Testosterone: A brief overview of the hormones functions

Testosterone: A brief overview of the hormones functions

Testosterone is an androgenic[g1] Anabolic[g2] steroid hormone[g3] produced in the body.

Men produce testosterone in the testes and in the adrenals[g4]

In women, testosterone is produced in small amounts directly from adrenals, the ovaries, and in large part from the conversion of androstenedione[g5][1] via the 17β[g6]-hydroxysteroid dehydrogenase enzyme or from DHEA via the 3β-HSD enzyme.[2][4]

Testosterone production is tightly regulated through a myriad of systems of checks and balances throughout the human body.

Alongside the bodies’ production, testosterone comes in a variety of preparations for medical use like hormone replacement therapy packages as well.

Throughout this article, I’ll try to delve into as many relevant systems and functions that occur in the context of general health/wellbeing/ and briefly on some performance enhancement aspects as seen fit.

This is NOT meant to be incredibly exhaustive, but to give a comprehensive BASELINE of information to branch out and start your independent research on the matter.

Without further ado, let’s get into it.

Testosterone production

Though testosterone is made by a few different pathways for each of the sexes, the starting process to signal testosterone is actually the same for both men and women.

Through the HPG[g7] Axis, the stimulation of GnRH[g8] causes the let down of LH[g9] and FSH.[g10]

Secretion of GnRH is different in women as opposed to men.
The menstrual cycle[g11] leads to a change from “pulsatile”[g12] releases of GnRH to “Surges”[g13] of the hormone during the pre-ovulatory phase.[g14][3]

This in turn leads to a shift in the total production of LH and FSH in women.

For men, the stimulation of LH will signal the Leydig cells[g15] in the testes to undergo the metabolism of cholesterol into testosterone.

Here’s how this is done.

Cholesterol will be turned into pregnenolone by a single CYP450 group enzyme[g16]
CYP11A1, which essentially just cleaves off one of the side chains of cholesterol.

from here, pregnenolone undergoes hydroxylation into 17-OH-pregnenolone via the 17a-hydroxylase enzyme before being turned into DHEA by another CYP enzyme “CYP17A1.”

Also of note, pregnenolone can also be converted into progesterone by first undergoing 3β-HSD enzyme conversion before undergoing the same two enzyme reactions above.
As a result, progesterone will turn into 17-OH-progesterone and then subsequently androstenedione respectively.

It is then turned into testosterone via one of the β-HSD activities depending on what metabolite is produced.

In women, they will undergo a relatively similar process through their ovaries, by the ovarian hilus cells[g17] which mimic male Leydig cells.

However; it is important to note that women will produce MUCH LESS testosterone than men in general.

Alongside this, women see also equal parts of adrenal androgen production and ovarian production of androgens that are later converted into testosterone.

This is a stark contrast to men who seem to have a practically negligible amount of adrenal androgen production.

Also, it’s worthy to note that when adrenal androgens are being produced there is a slight shift in the preference for pathways in which the hormones are produced.
Progesterone is primarily created in the ovaries of women, whereas adrenal androgens produced in the zona reticularis have an environment that favors the production of DHEA.

This is due to the CYB5A gene, found in the adrenals causing preferential activation of the CYP17A1 enzyme to create DHEA.

Lastly, it is important to note that adrenal androgens are almost completely unbound.

Meaning that they are freely circulating throughout the body and able to act upon receptors without needing to be linked to a transporter protein to circulate.

The adrenal androgens that are bound don’t typically bind to SHBG[g18] like testosterone or other sex hormones do. (only ~5% of those androgens bind to SHBG with an even smaller portion binding to albumin or small transporter proteins [g19] instead.)[5]


Testosterone is produced from cholesterol and is signaled to be created by a few different pathways and a few different systems.

As a result, there are a LOT of co-factors involved with elevated or suppressed testosterone levels in both men and women.

The pathways and enzymes are listed so that you can research each of them individually and see if there is anything in your diet/lifestyle that triggers a specific enzyme or pathway to be inactive or suppressed. This DEEP level of examination would probably only be necessary for individuals who are against the administration of synthetic androgens, though.

if you’re wondering “Why do I have low testosterone?” Look into some of these pathways and ask yourself is there something you’re doing that could disrupt one of these?
Things like

  • Taking opiods
  • Drinking alchohol
  • Chronic cannabis use
  • Chronic stress
  • Hormonal birth control
  • Poor dieting
  • Poor sleep

Can be culprits to sub-optimal hormone profiles.

