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Brief Intro to Male Physiology (Might be NSFW)
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Brief Intro to Male Physiology (Might be NSFW)

With the unexpectedly warm response to my post on female menstrual physiology, I decided to follow up with the physiology of the male human.

In this post, you will learn about what makes men tick, biologically speaking.

This is a pretty detailed, and long datasheet, much longer than the female menstrual physiology post. This post is divided into the following sections:

EMBRYOGENESIS - where I talk about what makes a male genetics and how it is expressed
WHAT COULD POSSIBLY GO WRONG? - where I talk about all the weird things that can go wrong in the development of a baby boy
BALL GAMES - where I talk in detail about the testicle
TESTOSTERONE
SPERM
HORMONAL REGULATION
PUBERTY
ALTERNATIVE SOURCES, BINDING AND EXCRETION OF TESTOSTERONE
FEMALE HORMONES IN MEN
ENDOCRINE DISRUPTERS
SEMEN
ERECTIONS
CLIMAX
FERTILIZATION

By the end of this post, you should have a good working knowledge of the functioning and development of the human male with regards to his sexual characteristics.

I apologise in advance for spelling/grammar/stylistic/factual problems in this post. It is a rather long essay and though I have proofread it, I'm sure I have let a few bugs through. Feel free to point out any serious mistakes that you may notice.

We will start our beginning at the very beginning of life - conception.

From the very beginning, from the very point of conception, being a man is fraught with challenges. It all begins at the gene level at the time of conception, in the process known as...

EMBRYOGENESIS

So in human beings there are cells, and in cells are nuclei, and in the nuclei are genes, which are the programs that run the human body. These genes are grouped into 36 pairs of chromosomes. One of these chromosomes, referred to as the 'Y' chromosome, will run the program necessary for the body to become a man.

(In a bizarre cosmic coincidence, the Y chromosome actually does look like a Y during mitosis, under some low powered microscopes. But the Y chromosome was discovered and named before its shape was known.)

Upon this Y chromosome, is an extremely important region called the Sex-determining Region of Y chromosome, otherwise known as the SRY gene. This chromosome will eventually force various bits of a baby to become male. In the absence of the SRY gene, the default programming will be to create a human female. The Y chromosome, with the SRY gene, can thus only come from the father, as women should not contain it at all in their genetic code. Therefore, it is the father's genetic contribution to the baby that determines whether it will be male (which it should become IF the father contributes SRY genetic material) or female (which is the default program, should the father fail to contribute a Y chromosome, and therefore fail to contribute SRY genetic material).

For the first 7 weeks of pregnancy, though, there is no difference between the male and female baby. In fact, in this early stage the baby is a hermaphrodite, with 2 primitive sets of sex organs - Wolffian ducts (which can eventually become male sex organs; also known as mesonephric
ducts), Mullerian ducts (which can eventually become female sex organs; also known as paramesonephric ducts), a pair of generic gonads (which can become either ovaries or testes as they develop), and a generic genital region which can either develop into the female or the male external genitalia.

Somewhere between 6 - 8 weeks into the pregnancy, the SRY gene begins to make proteins that stimulate the primitive gonads to start making 2 hormones: Anti-mullerian hormone, and Testosterone. The gonads aso start to develop into testes.

Anti-mullerian hormone causes the Mullerian duct to die off, thus preventing the formation of female sex organs.

Testosterone causes the Wolffian ducts to mature, creating the the epididymus, vas deferens and the seminal vesicles - basically, all the plumbing required to connect your testicles to your penis.

Furthermore, Testosterone is converted by an enzyme in the body into dihydrotestosterone. The name of the enzyme involved is 5-alpha-reductase. Dihydrotestosterone works on the generic genitalia to cause it to turn into male genitalia - it basically forces the growth of a scrotum
and penis (in other words, a man's outside bits) as well as the prostate and urethra (in other words, all the bits of plumbing not covered by the Wolffian ducts).

If all those names and bits are confusing to you, here is a picture that shows clearly all the plumbing that has to develop in the adult male:
[Image: male+organ.jpg]

WHAT COULD POSSIBLY GO WRONG?

We are barely 8 weeks into the pregnancy and already there are numerous hurdles to jump over before a baby can become male. Remember, the default programming is for a baby to become female - so if there is a failure of any of the male development systems, the baby will become
female regardless of the presence of the SRY gene.

First of all, the SRY gene may be defective and simply refuse to activate. In which case you will have a female baby who is genetically male, but has none of the features of maleness.

This generally results in condition called Swyer's syndrome. Here is an article about one such person:
http://www.theguardian.com/lifeandstyle/...cally-male

But what if the SRY gene is fine but the gonad itself is defective? If the gonad doesn't respond to the proteins released by the SRY gene, then testes will not develop, and the result again is a female baby who is genetically male. This condition is referred to as gonadal dysgenesis, and it shares many features with Swyer's syndrome.

But what if the gonad does respond but fails to secrete hormones?

If it fails to secrete testosterone, then you will have a female who will be born with abdominal testicles instead of ovaries. This condition is referred to as testicular failure - testes formed in response to SRY proteins, but they failed to secrete the most important hormone for male sexual characteristic development.

Even if testosterone is secreted, there is another type of testicular failure - the failure to make anti-mullerian hormone. If this is the case, then female organs will develop alongside the male organs, leading to a baby boy who happens to also have a non-functioning uterus inside
his abdomen! In some boys, this condition may even remain undiagnosed until a sonar or ct scan discovers the female organs by chance. However, as the female organs may prevent testicular descent into the scrotum, this condition may be discovered as part of the workup for that
condition. This disease is referred to as Persistent Mullerian Duct syndrome.

Yet even if the testes are fully functioning, this will not help if there are no chemical receptors for testosterone to bind to. If testosterone is produced but fails to bind with the Wolffian ducts and other body tissues, then again you will end up with male testes stuck inside
a female body. This condition is called Androgen Insensitivity syndrome.

Yet more could go wrong though. What if there is deficiency in 5-alpha-reductase enzyme? Or a failure of that enzyme to create dihydrotestosterone? Then you may end up in a situation where
half your body is responding to testosterone, and therefore becoming male, while the other half continues to develop as female (since dihydrotestosterone is required to develop roughly 50% of male sexual characteristics, especially the external parts). This will end up causing a baby to be born with testes and the internal plumbing of men, while having none or only part of the external plumbing (penis, prostate, urethra) thus causing a weird combination of male and female sex organs to form. Often these babies will look female but may have boyish or manly characteristics as they grow up. This condition is referred to as Intersex. Caster Semenya, a South African female athlete with very masculine features, is thought to have this condition; this caused some understandable controversy - as she was genetically male, it could be argued
that she had an unfair advantage in terms of physical strength compared to female athletes.

Here is a picture of her, how do you think she'd compete against genetically 'pure' females?:
[Image: Caster_Semenya_1673848c.jpg]

For interest's sake, here is a list that includes other intersex 'female' athletes:
http://listverse.com/2015/10/25/10-famou...-athletes/

As you can see, there are several hurdles a baby has to jump through before it can become a boy. It's quite a challenge to be a male, even before birth!

One particular challenge, that can still go wrong is the failure of the testicle to descend into the scrotum. The testicle, as noted, begins its life in the abdomen, and must undertake a journey to reach the scrotum. Failure to achieve this journey is referred to as having an 'undescended testicle.' Let's take some time now to look at the testicle in more detail, before we talk about its pivotal role in the male physiology.

BALL GAMES - A CLOSER LOOK AT THE TESTICLE

Testicles are massively important for male characteristics in humans. The functions of the testicles can be summarised as 1) the production of Testosterone 2) the production of Dihydrotestosterone 3) the production of anti-Mullerian hormone and lastly but certainly not least, 4) the production of sperm.

In this section, I will briefly describe the embryology and anatomy of testicles.

