Sperm, testosterone and penises: Male reproductive health in crisis?

In an earlier blog I focused on reports of declining penis size in human males, declining sperm count, and even increases in brain size and changes in head shape. A follow-up blog explored reports that men are falling behind in a variety of areas including academic achievement, careers, and even parental choice of newborn gender–a possible change to preferring girl babies.

I had expected to close this small series out with some reflections on what all this might mean.  However, I made the mistake of digging a little deeper into the research on sperm count and penis size and found a sea (or maybe it is a swamp) of related research.  This blog was designed to focus on temperament, but I hope that interested readers will bear with some biology today.  Next week I will follow up on the various ways that all of this might be related to temperament and personality at least in men.

The first major study of sperm health reported that sperm counts in healthy males had dropped in those surveyed by over 50%, from 1938 to 1990, going from 113 million sperm per milliliter in 1940 to 66 million in 1990.*  This might still sound like overkill in the sperm department, but it is not.  A great many sperm in any sample are damaged or dysfunctional and thus unable to impregnate. (This problem is thought to be increasing also.) For this and other reasons, a count below twenty million/milliliter is considered to be somewhere between subfertile and effectively sterile. (It apparently takes an enormous number  of strivers to produce one winner.)

This ground-breaking research was published in 1992 and was a review of previous data on some 14,947 men in 61 different reports.  It first received huge publicity, then was ridiculed by other scientists for some aspects of its methodology.  However, studies by many respected researchers since that time have simply confirmed and added to these findings.  For example, a project in Edinburgh  similarly reported a drop from 100 million per milliliter to 50 million from 1950 to 1990.  Most sources are reporting average reductions between 1.5% and 2% per year.  As another example, a 2012 study done in Rochester New York, found that 24.6% of their sample had a sperm count that was below the commonly used cutoff for subfertility of 20 million sperm per milliliter These were all young men 18-22, nonsmokers, not overweight, and all had completed a physical exam and lab tests, so presumed to be in good health.**

Testosterone (T) is essential for the production of sperm, and findings on reduced T levels are also fairly widely reported.  In 2007, a peer reviewed study of American males reported “a substantial age-independent decline in T  that does not appear to be attributable to observed changes in explanatory factors….The estimated population-level declines are greater in magnitude than the cross-sectional declines in T typically associated with age.”  Declines due to normal aging effects were found to produce a drop of .04% per year, while population declines (all ages compared at different points in time) were found to drop 1.4% per year in the 20 year period studied.***

A second study, also done in 2007  looked at T levels in 5350 Danish men, again, both by age and by the population values for all ages at each point in time, and reported similar though not identical values.”**** These studies and many others have been reported in scientific journals and picked up in blogs and popular journals over the years.  It seems clear that these are real and serious findings.

Well, how about shrinking penis size?  The 2012 report I noted in a previous blog was dramatic, suggesting a 10% drop in the population studied.  Although I didn’t uncover further studies centered  on that single aspect of male reproduction, there are many references looking at penis size changes as one of a number of variables that are all linked to chemical substances in our environment.  There have been reports for years on reproductive problems in aquatic animals of many kinds.  PCBs which are industrial chemicals that have been used in many types of electrical equipment can cause male turtle eggs to revert to female eggs, and can do the same in alligator eggs.  Alligators that live in contaminated lakes in Florida are known to have very small and dysfunctional penises.  Moving from water born animals, it is reported that panthers in Florida, who eat raccoons, which in turn eat fish in that area, are reported to have undescended testicles, and poor sperm production.*****

This same paper reports the following about humans:  “It is now evident that several aspects of male reproductive health have changed dramatically for the worse over the past 30 to 50 years….These observations [including declining sperm, enlargement of the prostate gland, testicular cancer, etc.] suggest that male reproductive health has declined progressively since the Second World War as a result of changes in environmental or lifestyle factors.  While the etiologies underlying these apparent changes are currently unclear, both clinical (i.e. human) and laboratory (i.e. animal) research suggests that all of the described changes in male reproductive health appear interrelated and many have a common origin in fetal life or childhood.  This means that the increase in some of the disorders seen today originated 20 to 40 years ago, and the prevalence of such defects in male babies born today will not become manifest for another 20 to 40 years or more.”