Testosterone transportation.

Testosterone has hundreds of practical applications and impacts thousands of complex interactions in the body, but it needs to find its way into circulation.

For the sake of brevity, I’ll focus this section of the discussion on how circulates and to a minor extent how it regulates its biological presence before we talk about its implications.

Testosterone its self is found in two main forms in our blood, “free” and “bound”.

Free vs bound are used to describe the transport systems accompanying the hormone

Free” testosterone is the hormone that is circulating throughout the body and can be used as a chemical messenger at any point in time when it is necessary.

Bound” testosterone is testosterone that is linked to a transporter protein that will allow it to circulate at a higher concentration than what is otherwise possible.

Testosterone is bound primarily by SHBG (roughly 66% of testosterone is SHBG bound in normal physiological conditions) with the rest being linked to albumin, and other small proteins.

There is a train of thought that “bound” testosterone is biologically inert and therefore not of significant importance, however; this has been proven to not necessarily be the case. [6][7][8]

It seems that there are specific receptors for SHBG bound hormones that allow them to exert biologically relevant effects on the body at the site, meaning that there is still some utility in these bound hormones even if it’s not entirely understood as of yet.

The extent to which the effects that testosterone itself can affect androgen receptors or perform its function indefinitely face an impact, but it’s not entirely useless to examine the “bound” testosterones functionality in the overall context of your body.

Having only information about “free testosterone” can leave questions as to whether or not you could optimize further by having a reduction in SHBG through lifestyle interventions.

The necessity for both free circulating and bound testosterone is important to maintain a sensitivity to receptors and to prevent their excessive and potentially unnecessary stimulation of these sites inside of the body. (like leaving a light switch on 24/7 vs turning it on and off when you need to use it to prevent a burnt-out light bulb.)

Also, checking to see if there is a heightened level of SHBG in tandem with below-average total testosterone and even lower free testosterone could be indicative of health problems.

Though in the context of performance enhancement, it is FAR more favorable to examine SOLELY the benefits of free testosterone as this is the portion that can most easily signal for protein expression in the muscle cells to promote anabolism and signal to down-regulate the catabolism of muscle.

An overview of testosterone’s interactions with the body

This is the section that I’m sure most of you are here for.
The portion on how testosterone interacts inside the body and leads to virilization or enhanced muscle growth.
I’d like to take a second to outline that while androgenic anabolic steroids CAN promote the development of muscle growth and could potentially lead to masculinization,
there’s a dose-dependent responsible that is different for EVERYBODY.
Just because someone sees results at a higher or lower number, it doesn’t mean that you’ll see the exact same results.
Muscular growth, virilization, and pronounced effects of testosterone have a myriad of underlying factors that will lead to changes in the gradient of doses necessary for everyone.
I’m going to section this part out into each group I think you may end up on here through different avenues of googling or searching.

So the section on muscle growth, heart, liver, prostate, masculinization through the androgens, etc will be sub-headings letting you skip to your favorite part.

Testosterone and Muscle Tissue

Testosterone usage for the accrual of muscle mass is notorious.
(See… featured image)

The association between heavily muscular individuals and steroid users is relatively commonplace and isn’t defined solely by professional athletes or bodybuilders anymore.

(This is due to the prevalence of testosterone and other steroids being made widely available.
Either through hormone replacement therapy clinics, a higher frequency of prescription by physicians, or from online black markets.)

Testosterone is theorized to affect muscular development by being able to increase muscle protein synthesis as well as preventing muscle breakdown through a few different mechanisms of action.

Most notably through its role in stimulating androgen receptors in the muscles and allowing for gene transcription factors to assist in muscle accrual.

Testosterone will illicit the upregulation[g20] of RNA transcription factors that promote higher levels of protein synthesis, muscle anabolism as well as incur a localized effect of IGF1[g21] that makes the muscle tissue grow faster.

It’s thought that testosterone can activate muscle satellite cell[g22] hyperplasia. This hyperplasia is perhaps responsible for leading to the overall development of more muscle mass through hypertrophy of newly created AND previously acquired muscle.[11,12,13]

There is one thing I’d like to point out:

People have this idea of the gradient between muscle accrual AND retention based on the gradient of testosterone levels:
(such as too low of testosterone levels making muscle accrual more difficult and elevated testosterone creating a more favorable environment.)

