Men don’t need female hormones for fat loss

There has been a resurgence of estro-philes (estrogen lovers) lately who have been actively parading the internet from nook to cranny, aggressively throwing studies around to try and prove the essentially of estrogen for fat loss. Like really, let’s not get hyper-emotional about this. 

I’m not trying to say estrogen is not needed at all, there is a reason why men do express aromatase. We do need some. And by that I don’t mean we need a lot. We aren’t women, so let’s just get some perspective for a moment.

The purpose of this article is to shed light on how much estrogen is actually needed; what the optimal level is and should be in order for us as men to stay healthy and manly.

Let’s discuss a few side effects of elevated estrogen and how it’s actually involved in fat gain, obesity and diabetes.

#1 Estrogen promotes fatty acid synthase

Fatty acid synthase (FAS) creates fats from glucose and elongates other shorter chain fats, such as butyrate, the MCTs and so on (R).

FAS is usually not that active, but when boosted by elevated estrogen and hyperinsulinemia, it contributes to elevated free fatty acids and triglycerides in the blood; all of which are elevated in obesity, cancer, diabetes, etc.

Estrogen also causes the retention of iron which, when in excess, also promotes lipogenesis and oxidative stress. People with elevated iron usually have elevated cholesterol as well as triglycerides and inflammation.

#2 Estrogen promotes adipogenesis

Estrogen is a known carcinogen (cancer promoter) which messes with cellular function and promotes excessive growth (proliferation).

One such form of growth is adipogenesis (R), which is the creation of new fat cells. The increased amount of fat cells release more estrogen and leptin in turn, both of which synergistically promote the aromatase.

#3 Estrogen promotes lipolysis

Estrogen promotes lipolysis and estrogen supplementation leads to elevated free fatty acids (FFAs) in the blood.

As mentioned above, elevated FFAs interfere with proper glucose oxidation and promotes insulin resistance.

Estrogen is thought to upregulate the anti-lipolytic α2A-adrenergic receptor expression in subcutaneous but not visceral adipose tissue, which leads to increased fat storage in the subcutaneous fat stores and less in visceral fat (R).

Men, who have less estrogen than women, have less subcutaneous fat, but are prone to accumulation of visceral fat, but that is due to elevated cortisol and low androgens, not due to low estrogen.

Additionally, DHT supplementation improves insulin sensitivity while lowering estrogen to very low levels (R). DHT was even more potent than testosterone supplementation in this regard.

Some might say that there are lots of studies that show that estrogen improves insulin sensitivity. Yes, they are all short term. 6 months to a year or 2 is short term. But if you look at it in the long run, estrogen promotes insulin resistance.

As shown here (R):

“…estrogen use was associated with lower fasting glucose (0.2 mmol/l lower) but higher 2-h glucose levels (0.4 mmol/l higher) compared with never users. It was not significantly associated with the risk of type 2 diabetes compared with past and never users, based on American Diabetes Association or World Health Organization definitions of diabetes or on only a 2-h glucose level ≥11.1 mmol/l. However, the risk of type 2 diabetes increased with increasing duration of estrogen use among current users, with an odds ratio of 1.10 per year of use (95% CI: 1.01–1.19).”

#4 Estrogen increases cortisol

Estrogen stimulates the hypothalamic-pituitary-adrenal (HPA) axis. Having high estrogen will lead to chronically elevated cortisol (which is catabolic), it will slow the metabolism, create visceral fat, induce insulin resistance, lower thyroid and steroidogenesis, etc.

Estrogen also reduces the clearance time of cortisol, causing cortisol to be elevated for longer (R).


#5 Estrogen and the metabolic rate

Short term estrogen supplementation in the presence of low estrogen does not restore the metabolic rate (R), however, androgen supplementation does (R).

Blood levels of estrogen are not an accurate indication of tissue estrogen, as the aromatase is expressed inside the tissue and not outside. So, although blood levels of estrogen in men are low compared to women, local concentrations in the tissue might be much higher and physiologically relevant at the site of production and/or action, where they may reach micromolar concentrations. Which is a lot!

Moreover, increased estrogen levels can create a hypogonadal state in men, because it potently suppresses steroidogenesis. Estrogen is one of the most potent suppressors of testosterone synthesis.

A testosterone deficiency, due to elevated estrogen, may aggravate the development of obesity and hyperinsulinemia, which, in turn, will suppress testicular androgen synthesis even further, resulting in a vicious cycle (R).

If estrogen was anti-obesity, all that estrogen created by the fat tissue would have made people lean. Which is clearly not the case.