Primitive gonads in the embryo become testicles under the influence of Testosterone. Oddly, the testes are first located in the abdomen, roughly at the level of the kidneys; they then have to go on a long and perilous journey to reach the scrotum, pulling down their blood supply and support structures with them. This journey is triggered by rising levels of Testosterone; without Testosterone, or if the levels of Testosterone are too low, then the testicles will simply not descend.

Sometimes, this process is not even complete by birth, but usually by one year of age the testes have finally settled in their final destination. If the process fails to complete, the testes are referred to as 'undescended' and either surgery or testosterone injections may be required to move them into their proper positioning. This is important, because the temperature within the abdomen is too high for testicular tissue, and will lead to long term damage, causing infertility and sometimes even cancer.

At this point, let's discuss the scrotum. The exact reason why humans have developed a scrotum is unknown. Many male mammals have abdominal testes which are perfectly fine with high abdominal
temperatures, and not only that, but they are nicely protected within the abdomen. Why it is an evolutionary advantage to put these precious organs in a sac outside of the body is unclear - it seems, logically, that is has less protection, does it not?

And yet, testicles are indeed put in harm's way by putting them in the scrotum. Not only that, but the human testicle is designed to function best at a temperature of 35 degrees celsius - which is almost 2 degrees
celsius lower than your typical human's body heat. In other words, they have lost the ability to exist within the abdomen, and must be actively cooled down to remain at a temperature lower than the rest of the body.

Besides hanging outside of the body, which in and of itself helps cool down the scrotum, the blood supply into the scrotum forms what's called the 'pampiniform plexus', whereby warm blooded arteries going into the scrotum are bolted down to cooler veins leaving the scrotum - causing a lot of heat loss from the arteries into the veins. This prevents warm abdominal blood from overheating the scrotum.

If the scrotum is allowed to regularly overheat, either due to poor heat loss mechanisms or due to much heat being applied (for example from having too many hot steamy baths) then this can cause loss of testicular function and fertility, which in some cases may even be permanent.

However, the testes don't work very well at cooler temperatures than 35 degrees celsius either.

So the human scrotum has 2 interesting mechanisms to conserve scrotal heat whenever things get cold down there: 1) the cremaster muscles pulls the testicles upwards, getting them closer to the warmer abdominal area 2) the dartos muscle scrunches up the scrotal skin, reducing it's
surface area, kind of like deflating a balloon. You can easily witness this effect on yourself by dipping your package into ice cold water - it will cause your balls to retreat and your scrotum to shrivel.

This picture from the classical Gray's Anatomy shows the two muscles:
[Image: image1143.gif]

Moving back to the testicles, let's briefly go over the anatomy of the human male testicle.

The outside of the testicle consists of a fibrous capsule that forms the wall of the testicle.

Inside, the testicle divides into somewhere between 250 - 300 compartments of coiled tubes; these are called the semniferous tubules. About 80% of a testicle's mass is actually made up of these tubules.

Between the tubules, there is a special type of tissue that contains blood vessels and Leydig cells (the cells that make hormones). This tissue is called interstitial tissue (which literally means 'inbetween the spaces' tissue).

The coiled tubules extend out of their compartments in order to join up together in a coiled supertube called the epididymis, which in turn then becomes an uncoiled tube called the vas deferens (also known as the ductus deferens). The vas deferens from each testicle joins up
with the seminal vesicle duct in the prostate to create an ejaculatory duct. The ejaculatory duct joins up with the urethra, which leads to the outside world.

Another picture from the classic Gray's Anatomy demonstrates the testicle's inner anatomy:
[Image: image1149.gif]

TESTOSTERONE

At this point, I'd like to give a brief very very very short summary of how Testosterone is actually made and its effects on the human body.

Testosterone, skipping a few biochemical steps, can be said to made from cholesterol.

Cholesterol is made by the liver by mixing fats with proteins (a small percentage of cholesterol is, however, absorbed from our diets). So adequate cholesterol levels are required to make enough testosterone. This cholesterol makes it's way to the testicle, where it is absorbed by Leydig cells which then convert the cholesterol to Testosterone.

Testosterone is part of the steroid hormone group of hormones. All steroid hormones work in a similar manner. The main mechanism of action is as follows: once the steroid hormone penetrates the cell, it migrates to the nucleus, where it forces some genes to become more active while causing other genes to become less active. Steroid hormones are in essence regulators of genetic expression. As a minor side mechanism, steroid hormones can also interfere with cell processes, altering the activity of some enzymes.

Testosterone, as we have seen above, is necessary for the creation of male organs during a pregnancy. These organs are referred to as the primary sexual characteristics - that which distinguishes boys from girls.

After birth, Testosterone production remains dormant for most of a boy's life but kicks in again at puberty. Testosterone then has effects on multiple areas of the body, changing the way they grow and develop. These changes in the body are referred to as secondary sexual characteristics - that which distinguishes men from women. The characteristics include: heavier and denser musculature, the growth of a beard, broadening of the shoulders, narrowing of the hips, growth of relatively more body hair, thickening of the vocal cords (which causes a lower voice pitch) and hair line changes (which may eventually lead to baldness).

In addition, testosterone works on the brain to alter behaviour, leading to a more driven approach to finding sex, increase use of aggression and expression of anger, a decreased subjective capacity to feel fatigue, an increased desire for thrill seeking behaviour even in the presence of increased risk (such as with addiction), and improved self-esteem.
Perhaps this is why women are attracted to horny violent drug party-animal drug addicts with narcissistic traits - perhaps because these traits may be signalling for relatively high testosterone levels?

When people take extra Testosterone, such as body builders might do, there are some predictable effects based on the above: obviously, their bodies grow more muscular; but it might also trigger aggressive outbursts (the so called Roid Rage) as well as addictive tendencies. The liver also has to detox all that excess testosterone which may lead to liver damage, and many tumours may respond quite happily to the growth stimulating effects of testosterone, which may explain why bodybuilders seem to have higher rates of liver cancer. It should also be noted that prostate cancer is thought to be especially stimulated by Testosterone and that having this cancer is a contra-indication to getting Testosterone treatment.

So Testosterone is very much the hormone that makes the man. It's made by the testicles, specifically the Leydic cells of the testicles, under a somewhat complicated system that is regulated by the brain. But before we further discuss the role of the testicle in male hormones, let's first find out about the other function of the testicle, namely

THE PRODUCTION OF SPERM

The story of sperm actually begins before puberty, indeed, it starts before birth. In the embryo, special sperm 'factory' cells are present that will produce sperm after puberty. They are referred to as germ cells or spermatogonia (female embryos also have germ cells, but they
are called oogonia).

These germ cells are constantly reproducing throughout a man's life through a process of cloning themselves, which is referred to as mitosis. Mitosis of these germ 'factory' cells continues through a boy's and later a man's life, although it is less in the extremes of age.

What this means is that your sperm factories are constantly making new, fresh clones of themselves - in other words, a man's ability to create sperm should last well into his old age. This is very much unlike female eggs - if you read my previous datasheet on the female menstrual cycle, you will know that a woman is born with a finite number of egg germ cells and they slowly die off until none of them are left, which then leads to menopause. Men, on the other hand, are constantly making new germ cells - regularly rebuilding their sperm factories, so to speak. As such, men pretty much preserve at least some of their fertility till the day they die, practically speaking.

Of course, germ cells are only factories for sperm, so a different process kicks in at around puberty that will trigger germ cells to become sperm.

So, to oversimplify things, a whole bunch of germ cells will clone themselves; then some of these clones will continue the tradition of being germ cells and will clone further generations, preserving the germ cell line
in the male body.

Some of the clones, however, will instead divide under a process called meiosis. This is the first step in the process of making sperm. Each germ cell can potentially generate 4 sperm cells.

I will briefly describe what happens in meiosis:
- First, the genetic material in the germ cells bundles up into groups that we callchromosomes. There are 46 chromosomes in the normal human cell (23 of them are inherited from your mother, and 23 of them are from your father).

- Then, the genetic material duplicates itself, so for a short while you have a cell that has way more chromosomes than normal: 92 chromosomes, to be specific. With this transformation of chromosomes, the germ cell is said to have become a primary spermatocyte.

