The evolutionary development of males provides critically important understanding and insight into the biological vulnerabilities of males.
Book excerpt from Your Inner Fish
Shark Past: Hernias
“Our propensity for hernias near the groin, results from taking a fish body and morphing it into a mammal.
Fish have gonads that extend toward their chest, approaching their heart. Mammals don’t, and therein lies the problem. It is a good thing that our gonads are not deep in our chest and near our heart (although it might make reciting the Pledge of Allegiance a different experience). If our gonads were in our chest, we wouldn’t be able to reproduce.
Slit the belly of a shark from mouth to tail. The first thing you’ll see is liver, a lot of it. The liver of a shark is gigantic. Some zoologists believe that a large liver contributes to the buoyancy of the shark. Move the liver away and you’ll find the gonads extending up near the heart, in the “chest” area. This arrangement is typical of most fish: the gonads lie toward the front of the body.
In us, as in most mammals, this arrangement would be a disaster. Males continuously produce sperm throughout their lives. Sperm are finicky little cells that need exactly the right range of temperatures to develop correctly for the three months they live. Too hot, and sperm are malformed; too cold, and they die. Male mammals have a neat little device for controlling the temperature of the sperm-making apparatus: the scrotum. As we all know, the male gonads sit in a sac. Inside the skin of the sac are muscles that can expand and contract as the temperature changes. Muscles also can expand and contract as the temperature changes. Muscles also lie in our sperm cords. Hence, the cold shower effect: the scrotum will tuck close to the body when it is cold. The whole package rises and falls with temperature. This is all a way to optimize the production of healthy sperm.
The dangling scrotum also serves as a sexual signal in many mammals. Between the physiological advantages of having gonads outside the body wall, and the occasional benefits this provides in securing mates, there are ample advantages for our distant mammalian ancestors in having a scrotum.
The problem with this arrangement is that the plumbing that carries sperm to the penis is circuitous. Sperm travel from the testes in the scrotum through the sperm cord. The cord leaves the scrotum, travels up toward the waist, loops over the pelvis, then goes through the pelvis to travel through the penis and out. Along this complex path, the sperm gain seminal fluids from a number of glands that connect to the tube.
The reason for this absurd route lies in our development and evolutionary history. Our gonads begin in development in much the same place as the shark’s: up near our livers. As they grow and develop, our gonads descend. In females, the ovaries descend from the midsection to lie near the uterus and fallopian tubes. This ensures that the egg does not have far to travel to be fertilized. In males, the descent goes farther.
The descent of the gonads, particularly in males, creates a weak spot in the body wall. To envision what happens when the testes and spermatic cord descend to form a scrotum, imagine pushing your fist against a rubber sheet. In this example, your fist becomes equivalent to the testes and your arm to the spermatic cord. The problem is that you have created a weak space where your arm sits. Where once the rubber sheet was a simple wall, you’ve now made another space, between your arm and the rubber sheet, where things can slip. This is essentially what happens in many types of inguinal hernias in men. Some of these inguinal hernias are congenital—when a piece of the gut travels with the testes as it descends. Another kind of inguinal hernia is acquired. When we contract our abdominal muscles, our guts push against the body wall. A weakness in the body wall means that guts can escape the body cavity and be squeezed to lie next to the spermatic cord.
Females are far tougher than males, particularly in this part of the body. Because females do not have a giant tube running through it, their abdominal wall is much stronger that a man’s. This is a good thing when you think of the enormous stresses that female body walls go through during pregnancy and childbirth. A tube through the body wall just wouldn’t do. Men’s tendency to develop hernias is a trade-off between our fish ancestry and our mammal present.” – pages 193 – 196
As you can see male evolution leads to biological vulnerabilities. Hormones were critically important in the evolution of male reproductive morphology from their fish to mammal development. Those hormones played the staring role in the descent of male testicles from their abdomen to their current location. What happens when those hormones are disrupted and those testicles don’t descend?
My 12-year-old son commented, “Mom, Oscar stayed a fish!” That was his statement while we were watching, “Your Inner Fish.” (He’s a smart little bugger) I explained to him why his cousin’s health was altered when he had an undescended testicle and why the doctors should have removed it altogether. It would immediately prevent and lower his cancer risks and here’s why.
Our Stolen Future provided much understanding.
“British researchers report a doubling in the number of cases of undescended testicles in England and Wales between 1962 and 1981, and similar increases have been reported in Sweden and Hungary. Men with undescended testicles have a higher risk of testicular cancer and typically have lower sperm counts and more abnormal sperm. There also appears to be an increasing incidence of the genital defect hypospadia.