The shrinking penis phenomenon  turns out to have been noticed in a number of older reports on humans.  Again, data on this tends to be incorporated in studies on the agents being studied for their effects on general reproductive health.  The assumption is that since the changes have occurred in many (probably most) Western, developed countries, and with dramatic decreases over a relatively short period of time, that they are mainly due to toxins in the physical environment rather than any sort of genetic alteration. One agent in particular (known as DEHP and classed as a phthalate) can be found commonly in the human bloodstream, and where found in pregnant women is “significantly associated  with the decreased penis width, shorter anogenital distance and the incomplete descent of testes of their newborn sons, replicating effects identified in animals….Approximately 25% of US women have phthalate levels similar to those in the study.”******  DEHP is an industrial chemical very widely used as a “plasticizer”, meaning that it is added to plastic products to promote flexibility and  related plastic properties.  Of particular concern is its use in many medical devices, such as lines carrying fluids of all kinds to patients, including neonates in intensive care.

Another agent of concern is Bisphenol A or BPA–widely used in plastics including children’s baby bottles and sippy cups.   BPA is also a “plasticizer” used to add strength to plastic containers, but also used in the lining of food and beverage containers.  It is capable of being ingested by contact with the skin and through the food contacting it in cans and bottles.  In a study involving 2000 people it was found that 90% of them had BPA in urine.  It is one of many industrial compounds (including DEHP) that have been classed as “endocrine disruptors”, meaning that they are able to act on many of the hormones we produce, including sex-related hormones.  Many of these, including BPA, have their disruptive effect by having, at least weakly, the actions of the female hormone, estrogen.  Animal studies clearly show these disruptive effects in virtually all reproductive areas, from predisposition to breast cancer and prostate and testicular cancer, to decline in testosterone. and permanent changes in genital structures.

PCBs, referred to earlier, were dumped into the environment in huge quantities from 1929 to 1979 in many countries, and in Russia until 1990.  They were used in massive power transformers, and in smaller electrical equipment, but also were found in the 60ssuch everyday products as wood floor finishes and may still be found in higher quantities in the bloodstream of persons with such flooring.   They had many destructive effects, including actions on the reproductive system.  What is more, they are highly stable compounds and can exist for dozens of years, reaching us through dust, and water and even plants that absorb the dust. Scattered reports of effects on penis size include a finding from Taiwan where pregnant mothers exposed children to PCBs because they unknowingly consumed severely contaminated rice oil in 1979,  The children were exposed only prenatally and perhaps postnatally in breast milk, but did as a group have smaller penises than non-exposed boys, as well as other birth defects and developmental problems.  It is reported that a similar contamination occurred in Japan in 1968.*****

There are many, many candidates for endocrine disruption including the now-banned pesticide, DDT.   The various types of plasticizers turn up in many, many kinds of household products, from vinyl shower curtains to floor finishes.  A Wikipedia article on endocrine disruptors noted that “if a consumer used the alternative surface cleaner tub and tile cleaner, laundry detergent, bar soap, shampoo and conditioner, facial cleanser and lotion, and toothpaste [he or she] would be exposed to at least 19 compounds.

In addition to industrial products (including many pesticides) there are also plant-based compounds called phytoestrogens–again acting at least weakly on estrogen production.  Perhaps the best known and most widely used example of this is soy, which, on the positive side, has been recommended for estrogen-like actions in women who are struggling with menopause symptoms.  It is very widely used in daily foods, both as a meat substitute (tofu) and as a protein addition to many products.  During pregnancy, the concentrations in the fetus’ umbilical cord has been found to be similar to that in the mother’s blood stream.  More importantly, however, we have seen a major trend for the use of soy milk formula for infants in place of cow’s milk.

One major review of phytoestrogens stated that “infants fed soy formula have circulating phytoestrogen concentrations  [that are} 13,000 to 22,000 times higher than their own estrogen levels.” ******* Soy milk was available as early as1929, but only gained wide acceptance after the mid-60s when an improved form was developed.  It is estimated that some 40% of all formula in the US today is soy based.  Although there has been a great deal of research on soy and general health, and most of this positive, reproductive health has had little study as yet.  The authors of this review state that “infants fed soy formula have the highest exposure to any nonpharmacological source of estrogen-like compounds, yet we know virtually nothing about how the use of these phytoestrogen-rich formulas might impact their future reproductive health.  Although relative few adverse effects have been detected, that may simply be because a surprising paucity of large-scale comprehensive studies have been undertaken to address this issue, especially in boys.”

