|This is definitely not the fault of BCPs|
Male reproductive health is in decline.
Bear with me, readers. This one is a doozy. A REALLY LONG doozy. I’ve tried to break it up for you, but it’s still long. So beware.
In this episode of debunking 1Flesh, we’re taking a look at their claims that oral contraceptives are leading to the end of civilization as we know it by causing male sterility. (Okay, so they didn’t actually SAY those exact words, but they’re definitely inferred).
If you want the short version, just know that your oral contraceptives aren’t causing a massive decline in male fertility or sperm counts. Fin.
The long version, though, is full of awesome information about semen, sperm, birth control pills, estrogen, and wastewater treatment plants. And, yes, they’re all connected, so if you want to learn how, and see me show 1Flesh just how wrong they are (including the use of some awesome gifs), settle in with a cup of tea and get to reading.
*Note: As always, full paragraphs/lines in italics are taken directly from 1Flesh’s site.
A recent study of 26,600 samples found that the average sperm count of a man living in France has dropped by a third between 1989 and 2005.
Okay, first, here’s a link to the actual study so y’all can read it for yourselves. Second, let me point out that this subject is HIGHLY contested. While this study shows a decline in sperm count, many other studies have shown no decline, and one in Italy has actually shown an INCREASE (I’ll detail more studies of this nature below).
Finally, the study could not offer a reason for the alleged decline. And as I’ve stated time and again:
It really would behoove you, 1Flesh bloggers, to tattoo that somewhere on your bodies to help you remember it.
Once considered a global problem by the 1992 study “Evidence for decreasing quality of semen during past 50 years,”
And yet another sketchy study. Luckily, I found a review published in 2008 disproving this very study, and the myth of the global decline altogether. Aside from pointing out the many, MANY, MANY flaws with the Carlsen study, Dr. Fisch conducted a re-evaluation of the Carlsen data controlling for geographic variation. This re-evaluation showed NO decline in sperm counts, once studies conducted entirely in New York – which accounted for 80% of the studies prior to 1970 but only 3 studies after 1970, and where sperm counts were (and are) highest – were excluded.
|The circles indicate the size of the subject pool.|
Dr. Fisch then conducted his own meta-analysis, reviewing the 31 major studies published after Carlsen that reported on time trends of semen parameters. Of these 31 studies, only SIX showed clear evidence of a decline in either sperm counts, or sperm counts and other semen parameters in a given time period. These six studies had a combined total number of participants of 9215, with declines ranging from 16% to 31.5%.
SIXTEEN of the studies, unambiguously showed no decline (either no change or an increase) in semen parameters. These sixteen studies had a combined participant N of 103,313.
Finally, five of the studies showed ambiguous results, including studies in which some semen parameters experienced a decline, but others did not among the same population.
Somehow the idea that the world’s sperm is under attack doesn’t seem quite so plausible anymore, does it?
it has been shown — by the 2000 study by Swan et al
Unfortunately, this study (primarily a re-evaluation of the Carlsen study, with the addition of certain other studies) fails for many of the same reason the Carlsen study fails. While Swan’s study attempted to control for variability in methods and protocols for semen collection and analysis and abstinence time, it failed to control for lifestyle and socioeconomic factors (such as smoking or drug use) or for geographic regions (beyond continental regions, see the New York examples above as to why this was important). It also primarily used the same flawed statistical analysis – a linear regression model – which is inappropriate for analysis of such non-uniform data.
and subsequent studies – that the massive decline in semen quality is largely limited to Western countries, and to Caucasian males.
By” studies.” I’m assuming you mean “study,” singular? Because that’s what this links to. A single study showing no decline in sperm count or motility in India. Also, based on the Carlsen and Swan studies, it would be incredibly difficult, if not impossible, to determine whether or not a possible decline in semen parameters was different within Western nations than without. To explain, the Carlsen study only included 12 studies from non-Western nations (out of 61 – so less than 20%) with a N of 3525 (out of a total N of 14947, or less than 24%). The Swan study only further exacerbated this problem. That study included 18 studies of non-Western nations (out of 101 studies, so less than 20%) with an N of 4885 (out of a total N of 18945, or less than 26%). Making such broad-sweeping comparisons based on a 75/25 ratio of Western to non-Western nations should be considered highly suspect.