This dynamic does NOT necessarily favor increasing the amount of testosterone being exogenously administered as a “take more to gain more” spectrum of application that can go without risks or adverse effects.

Although there IS a dose-dependent increase in body mass associated with increases in testosterone, there is always a rate of diminishing returns and it’s compounded by innumerable co-founding factors.


Just like your arms and legs, the heart is a muscle!
though it’s not a skeletal muscle, it’s actually got its own category as a “Cardiac” muscle.

Pretty much, unlike skeletal muscle that you can choose to move, your heart (luckily) never stops beating and does so involuntarily.

Now, given that we know contracting and exercising your biceps with testosterone in your system can lead to them getting bigger, we can see what can potentially happen to your heart.

The same way your biceps can grow, so can your heart, which can be dangerous.

LVH (left ventricular hypertrophy) is when your heart’s main chamber for blood begins to grow and thicken.

This is incredibly dangerous as it can lead to numerous complications if left untreated.

you can begin to have restricted blood flow, poor oxygen capacity to the heart, and even have a stroke/ heart attack as a result of improper function.

Now, I MUST note, this is typically not SOLELY due to testosterone in our body.

Rather this is a potential side effect of supraphysiological amounts of free circulating testosterone in tandem with poor dieting, high blood pressure, and excessive stressors on the heart (like being overweight/obese)

High amounts of testosterone can also cause issues with lipids that can lead to heart problems.

AAS use can lead to reduced HDL and increased LDL cholesterol levels through the hepatic stressors that I’ll be touching on briefly.

Alongside this, androgens will lead to sodium retention, which in turn lead to higher blood pressure and can contribute to LVH that we talked about earlier

Conversely, it’s important to note that having LOW testosterone levels also carries a significant burden on your cardiac health. [14]

This is more so due to the associations with lower muscle mass and increased amounts of visceral (abdominal fat) which leads to complications like obesity and types 2 diabetes that interplay with co-factors relating to heart disease.

Considering that both ends could potentially increase the risk for harm, it seems the most rational decision is to always be mindful of your cardiac health and to err on the side of caution.

The Gonads and Testosterone

When it comes to testosterone and the gonads we have covered a decent bit of ground on its production and interactions.
Alongside this, it’s easy to imagine the impact of exogenous or otherwise elevated/underwhelming amounts of testosterone has on the feedback systems for the gonads.

(The shutdown of endogenous production when outside excessive testosterone is supplied, or the encouragement of production when a GNRH agonist or LH is introduced. For instance.)

So instead, I’ll focus on the main concerns for both men and women here briefly with elevated testosterone.

The most common incident of elevated androgens and testosterone in women is present in a condition called “PCOS” or “Polycystic ovary syndrome.”

PCOS causes hyper-androgenic activity in the female body.
It’s responsible for the excessive production of pre-androgens, androgens, and testosterone, leading to some potentially deleterious outcomes.

This disease is not solely an issue where women are suddenly appearing more masculine due to virilization.

The impact of PCOS can lead to infertility, amenorrhea, insulin resistance, (which can lead to gestational diabetes), depression, irritability, and if left untreated, things like uterine cancer/ high likelihood of miscarriages can occur. [15]

It’s worth mentioning, however; outside of PCOS these issues alongside secondary amenorrhea are still a very serious concern for female use of exogenous testosterone.

This is due to the interplay between feedback systems in the body leading to a dysregulation of the normal menstrual cycle.

In men, elevated testosterone can lead to infertility as well, through the same mechanisms.

Alongside this, the reduction in the size of the testes can occur as a result of the atrophy and loss of testicular germ and Leydig cells.

As mentioned earlier, there is a concern for infertility in men with excessive androgenic anabolic steroid use and the scarring that can occur as a result.
It is to be noted though, AAS-induced hypogonadism can most often be reversed after the cessation of exogenous use alongside the potential intervention including agents like GnRH agonists or by following the administration of a SERM [g25] in tandem with other forms of drug interventions.

The liver

The metabolism of steroid hormones in both your liver and kidney can NOT be understated.

In fact, these two are probably the most hardworking organs in your entire body.

Your liver not only deals with alcohol but also drugs and steroid biosynthesis.

