuals with estradiol resuled in increased subcutaneous fat on the original male subjects (Elbers et al., 1999). However, a recent comprehensive review of the role of estrogen and estrogen receptor alpha in male adipose tissue (Cooke et al., 2001) suggests that estrogen is higly implicated in regulating white adipose tissue in male, and that males who lack both ER alpha and beta receptors show increased fat gain/retention. They further postulate that since this is not due to hyperphagia (the fat gain) that estrogen acts on the male body in a myriad of ways, primary amongst which one is controlling basal metabolis rate. They also offer the following seemingly surprising points:

1)…"Although both human and animal studies suggest estrogen may affect glucose tolerance and insulin resistance in females by direct actions on adipocytes to increase insulin receptor expression (references)…Estrogen also appears to act on WAT (White Adipose Tissue) through alteration of leptin production and hypothalamic leptin expression

2)…"The altered glucose tolerance and insulin resistance in the ERalpha knockout mice could be a major factor in the etiology of the increased WAT in both sexes. The insulin resistance and impaired glucose tolerance, as well as the increase in male WAT, in mice lacking ERalpha was similar to those reported for the aromatase knockout mouse and the insulin resistance and glucose tolerance findings in alpha ERKO and ArKO mice parallel observations in humans lacking ERalpha or aromatase.

3)**"There has been intense recent interest in the potential benefits of phytoestrogens, estrogenic compounds found in soybeans and other plants. These compounds may also be beneficial in regulating WAT in humans…The primary phytogestrogen in soy is the isoflavone genisten…genisten and some other isoflavones act as weak estrogens…could the ability of genisten and other phytoestrogens to signal through ERalpha be one contributor to the lower obesity levels seen in populations that consume higher amounts of these compounds? Nogowski et al. (1988) have shown that genisten can act on adipocytes to strongly depress both their basal and insulin-induced lipid synthesis and that genisten can have effects on triglyceride and free fatty acid concentrations in the serum.

Returning to the original study pointed out by K. Stark, the male-female transexuals were treated with both estradiol and an anti-androgen. Perhaps it was the anti-androgen, not the estradiol that allowed for the increase in subcutaneous body fat. After all, T is a major regulator of subcutaneous body fat, and its reduction would most likely act to increase the turnover of that particular type of fat. Furthermore, it has been demonstrated that animals treated with estrogens such as estradiol or the synthetic estrogen zeranol have both decreased fat and incrased lean muscle mass.

In conclusion, I might state that I continue to be confused by the role of E in what may be subcutaneous body fat retention and patterning in males. Perhaps there is none, although anecdotal reports of cycles of clomid and other anti aromatases and estrogens indicate that they greatly reduce fat, particularly around the umbilical region. Then again, this may be due to the fact that renal sensitivity to AVP may be lower during E due to intrarenal effects on water and sodium as estrogen/progesterone treatment has been shown to increase sodium retention and renin-angiotensin-aldosterone stimulation.


#3 is a bit… perplexing. :slight_smile:

wow, there was lotsa big words in that one!
its far to late for any of that to sink in, did it pretty much say, V68, we still dont know how E affects fat loss?

This post falls more under the minutia area although it is something that interests me greatly…when shedding that last bit of body fat, often we talk of estrogenic fat being the hardest to rid (personally, a tiny bit of a roll right around the navel which seems more water retention than fat, as it is not as noticeable in the am).

At any rate, it appears estrogen does not lead to fat retention necessarily and that it may actually assist in the prevention of fat gain. However, estrogen has been shown to increase both AVP and fluid retention (mainly via sodium pathways) which would result in subcutaneous water retention giving that sometimes soft and puffy “sponge-like” surface fat.


cheer bro, this reading thing is new to me, i normally just post without taking in much of what anyone has said :wink:
HAs anyone that you know of tried M on the last stretch of a diet and noticed anything cool?


Thanks for this post. I’m very interested in this subject area as well, I just don’t seem to ever have the time to dive deep enough into research to find these ‘morsels’.

Anyway, I also have that fat store just beneath my umbilicus that appears to be lowest in the A.M., just after waking. I had always assumed this had little to do with estrogen. You’re suggesting different, which does make some sense to me.