Further, I think we’ve shown by now that there actually HASN’T been a “massive decline in semen quality.” Yes?
Finally, not to be pedantic, but I just cited a study above showing that sperm counts weren’t falling in the US – when did we become a non-Western country?
Specific studies, largely carried out in the 90′s, showed falling sperm counts in Belgium— where the “percentage of candidate donors with sperm characteristics below the 5th percentile cut-off value of a normal fertile population increased from 13 to 54% during the [19 year] observation period” —
Um, I know y’all go to a Franciscan college, and perhaps your sexual education curriculum isn’t what it should / could be, but sperm COUNT is not the same as semen CHARACTERISTICS. What this study ACTUALLY showed was that semen volume increased slightly, the mean concentration declined by 12.4m/mL, normal morphology decreased from 39.2% to 26.6%, but the sperm count was unchanged.
I’ve said it before, and I’ll say it again:
Or at least it does when you’re searching for the truth and not just trying to scare impressionable people into buying into the Creighton Method because they’re afraid their somehow sterilizing their partners through the use of oral contraceptives.
Further, a more recent (and larger) study on Belgium, published in 2007, indicated, “[t]otal sperm count did not change significantly with time” and “continuing decline in sperm morphology with time is confirmed, statistically unrelated to pollutants.”
in Canada — where overall sperm quality showed “a significant downward trend in sperm concentration among 48,968 samples from Canadian men”
Only telling part of the story again, you naughty birds, you? What the study actually found was that a linear regression of the means of each of the 11 districts studied showed no significant trend. It is only when ALL of the centers were combined (a big no-no, given what we know about geographical influences in semen parameters) that a decline appears.
— in Spain – which showed “a statistically significant decline was observed in the percentage of normal spermatozoa” between 1960 and 1996,
And again with only part of the story. In this study, while there was a 3.6% decline in normal sperm, and a 0.2% decline in volume, there was a .04% increase in sperm count, and a .4% increase in motility.
Hey, look! One of the six studies that actually DID show a decline in sperm count! Good job 1Flesh. Here’s a cookie:
and in Denmark – to name a few.
Um, that study in Denmark (here’s the full study) didn’t look at trends in semen parameters over time. So it’s not really useful for you’re analysis. Just thought you should know.
In the same places, and over the same time periods, there have been noted increases in male reproductive diseases. A 2003 study showed that the rate of testicular cancer doubled over the last 30 years “in the majority of industrialized countries in North America, Europe and Oceania”.
This study also noted that surprising difference in incidence rates were found between neighboring countries – e.g. Finland: 2.5/100k cases, Denmark: 9.2/100k cases – and even regionally within a single country, e.g. rates 2.8 to 7.9 per 100k in France. Keep these intra-country differences in mind; they’re important.
A review of multiple studies — “Are Male Reproductive Disorders a Common Entity?” – found evidence for “high and possibly increasing frequencies of undescended testis and hypospadias” as well.
I thought it might be useful here to point out that the authors of this review, a year later, published this study, stating that androgen abnormalities (NOT estrogen abnormalities) were the cause behind TDS.
Given that the problem is largely limited to Western countries, it is generally conceded that the decline in male reproductive health is the result of environmental influences. But what influences?
Since the 1995 study “Do environmental estrogens contribute to the decline in male reproductive health?” it has been debated that artificial estrogens — such as those found in hormonal contraception — may be the primary factor.
First, we’ve shown above that the data is inconclusive as to whether a possible decline in semen parameters is “largely limited to Western countries.” As for it being generally conceded that the “decline” is the result of environmental influences, or more specifically that artificial estrogens may be the primary factor, well…that’s actually not true.
