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Why Transitioning with Testosterone Tends to Transform Transmen’s ScenT

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A trans guy asked me once, “Can you write about why my scent has changed since I went on testosterone?  My girlfriend wants to know.”

Of course she does.

I’d heard of this phenomenon before, enough to make me believe that there was something biological behind it.  And to be honest, I was happy to get the question.  After multiple posts and over a month of reading and writing on the previous scientific topic, this one looked like a relative piece of cake.  I thought, “Heck yeah!  This won’t require much work at all!”

That’s what I thought anyway, because I figured I already knew the answer:

Pork chops.

Yes, pork chops.  I know, that’s so obvious, right? (he says, tongue-in-cheek)  But, like a lot of topics I’ve set out to write about, this one became more complicated than I first anticipated.  You’d think I’d learn…

Anyway,  let me take you through my initial line of thinking.

Pork, the Other White (and Potentially Stinky) Meat
Standard hog farming practices in many countries include castration of male pigs relatively soon after birth.  It’s not that the farmers really want to indulge in this practice because, in addition to the animal welfare considerations, it also hurts the farm’s bottom line.  Castration removes the growing male pigs’ source of testosterone, so they grow slower, have a lower feed efficiency (pounds of feed required to produce a pound of pig) and have more fat deposition compared to testicle-intact male pigs and even female pigs.

Well, if castrating baby male pigs causes so much trouble, then why do it?

Because if male pigs, known as boars, were raised with their testicles intact, very few people would want the meat.  The reason?  An issue called “boar taint” (Duijvesteijn et al. 2010; Robic et al., 2008).

There are particular steroids produced by boars that go into the fat and the muscle so that when boar meat hits a hot skillet, the odor is, well, downright unpleasant.  It’s a musky, urine-like scent that some people can detect better than others.  (These steroids contribute negatively to the flavor of the meat as well, but this post is about scent.)

There is actually a good amount of research about boar taint because farmers don’t want to castrate all of those little baby male pigs, some governments forbid the castration of all those little baby male pigs, and a whole lotta people don’t want to eat (or smell) boar-tainted meat.  Some scientists have been determining the genes responsible for boar taint so they can remove the problem through breeding (Duijvesteijn et al. 2010).   No more boar taint, no more male piglet castrations.

The main steroidal culprits for boar taint are 16-androstenes, which are known piggy phermones.  [Boar taint is also caused by an indole called "skatole"  that's produced in the lower gut of male pigs from bacterial metabolism of the amino acid tryptophan.  Skatole diffuses from the pigs' intestines into the fat tissue and lends a wonderful fecal aroma to the boar meat which everyone seems to be able to smell. No one knows why skatoles are produced in intact male pigs but not in female or castrated male pigs.  Fortunately, skatoles are not a problem in humans.]

From.Robic et al., 2008

I can tell you from first-hand experience that even on the hoof, boars are quite odoriferous.  It’s like this smelly stuff is coming out of their pores!  If you give a friendly pat or a scratch behind the ear of a post-pubertal boar, that stink gets in your skin and it doesn’t wash off easily.

But I digress.

So my line of thinking was that, okay, steroidogenesis in the human testis is similar to that in the boar testis, and 16-androstene steroids are produced in the human testis, and so human males have this contribution to their scent as well, but at lower level than in pigs (Smals & Weusten, 1991).

And then, I hit the wall.

You’re all ahead of me out there, aren’t you?  Of course, trans men don’t have testes!

D’oh!

I thought, well, something must contribute these smelly steroids that change the scent of trans men who take testosterone therapy.  So I took a look at where human scent comes from.

Sweat Glands

There are four different types of glands in the skin, three of which are sweat glands.  The non-sweat glands are the sebacious glands – they are associated with hair follicles and secrete the oily, waxy sebum that lubricates the hair shafts and the skin itself.  Regarding the sweat glands, there are three types: eccrine, apocrine and apoeccrine (see Wilke et al., 2007 for a review of sweat gland biology).

Eccrine glands are associated with sweating for regulating body temperature (thermoregulation) and from emotional reactions.  They consist of a coiled tubular structure that is located in the dermis with a duct that extends to the surface of the skin.  Developed at birth, eccrine glands are found over the entire body except for the lips and glans of the penis.  Although secretions by eccrine glands are variable depending on, among other things, the area of the body, they mainly produce sweat that is about 99% water and the rest is made up of ions and salts and some proteins.