In the beginning, your liver will either utilize the cholesterol inside of your body or make its own through an incredibly energy-expensive process called “cholesterolgenesis

Explaining the process of internal production from start to finish would add ATLEAST 3000 words to this article.

To save me from going insane and to also make this article UNDER 8000 words, please refer to THIS article if you would like more information on the entire process of converting things like squalene into cholesterol before converting cholesterol into steroid hormones like testosterone through the aforementioned processes above.

Once the cholesterol is produced/utilized, it will then send out the product to the body where steroid hormone interactions occur.
(though we’ll be almost immediately returning to the liver)

After testosterone is produced, the metabolism process of the steroid begins here as well.
The production of steroid metabolites like DHT through 5α-Reduction enzyme type 1 will occur in the liver.
Alongside this, estrogen metabolism and other forms of steroid hormones/drugs will be detoxified or need to be processed by the liver.

One important thing to note is that low testosterone is associated with increased levels of Visceral fat.

Visceral fat is MUCH more concerning the regular adipose tissue. Fat stored around your arms might be unsightly, but this form found in your abdomen is the fat that is surrounding your organs and leads to an unbelievably high amount of health complications. [21]

A few of these complications are impairment of glucose regulation, lipid metabolism, and things like “Non-Alcoholic Fatty Liver Disease,”[22] [23]

For quick reference

Fatty Liver Disease (also sometimes interchangeably called steatosis in older literature) is an ailment in which the build-up of fats inside of the liver exceeds the normal healthy allotment that typically compromises the organ.

Over time the exacerbation of this leads to high levels of inflation and potentially scarring and fibrosis, before eventually causing a shut-down and death of the organ altogether if intervention is not introduced in time before a transplant or the progression becomes worse enough.

One more thing to quickly note is that there IS a difference between NAFLD and Non-Alcoholic Steatohepatitis or (NASH) [24]

NASH is a progressively WORSE form of NAFLD in which there is damage done to the liver and concurrent high levels of inflammation, the interchangeable use between those just seems to be commonplace for the average joe.

Alongside low testosterone potentially harming the liver, having a liver in poor health can cause lower testosterone levels.

We know the liver produces SHBG and is responsible for metabolizing the sex hormones.

If there is an issue with the livers’ ability to function, like say we develop cirrhosis of the liver, it’s been found that testosterone levels can plummet as much as 90% in men.

Why is that? because your liver is already under enormous strain to just survive.

The lack of healthy normal function to fight off inflammation means that the rate of non-necessary functions like producing steroid hormones such as testosterone will become impaired.

Speaking of testosterone and impaired bodily function, this next section might be a little hard for some people to come to terms with.

Testosterone is bad for your Kidneys. Plain and Simple.

Much like your liver, the kidney plays an incredible role in homeostasis.

your kidney is a HIGHLY complex filtration system that has to put up with a lot of work.

The kidneys have a filtration system called the glomerulus, they’re a bunch of capillaries at the end of the kidney that prevents a LOT of junk from entering our body.

Think of it as a fine-mesh sieve that’s preventing pulp from getting into your orange juice.

Over time, if you push too hard you could eventually damage things and end up getting pulp that leaks into your orange juice, or for other recipes, you can get big unwanted chunks ruining your recipes.

Now, instead of tearing a hole in a sieve, you can cause “Glomerulosclerosis”

which means you’ve caused scarring on the filtration system that can lead to things like fluid build-up in your extremities, protein leaking into your urine, and high cholesterol [24]

17β-Estradiol (also known as E2) is found to be protective against glomerulosclerosis, whereas testosterone is found to be damaging to the glomerulus.

It was thought to be the case that the protective effects of E2 were a result of the prevention of apoptosis (cell death) of the podocytes[g26] inside of the kidneys [25]

Whereas the introduction of any level of testosterone (normal endogenous levels, and especially in the instances of exogenous intervention) would elicit a response by the androgen receptor to aggravate and damage the kidneys’ filtration system via the inverse reaction estrogen has (testosterone and androgen receptor activation encourages the apoptosis of podocytes.)

Why is this the case?
Because androgens are damaging to kidney health.[27]

The above case is an example of kidney damage caused by steroid use, BUT this is not solely a matter of supraphysiological levels of testosterone and other highly androgenic compounds causing renal damage.

This could occur from the introduction of “therapeutic” amounts of exogenous testosterone that would put you in a range higher than what you could reasonably handle while still being in the reference range.