I recently have been cutting my bodyfat down. Summer seems to lend itself to that goal here in Toronto due to the longer days and hotter weather. I digress. I’ve added M to the end of my first ‘wave’ of fat loss and I’ve found that the decrease in fat has been both much more rapid and more noticeable in the supra-iliac area.

Nevertheless, the fat deposit around and below the umbilicus is the most difficult to get rid of. I’ve toyed with the idea of topical Yohimbe. What are your thoughts? Yohimbe has an effect on the conversion of Brown Adipocytes to White and a faster oxidation of WAT, correct?

Yohimbe does not change or convert brown adipocytes to white adipocytes. Yohimbe, more particularly the alkaloid yohimbine binds to the A2 receptors and antagonizes them, thus shutting them off so to speak. This allows them to be mobilized (the fat cells of the alpha 2 variety) more easily. They are the hardest to rid, becuase unlike beta receptors, they are not moblized when agonized or “turned on” by sympathetic responses (i.e., epinephrine, norepinephrine etc.)

In regards to estrogen however, there must be a different issue. Interestingly, estrogen receptors on adipose tissue appear to be of the alpha variety. Perhaps there is an interaction?

One possible notion is that becuase a half-maximal dosage of insulin is so anti-lypolytic in vitro, perhaps this is the case in situ. In other words, it would require a drastic reduction in insulin (i’m talking not just less carbs, but less food sources that spike insulin such as certain proteins and fats) in order to rid that umbilical fat. Any insulin response at all would make it harder to rid this fat it would seem.

This is one possibility. The other is that clearly this umbilical region is somewhat water retention, as noted by the lowered retention in most mornings. As noted above, this may be more due to estrogens role in sodium retention as opposed to fat retention. I want to make the statement here to that when I speak of umbilical fat, I am assumming the person is already highly shredded for the most part…certainly at 7% or lower.


Not highly scientific, but maybe of interest -
I’m a woman with PCOS. As such, I overproduce androgens. Although my T levels are, according to my doctor, roughly half that of a healthy man my age (31), they are far higher than an average woman’s. To correct my hormonal imbalance, I have been taking an anti-androgen, a synthetic estrogen, and every 3 or 4 months, a two weeks cycle of progesterone to induce menstruation. Having heard repeatedly that estrogen was the devil when it comes to fat loss, as part of my ongoing fat war I decided to stop my hormone replacement. Although I changed nothing else but this one factor, I have since seen measurable increases in leanness, contributed to by both fat loss and increased muscle mass, both happening more rapidly than my previous efforts. In the past 18 months I’ve lost 120 lbs of fat mass and gained 55 lbs of lean mass. After my initial massive fat loss, since I began weight training, my weight has been stable, with fat lost and lm gained balancing out. Since I stopped my HRT, I have lost 6.5 lbs of fat and gained 12 lbs of muscle. Although this doesn’t in any way solve the relationship between fat and estrogen, it does show a definite link.

did you discontinue only the synthetic E or did you also discontinue the anti-androgen…that is a key question, as we are going to need to separate one effect from another.


Vain - I discontinued both simultaneously, so don’t know which one the effect was from. Sorry. I suppose for the sake of science I could try just taking one or the other for a while and see what kind of results I get. Of course, a sample group of one doesn’t give you much proof, but would still be interesting. As a teacher I’m off for the next 2 months anyway, so I’m up for experiments.

Absolutely. You could be a case study. When you discontinue your cycles or titrate your dosages, make sure that if you drop E to keep the anti-androgen or vice versa…I think this is the key here to determine whether its E or the anti-andro that is causing the issues I have pointed out. It could be an interaction but I doubt this.


Vain - You’re the scientist here, not me, but I’m willing to be a guinea pig. Any preference which I should take solo first, for how long, any other protocols to go along with this? Both pills are enterically coated, time release things, which makes modifying the dosage difficult. I suppose it has to be an all or nothing thing. Anyway, you’re one of the body manipulation gurus here, and my body is in continued need of manipulation, so I’m interested in an experiment.

if possible, drop the anti-androgen and keep the E for a bit.
I would like to see your thoughts after some time of this protocol.

As long, of course, there are no contraindications with doing this.

I would like to see the effect of E en absentia of the anti-androgen.