As many as one in five healthy young men between the ages of 18 and
25 produce abnormal sperm counts. Even the sperm they do produce is
often of poor quality. In fact only between 5 and 15 per cent of their
sperm is, on average, good enough to be classed as "normal" under strict
World Health Organisation rules – and these are young, healthy men. By
contrast, more than 90 per cent of the sperm of a domestic bull or ram,
or even laboratory rat, are normal.
Human males also suffer a disproportionately high incidence of
reproductive problems, from congenital defects and undescended testes to
cancer and impotency. As these also affect fertility, it's a minor
miracle men are able to sire any children at all. In fact, an increasing
number of men are finding themselves childless. Among the one in seven
couples now classed as infertile, the "male factor" has been found to be
the most commonly identified cause.
Next year marks the 20th anniversary of the WHO conference where a
Danish scientist first alerted the world to the fact that Western men
are suffering an infertility crisis. Professor Niels Skakkebaek of the
University of Copenhagen presented data indicating sperm counts had
fallen by about a half over the past 50 years. Sperm counts in the 1940s
were typically well above 100m sperm cells per millilitre, but
Professor Skakkebaek found they have dropped to an average of about 60m
per ml. Other studies found that between 15 and 20 per cent of young men
now find themselves with sperm counts of less than 20m per ml, which is
technically defined as abnormal. In contrast, a dairy bull has a viable
sperm count in the billions.
Experts in human reproductive biology were astonished by the Danish
study. The declining trend seemed to indicate that men were on a path to
becoming completely infertile within a few generations (although recent
studies suggest the fall in sperm counts may have bottomed out).
Professor Skakkebaek could offer no explanation for the trend other than
to suggest that the fall may have something to do with the equally
alarming rise in other reproductive disorders, such as cancer of the
testes and cryptorchidism, the incomplete descent of the testes into the
scrotum.
Experts began to talk of a new phenomenon affecting the human male, a
collection of disorders known as testicular dysgenesis syndrome. They
wanted to know what was causing it, because the changes were occurring
too quickly to be a result of genetics. It must have something to with
changing lifestyles or the environment of men, and almost everything was
suggested, from exposure to chemical pollutants to the modern fashion
for tight underpants. There is now an emerging consensus among some
experts that whatever it is that is exacerbating the problems of male
infertility, it probably starts in the womb. It is not the lifestyle of
men that is problem, but that of their mothers.
The process of sperm production, called spermatogenesis, starts in
adolescence, but the groundwork is laid down in the few months before
and immediately after birth. An increasing number of studies point to a
crucial "window" of testicular development that begins in the growing
foetus and ends in the first six months of life. Interfere with this
critical developmental period, and a baby boy will suffer the lifetime
consequences of being a suboptimally fertile man.
So are we anywhere nearer to finding an explanation for why are so many more men today are suffering from reproductive problems?
"It's most likely a reflection of the fact that many environmental
and lifestyle changes over the past 50 years are inherently detrimental
to sperm production," says Professor Richard Sharpe, fertility research
expert at the Medical Research Council. "It may be that different
factors come together to have a combined effect." A number of studies
point to a connection between early development in the womb and male
reproductive problems in later life, especially low sperm counts. For
example, men whose pregnant mothers were exposed to high levels of toxic
dioxins as a result of the 1976 industrial accident in Seveso, Italy
have been found to have lower-than-average sperm counts. But men exposed
to dioxins in adulthood showed no such effect. Another study found
women who ate large amounts of beef during pregnancy, a diet rich in
potentially damaging chemicals called polycyclic aromatic hydrocarbons
(PAHs), had sons with relatively low sperm counts. But eating beef as an
adult man shows no similar impact.
Meanwhile, studies of migrants between Sweden and Finland, showed
that a man's lifetime risk of testicular cancer tends to follow the
country he was born in rather than the country where he was brought up.
It was his mother's environment when she was pregnant with him, rather
than his own as a boy or as an adolescent, that seems to have largely
determined a man's risk of testicular cancer.
One of the strongest pieces of evidence in support of this idea comes
from studies of people who smoke. A man who smokes typically reduces
his sperm count by a modest 15 per cent or so, which is probably
reversible if he quits. However, a man whose mother smoked during
pregnancy has a fairly dramatic decrease in sperm counts of up to 40 per
cent – which also tends to be irreversible.
Professor Sharpe said such findings can be explained by understanding
how the first cells of the testes form. Sertoli cells, which in the
adult act as guardians for the development of sperm cells, are the very
first cells to form from a "genital ridge" of the human male foetus. The
number of sperm that can be produced in an adult man is critically
dependent on the number of Sertoli cells that develop in his foetus, so
anything that interferes with the formation of Sertoli cells in a
mother's womb will affect sperm production many years later.
"Maternal-lifestyle factors in pregnancy can have quite substantial
effects on sperm counts in sons in adulthood, and the most logical
mechanism by which this could occur is via reducing the number of
Sertoli cells," Professor Sharpe says.
But the key question now is to identify the relevant lifestyle and environmental factors.
This is proving tricky. Obesity, for instance, is a growing problem
and it has been linked with reproductive problems in both men and women.
One study has also indicated that overweight pregnant women tend to
produce sons with poor semen quality. But is it being fat that is the
cause, or the environmental chemicals stored in fat?
There has been a lot of interest in chemicals in the environment,
especially those that can either mimic female sex hormones – oestrogenic
chemicals – or block male sex hormones, specifically testosterone which
plays a critical role in stimulating the development of Sertoli cells
in the womb. So far, the Seveso study provides the clearest link between
human foetal development, low sperm counts and prenatal exposure to an
environmental chemical. But the dioxin concentrations from this
industrial accident were exceptionally high.
It is more difficult trying to establish a similar, significant link
between male reproductive problems and exposure to low concentrations of
the many other environmental chemicals that may have weak oestrogenic
or androgen-blocking properties, including substances as wide-ranging as
pesticides, traffic fumes, plastics and even soya beans. Professor
Sharpe says that much of the evidence to date is weak or non-existent.
"Public concern about the adverse effects of environmental chemicals
on spermatogenesis in adult men are, in general, not supported by the
available data for humans. Where adverse effects of environmental
chemicals have been shown, they are usually in an occupational setting
rather than applying to the general population," he says.
So although scientists are closing in on the critical window of
foetal development in the womb that determines a man's fertility status
in later life, they are still not sure about what it is that could be
affecting this change in his reproductive status. But one thing is
clear, it is his mother who almost certainly holds the key.