As noted in the citation above this section, estrogen is protective in terms of kidney health. Luckily the introduction of testosterone in any capacity means that it will also become aromatized into estrogen as well.

This means that there is still a reasonable level of safety for the introduction of TRT/HRT depending on one’s necessity.

If you and your doctor find that the increase in quality of life is worthwhile, and you don’t have some kidney ailments that are preexisting it could be a reasonable addition, but not a lot of discussion about kidneys and testosterone is made very popular.

This is incredibly pertinent to note for anyone with pre-existing kidney issues to consider before trying to elevate their testosterone, as there may be a necessity for other things like ACE inhibitors[g27]/ ARB’s [g28] to help alleviate the strain.
(to note, this won’t help prevent or reverse damage caused by the androgens, but rather MAY prevent damage to the capillaries inside of the kidneys due to high blood pressure.)

The Prostate

The development and maturation of the prostate gland is due to its utility of androgen-based transcription factors.

Since androgens are transcription factors necessary for the growth and development of the prostate, it follows logically that the eventual cause of carcinoma has to be implicated by androgens.

Prostate cancer is of CONSIDERABLE concern for older adult men.

This is because of how fatal prostate cancer is for men.

Now, I am going to HEAVILY outline some things before I dive into testosterones’ role in the prostate.

This is because a LARGE portion of you guys are men in the US aged from 20-50 years old.

It will NOT be INCREDIBLY comprehensive, due to the already long-winded nature of this post, but it is VERY important to have some general information.

I may circle back to this section if I get any emails/comments encouraging me to do so, but for now, here’s the quick run-down.

Typically, screening for prostate cancer in middle-aged men is a simple practice.

Most men are familiar with the D.R.E or “Digital Rectal Examination”

If you’re not familiar with it by name, simply put it’s the prostate exam where a doctor will glove up, put a finger inside of your butt, and feel around for anything odd.

A lot of people are opposed to this practice, as it can miss prostate cancer pretty frequently, but it still exists.

Alongside this, there’s something called a “PSA” biomarker that will often be checked for.

PSA (prostate-specific antigen) is an androgen-regulated serine protease.
PSA circulates in relatively low amounts throughout the body.
Over time when there is too much being freely let into the blood, it can be indicative of prostate damage/poor health.

There is a relative scale that is used to check for prostate health, roughly a ratio of ~4.0ng/ml is seen as moderately safe. [28]

Typically any point over 4.0 ng/ml to 10.0ng/ml in the blood is seen as a risk factor for prostate cancer and could merit a screening or biopsy if your physician is so inclined to.

Any point OVER 10.0ng/ml is seen as highly concerning and will most likely lead to a definite screening

(any PSA level over 10 carries above a 50% chance of having prostate cancer) [28]

Now, there is a LOT of talk about issues and the necessity for FURTHER examination of the prostate because a lot of these general practices have false positives, false negatives, or just aren’t good PREDICTORS of prostate cancer.

Other tests that are commonly recommended to be done are ones such as other Kallikreins, doing PHi testing, or looking into genetic transcription factors like PCA3 (Prostate Cancer Antigen-3) to see if there is a predisposition to the likelihood of developing Prostate Cancer.

BUT largely put, there is a LOT of just general speculation about actively determining how to effectively predict prostate cancer.

the only DEFINITIVE way to be diagnosed with prostate cancer is a biopsy, which can still miss Prostate cancer on occasion as well.

Testosterone suppression and androgen deprivation as a temporary solution to prostate cancer.

It has been made very commonplace in the medical community that testosterone levels and androgens (namely DHT/DHEA) are the catalysts for the progression and development of Prostate Cancer.

This is because of the necessity for these hormones to cause the development in the first place.

In the very beginning, during the “production of testosterone” section I talk discussed GnRH and its role in stimulating LH & FSH.

This now becomes incredibly important for this section, as we introduce things like GnRH agonists and their role in testosterone suppression to prevent androgenic activity and promote chemical castration in men.

Now, it follows logically that if androgens cause prostate cancer to develop and worsen, that the removal of androgens would suppress the progression of this, right? Sort of, this works in theory, and I’ll touch on this later. [29,30,31,32]

But the typical means of treating Advanced Prostate cancer development is to shut down testosterone and androgen production COMPLETELY.