For example, Dr. Stephen Safe (who has been studying the possible role of endocrine disruptors on male reproductive health since the early 1970s), in discussing research conducted by Dr. Fisch and associates on vasectomy clinics in New York, California, and Minnesota, highlighted the fact that there was no change in sperm count, volume, or motility between 1970 and 1994. What Dr. Fisch DID discover, however, is that there was a great deal of difference in sperm counts BETWEEN the three locations (and here we come back to the importance of intra-country geographic differences), conclusions that have been verified in research of other countries. According to Dr. Safe, these and other studies indicate that “persistent organic pollutants (POPs)…are unlikely to be causative agents for decreases in sperm counts (geographic or temporal) because human levels of these contaminants tend to be similar within most countries.” He further states that, “humans are exposed to high levels of dietary endocrine-active compounds in fruit, vegetables and other food products and therefore, lower and even trace levels of contaminant EDCs would have a negligible impact on overall EDC exposure and impact.”
It is a scientific fact that in utero exposure to artificial estrogens negatively impacts male reproductive health. (For those interested in the science behind the effect, the 2006 study “Estrogen effects on fetal and neonatal testicular development” clearly demonstrates “that fetal and neonatal testes are very sensitive to estrogens”
Actually, no, it’s not a “scientific fact” that in utero exposure to artificial estrogen negatively impacts male reproductive health. Except maybe in mice. Or if you’re talking about DES. This study talks about E2 – you know, the estrogen that ALL HUMANS SECRETE NATURALLY, and DES, which is no longer used because of the damage it caused, particularly to females in utero. It doesn’t say a single word about EE2, which is what y’all have been harping on since you set up shop.
while the 2003 study “Environmental estrogens and sperm counts” shows that “based on both animal and human data with DES, it is biologically plausible that in utero exposures to exogenous estrogenic compounds are capable of reducing sperm production in adult men.”)
|Lesson for 1Flesh? Read ALL of the study you’re citing and not just the abstract.|
In humans, in utero exposure to DES has indeed been found to have negative impacts on male reproductive health. However, while these authors agreed that clinical data suggests that in utero exposure to DES can result in decreased sperm count, they also stated that the magnitude of these effects were not large, demonstrating that even ”an estrogen as potent as DES does not produce a decrease in mean sperm counts approaching the levels at which fertility might be affected.” The authors also stated, “the apparent existence of a maternal dose threshold for DES-induced effects on sperm count undermines the likelihood that environmental estrogens, which are substantially less potent, are capable of causing similar effects.”
Also, since y’all seem to be most concerned about the impact or oral contraceptives, I’ll share with you that, while there have not been many studies conducted on the impact of exposure to EE2 in utero, particularly on humans, there have been some. For instance, a 1991 study conducted by exposing pregnant women to .04mg of EE2 discovered no difference in the enzyme activities of testes between the experimental and control groups.
Another study, using mice to examine the impact of EE2 and BCP in utero,attempted to extrapolate their findings of negative impacts on male reproductive development to humans. However, the amount of EE2 needed to produce any negative impact on humans in utero was estimated to be 100 – 5000 μg/day. The amount of EE2 in most modern oral contraceptives? 30μg. And the amount of EE2 in drinking water? .002μg/L
Finally, there actually has been a study, involving humans, talking about the impact of the exposure to oestrogens in utero to sperm counts in adulthood. These researchers discovered that higher concentrations of estrogen in utero were not related to reduced sperm count in adulthood, based largely on the fact that they “did not find lower sperm counts in twin brothers; both the concentration and potency of oestrogens during pregnancy with twins are greater that for most environmental oestrogens.”
We know that male reproductive health is on the decline.
Well…based on the evidence above…not really. We know that incidences of testicular cancer are on the rise, but that’s about it.
We know that artificial estrogens have the capacity to negatively influence male reproductive health.
We know that CERTAIN artificial estrogens have the capacity to negatively influence male reproductive health – namely DES and PCBs. And we know that EE2 can negatively impact human males in utero at daily dosages between 3 and 167 TIMES the amount of EE2 found in today’s oral contraceptives.
We know that the prevalence of environmental estrogens — via hormonal contraceptives, industrial waste, and even milk — has increased, and over roughly the same time period as the observed decline in male reproductive health. So what’s the problem? Can we not, with some degree of confidence, state that hormonal contraceptions are having an environmentally negative effect on male reproductive health?