- Then some gene swapping occurs at random within this primary spermatocyte. Basically, chromosomes join up in groups of four, creating 23 groups of tetrads, and then they go into this orgy of swapping genetic material, especially between the female-inherited and male-inheritied chromosomes. The result is brand new random combinations are created; this helps to ensure that the child you father is a unique random combination of your own ancestral lines from both your parent's sides.

- Then after the gene swapping, random pairs of chromosomes hook up together; and then the cell splits into two. (The randomization of the pairs in and of itself helps to contribute to the genetic uniqueness of sperm). Pairs of chromosomes are dumped into each of the two parts, leading to the creation of two cells that have 46 chromosomes each. These cells are referred to as secondary spermatocytes

- Then these secondary spermatocytes divide again into two cells, which we call spermatids; the pairs of chromosomes are randomly torn apart to create two spermatids that each have 23 chromosomes. (Again, the randomization helps to contribute to genetic uniqueness). These spermatids will mature into sperm, and they represent a man's contribution
to the genetic code of his child. These sperm consists of random mashups of a man's paternal and maternal genetic codes that he himself inherited at conception, with a few mutations thrown in.

To summarise: Germ cell (46 chromosomes) duplicates its genetic material to become a primary spermatocyte (92 chromosomes). One primary spermatocyte will then divide into two secondary spermatocytes with 46 chromosomes. These two secondary spermatocytes will also split, creating
four spermatids of 23 chromosomes each from the original germ cell. Each of these spermatids have unique genetic material due to the genetic shuffling that occurs in the meiosis process.

Meiosis may also lead to accidental errors happening the genetic material - these we call mutations. Mutations may be harmful, helpful, or neutral - there is no way to tell until the baby is made and the stresses of life are thrown upon it.

Spermatids migrate to the semniferous tubules, and there they grow a tail, and become fully-fledged sperm. Upon ejaculation, this tail, or flagellum to use the more correct term, will flail furiously and propel the sperm forward. However, in the tubules, the tails stay dormant and lifeless for now.

A possible problem arises, however. Your immune system is designed to attack foreign genetic material. After all, foreign genetic material usually represents a bacterial or viral invasion, and these bugs should certainly be destroyed. But remember, each spermatid has a unique genetic code which is very different from your own - that means your immune system will probably regard your spermatids as being 'foreign' genetic material. Therefore there must be a way to protect your fragile, genetically unique spermatids from the powerful immune system.

This is done through a blood-testicle barrier. This barrier is formed by Sertoli cells, which lovingly grow around maturing spermatids and shelter them from the body's immune system, as well as filtering potentional toxins out of the way of the spermatids. This they do until the spermatids migrate into the semniferous tubules and become sperm. This barrier also prevents reverse traffic - in other words, sperm DNA material is prevented from leaking into the host body and thereby causing an inflammatory response - after all, although you made the sperm, each sperm has its own unique genetic code, and is therefore a unique little lifeform all on
its own, derived from you but unlike you.

The sperm in the tubules are constantly pushed out by new spermatids coming in - so the sperm migrate further, entering the epididymus. The epididymus secretes special proteins which cause the sperm to mature further and also kickstart the sperm's tail mechanisms, giving the sperm
the ability to propel itself forward.

The entire process from germ cell to sperm takes about 70 days. Sperm production starts at puberty, and a young adult male will produce about 300 000 sperm a minute, or about 4 million sperm per day, each sperm genetically unique due to random gene shuffling and mutation during
meiosis.

Let's take a brief look at the structure of sperm, as we will need to be familiar with it in order to understand fertilization.

THE ANATOMY OF A SPERM

A sperm consists of 3 parts: the head, the midpiece, and the tail (also known as the flagellum).

[Image: 350px-Complete_diagram_of_a_human_sperma...en.svg.png]

The head is mostly composed of a dense mass of genetic material. At its tip it has a bubble filled with enzymes, called an acrosome. This bubble bursts in the present of an egg cell, releasing the enzymes and triggering off a chemical chain reaction that allows the sperm to fuse with the egg.

The midpiece consists of 2 major components: the mitochondrial spiral and microtubules. The mitochondrial spiral is sort of the engine of the sperm - it's job is to generate adenosine triphosphate (also known as ATP), which is the fuel that triggers off the majority of cell processes in the human body. The ATP molecules cause the microtubules to lengthen and shorten,
and this process causing the tail of the sperm to flip from side to side.

The tail consists mostly of microtubles, which originate in the midpiece. The tail is divided into an anterior, or front, compartment and a posterior, or back compartment. The microtubules of these compartments take turns contracting, and this causes the tail to dart back and forth
like a whip. This whip-like motion causes the sperm to propel forward.

Okay, so your children will begin as germ cells in your body, then they become sperm, then they have to be launched into a woman to make a new baby. But before we go into that, let's take about how the human male body supports sperm production and maleness during adult life. In otherwords, let's talk about hormones.

HORMONAL REGULATION OF MANLINESS

Men are men because of the effects of hormones on the body. We have already seen how important male hormones are for the formation of a baby boy. Once a boy is born, however, male hormones such as testosterone fade away as the male organs become dormant, at least until puberty.

It is the brain that controls the hormonal balance of the body - especially a part of the brain known as the hypothalamus. The hypothalamus is, in essence, the regulatory control centre of the body, controlling not only hormones, but diverse processes such as body temperature, thirst, hunger, the sleep-wake cycle, and so forth.

[Image: 800px-1806_The_Hypothalamus-Pituitary_Complex.jpg]

The hypothalamus regulates male sexual hormones through a hormone known as Gonadtropin Releasing Hormone, or GnRH for short. This hormone is released in pulses every 1 to 3 hours.

GnRH then binds to receptors in a nearby region of the brain called the anterior pituitary gland, also known as the adenohypophysis. A peculiar feature of these receptors is that they become fewer and fewer under continuous stimulation. What that means, practically speaking, is
that in the presence of continuous and non-pulsatile GnRH release, the receptors all die off and then the GnRH floats uselessly about not doing anything. In essence, continuous GnRH secretion causes chemical castration of the male at the brain level, and indeed it is used as such for some medical conditions.But because the hypothalamus releases GnRH in pulses, the receptors do not downregulate, because they are given short bursts of stimulation rather than continuous stimulation, and as
long as the stimulation is not continuous the receptors will remain. (I have explained this phenomenon in detail because it is essential in understanding puberty, which I will discuss in the next section).

After GnRH binds to receptors in the anterior pituitary, the anterior pituitary gland then produces two hormones: Follicle Stimulating Hormone, and Luteinizing Hormone. You may recognise these names if you read my explanation of the menstrual cycle. Although men do not
have follicles or luteums, nevertheless these are the exact same hormones and the names, which reflect their respective roles in the female menstrual cycle, have stuck. If the hormones had first been discovered in men, then perhaps they might have been called other things (perhaps
Sperm Stimulating hormone and Testoronizing hormone, but I digress).

The two hormones are also called the gonadotropins (which, translated into English from the Latin, literally means 'that which makes the genitals strong'). For convenience, I shall refer to Follicle Stimulating Hormone as FSH and Luteinizing hormone as LH.

The anterior pituitary makes FSH and LH and then releases them into the blood stream, where they will eventually drift into the testicles.

FSH goes into the Sertoli cells of the testicle, where it stimulates the production of sperm and also the production of Androgen Binding Protein. Androgen Binding Protein causes testosterone to accumulate in the Sertoli cells and in the Epididimus, where testosterone is necessary for maturation of the sperm. Without FSH, not only would no sperm be produced, but
without Androgen Binding Protein, there would be no testosterone accumulation to promote sperm maturation.

LH on the other hand goes into the Leydig cells of the testicle. Leydig cells have one main job: to make testosterone. This testosterone then either gets sucked into Sertoli cells (due to the effects of Androgen Binding Protein) or else diffuses into the blood stream in order to have effects on the body.