Typically there are things like Triptorelin (name brand Trelstar®) that are used to essentially “fry” the GnRH receptor via excitotoxicity.

Pretty much, this form of triptorelin is a GnRH agonist that is so potent it causes the suppression of LH/FSH. The suppression of these two hormones stops the total production of testosterone and downstream with prevent androgen production.

It has been noted in their studies that in animals Trelstar® is over 13 fold higher in producing LH activity and more than 21 fold higher in FSH activity, making it the preferred method of GnRH agonism for testosterone suppression in men with advanced prostate cancers.

After an initial bump of serum testosterone caused by the letdown of FSH/LH, the testosterone levels plummet and concurrently remain low for a period of time depending on administration dosing protocols.

Now, remember earlier how I mentioned this method “Sort of” works?

That’s because although androgens are the suspected culprit of worsening prostate cancer development, there exists another form of prostate cancer that can arise from this subset.

A significant portion of men who undergo the androgen deprivation therapy can develop something called CRPC (Castration Resistant Prostate Cancer) which is speculated to develop by either upregulation of androgen receptor transcription activities, mutations of AR receptor or intratumor based steroids synthesis that causes the production of DHT responsible for its resistance.[29,30,31]

for those who still face these issues, they recommend a complete blockage of androgens by the utility of antiandrogens like enzalutamide and GnRH agonism as well.

Now, even with all of those means listed above…there is, unfortunately, ANOTHER variation of this variation called Neuroendocrine prostate cancer which mutates in response to androgen receptor signaling inhibition. [32]

Again, in the interest of NOT derailing this topic on testosterone into prostate health concerns, I’ll wrap it up by saying this.

While androgens are important for the development and function of the prostate, they are, by nature a risk factor for prostate cancer, with seemingly no real remedy to prostate cancer once it develops.


I feel compelled to put this section here for two reasons.

Firstly, I often only see testosterone being either abused by athletes or being used as a means of therapeutic replacement for older men who don’t produce adequate amounts.

Very seldom do I see any outlines for biological women who are interested in testosterone’s effects on their bodies.
(which is why this post isn’t just including information for men)

Secondly, I also think it’s of decent importance to provide information for individuals who are transitioning from one sex to the other to have a decent baseline understanding of the impacts it has on their bodies.

Without further ado, here’s how testosterone and androgens lead to masculinization in the body.

In women, raising testosterone will cause an elevation of total androgens in the body that slowly can start to lead to virilization. [16][17]

Androgens are responsible for things like facial hair growth, increased sebum production, male-pattern baldness, as well as increased bone mineral density.[16][17][18]

Alongside this, things like deepening of the voice, as well as increased musculature could be noted in individuals who have elevated testosterone levels.[16][17]

(though the deepening of the voice is not always guaranteed with exogenous hormone use, a perfect example of this… my high pitched voice, alongside this iconic video of Ronnie Coleman)

Those undergoing administration of testosterone in hope of transitioning in line with their correct sex should note that after roughly 4-6 months of time the bolus administration of testosterone seems to not create additional benefits in terms of faster virilization. [17]

The mechanism by which this virilization rate picks up and halts around this point isn’t known, but as time goes on we find out more and more through proper research studies.
(anecdotally I think it’s due to a peak saturation level from the bolus administration.)

When it comes to problems caused by testosterone we can see that these problems exist in individuals choosing to undergo testosterone administration, such as hair/skin problems

So far, we understand that the “Male Pattern Baldness” may occur as a result of testosterone being 5α-Reduced to 5αDihydrotestosterone (DHT) which is a highly androgenic hormone that is speculated to be responsible for androgenic alopecia.

Alongside this, the rise in acne which one may incur is due to the elevation of DHT and testosterone as noted earlier with the mention of increased sebum production. [16][17][18]

Assuming that the incorporation of testosterone is not accompanied by another drug like an anti-androgen or any sort of anti-estrogen as well, then the increase in bone mineral density could potentially be included as a potential benefit.

(it’s noted heavily that things like anastrozole and other aromatase inhibitors are associated with a loss of bone mineral density, most likely due to their role in preventing sufficient estrogen production/ removing estrogen from the body)[20]

Considering that the face is comprised of numerous muscles, we can also see that there is often a change in facial structures with testosterone administration.

Alongside this, there is a differential distribution of body fats as a result of the administration of testosterone that creates a more masculized appearance.