No, we can’t. Because of all of the reasons I cite above, and below.
The problem is that there is no accurate data on the extent to which we are exposed to these artificial estrogens.
False– please read below to see a review of LOTS of data.
Reviews, looking at the studies of this issue, have commonly expressed this.
I’m questioning their scientific technique.
In the review ”In utero exposure to environmental estrogens and male reproductive health: a systematic review of biological and epidemiologic evidence“ it was stated that “the results do not support with certainty the view that environmental estrogens contribute to an increase in male reproductive disorders, neither do they provide sufficient grounds to reject such a hypothesis.”
Hmmm….here’s a more slightly more recent article on the topic that determined – after reviewing all of the epidemiological literature on the topic for evidence linking indicators of prenatal serum levels of maternal estrogens (including direct measurements; recorded intake of DES, oral contraceptives, and estrogens; pregnancy conditions with known deviant estrogen levels, such as twin pregnancies; and some environmental exposure) with male reproductive health – that, “with the possible exception of testicular cancer there is no strong epidemiological evidence to indicate that prenatal exposure to estrogen is linked to disturbed development of the male reproductive organs.”
In the 2003 review ”The ‘oestrogen hypothesis’– where do we stand now?” it was admitted that “whatever the truth emerges to be, it is as clear today as it was in 1993 that foetal testicular hormones, whether androgens or oestrogens, will figure prominently somewhere in the cascade of changes that leads to male reproductive developmental abnormalities.”
Wait – you mean reproductive hormones can cause changes in reproductive development? I’m shocked!
The authors also said this, “Although many new environmental oestrogens have been identified, their uniformly weak oestrogenicity excludes the possibility that they could induce the above disorders.
But, with regards to the effects of hormonal contraception “it is considered that human exposure to ethinyl oestradiol, or to other oestrogens, via drinking water is unlikely to result in sufficient exposure to induce effects.”
But this opinion — that we are exposed to a negligible amount of artificial estrogen in drinking water and that the increase in male reproductive disorders comes from elsewhere – neglects the consideration that artificial estrogens may also be passed up the food chain, and is otherwise hotly contested. From our discussion of the environmental impact of hormonal contraception:
The study Fate of Estrogens in a Municipal Sewage Treatment Plant found that EE2 levels were reduced by 90% by modern sewage plants, down to 3 parts per billion of EE2.
Why must you lie? No, really. Why.must. you.lie?
Sensitive readers: Please cover your eyes.
Fuck this dishonest bullshit you keep spewing! No, seriously:
QUIT FUCKING LYING.
Sensitive readers, you can return now.
What the study ACTUALLY says is that, “the steroid estrogen concentrations were always below the quantification limit of 1 ng/L.” That would be ONE part per TRILLION. Also, this was from a study in Germany, in case you were wondering.
If you want to talk about the US, let’s use data from the US. A 2009 study of surface water looked at source water around 19 different water treatment plants and found EE2 in only ONE of those sources, at a level of 1.4ng/L (again, parts per TRILLION). EE2 wasn’t discovered in any other source water. Further, after treatment at the one area where EE2 WAS discovered in excess of the 1ng/L MRL (method reporting limit), the results after treatment were BELOW the level of detection.
If you want to know more about how wastewater treatment plants work to reduce the level of EE2 in effluent, you can read this study, wherein you’ll find an examination of effluent from 6 different types of US treatment plants. This study found a mean level of 3.8ng/L of EE2 at a secondary treatment plant; 0.7ng/L at a plant employing a trickling filter; 0.3ng/L at a plant equipped with biological nutrient removal and effluent filtration; 0.14ng/L from an advanced treatment plant with microfiltration; 0.1ng/L at a reverse osmosis plant; and 0.07ng/L at an engineered wetland.