#6 Estrogen increases leptin

Leptin has always been thought to be a good hormone which stimulates the metabolism and steroidogenesis while reducing appetite.

However, estrogen stimulates fat cell production and fat cells release leptin. Estrogen and leptin synergistically upregulate 11β-hydroxysteroid dehydrogenase type 1 (the enzyme that converts inactive cortisone into active cortisol). This leads to significantly increased intracellular cortisol, which upregulates the aromatase some 9-fold (R).

Under stress, the increased cortisol and leptin output increases compensatory eating and the desire to increasingly consume poor quality, high glycaemic ‘‘foods’’, only to increase insulin production and further up-regulate the aromatase another 6-fold (R).

Additionally, hyperleptinemia and hyperinsulinemia potentiate the effect of estrogen on the receptor, strengthening its effects (R).


#7 Estrogen and insulin secretion

Estrogen and its metabolite stimulating insulin secretion, with 2-Hydroxyestrone being the most abundant and efficacious endogenous estrogen metabolite (R). 

Elevated estrogen, free fatty acids, cortisol, insulin and leptin leads to diabetes, fat gain and cancer. Elevated estrogen and insulin synergistically further promote the aromatase in a feed forward loop.

Some people think that there is an estrogen deficiency in conditions of excess hair growth, or during diabetes, but in fact, the elevated insulin stimulate testosterone production and its conversion to DHT and estrogen itself. So these conditions is not caused by a “deficiency”, but rather an excess of estrogen. Keep in mind that estrogen, as well as cortisol, can be mostly intracellular, so blood tests might reflect a deficiency, when in fact the tissue in overflowing with estrogen and cortisol. 

Also, most doctor test only estradiol and in some cases estrone, when in fact there are 15 different metabolites (or more) of estrogen. How can you get an accurate measure of the total estrogenic burden on the body, or conclude you have low estrogen, when only one metabolite is measured?

Research indicates that a deficiency in the enzyme dopamine β-hydroxylase, which converts dopamine to norepinephrine, leads to hyperinsulinemia (R).

So before dismissing the fact that estrogen is not that crucial, there are many other possible explanations as well. 



Estrogen, in excess, promotes insulin resistance and fat gain, while triggering the stress response, sending the body into a catabolic mess.

Mice given estrogen through their life initially gained more weight than the control group, but later in life ended up much more catabolic with increased late-life frailty (R).
This most likely happened as a result of androgens dropping too low and elevated cortisol being unopposed.

A human study showed that diabetes and estrogen are correlated. Here is a quote from the study (R):

“Obesity, increased fat, elevated BMI and larger hip circumferences are all closely linked to raised oestradiol levels and to the incidence of type 2 diabetes, such that women with low oestradiol levels have 80% less risk of developing type 2 diabetes, and men have 52% less risk.”

Estrogen is a powerful inducer of serotonin, which is known to slow the metabolism, inhibit steroidogenesis and promote obesity, diabetes, and a whole host of other conditions.

Now I can already hear a few people screaming: “Gimme the human studies bro!!!”.

Apart from the few mentioned above, here are a few more:

From this study (R):

“E2 (estradiol) between 14.0 and 17.4 pg/ml is associated with the best body composition, i.e., lowest total and % FM and highest % FFM”.

For those who don’t know, 14-17pg/mL is on the low side of the range, with the normal range being 10-40 pg/mL.

And in this study (R), the researchers gave one group of men TRT and the other TRT plus and aromatase inhibitor (AI).

Surprisingly (or was it), only the TRT + AI group gained muscle mass, whereas both groups lost the same amount of fat.

Now the AI didn’t crush estrogen of course, that’s not the point. The point is that high estrogen is not needed for fat loss.

Lastly, men who supplemented DHT for a period of time crushed their estrogen and they experienced no increase in fat gain, but actually experienced fat loss (R, R, R). Again, you don’t need lots of estrogen to get fat loss.
You can be optimally healthy and have the benefit of fat loss with low estrogen, but increasing estrogen will only cause a plethora of side effects, namely frailty, cancer, degeneration, fibrosis etc. 

I don’t think using DHT alone to crush your own steroidogenesis is a good idea, but if you want to take DHT, use it with a little pregnenolone, DHEA, testosterone and maybe a little progesterone as well, because these hormones are very important and are significantly lowered when your own steroidogenesis shuts down.

As always, thanks so much for reading my article.
If you found it helpful and insightful please like and share so others can also benefit from this information and feel free to leave a comment down below if you have any questions for me.

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