A reduction in estradiol and increase in testosterone changes fat storage and distribution around the hips/thighs.
Resulting in a lower hip circumference and body composition. [33]

Lastly, clitoral enlargement as a result of androgen exposure can be of note in women with continued exposure to either synthetic androgens or continuously high serum testosterone/androgens as a result of PCOS or other means of elevation in the body.

Any further questions on testosterone you want to see covered?

If you have any questions about the content posted, please feel free to leave a comment down below!
If it’s an interesting or broad enough topic that wasn’t covered here or in another post I’d be more than happy to do a follow-up in another post!

If there’s something you believe I missed that should be covered in this article, let me know! I’d be more than happy to accredit you with the inclusion in the article as well if I feel it’s an appropriate fit.

Alongside this, if you have a question you’d like to ask me personally, feel free to check out the contact page on the blog or send me a DM via Instagram @damonisvegan.

I try to keep these pillar posts as objective and fact-based as possible, whereas anecdotal stories and experiences have a far more laid-back view of the topic.

Below I’ve created an outline to reference in terms of citations as well as a glossary to refresh your memory or for clarity in some of the jargon posted.

Hope you’ve enjoyed the article! Toodles.

Glossary [g]
  1. Androgenic: describing something as an having androgen related properties. “Androgens” are defined medically as male sex hormones. If something is androgenic it is defined as a hormone pertaining to the development or maintanence of masculine characteristics.
  2. Anabolic: refering to anabolism, the process of metabolic activity which focuses on synthesizing simple substances to promote growth and repair. In the context of this article and in steroid use, “Anabolic” steroids refer to a steroid hormone that illicits recovery, repair of body tissues, and promotes muscular development and growth.
  3. Steroid hormone: in this article refers to the sex hormones, Hormones that are sythesized from cholesterol and utilized for a myriad of complicated intra-cellular interactions throughout the body that may cirulate freely to regulate physiological functions.
  4. Adrenals: referring to the adrenal glands (interchangable called supra-renal glands in literature, as they they are located above [supra] the kidneys [renal])
  5. Androstenedione: A weak androgen source alongside DHEA in women that is produced by the adrenal glands. It is responsible for the majority of testosterone production in normal healthy women.
  6. β: Pronounced Beta used to distinguish between other groups of receptors, classes, or in some instaces positions of atoms such as alpha(α), delta(Δ) or gamma (γ)
  7. HPG: Hypothalamic-Pituitary-Gonadal axis: refers to the hypothalamus, the pituitary and gonadal glands as one interlinked set of endocrine glands, due to the fluction in one set of hormones disrupting and regulating the production of others in the axis as well as inside of the body.
  8. GNRH: Gonadotrophin-releasing hormone, is the hormone responsible for releasing the reproductive hormones from the Gonads, like LH and FSH
  9. LH: Lutenizing Hormone
  10. FSH: Follicle stimulating hormone
  11. Menstrual Cycle: (often referred to as a womans “Period”) is used to describe the process of menstration which has four phases:
    P1. Menstruation.
    P2. The Follicular/Pre-ovulatory Phase.
    P3. Ovulation.
    P4. Luteal Phase.
  12. Pulsatile: Referring to the secretion of hormones, an easy way to think of Pulsatile vs Surges think of this as the same way that the heart beats: there’s one push of blood, and then a quick cessation, followed by a second push of blood that aligns in a rhythm. In this instance pulsatile is a rhythmic and steadily regulated release of hormones
  13. Surge: Referring to the secretion of hormones, a surge is a bolus non-rhymic release of hormones often prompted by a sudden elevation of hormones. (in this article and referring to GNRH pulsatility, the surge of GNRH hormones due to pregnancy and menstration occur naturally in women.)
  14. Pre-ovulatory phase: Following the Menstration Phase, and before the beginning of ovulation in the menstrual cycle, this phase is associated with noticable increases in LH and as a result elevated estrogen.
  15. leydig cells: located in the male testes, leydig cells are responsible for the production of testosterone and the masculinization of the brain.