Sidenote: Go engineered wetlands! I actually built one using duckweed on a minor scale for an eight grade science project to prove engineered wetlands could better treat wastewater that traditional sewage treatment plants. Apparently I was some kind of visionary. 😉
In reading these numbers, keep in mind that in the last decade, almost the entirety of the US has moved to at least tertiary (i.e. a biological nutrient removal plus effluent filtration) ,if not a more advanced, wastewater treatment, so the true levels of EE2 in wastewater effluent in the US most likely range from .14ng/L to .3ng/L; this information correlates with the 2009 study showing no levels of EE2 above the MRL in 18 of 19 source samples.
1 part per trillion of EE2 is enough exposure to alter the reproductive systems of the flathead minnow, as the study “Effects of 17alpha-ethinylestradiol in a fathead minnow (Pimephales promelas) gonadal recrudescence assay.” points out: “The lowest observed effective concentration (LOEC) of EE2 for plasma VTG induction in both sexes and for ultrastructural changes in the testes and livers was 1 ng/L [parts per trillion]”
First, readers can download full article here. Second, in case y’all didn’t notice, these are FISH, not people. Third, if you read the study I cited above, you would know that all of the available information indicates that in utero exposure to oestregens other than DES have no impact on adult HUMAN males other than a POSSIBLE link to testicular cancer.
The same was found in a 2006 study of zebrafish and Japanese medaka.
No, the same thing was NOT found. This study found that feminization and VTG effects occurred at 10ng/L. That’s thirty-three to more than SEVENTY times the levels of EE2 found in US source water, and more than FIVE THOUSAND times the amount found in US drinking water.
So even after up-to-date sewage treatment, there is an environmentally damaging amount of EE2 present in our drinking water.
FALSE. Again, the levels of EE2 found in wastewater effluent is somewhere in the range of 0.14ng/L to 0.3ng/L (levels which are below the MRL, and below the levels shown to impact even aquatic species).The levels in our drinking water are even further below the MRL at 0.002ng/L. For those keeping track, that means that the mean level of EE2 found in US drinking water is 0.2% of the level found to impact FISH.
More research is needed to determine whether this amount of EE2 present in our drinking water has the capacity to harm human reproductive systems (especially in the unborn, who are very sensitive to the influence of hormones).
That research is ongoing, but so far the consensus is that .002ng/L of EE2 has no impact on human reproductive systems, either in born persons or in humans in utero.
But ultimately, the significance of EE2 in drinking water pales in comparison to other ways in which we might be intaking the pollution.
I just gave you a recent study showing that EE2 and other environmental factors do not impact humans, but let’s play along, shall we?
The EE2 that has been polluting our waterways and disrupting the reproductive patterns of amphibians and fish is passed up the food chain, growing in potency as it does. Thus the dissertation “ points out that “EE2 has the potential to be transferred via the food chain since it accumulates in biota from the basis of the web. Therefore, it is important to improve and extend monitoring programs including organisms of different trophic levels, sediments, and suspended material.” It specifically states that this process ” indicates risks of EE2 uptake for fish consuming human[s].”
Let’s delve a little deeper into this study. While the authors do give us uptake information and BCF information, they do not give us information on precisely what levels of EE2 were used to spike the water, the algae, or the sediment. So while we know that the bioconcentration factor (BCF) of the secondary consumer (in this case, a zebra fish) was 960 L/kg – a moderate level – we do not know how much EE2 was required to produce this level of BCF – a MAJOR limiting factor.
A more useful study was recently conducted in Canada, using field research to examine EE2 bioaccumulations in fish near the Stag Island wastewater treatment plant near Ontario Canada. Researchers found concentrations of EE2 in approximately 50% of the fish (shorthead redhorse suckers) samples collected; with an average of 1.6ng/g ww (water weight) for males and 1.43ng/g ww for females. While we don’t know the exact amount of EE2 present in the St. Clair river near the Stag Island wastewater treatment plant, we DO know that Stag Island is only a secondary treatment plant, meaning that the levels of EE2 found in effluent were likely 667% to 1428% higher than the levels of EE2 found in effluent from a US wastewater treatment plant. It stands to reason that fish exposed to much, MUCH lower levels of EE2 would have much, MUCH lower levels of EE2 bioaccumulation.