In his earlier work, Skakkebaek had slowly accumulated evidence that all these abnormalities stem from developmental errors that take place in the womb, leading him to suspect they might have a common cause. He first found signs that prenatal event might play a role in testicular cancer while exploring the causes of male infertility. Examining tissue samples taken from the testicles of infertile men, he noticed strange-looking cells resembling the fetal germ cells that evolve during normal development into the testicular cells that produce and nurture sperm in mature males. The next clue came when some of the infertile men with aberrant cells later developed testicular cancer. Then he found the same abnormal cells in a boy with undescended testicles, who also developed cancer a decade later. It appeared that the abnormal cells had given rise to the testicular cancer and that men suffering from infertility or certain genital defects were at greater risk of having such cells.
At the same time that Skakkebaek was conducting his review of sperm numbers, another researcher in Edinburgh, Scotland, was also puzzling about the increase in male reproductive problems. Richard Sharpe of the Medical Research Council’s Reproductive Biology Unit was exploring possible explanations for the increase in undescended testicles and the drop in human male sperm counts. He, too, began to suspect that prenatal events might be responsible.
When Sharpe and Skakkebaek met at a conference and discovered they were thinking along similar lines, they began collaborating. In May 1993, they published a paper in the distinguished British medical journal The Lancet, proposing that the cause of the falling sperm counts and increased reproductive abnormalities in men was increased exposure to estrogens in the womb. They cited the DES experience and laboratory studies as support for this hypothesis, noting that prenatal exposure to elevated levels of synthetic or natural estrogens resulted in reduced sperm counts and an increase in the incidence of undescended testicles, hypospadias, and possibly testicular tumors in male offspring.
Animal studies had also provided an insight into how elevated estrogen levels in the womb might limit the number of sperm a male produces in adulthood by inhibiting the multiplication of key cells in the testicles known as Sertoli cells, which orchestrate and regulate the production of sperm. Since each Sertoli cell can support only a fixed number of sperm, the number a male acquires early in life will ultimately limit the number of sperm he can produce as an adult. During male development, the pituitary gland secretes a follicle-stimulating hormone and thereby limits the growth of Sertoli cell numbers.
Of course, one has to bear in mind that many chemicals can undermine male fertility, acting not just before birth but during childhood and adulthood as well. Prenatal exposure to synthetic estrogens is just one of many assaults on male reproductive potential. As we’ve seen, U.S. Environmental Protection Agency reproductive toxicologist Earl Gray has discovered that some synthetic chemicals act as potent androgen blockers and may pose an even greater threat to males than estrogen chemicals. Nevertheless, Sharpe and Skakkebaek’s theory offers an eminently plausible explanation of how estrogens might be having a major impact of male fertility by disrupting development….
The latest sperm count studies, however, add weight to the theory that the cause of the precipitous drop in sperm counts in some prenatal event rather than later damage caused by chemical contaminants or bad habits. If sperm counts were dropping because of adult exposure to increased contamination, smoking, or alcohol or because of venereal disease, they would be dropping in older men as well as younger men. The fact that the sperm counts are lower in younger men and correlate inversely with date of birth argues that the damage was done in the womb.” – Our Stolen Future by Theo Colborn (pages 175 – 177)
And males, that’s why you should care a great deal about female health because your first home is a womb and it’s being destroyed which directly impacts your own health. Dr. Theo Colborn rightly called our ruling class industrialists “womb terrorists.” They certainly know how to manufacture many kinds of terrorists all across our globe and they cause much destruction.
Biological development is a remarkable orchestration that makes a symphony boring in comparison. The sonic hedgehog gene is responsible for building the hand. The gene is like first violin and when it gets turned on, it chemically alerts the entire string section to play so all the digits form properly. Sniper fire from an organochlorine munition like thalidomide silences the sonic hedgehog gene and many other critically important genes during development so the entire string section remains silenced and no limbs are formed.
Some genes like the Sox9 are triggered to play by hormones so instead of the strings playing, the trumpets belt it out and males form. Unfortunately for some males, their development is altered by munition technologies from the benzene branch and they are feminized or suffer from teeny weeny syndrome and more…
Sox9? That’s the best name they could come up with for such a critically important gene? (Poor males! That’s not going to stick in anyone’s brain! Rocket launcher gene…)
Hormones: Chemical Messengers That Work in Parts per Trillion From Our Stolen Future Theo Colborn
Sex determination is regulated by the Sox9 gene. During testis differentiation, this gene is directly targeted by the product of the Y chromosome–encoded gene Sry. The regulatory region of Sox9 is complex, which is typical of genes with multiple roles in development. Gonen et al. find that a single far-upstream 557–base pair element is critical for up-regulating Sox9. Without it, XY mice develop as females instead of males. The 557–base pair enhancer is conserved, likely to be relevant to human disorders of sex differentiation, and probably essential because it acts early in a time-critical process, and any failure allows ovary-specific factors to dominate.
http://discovery.ucl.ac.uk/10059532/
Sex reversal following deletion of a single distal enhancer of Sox9
https://science.sciencemag.org/content/360/6396/1469
Their technologies have hijacked and destroyed so much life and health. When will you wake up and stop attacking victims and focus on the capitalist ruling class perpetrators and their technologies destroying us all?