Apocrine glands are coiled tubular structures like eccrine glands but they open into the canal of the hair follicle, similar to sebacious glands. Because they are associated with hair follicles, they are mainly found in the axilla (arm pit), chest and genital areas of the body.  Although present at birth, apocine sweat glands do not become active until puberty.  They have oily secretions made up of lipids and proteins and they respond to emotional stimuli.  In general, males have fewer apocrine glands than females.

Apoeccrine glands are similar to and might even be derived from eccrine glands.  Apoeccrine glands have the highest fluid production rate of the three types of sweat glands and have secretions that are very similar to those of eccrine glands.

Now that we know a little bit about the glands in the skin and their secretions, let’s look at how they can be affected by hormones.

Effects of Sex Steroids on Skin

It’s probably obvious to most, if not all of you readers out there that males and females have some differences in the characteristics of their skin.  As you can imagine, androgens play a significant role in these sex-based differences, but estrogens have effects as well (Zouboulis et al., 2007).

Androgens produced at puberty stimulate enlargement of the sebaceous glands, an increase in production of sebum, growth of the hair follicles in the skin of androgen-sensitive areas (such as the beard and axillary areas), miniaturization of scalp hair follicles in people pre-disposed for male-pattern baldness, and an increase in skin thickness due to stimulation of the proliferation of skin cells.

Androgen-stimulated sebum production, combined with conversion of testosterone to dihydrotestosterone by 5-alpha-reductase in the skin, plus localized inflammation, results in an increase in or exacerbation of acne.  This is no surprise considering the problems with acne experienced by pubescent boys and trans men on testosterone thereapy.

Androgens also augment sweating, with one potential mechanism being the conversion of eccrine sweat glands to apoeccrine glands, the latter of which have a sweat production rate that is roughly seven-fold greater than the former.

Estrogens are thought to have protective effects on skin, determined mainly by comparing the skin of pre- and post-menopausal women.  Estrogens retard skin aging by maintaining elasticity, thickness and hydration.  Through direct and/or indirect mechanisms, estrogens promote wound healing, reduce local inflammation of the skin and stimulate scalp hair growth by lengthening the cycle of the hair follicles.

Okay, now that we know some of the fundamental sex-based differences of skin, let’s talk about scent.

The Scent of a Man

The study of human scent is part of a relatively involved area of research, which is easy to understand if we consider just what we see on television commercials.  Ads for underarm deodorants, breath fresheners and foot odor would have us believe that we are fairly stinky creatures.  (And don’t forget the Beano!)

The irony is that the secretions of the human skin are odorless.  It’s true.  Human sweat, when it is secreted from the sweat glands, has no scent.  It’s the bacteria that live and feed on our surfaces that cause the odor problems.  To quote Troccaz and coworkers (2009):

“The generation of malodor on various sites of the human body, for example, foot, mouth, or armpit, is mainly caused by microbial transformation of odorless natural secretions into volatile odorous molecules.”

Now, “volatile” odorous molecules are not part of a cranky personality trait.  Volatile chemicals are those that evaporate (liquid phase to gas phase) at relatively low temperatures, such as body temperature.  When volatile odorous compounds evaporate, they waft through the air and right up the ol’ nose pipes, and voilà, you’ve got detection of human scent.

So, how are the volatile steroids in sweat derived?  The bacteria that live in the axilla (underarm areas) have the enzymatic machinery capable of metabolizing low-odor 16-androstene steroids into volatile, odorous steroids (androstenone, androstenol, androstadienone) that are like those that cause boar taint (Mallet et al., 1991; Gower et al., 1994), and these volatile steroids are known to contribute to a person’s malodor (Gower & Ruparelia, 1993).

From Gower & Ruparelia, 1993

However, there is a gap in the data.  Although human axillary microflora are capable of producing the volatile 16-androstenes, they’re not capable of making their non-volatile precursors.  In addition, the  axillary bacteria are not able to convert testosterone into the 16-androstene steroids (Austin & Ellis, 2003).

When I learned this, I considered that testosterone might be converted in other ways into the 16-androstene steroid precursors, like perhaps in the liver.

What I found in the literature, however, was that metabolism of testosterone and dihydrotestosterone (DHT) by the liver into hydroxylated forms of testosterone and androstenedione and 5- and 3-alpha-reduced androstanes, respectively, does not provide the 16-androstene steroids needed by skin bacteria to convert into volatile, odorous androstenone and androstenol (Meikle et al., 1987; Pirog & Collins, 1999; Tachibana & Tanaka, 2001).