Note that to have manly characteristics, all you need is LH and functioning Leydig cells. If for some reason you only make LH but not FSH, you will have all the manly characteristics - but no sperm! This is one of many ways that men can be infertile.

The testicle can offer feedback to either increase or decrease FSH production. It does this through the production of various hormones which for convenience sake are divided into 'Inhibins' and 'Activins'. The testicle produces Inhibins in the presence of too much FSH, and these inhibins migrate through the blood stream until they find the anterior pituitary, where they suppress the release of FSH. On the other hand, if there is too little FSH, the testicle produces Activin, which stimulates the release of FSH. Activins also help stimulate sperm production.

Besides Inhibin and Activin, Testosterone itself provides feedback to the brain. Testosterone works on the hypothalamus and anterior pituitary to supress GnRH, FSH and LH release. In effect, in the presence of too much Testosterone, the entire hormonal support structure for maleness shuts down; this throttles the production of Testosterone, so Testorone levels drop; as Testosterone drops, the brain fires up again and releases GnRH, FSH and LH. The result is that Testosterone naturally follows a daily up and down rhythm, generally being lowest in the morning and highest in the afternoon.

The interaction between the hypothalamus, pituitary gland, and testicles is described in medical textbooks as the 'hypothalamic-pituitary-testis axis'. It is the hormonal foundation of manliness.

The axis can easily be disturbed. For example, taking external testosterone will cause that extra testosterone to shut down the axis. As long as there is excess extra testosterone being put into the human body, there will be no production of FSH or LH, and thus no internal production of testosterone. Since FSH is required for sperm production, what you end up having is a man with excessive manly characteristics but who are infertile. Hence you have huge, muscular body builders who go into roid rage at a moment's notice... but they have no sperm!

Sperm production can in fact take up to a year to return after stopping external testosterone intake, since the axis may take some time to recover from its shutdown. So, if you ever feel inadequate looking at those huge roided bodybuilders in muscle magazines, just remember, at least you have sperm!

So that's basically the sexual hormones in the adult male human; it's relatively simpler than the cyclical female hormonal cycle. However, through most of boyhood the hypothalamic-pituitary-testicular axis remains dormant. Let's have a look at how it activates to transition into adult functioning; in other words, let's talk about...

PUBERTY

As noted above, GnRH is released in pulses. If released continuously instead, then you get chemical castration. This is inf act what happens in boys before they hit puberty. Throughoutboyhood, GnRH is released in a constant, steady stream. The anterior pituitary gland's GnRH receptors are downregulated (die-off) to a point that the gland doesn't respond to GnRH at all. You can think of the anterior pituitary gland as becoming 'tolerant' to the GnRH, like the way drug users become increasingly tolerant of the drugs they take so that the drugs slowly stop working for them.

At puberty, through an as yet unclear mechanisms, this continuous GnRH release suddenly switches to pulsatile release. This causes GnRH receptors to start spawning in the anterior pituitary, which in turn kicks start the entire hormone production system of FSH, LH, and Testosterone.

Strictly speaking, medically, puberty in boys is the onset of viable sperm. Even if a man has clear male characteristics, such as a beard and deep voice, if he has never had sperm production then technically speaking he has not hit puberty. By definition, if a boy has not had any sperm production by the age of 20, then he has delayed puberty. If a man develops secondary male characteristics (increased muscle mass, beard, deep voice, etc) but has never had sperm, he is referred to as having a type of delayed puberty called eunuchoidism. Eunuchoidism can occur if LH and Testosterone production are normal but for whatever reason either FSH is not produced or FSH is utterly ineffective, perhaps due to a lack of receptors at the Sertoli cell.

In some cases delayed puberty is due to the failure of the brain to produce GnRH. These children are treated with spaced doses of GnRH to kickstart the hypothalamic-pituitary-testicular axis. The doses are spaced to mimic the body's pulsatile secretion of GnRH - it would be useless to give these boys continuous infusions of GnRH, that would just chemically castrate them!

Medically, premature puberty is the onset of sperm before the age of 9. This is often due to hormone-secreting tumour growths in the body or brain, and generally these boys must be thoroughly investigated to exclude cancers. Sometimes, a severe infection of the brain can also cause premature puberty. It is speculated that there is a specific area of the
hypothalamus that is designated to prevent pulsatile GnRH release, and that it is sensitive to damage by infection. If a boy gets a severe brain infection, otherwise known as encephalitis, this area can die off and when the boy recovers he ends up having pulsatile GnRH release and therefore puberty sets in.

If for whatever reason puberty must be delayed, GnRH can be given as a continuous infusion to cause chemical castration.

ALTERNATIVE SOURCES OF TESTOSTERONE

Testosterone isn't entirely made by the Leydig cells. About 5% of a man's total Testosteroneis made by the adrenal cortex, also under the influence of LH. The adrenal cortex will not make Tesosterone in the absence of LH. Excess testosterone in and of itself can suppress the production of testosterone in the adrenal cortex.

BINDING OF TESTOSTERONE

In the blood there is a molecule called sex hormone binding globulin. It loves to hunt down Testosterone and sticks to it, which makes the hormone useless. In fact, 98% of testosterone in the blood stream is stuck to sex hormone binding globulin. It is the 2% of testosterone left over that actually has an effect on the body.

That is why it is not accurate to take blood and measure the total Testosterone level in a sample, since most of a sample's Testosterone is inactive, bound Testosterone. To get an accurate picture of Testosterone levels, it is necessary to measure the free amount of Testosterone. Therefore when testing testosterone levels, it is better to test for both total and free Testosterone, which gives the most accurate picture of what is happening in the body.

Sex hormone binding globulin can rise in certain disease conditions, such as liver disease. In such disease states, the rising levels of globulin can neutralise what remains of the free Testosterone. Such patients may end up have normal total Testosterone levels, but will have abnormally low free Testosterone levels - so it is as if they did not have any testosterone at
all!

EXCRETION OF TESTOSTERONE

Alas, all things eventually break down and get used up. Most Testosterone is eventually broken down into what are called ketosteroid molecules. These ketosteroid waste products are eventually excreted in the kidneys through urine. Basically, every time we go to the toilet to pee, we piss away a part of our manhood.

THE EFFECT OF STRESS ON TESTOSTERONE

A short word on what stress does to the hypothalamic-pituitary-testicular axis. By definition, stress is the presence of increased cortisol levels in the blood. This increase may be triggered by a huge number of things - psychological stress, fear, depression, being physically assaulted, being infected with a flu virus, having major surgery, sleep deprivation,
starvation, etc. Any psychological or physical strain on the body can translate into stress, leading to that increased level of cortisol.

Now cortisol has a number of both good and bad effects, but let's limit the discussion to the effect of the male hormonal axis. Basically cortisol inhibits the entire axis. Cortisol suppresses the production and release of GnRH in the hypothalamus; in the anterior pituitary, it suppresses FSH and LH production and release. Not only that, but Cortisol also suppresses
the prodution of chemical receptors for GnRH, FSH, LH; that means even if the hormones are present, they are less likely to activate at their target organs and therefore drift uselessly about. The testicle, therefore, becomes less responsive to FSH and LH due to this receptor
downregulation; but in addition, Cortisol actually interferes with the production of Testosterone in the Leydig cells.

And it doesn't end there. Not only is there less Testosterone, but Cortisol downregulates Testosterone receptors in the whole body and also intereferes with Testosterone activity inside human cells - so even if the remaining Testosterone finds a receptor, it still has to overcome
Cortisol to activate properly.

I'll just give one good example of the consequences of this: Testosterone is necessary for maintaining heavy, strong muscles. So under chronic stress, what happens? Well, there will be less Testosterone, fewer Testosterone receptors at the muscle, and even if Testosterone gets in that muscle, it will face a lot of resistance to its effect. So one effect of chronic stress
is a drop in muscle mass and more difficulty in gaining muscle at the gym.

INVESTIGATING LOW TESTOSTERONE LEVELS

What if Testosterone levels just happen to be low? There are a couple of tests that a doctor can do to get some clues as to why the body is not making enough testosterone.