  16. CYP450: Referring to the “Cytochromes P450 family”, they are a group of enzymes that metabolize a range of hormones, fatty acids and medications in the body.
  17. Ovarian hilus cells: interchangable referred to as “interstitial ovarian cells” they are the female equivalent to the “leydig cells”
  18. SHBG: Sex Hormone Binding Globulin is a gylcoprotein that is responsible for binding to androgens and estrogens in the body (most notably testosterone and estrodiol) to transport them throughout the blood.
  19. Transport proteins: they are a class of proteins produced in the body meant to carrier specific molecules throughout the body.
  20. upregulation: referring to the marked increase of either senstivity to a response or by the increase in the number of cell density on a surface. (in this context, upregulation of protein synthesis factors would include things like increased rates of nitrogen retention and promoting factors that will prevent leucine oxidation/breakdown)
  21. IGF1: Insulin Like Growth Factor 1
  22. Satelite cells:   are precursors to skeletal muscle cells. essentially allowing for more muscle cells to be created over time allowing for more muscular hypertrophy.
  23. (Testosterone) Cypionate: Cypionate refers to the “ester” attached to the molecular of a compound to prevent its immediate release into the blood stream. Common examples are acetate, propionate enanthate, deconoate
  24. gynecomastia: simply put, the development of breast tissue in men (sometimes in boys during puberty due to the elevation in testosterone being aromatized into estrogen)
  25. SERM: Selective Estrogen Receptor Modulator, a form of drug that has a high affinity to bind to specific estrogen receptors in the body.
  26. Podocytes: specialized epithelial cells that cover the outer surfaces of glomerular capillaries. 
  27. ACE inhibitor: Angiotensin-Converting Enzyme inhibitors prevent the production of angiostensin II, which is a chemical that narrows your blood vessels.
  28. ARB: Angiotensin II receptor blockers, they activate the angiotensin II type 2 (AT2) receptors, which causes vasodilatation in the small vessels and presumably leads to additional cardiac and renal protection.
  1. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/aromatization
  2. https://www.ncbi.nlm.nih.gov/books/NBK279000/
  3. https://www.ncbi.nlm.nih.gov/books/NBK279070/
  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636985/
  5. https://www.fertstert.org/article/S0015-0282(02)02985-0/fulltext
  6. https://www.researchgate.net/publication/12880575_Sex_hormone-binding_globulin_mediates_steroid_hormone_signal_transduction_at_the_plasma_membrane
  7. https://www.sciencedirect.com/science/article/abs/pii/096007609190307Q?via%3Dihub
  8. https://pubmed.ncbi.nlm.nih.gov/10323678/
  9. https://pubmed.ncbi.nlm.nih.gov/2055206/
  10. https://www.ncbi.nlm.nih.gov/books/NBK278929/
  11. https://pubmed.ncbi.nlm.nih.gov/2917954/
  12. https://www.researchgate.net/publication/47500270_Anabolic_Processes_in_Human_Skeletal_Muscle_Restoring_the_Identities_of_Growth_Hormone_and_Testosterone
  13. https://journals.physiology.org/doi/full/10.1152/ajpendo.00502.2001
  14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5512682/
  15. https://academic.oup.com/edrv/article/18/6/774/2530788
  16. https://academic.oup.com/jcem/article/85/8/2913/2853998
  17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5182227/
  18. https://www.thelancet.com/journals/landia/article/PIIS2213-8587(16)00036-X/fulltext
  19. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2604138
  20. https://pubmed.ncbi.nlm.nih.gov/18309940/
  21. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3473928/
  22. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513682/
  23. https://bmcgastroenterol.biomedcentral.com/articles/10.1186/1471-230X-12-69
  24. https://www.kidney.org/atoz/content/focal
  25. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4775100/
  26. https://www.frontiersin.org/articles/10.3389/fendo.2014.00160/full#:~:text=Podocytes%20are%20specialized%20epithelial%20cells,connect%20adjacent%20podocyte%20foot%20processes.
  27. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2799287/
  28. https://www.cancer.gov/types/prostate/psa-fact-sheet
  29. https://www.cancer.gov/news-events/cancer-currents-blog/2017/prostate-cancer-resistant-new-subtype
  30. https://www.dovepress.com/a-review-of-the-pathophysiological-mechanisms-underlying-castration-re-peer-reviewed-fulltext-article-RRU
  31. https://www.nature.com/articles/s41598-021-87441-2
  32. https://www.frontiersin.org/articles/10.3389/fonc.2020.571308/full
  33. https://eje.bioscientifica.com/view/journals/eje/178/2/EJE-17-0496.xml

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