What about other bodily sites where androgens are metabolized?  We’ve known since the 1950s and 1960s that skin itself can metabolize androgens.  Keratinocytes, hair follicles, sebaceous and sweat glands all have the enzymatic machinery to not only metabolize androgens such as testosterone, but also to produce them from cholesterol (reviewed in Chen et al., 2002);  however, I cannot find evidence in the literature that the skin itself is the site of 16-androstene production, whether de novo from cholesterol (the starting material for all steroids) or metabolized from testosterone or adrenal steroids such as dihydroepiandrosterone (DHEA).

The bottom line is that the source of 16-androstenes in humans is likely from the gonads (testes and ovaries), although an adrenal source is possible as well (reviewed in Gower and Ruparelia, 1993).  If these steroids come from testes in males, and trans men have no testes, then do the volatile steroids even exist in the sweat of trans men, and if not, what contributes to the change in scent of transitioning trans men?

Well, it turns out that volatile 16-androstene steroids are not the only contributors to a person’s scent.  Although they might be important as porcine pheromones (and thereby, piggy-to-piggy attractions), the volatile 16-androstenes make a relatively minor contribution to the scent of a man (and even less to the scent of a woman).

Okay then, what are the chemicals that contribute to human scent and what influences their production?

Sweat-Eating Bacteria

Consider that the normal microflora of the human skin uses odorless constituents of sweat and sebum as nutrients and generates volatile, odorous by-products in the process (Labows et al., 1999).  In the axillary (underarm) area, the main bacterial culprits of these processes are species of Corynebacteria and Staphylococci, and their smelly products are C6-C11 volatile fatty acids (Zeng et al., 1991, 1992).

These malodorous volatile acids are present in sweat at significantly greater concentrations than the volatile 16-androstene steroids (Gower & Ruparelia, 1993; Zeng et al., , 1992, 1996) and are now known to be major contributors to human odor.  In particular, volatile acids in human sweat include (E)-3-methyl-3-hexanoic acid (E-3M2H; Zeng et al., 1996), it’s hydrated form (R)/(S)-3-hydroxy-3-methylhexanoic acid (HMHA; Natsch et al., 2003, 2006) and (R)/(S)-3-methyl-3-sulfanylhexan-1-ol (MSH; Hasegawa et al., 2004; Natsch et al., 2004; Troccaz et al., 2004).

Now that we know about the system, we can ask how it is affected by sex.  There are clear differences in these system components between males and females, although the actions of sex steroids upon them may be direct or indirect, and there are genetic elements at play as well (Emter & Natsch, 2008; Savelev et al., 2008).  We can likely be safe with an assumption, however,  that when trans people replace the predominance of one sex steroid hormone with another, they are changing the constituents of their sweat, the abundance and type of dermal microflora and the products produced by those bacteria.

First, considering the glands of the skin, we know that males have a greater production of sebum and sweat than females and also have 2-to-5-fold higher concentrations of glucose in their sweat, which can act as an energy source for some types of bacteria (Troccaz et al., 2009).

Second, we know that the Corynebacteria that produce the volatile fatty acid HMHA are in greater abundance in the axilla of males versus females than Staphylococci, which produce MSH (Labows et al., 1982; Jackman & Noble, 1983).

Third, we know that the ratio of HMHA-precursor to MSH-precursor is roughly three-fold higher in males than females (Natsch et al., 2003; Starkenmann et al., 2005; Troccaz et al., 2009).

Taking all of these sex-specific conditions together, we would predict greater levels of HMHA in the sweat of males versus females.  As described by Troccaz and coworkers (2009), the trained assessors who evaluated the odor of sweat samples described HMHA as “animalic, cheesy, and rancid,” and the sulfur-containing MSH as “fruity and onion like.”

In other words, testosterone therapy may make trans guys go from smelling like onion-fruit salad to smelling like a wet dog that eats rancid cheese.  But don’t worry lads!!!  The odor assessors also reported that sweat from females had more intense (and unpleasant) sulfur odors!  (What?  That’s no consolation?)

Well, okay, I’m being facetious — the initial question wasn’t about why this trans guy’s scent became smelly or worse, but why it simply became different.  From these data we can see how trans people’s scent can change when they alter their hormonal status, whether it be trans men reducing their estrogen and increasing testosterone, or trans women doing the opposite.