The standard blood tests for low testosterone are: total testosterone, free testosterone, prolactin, FSH and LH.

A low FSH or LH level suggests a failure of the brain to create the hormones necessary to make testosterone. High prolactin levels suggest pituitary failure due to a brain tumour. These patients will need to be managed by an endocrinologist. If this is a new thing, then it will be important to exclude a brain tumour by doing a brain scan, as a brain tumour can present
with failure to generate FSH and LH. In cases of delayed puberty, this may indicate pituitary failure to respond to GnRH or to failure of the hypothalamus to excrete GnRH in a pulsatile manner, if at all.

If FSH and LH levels are high, or even if normal when testosterone is low, then this usually indicated the failure of the testicle to make testosterone. The hormones are there to stimulate the Leydig cells, but the Leydig cells for whatever reason simply will not work. In older men, this is almost always due to aging, and can be managed by generalist or family
physician with testosterone injections. If there is any doubt as to the cause of testicular failure, thought, especially in young men, then referral to an endocrinologist or urologist is necessary.

Sometimes total testosterone is normal or even elevated, but the is a virtual shortage of testosterone - because the testosterone that is available is inactivated by sex hormone binding globulin. This is why it's a good idea to measure free testosterone. Free testosterone levels
may be low even in the presence of high total testosterone levels. The most common cause of this condition is liver disease, but in any case these patients require further investigations to find out what exactly is the source of the excess sex hormone binding globulin, and that diseased source must be managed.

I think I've discussed Testosterone enough for now. But there are other sex hormones that play their part in the human male. Let's briefly look at Oestrogen and Progesterone.

FEMALE HORMONES IN MEN

Just as FSH and LH are present in both men and women, so too are Oestrogen and Progesterone present in men. Although these hormones are considered to be 'female' hormones, they are also essential, in small amounts, to the healthy correct functioning of the male body (just as small
amounts of testosterone are needed in the female body).

OESTROGEN IN MEN

Most Oestrogen in the male body is made from Testosterone. Testosterone is converted into Oestrogen through an enzyme called Aromatase. Most of this conversion occurs in the Leydig cells where Testosterone is produced, but aromatase is also present in other tissues, most notably fat cells and the brain. Unfortunately, this means that overweight, fat men are going
to convert a lot more Testosterone into Oestrogen due to the extra fat cells they have. Since Testosterone helps with physical drive, these fat man have lower physical drive and thus do not like to exercise, so they tend to stay lazy and fat!

Oestrogen also works on the brain just like Testosterone, to suppress the release of FSH and LH. Thus too much Oestrogen can shut down the hypothalamic-pituitary-testicular axis, in effect shutting down Testosterone production as well.

Which begs the question, why do men even have Oestrogen? Oestrogen's main role in the male body is to regulate sperm production. A lack of Oestrogen can in fact cause infertility. And that's about it, as far as medical science goes. It may have other effects on the male body that are not yet properly understood.

PROGESTERONE IN MEN

The other 'female' hormone is progesterone. I won't go into the exact biochemical process, but Progesterone is made from cholesterol (as is Testosterone).

The role of progesterone in men is poorly understood. It has anti-inflammatory effects, and it promotes sperm production. It suppresses testosterone production, and competes against
testosterone in some tissues, such as the prostate. Progesterone receptors are present in the kidneys, heart and blood vessels, and in fat tissue; but what exactly it does in these tissues in the male body is unclear.

Progesterone receptors are also present in the brain and progesterone has as yet poorly understood effects on male behaviour. High progesterone levels seem to cause sedation in men, as well as reducing sexual drive. In fact, progesterone injections are used in some cases to suppress deviant sexual behaviour. Progesterone also stimulates breathing and appetite (so the sexual deviants who get progesterone injections tend to gain a lot of weight... and they tend to breath heavily...)

XENOESTROGENS AND OTHER ENDOCRINE DISRUPTERS

So above we see that Oestrogen and Progesterone can suppress Testosterone production. But what happens if a man gets foreign Oestrogen-like molecules into his system? Oestrogen-like molecules, also called xenoestrogens, can mimic Oestrogen's effects and therefore suppress Testosterone, and are apparently quite common in plastics and industrial processes. If you eat something wrapped in cling plastic, you probably have ingested some of the xenoestrogens of the plastic that clung to the food.

In the 90's there was a big scare when a research team lead by Skakkebaek claimed that male fertility in Europe was dropping due to the effects of pollution and the presence of xenoestrogens in the pollution.

However, Skakkebaek's research was exaggerated, some might even say erroneous. Some of the most polluted areas on the planet also have the highest fertility rates and highest population growth rates, which goes against his hypothesis. Places like Bangladesh, for example, are heavily polluted and yet still breeding.

Evidence does however show that exposure to xenoestrogens to pregnant women can cause abnormalities in their baby boys - such as small penis length, small testicular size, and other abnormalities of the reproductive tract.

In adults, Indian and Chinese factory works who work in industries that generate a lot of xenoestrogen pollution have been found to have sluggish, weak sperm with low sperm counts.

But otherwise, there is little good hard science about the effect of xenoestrogens on the human male body. So it's impossible to make a recommendation, based on science, as to what pollutants or plastics to avoid specifically.

One type of xeonestrogen is the phytoestrogen - oestrogens from plants. Some plants, such as soy, are rich in oestrogen like compounds. It is still unclear whether these oestrogen like compounds can actually interfore with male hormone balance, the evidence is rather conflicting.

So medically speaking, there is not really enough evidence to say whether one should take or avoid foods with phytoestrogens.

Well, we've talked a lot about hormones, and we've also covered embryogenesis and sperm.

However, all that testosterone and sperm are not going to be useful in making babies if you don't have a transport medium for the sperm to get it into a woman. So for that we need...

SEMEN

Multiple glands surround the ducts that move sperm from the testicle to the outside world. These glands are referred to as the male accessory glands, and they are three: the prostate, the seminal vesicles, and the bulbourethral gland.

These glands make secretions, which combine with the sperm-containing secretions of the testicle to make semen. Actually, 99% of semen is made by the accessory glands; the testicle only contributes 1% of the fluid that makes up a man's jizz.

The different glands have slightly different functions.

The prostate specialises in making a secretion that is rich in nutrients. These nutrients provide food for sperm. The prostate secretion also contains pH buffers that neutralises the hostile acidic environment of the vagina (sperm are most active with a neutral pH of 7.5).

The seminal vesicles also secrete nutrients but they also secrete prostaglandins, chemicals which influence sperm movement, but also muscle contraction. The prostaglandins stimulate muscle fibres in the urethra and in vagina and uterus - this stimulation helps propel semen
forward.

The bulbourethral glands mostly make mucous, which acts as a lubricant and buffer against harsh vaginal acids.

The nutrients that are secreted are mostly fructose, citric acid, Vitamin C and carnitine.

These molecules are essential for sperm movement, and deficiency in any one of them can cause slow moving or even paralysed sperm.

Accessory glands also secrete antibacterial molecules, and thus contribute to keeping the male genital tract free of infection.

Besides the above ingredients, semen also contains enzymes that cause various chemical reactions in semen. These enzymes first cause semen to be sticky, then to clot, and then to liquify. This makes sense - semen first needs to stick to the cervix; than it needs to hunker down in the uterus and not fall out; then it needs to liquify so that it can spread up to the
ovaries. You can see these changes for yourself by collecting some jizz and watching how it changers over the course of about 30 minutes. Most men's semen will liquify by the 30 minute mark. Alonger liquification time is a problem, because it prevents the sperm from freely swimming - poor liquification can be a cause of male infertility.

The most famous enzyme is probably Prostate Specific Antigen. It is made by the prostate, and its production is stimulated by prostate cancer. Prostate cancer can stimulate Prostate Specifc Antigen so much that it spills into the blood stream. Rising levels of Prostate Specific Antigen in the blood can therefore indicate a possible cancer in the prostate.