Further, to combat the risk of uptake of EE2 by fish-eating humans, at least one studyhas determined the rates of uptake and bioaccumulation of EE2 by fish at varying temperatures, levels of salinity, and oxygenation to help wastewater treatment plants determine the best time and place to release effluent.
Similarly, it has been shown that EE2 has the potential to be taken up by plants: Given that we do not use drinking water to irrigate crops, but source water, this matters.
Let’s look at this study more closely, shall we? What these researchers were studying was the uptake of triclosan and EE2 by pinto bean plants. Each week for one month, the researchers spiked a soil patch and a sand patch in which they were growing pinto beans with 1ug/g (1 microgram per gram, aka 1 part per BILLION) of both triclosan and EE2.
Now let’s compare that amount to the amount of EE2 found in wastewater effluent. If you remember, above we discovered that most wastewater treatment plants in the US would leave anywhere between .14ng/L and .3ng/L in their effluent. That would be parts per TRILLION. So, effectively these researchers were applying ONE THOUSAND ng/L to both the soil and the sand when effluent would normally only contain 0.14ng/L to .03ng/L.
Applying these relatively MASSIVE quantities of EE2 to the plants, the researchers discovered that, in sand, the roots of the pinto beans contained 1424 mg/g of EE2, while the leaves contained 55 mg/g at the end of four weeks. In soil, the beans’ roots contained 32 mg/g, while their leaves contained 20 mg/g.
If we take these figures and examine what would happen if the researchers had used the typical amount of EE2 found in wastewater effluent, we discover that the plants’ roots and leaves would have contained .0002mg/g and .0000077 mg/g of EE2 in sand, respectively. In soil, the results would have been even more striking; roots and leaves would have contained .0000045 mg/g and .0000028 mg/g, respectively.
While I don’t disagree with 1Flesh that we should be carefully monitoring the levels of ALL pharmaceuticals entering waterways, I hardly find the possible presence of 2 ten thousandths of a milligramof EE2 per gram of pinto beans to be panic-inducing.
A greater exposure to artificial estrogens via hormonal contraceptions makes sense out of a study published in the BMJ last year – which found that countries with high oral contraceptive use have higher incidence and mortality rates of prostate cancer.
Seriously? You’re going to throw that out there again? After I already showed you howflawed it was? Trust me, dear readers, when I tell you this study was MAJORLY flawed, and even the authors conceded that, AT MOST, oral contraceptive usage could be correlated with LESS THAN 3% of the variation in prostate cancer mortality across countries. Further, the authors also stated several times in the study that, “we do not believe we have proved a cause and effect relationship.”
More research is needed.
You know me; I’m always up for more research.
To summarize where we currently stand:
1. We know that male reproductive health is on the decline.
True – well, at least somewhat.
2. We know that the artificial estrogens found in hormonal contraception have the capacity to negatively influence male reproductive health.
3. We know that the decline in male reproductive health is largely limited to Western countries.
False – not enough data to confirm.
4. We know that, like the decline in male reproductive health, the use of hormonal contraception is far more popular in Western countries.
True. Rates of hormonal contraceptive usage in the various world regions are as follows:Europe: 20.7%, Latin America and the Caribbean: 19%, North America: 22.3%, Oceania: 19.3%, Africa: 14.1%, Asia: 9.7%
5. We know that the prevalence of artificial estrogen pollutants have increased over roughly the same time period as the observed decline in Western male reproductive health — with the increase in the Western use of hormonal contraceptives, plastics and pesticides.
Are y’all seriously going to make me say it again? You are, aren’t you.
CORRELATION DOES NOT EQUAL CAUSATION!!!!!
It can be firmly suggested that hormonal contraceptives are having a significant negative effect on male reproductive health,
Given the evidence above, NO, it CAN’T.
but until there is definite data expressing the degree to which are exposed to these artificial estrogens, it cannot be proven. We await the data.
If you’re awaiting data, perhaps you shouldn’t publish blog posts with such misleading and inflammatory titles as, “Turns Out Artificial Estrogens Hurt Testicles”
Till next time,