And actually, it turns out that this whole human scent business is even more complicated than a couple steroids and a few fatty acids.

The Unique Scent Patterns of People

A person’s scent can be affected by their sex, as we have learned, but it can also be influenced by other factors, such as emotional status, ethnic background, health status, and physiological and environmental conditions (see references in Troccaz et al., 2009).  In addition, these factors can influence not only the scent of skin, but also that of saliva (breath) and urine.

Because of all of the influential factors involved, the scent of a person can be as unique as their fingerprints — in other words, an “odor-print” for each person.  Think about tracking dogs such as Bloodhounds and their ability to sort through scents and pick out the signature fragrance of a particular individual — aren’t the dogs really detecting the “odor-prints” of the individuals they’re tracking?

Not ones to let the Bloodhounds have all the fun, scientists and engineers are now making “electronic noses” that can measure human odor-prints.  These high-tech sniffers have the potential for detection and diagnosis of poor nutritional status, organ failure, and diseases such as diabetes, tuberculosis and cancer, to name a few applications in human medicine (Wilson & Baietto, 2009).  Well, what makes up these odor-prints?

To investigate the various chemicals that contribute to odor fingerprints, Penn and coworkers (2007) collected multiple urine, saliva and axillary sweat samples from almost 200 people.  They extracted the samples using a special method, followed by analysis via gas chromatograph-mass spectometry (GC-MS).   In doing so, they discovered that:

  • sweat had higher concentrations of volatile and semi-volatile compounds than did urine or saliva
  • few compounds were common to all samples, contributing to the unique nature of the sample constituents
  • not all of the chemicals in the samples could be identified
  • some of the compounds in the samples came from man-made products such as soap, cosmetics, perfumes, shampoos and tobacco

From Penn et al., 2007 (RT = "Retention Time)

Most importantly (for the purposes of this discussion), they found statistically significant sex-specific patterns of some of the compounds!

From Penn et al., 2007

Therefore, we can see that the sex of a person has a major impact on their odor-print from sweat, saliva and urine.  So how does this translate to trans folks?

When I look at data like these, I have to wonder whether trans people, if analyzed along-side of non-trans people, would contribute an additional group (or groups) to the sex-specific results.  Would the natal hormonal milieu of a trans person have an influence on the chemicals in their sweat, saliva and urine after they transitioned to a different sex and hormonal make-up and form an odor-print that’s different than those from males and females?  Or, would the pattern simply switch from that of one sex to the other (basing the question on the binary analysis at left)?

We may never know the answer, but from this discussion, we do have a better understanding of how transitioning with testosterone can transform trans men’s scent.  (And it really doesn’t have much to do with pork chops…)

–ATM

Note after posting:  The person-to-person variation in the studies cited in this post was significant when parameters such as the amount of sweat produced or the amount of the steroids or acids in the sweat were measured.  However, when a relatively large group of people were included in the studies, there were general trends and that’s what I described.  Therefore, it’s possible that on an individual level, there will be some trans men whose scent changes little (if at all) on testosterone therapy and others whose scent will change quite a bit.

References

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Chen, Thiboutot, Zouboulis, 2002.  Cutaneous androgen metabolism: basic research and clinical perspectives.  J Invest Dermatol 119:992-1007

Duijvesteijn, Knol, Merks et al., 2010.  A genome-wide association study on androstenone levels in pigs reveals a cluster of candidate genes on chromosome 6.  BMC Genetics 11:42-53

Emter & Natsch, 2008.  The sequential action of a dipeptiase and a β-lyase is required for the release of the human body odorant 3-methyl-3-sylfanylhexan-1-ol from secreted Cys-Gly-(s) conjugate by Corynebacteria.  J Biol Chem 283:20645-20652

Gower & Ruparelia, 1993.  Olfaction in humans with special reference to odorous 16-androstenes: their occurrence, perception and possible social, psychological and sexual impact.  J Endocrinol 137:167-187

Gower, Holland, Mallet, Rennie, Watkins, 1994.  Comparison of 16-androstene steroid concentrations in sterile apocrine sweat and axillary secretions:  interconversions of 16-androstenes by the axillary microflora — a mechanism for axillary odour production in man?  J Steroid Biochem Mol Biol 48:409-418

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