However other diseases, such as age-related prostate size increase or prostate infections, can also cause a rise in Prostate Specific Antigen.

Of note is that semen is rich in Zinc. It is unknown what zinc does in semen, or even how zinc even gets into semen. What is clear is that zinc deficiency causes infertility, so zinc must have a critical role to play in sperm and semen, but the exact nature of this role is still a mystery.

So now we have sperm, and semen to carry the sperm. It's almost like semen is a bus and the sperm are the passengers. Now we need a long, straight highway to get to the destination. We need an organ to that can become long and hard and penetrate deep into the female body, so that
the semen doesn't have to travel far to do deliver its passengers. For that, gentlemen, we have...

ERECTIONS

The penis is rich in blood vessels and in nerves. In fact, the penis has specialised blood vessels that act like massive sponges. When there is increased blood flow, these sponges soak up and fill up with blood, inflating like balloons. These specialised areas are called the
corpus spongiosum and the corpus cavernosum.

So really, erections are due to increased blood flow into the penis, filling up the corpus spongiusum and corpus cavernosum. As the fill up they inflate, cause the penis to become longer, harder, and stiffer. Also, as these vessels dilate, they exert a clamping effect on the blood vessels that take blood away from the penis, which further contributes to pooling of blood in the penis and contributes to the inflating effect.

[Image: Figure_28_01_06.jpg]

It is the nervous system that regulates this blood flow into and out of these areas. The nervous system is divided into 2 parts : the sympathetic nerve fibres and the parasympathetic nerve fibres. Sympathetic nerve fibres release adrenaline, which causes blood vessels in the penis to clamp down and become smaller, in effect throttling the blood supply into the penis and keeping it flaccid. Parasympathetic nerve fibres, however, stimulate the release of nitric oxide. Nitric oxide in turn causes the release of a molecule called Cyclic GMP, which causes blood vessels to dramatically dilate, forcing blood to gush into themselves.

Every erection has something of a built-in time limit due to the effects of an enzyme called Phosphodiesterase-5. This enzyme destroys cyclic GMP, which causes the blood vessels to contract again and then the penis becomes flaccid again. There are medications, such as Viagra, available that can block the action of Phosphodiesterase-5. By blocking this enzyme, more cyclic GMP becomes available for a longer duration, thus improving erection duration and strength. Cyclic GMP also has other functions in the human body, though, for example the detection of blue light in the eye. This is why some people who use drugs like Viagra will complain that their vision becomes blue-tinged - this is because the blue receptors in the eye become overactive. It is rather amusing that Viagra's side effect is to turn the world into a 'blue movie'. A more potentially devastating side effect, though, can occur if a patient is already taking nitric oxide for a heart condition (nitric oxide also increases blood flow into the heart, not just the penis. In fact, Viagra was first developed in order to be a heart drug). The combination of nitric oxide and Viagra-like drugs can cause sudden death due to a massive, sudden loss of blood pressure control, especially around the heart.

The triggering of an erection by the parasympathetic nervous system is referred to as the Erection Reflex. Interestingly, erections are controlled by the spine. There are special spinal nerves that exist to cause erections. That's why some paraplegic or quadriplegic patients can still have erections (and bear children) - even if the brain cannot reach the penis, as long as the spinal centre is intact, it has enough neurological computing power to cause an erection by itself. Sadly, such paralysed patient cannot feel their erections or other sensations coming from their penis, but at least they can have children the normal way and give pleasure to their significant others.

That said, these spine centres do not operate completely independently - they are willing to take suggestions from other parts of the body. Most obviously, the brain has direct connections to the spinal erection centres, so that psychological stimuli can cause an erection. Parts of the male body can also be directly hard wired to connect to the spinal centres. Therefore, touching of the penis, scrotum, lips, tongue, ear lobes and nipples can also cause an erection, as touch signals from these areas can go directly to the spinal erection centres and trigger off the erection reflex. However, exactly which body areas can trigger off an erection probably varies a lot from person to person, and depends a lot on
genetically controlled wiring patterns between the body and the spine. That is why one person may find it intensely erotic to have their ear lobes licked, while another person honestly cannot understand what the fuss is about ear lobes. Some people may find kissing more erotic than other people. Some people may have unusual 'trigger' areas connected to their spinal erection centres, like perhaps the feet. So erotic triggers can vary a lot from individual to individual.

Erections can also be triggered by the parasympathetic nervous system during sleep. There are phases in sleep when the parasympathetic nervous system throughout the body activates, and as a side-effect an erection can occur independently of the erection reflex. This can be rather troublesome if you have to pee in the middle of the night and you wake up in the middle of one of these parasympathetic phases.

As you can see, a good working blood system is required for an erection. Therefore, it is not unusual for men to have problems with their erection when their blood vessel systems are diseased. The most common blood vessel diseases are hypertension, diabetes mellitus, and cholesterol-deposition (atherosclerosis). These diseases all damage the lining of the blood vessel wall. This damage reduces nitric oxide production (because nitric oxide is manufactured in blood vessel walls) and it decreases the ability of the blood vessel walls to react to nitric oxide. So generally, when a patient complains of erectile dysfunction, a doctor should
first consider blood vessel wall disease and at the minimum check the blood pressure, blood glucose and blood cholesterol and treat these if they are abnormal, before tacking the erectile dysfunction itself. In Africa, another common disease that destroys erections is HIV. The HIV
virus likes to attack the blood vessel wall and damage it, so ironically it is a sexually transmitted disease that sometimes prevents its own transmission in the late stages of the infection.

So we now have the 3 male ingredients necessary to make a new baby - the sperm, the semen to carry the sperm, and the erection to carry the semen to its destination. Now we need to mix the 3 ingredients together, to get what is medically referred to as...

CLIMAX

By defintion, sexual climax in men consists of emission and ejaculation.

Emission is the movement of sperm out of the vas deferens into the urethra. This movement is due to contractions of a type of muscle called smooth muscle, that lines all the piping in the male sexual system.

Ejaculation is when semen is expelled through the urethra at speed. This
movement is due to contractions of the bulbocavernosus muscle, a type of muscle that is called skeletal muscle (because it is connected to the skeleton). Ejaculation is allegedly accompanied by a pleasurable sensation, that scientists have termed 'orgasm'.

In order to prevent back wash into the bladder, the bladder sphincter contracts at the time of ejaculation, prevent accidental ejaculation into the bladder instead of to the outside world.

In some men, the force of the bulbocavernosus muscle is strong enough to cause semen to squirt forcefully; however, in many men the force generated is not enough to cause squirting and instead the semen dribbles out. Therefore some men are squirters, and some are dribblers.

Since human men have rather long penises compared to many other mammals, whether a man is squirter or a dribbler is irrelevant - the penis is long enough that the head of the penis will push the semen pretty much to the end of the vagina, which is all that is required. Some animals have
short penises (relative to the vagina of their female counterpart) and then squirting is required, otherwise the semen won't reach the end of the vagina; but in humans this is an evolutionary leftover that is no longer required.

Strangely, the contractions of the muscles involved in climax are stimulated by the sympathetic nervous system. During climax, the sympathetic nervous system activates throughout the penis.
However, this works to oppose the activity of the parasympathetic nervous system which was causing the erection in the first place, and therefore climax is usually also accompanied by contraction of the blood vessels and a sharp reduction in penis blood flow, leading to a loss
of the erection and a return to flaccidity.

In a sense, achieving climax causes a race to occur - once started, the process will cause the penis to go flaccid, so the semen needs to urgently escape the penis before the erection is lost.

After climax, it takes a while for the sympathetic nervous system to shut down and the parasympathetic nervous system to recover, meaning it is difficult for the short time period after climax to have an erection.

Well, we are almost at the end of this exploration of male physiology. Let's close the circle - we started with embryology, and having deposited some semen into the vagina, let's go back to where we started, embyrology.

FERTILIZATION

Once deposited into the female genital tract, sperm can survive for approximately 6 days.