Lastly, studies have begun on the effects of these various agents on  behavior in males, apart from reproduction.  Testosterone in rats, primates and humans is known to promote masculinized development in the male brain well before birth  It has also been known for some time that unborn rats exposed to DEHP and other related endocrine disruptors during a critical period of development will experience a reduction in prenatal testosterone as a result and show various problems postnatally including reduced genital size, later reproductive problems and feminized behavior.  This leads to the question of whether masculine behaviors in general could be disrupted in a similar way.

There are gender differences in male and female play behavior that are true for young rats, non-human primates and for humans.  For rats and non-human primates there is more rough and tumble play and more play-fighting, and this is probably true for boys also. The authors of a relevant 2010 study comment that “Young male rhesus monkeys, like boys, also show distinct preferences for toys with wheels, and vervet monkeys show sex differences in toy preferences similar to those shown previously in children.”  Some work was done in in 2002 measuring play behavior in human children exposed to varied endocrine disruptors, with the result that there appears to be a relationship between these agents and less masculine play behavior in preschoolers.

In the 2010 study******** DEHP was the agent and the levels found in the urine of the pregnant mothers were used to measure each child’s prenatal exposure.  Each child’s later play behavior at age 3-6 was measured on a standardized instrument that is widely used for this in many different situations.  It has 24 questions about choice of toys, types of activities, and general characteristics of the child.  In this study it was taken by the mother.  The overall result was that typical prenatal exposure to DEHP from the mother produced no significant relationship between DEHP level and play behavior in girls, but did significantly reduce masculine scores for boys.  The authors conclude “This study is the first to relate complex sexually dimorphic behavior to phthalate [DEHP, here] exposure.  Although our results are based on a relatively small sample [150 participants], their internal consistency and their compatibility with current knowledge about how gonadal hormones mold sex differences in brain and behavior support their plausibility.  Their implications warrant extensive investigation.”

It is the massive and corroborative nature of all these findings that first startled me and then shocked me.  We know we live in a heavily industrialized world in which toxic chemicals turn up with mind-numbing regularity.  Any half dozen of these reproductive studies might turn up and be partly true, partly false, and perhaps only for a limited number of susceptible persons or only in unusual or extreme circumstances. But that is not what we are looking at here.  Whether researchers have identified the principle agents here, or much more remains to be discovered–when human sperm count is dropping as much as 2% every year, and testosterone levels as much as 1% or more per year and all this is happening slowly but steadily over 50 or 60 years. that is simply a stunning finding.  When, if this continued at the same rate, large portions of the human race might be effectively sterile, and not in too many years–and there is no massive outcry–I find myself simply amazed.  If global warming were increasing at 2% per year the whole world would be in total panic.  What’s it all about, Alfie?

 

 

SELECTED REFERENCES

* Dindyal, S. (2004).  The sperm count has been decreasing steadily for many years in Western industrialised countries:  Is there an endocrine basis for this decrease?  The Internet Journal of Urology 2(1).

**Mendiola, J. et al. (2011).  Shorter Anogenital Distance predicts poorer semen quality in young men in Rochester, New York. This is available online at http://dx.doi.org/

***Travison, T. G., et al. (2007)  A Population -Level Decline in Serum Testosterone Levels in American Men.  Journal of Clinical Endocrinology and Metabolism 92(1) 196-202.

****Anderson, A.,  et al. (2007)  Secular Decline in Male Testosterone and Sex Hormone Binding Globulin Serum Levels in Danish Population Surveys.  Journal of Clinical Endocrinology and Metabolism 92(12) 4696-4705.

*****Chemicals and Male Reproductive Health.  (This is a summary report on an extensive National Institute of Environmental Health Studies paper.  It can be found online at http://ces.iisc.ernet.in/hpg/envis/maldoc104.html)

******Swan S. (2008).  Environmental phthalate exposure in relation to reproductive outcomes and other health endpoints in humans.  Environmental Research 108 (2) 177.

*******Patisaul, H. B. & Jefferson, W. (2010).  The pros and cons of phytoestrogens.  Front Neuroendocrinology 31(4) 400-419.

********Swan, S. H. et al. (2010) Prenatal phthalate exposure and reduced masculine play in boys. International J of Andrology 33(2) 259-269.

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