Semen contains a variable amount of sperm, but generally there are about 50 - 120 million sperm per millilitre of semen, with the typical ejaculate being 2 - 5 millilitres (It's an interesting thought - with just one ejaculation, there are up to 600 million unique individuals that a man can father!).

However, the female genital tract is a hostile, strange and vicious land for sperm. Most sperm die, or get trapped in female genital secretions, and some are destroyed by the woman's immune system. Some sperm even get lost, swimming away from the egg cell instead of toward it.

A few sperm eventually reach the egg cell in a region known as the fallopian tube. These few remaining survivors, perhaps numbering only a few hundred (of the original millions) must know compete with one another to fertilise the egg. Usually only one sperm will get the prize. A sperm must first penetrate the tought outer layers of the egg cell. It does this by releasing the enzymes from the acrosome on its head, and these enzymes dissolve a passage down into the core of the egg. Once a sperm reaches the cell membrane of the egg cell, which lies just beneath the tough outer layers, the sperm's head then fuses with the membrane of the egg. Two things then happen - first, a reaction is triggered off in the egg cell's cell membrane, which releases molecules that cause a rapid, almost instantaneous hardening of the egg cell outer layers and membrane. This prevents any further sperm from being able to penetrate deeper into the egg. Secondly, the sperm's head bursts open and the genetic cargo of the sperm is released into the egg cell, where it fuses with the genetic material of the egg. Once this process begins, the egg is now referred to as a zygote. The zygote will migrate into the uterus, implant on the uterine wall, and become an embryo, and then a baby.

And so we end off more or less where we started. The circle is complete.

Anyway, I hope you found this informative and maybe even mildly entertaining. Any questions?
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#2

Brief Intro to Male Physiology (Might be NSFW)

Why go to college when there's scholar dudes like you on the forum...
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#3

Brief Intro to Male Physiology (Might be NSFW)

Thank you for taking the time to make such a meticulous post.

I am probably being stupid - it happens at the best of times - and I am no scientist, but in the first section you talk about there being genes in the cell nucleus, with each gene being made up of chromosomes. You then talk about the SRY gene as a chromosome. My understanding is that it is a gene, and that it releases certain proteins which binds DNA. But how can it be a gene, which forms part of the region of a chromosome according to your explanation, which is itself a tiny constituent part of a gene? Could you explain that part a little more when you have a moment? It was a fascinating and informative post from start to finish, and I am very pleased to know all sorts of interesting things I didn't a few minutes ago.
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#4

Brief Intro to Male Physiology (Might be NSFW)

Quote: (07-06-2016 04:27 PM)H1N1 Wrote:  

I am no scientist, but in the first section you talk about there being genes in the cell nucleus, with each gene being made up of chromosomes. You then talk about the SRY gene as a chromosome. My understanding is that it is a gene, and that it releases certain proteins which binds DNA. But how can it be a gene, which forms part of the region of a chromosome according to your explanation, which is itself a tiny constituent part of a gene? Could you explain that part a little more when you have a moment? It was a fascinating and informative post from start to finish, and I am very pleased to know all sorts of interesting things I didn't a few minutes ago.

I think the bold part above is where you have made an error. Chromosomes are made of genes (by genes, I mean strands of DNA), not the other way round. This picture from wikipedia illustrates it well.

[Image: Eukaryote_DNA-en.svg]

Now, on a specific chromosome called the Y chromosome, there is a special strand of DNA called the SRY gene. This strand of DNA triggers off maleness in the embryo. It does this by creating certain proteins, and these proteins in turn cause a chemical cascade of reactions, that alter how cells work.

So basically, out of your 46 chromosomes, there is only one chromosome that has the genes (the DNA) for your maleness. In fact, that maleness DNA is only a tiny region on the Y chromosome. So the only thing that stood between you and becoming a female was a few tiny threads of DNA on a tiny region on an already tiny chromosome! Here is an electron microscopy photography of a normal and a Y chromosome sitting next to each other - the Y chromosome is on the right. Note how tiny the SRY region is on the chromosome:
[Image: XYchromosome.jpg]

As an interesting side note: although bizarrely X and Y chromosomes actually look like an X and Y, as seen on the photo above, they were named long before their shapes were discovered. In the 19th century, scientists where trying to figure out how sex was determined, and there was a belief that some sort of specific mystery factor determined gender. This mystery factor was labeled by someone as 'Factor X', and the name stuck. Eventually someone figured out that there must be a second factor, and since Y follows X, it was called 'Factor Y'. This was before powerful microscope techniques confirmed the existence of these things.

What I didn't get into, because I wanted to keep the explanation as simple as possible, is the fact that the Y chromosome must always buddy up with an X chromosome to work, which is why men are referred to as being genetically XY. If an X chromosome fails to buddy up, then the embryo is referred to as being OY, which as far as I know is incompatible with life and will cause a miscarriage.

Women, in general, have two X chromosomes that buddy up. Therefore women are referred to as being genetically XX.

Interestingly, though, it is possible for a baby to have only one X. In other words, to be XO, with an X chromosome that isn't buddied up to another X or Y. But although it is possible for a baby to be born with such a make-up, these type of genetic conditions usually have severe consequences on the child's development (more often than not there is mental retardation, for example) and they are generally infertile.

On occasion, an extra chromosome partner may jump in, causing bizarre combinations such as XYY or XXY. Which again, is usually associated with severe consequences.

Complicating the picture is the fact that women can express mosaicism. Women are capable of having multiple genetic codes in their bodies that are randomly assigned across the body. It is unclear as to why this happens but it is thought that in some twin pregnancies, the one twin may parasitically devour the other twin and incorporate its body into itself. This can cause weird situations where a woman may have scatterings of XY tissue in an otherwise XX body, if they devoured a twin brother; alternatively, they can have two sets of XX if they devoured a twin sister. Women of this type can often be reasonably healthy and functioning and even have children, but if there is a lot of XY tissue scattered in their bodies they may be somewhat masculinised.
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#5

Brief Intro to Male Physiology (Might be NSFW)

[Image: clap.gif]
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#6

Brief Intro to Male Physiology (Might be NSFW)

I have a question regarding rawdogging.
Assuming that one pulls out before every ejaculation, could there be any truth to the idea that urinating between rounds kills any sperm that might be left in the pipes/precum for the next round?
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#7

Brief Intro to Male Physiology (Might be NSFW)

^ Urinating should clear out any residual sperm in your urethra. But obviously if you cum again your testes will produce and send out more.

Precum, technically, does not and should not contain sperm, but sometimes does.

The cowper gland produces pre-cum, which is completely separate from the testes, prostate, and the rest of semen production. So precum by itself is sperm-free.

I think what happens is a man might have leftover sperm from a prior ejaculation somewhere in the urethra, so when the next round of precum comes out, it can impregnate. So you get misleading answers, even from doctors who might say 'precum sometimes contains sperm', when the real answer is IF it picks up residual sperm along the way.
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#8

Brief Intro to Male Physiology (Might be NSFW)

Quote: (07-07-2016 06:57 PM)Nightfled Wrote:  

I have a question regarding rawdogging.
Assuming that one pulls out before every ejaculation, could there be any truth to the idea that urinating between rounds kills any sperm that might be left in the pipes/precum for the next round?

I've answered this question somewhere before on this forum in another thread, but:
- if you was your penis of any semen that might still be sticking to it
- and you urinate

then the chances of being able to impregnate anyone without ejaculating again are very slim. Not impossible, but nearly impossible.

I think the confusion with regards to pre-cum stems from the fact that if you ejaculate, and then immediately go back in, then the pre-cum on your penis tip can contain sperm. Sperm can survive on the penis tip for a few hours and have been found on the penis tip after ejaculation. That's why if you are practicing the withdrawal method, and you want to raw dog for round two, you have to wash the penis and urinate.
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#9

Brief Intro to Male Physiology (Might be NSFW)

Thank you very much for pointing out my error, and for giving such a patient and thorough explanation. I've learned a lot from your thread.
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#10

Brief Intro to Male Physiology (Might be NSFW)

Thomas, thank you for the great post.

I have a few questions.

Quote: (07-06-2016 01:19 PM)Thomas the Rhymer Wrote:  

It should also be noted that prostate cancer is thought to be especially stimulated by Testosterone and that having this cancer is a contra-indication to getting Testosterone treatment.

Although this is still the point of view thought in medical school, more recent work seems to reject this notion.

http://www.lifeextension.com/Magazine/20...er/Page-01

Saturation explains the paradox in this way. At very low levels of T, near the castrate range, prostate growth is very sensitive to changes in T concentration. Thus, severely lowering testosterone will definitely cause prostate cancer to shrink; adding testosterone back will cause the cancer to regrow. However, once we get above the point where the prostate is saturated with testosterone, adding more testosterone will have little, if any, further impact on prostate cancer growth. Experimental studies suggest the concentration at which this saturation occurs is quite low.
In other words, the old analogy I learned in training was false. Testosterone is not like food for a hungry tumor. Instead, a much better analogy is, “Testosterone is like water for a thirsty tumor.” Once the thirst has been satisfied, prostate tumors have no use for additional testosterone. And the vast majority of men with low testosterone appear to have prostates that are not particularly thirsty.


A rat study I’ve seen suggested that prostate cancer was stimulated by estradiol, but not by testosterone.
What is your take on this?

Quote: (07-06-2016 01:19 PM)Thomas the Rhymer Wrote:  

Of note is that semen is rich in Zinc. It is unknown what zinc does in semen, or even how zinc even gets into semen. What is clear is that zinc deficiency causes infertility, so zinc must have a critical role to play in sperm and semen, but the exact nature of this role is still a mystery.

I thought that zinc was important for the proteins that influence the transport of cholesterol to the mitochondria (like StAR), where the cholesterol is converted to pregnenolone, but I might be wrong.

Quote: (07-06-2016 01:19 PM)Thomas the Rhymer Wrote:  

The most common cause of this condition is liver disease, but in any case these patients require further investigations to find out what exactly is the source of the excess sex hormone binding globulin, and that diseased source must be managed

Can you explain the hepatic metabolism of SHBG or is this process still unknown?

I am in this case and alternative therapies serve me well, but I would like to have a deeper understanding. Unfortunately I cannot find any text/papers that discusses SHBG metabolism; they all seem to focus on the correlation between SHBG/insulin/diabetes.

Thanks again for the very informative post!
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#11

Brief Intro to Male Physiology (Might be NSFW)

Quote: (07-07-2016 08:21 PM)Disco_Volante Wrote:  

^ Urinating should clear out any residual sperm in your urethra. But obviously if you cum again your testes will produce and send out more.

Precum, technically, does not and should not contain sperm, but sometimes does.

The cowper gland produces pre-cum, which is completely separate from the testes, prostate, and the rest of semen production. So precum by itself is sperm-free.

I think what happens is a man might have leftover sperm from a prior ejaculation somewhere in the urethra, so when the next round of precum comes out, it can impregnate. So you get misleading answers, even from doctors who might say 'precum sometimes contains sperm', when the real answer is IF it picks up residual sperm along the way.

Yes, it is the same principle as the dynamic flow of urine "washing out" bacteria. Longer urethra in males (longer way to travel and high flow) with flow of anything disables bacteria in that they can't stick as easily to the walls and climb into the bladder for example. Similarly, if you theoretically piss enough, you'll wash the existing sperm out/acidify them/make the whole situation less hospitable for them to stick around as viable.
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#12

Brief Intro to Male Physiology (Might be NSFW)

Quote: (07-08-2016 08:47 AM)PhDre Wrote:  

Thomas, thank you for the great post.

I have a few questions.

Quote: (07-06-2016 01:19 PM)Thomas the Rhymer Wrote:  

It should also be noted that prostate cancer is thought to be especially stimulated by Testosterone and that having this cancer is a contra-indication to getting Testosterone treatment.

Although this is still the point of view thought in medical school, more recent work seems to reject this notion.

http://www.lifeextension.com/Magazine/20...er/Page-01

Saturation explains the paradox in this way. At very low levels of T, near the castrate range, prostate growth is very sensitive to changes in T concentration. Thus, severely lowering testosterone will definitely cause prostate cancer to shrink; adding testosterone back will cause the cancer to regrow. However, once we get above the point where the prostate is saturated with testosterone, adding more testosterone will have little, if any, further impact on prostate cancer growth. Experimental studies suggest the concentration at which this saturation occurs is quite low.
In other words, the old analogy I learned in training was false. Testosterone is not like food for a hungry tumor. Instead, a much better analogy is, “Testosterone is like water for a thirsty tumor.” Once the thirst has been satisfied, prostate tumors have no use for additional testosterone. And the vast majority of men with low testosterone appear to have prostates that are not particularly thirsty.


A rat study I’ve seen suggested that prostate cancer was stimulated by estradiol, but not by testosterone.
What is your take on this?

Testosterone clearly drives prostate cancer, given that anti-testosterone treatments usually causes dramatic reductions in prostate cancer growth. However, the 'rate-limiting factor' is not testosterone, but testosterone receptors. In other words, it's the interaction between testosterone and testosterone receptors that determines growth of prostate cancer, not simply the level of testosterone.

This is the 'saturation' model of prostate cancer and it evolved to explain why massively high doses of testosterone do not seem to increase the risk of prostate cancer.

This model is still theoretical and it is unclear what the clinical significance of it is. In other words: If I give a patient testosterone, to what extent a am I slaking the tumour's thirst? As a generalist doctor, I don't know. Hence, for now, I would still not give testosterone to a known prostate cancer patient unless it was under a specialist urologist's recommendation.

Oestrogen could very well play a role in prostate cancer (the actual chemical reactions that trigger it are still unknown, after all) but given that anti-testosterone drugs work so well in prostate cancer, it's generally accepted that testosterone is the main culprit. Obviously, medical knowledge is continuously changing and new data may change our understanding over time.


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Quote: (07-06-2016 01:19 PM)Thomas the Rhymer Wrote:  

Of note is that semen is rich in Zinc. It is unknown what zinc does in semen, or even how zinc even gets into semen. What is clear is that zinc deficiency causes infertility, so zinc must have a critical role to play in sperm and semen, but the exact nature of this role is still a mystery.

I thought that zinc was important for the proteins that influence the transport of cholesterol to the mitochondria (like StAR), where the cholesterol is converted to pregnenolone, but I might be wrong.

This is plausible but as far as I know there is no proof of this. There are multiple theories of zinc's role in sperm and none of them are properly proven.


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Quote: (07-06-2016 01:19 PM)Thomas the Rhymer Wrote:  

The most common cause of this condition is liver disease, but in any case these patients require further investigations to find out what exactly is the source of the excess sex hormone binding globulin, and that diseased source must be managed

Can you explain the hepatic metabolism of SHBG or is this process still unknown?

I am in this case and alternative therapies serve me well, but I would like to have a deeper understanding. Unfortunately I cannot find any text/papers that discusses SHBG metabolism; they all seem to focus on the correlation between SHBG/insulin/diabetes.

Thanks again for the very informative post!


Liver disease is the common example simply because the liver makes so much of SHBG. Other tissues can also make SHBG too.

Liver diseases have odd effects at times - other organs tend to shut down when sick, whereas the liver at times overcompensates when sick. So it starts manufacturing too much SHBG in the presence of liver disease. Other glonulins are also released too much, so it's not only SHBG. The exact mechanisms why the liver does this are still not entirely understood.

Another mechanism that enhances the effect of SHBG is the fact that the liver production of albumin drops when the liver is diseased. Albumin binds harmlessly to testosterone and helps transport it from place to place. Unlike SHBG, it does not inactivate testosterone. So when albumin level drop, there is less competition for SHBG and it is allowed to inactive more testosterone. This is referred to as an altered albumin-globulin ratio.

Once made by the liver, SHBG goes into the blood stream and then rapidly goes into tissues all over the body. Once there, it probably slowly degrades with time by spontaneous chemical breakdown.
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