Welcome, dear readers, to another installment of my series defending contraception from the lies and inaccuracies spewed by 1Flesh. This week, we’ll be talking about how birth control pills do not, in fact, cause prostate cancer. As always, paragraphs in italics below are taken from their site. Enjoy!
The Pill and the Prostate
A fascinating study published in the BMJ last year found that countries with high oral contraceptive use have higher incidence and mortality rates of prostate cancer, the second leading cause of death in American men.
A glaring inaccuracy in your VERY FIRST SENTENCE. I know I shouldn’t be shocked, but I am.
In 2009 (the most recent year for which full data is available), 307, 223 men died from heart disease in the US; 88, 541 men died from lung cancer; 76, 680 men died from accidental causes; 35, 346 men died from diabetes; and (while exact numbers are hard to get do to reporting errors) it would appear that at least 30,000 men died from influenza. How many men died from prostate cancer, you might ask? That would be 28, 471.
So, while prostate cancer is the most prominent form of cancer for men, (though not the most deadly), and cancers overall are the second leading cause of death for Americans, prostate cancer is not the second leading cause of death for American men.
It would be better for you to correct this to say that prostate cancer is “a” leading cause of death in American men.
Now on to the actual study. What is intriguing about this study is that the authors stated SEVERAL times that, “we do not believe we have proved a cause and effect relationship.” It’s important, 1Flesh students, to keep in mind the old adage of “correlation does NOT equal causation” whenever you present a research article as proof of something. Particularly when the authors themselves indicate that they have not proven causation.
I think it would also behoove your readers to check out the comments to this article, wherein other scientists pointed out flaws in the article, such as the lack of controlling for known prostate-cancer risk-modifying factors, such as dietary factors and the prevalence of apolipoprotein E epsilon 4, and errors in the data analysis of the article (which the authors acknowledged and attempted to fix in their analysis). These responders also pointed out that even under the new analysis, OC usage was correlated with something less than 3% of the variation in prostate cancer mortality rates across countries.
Further, I am particularly fond of this response to the article:
Our main concern about the Margel and Fleshner paper  stems from the extensive coverage that it has received in the lay press and the likelihood that the erroneous findings have been widely interpreted as being causal. For example, we note that in the British Daily Mail newspaper the study was reported with the headline ‘Rise in prostate cancer due to use of the Pill which increases men’s exposure to oestrogen’ . We accept that many research publications ultimately turn out to present false conclusions ; that there is a need for researchers to float interesting ideas; and that researchers are not responsible for over -interpretation by the press. However, we believe that it is of prime importance that scientists endeavor to frame their results and their speculations in ways that limit the potential for misinterpretation. Margel and Fleshner did not do this: the original data were wrong; the authors’ analysis and interpretation of the correct data remains unconvincing; and the title of their paper is misleading.
From your piece, it would seem like these scientists’ concerns were valid.
Precisely how oral contraceptives have this effect remains unknown, but it was suggested that this “OC effect may be mediated through environmental oestrogen levels,” through the increased amount of artificial hormones released into the water supply.
Suggested, but not proven. Because this was an ecological study. Like the authors repeatedly said.
This makes sense. A 2005 study found that artificial estrogens have dangerous effects on the prostates of fetal mice, and determined that “acceleration in the rate of proliferation of prostate epithelium during fetal life by small amounts of estrogenic chemicals could permanently disrupt cellular control systems and predispose the prostate to disease in adulthood.”
First, here a link to the full study. Then, let me just point out that this study only concerned itself with the possible effects of oestrogens on male fetuses, and let me also point out that they fed the mice not only EE2, but also bisphenal-A, which has ABSOLUTELY NOTHING to do with oral contraceptives.
The BMJ study points out that “OCs were made publicly available in the 1960s, and have been widely used since the 1980s, hence the exposure to these substances, even in small quantities, may be chronic enough (20–30 years) to have a clinically significant effect.”
They also point out that “the correlation with OC was independent of a nation’s wealth”.
I’m just going to point readers here again to the fact that the BMJ authors EXPLICITELY state that their research did not indicate causation, and to the responses to the article linked above.
The idea that OCs may have a significant environmental impact is often met with the criticism that OCs are only one of many sources of artificial estrogen pollution. The study “Are Oral Contraceptives a Significant Contributor to the Estrogenicity of Drinking Water?” is used to claim that OCs only contribute to 1% of total pollution.
Let’s make this a little more clear, shall we? What the researchers in this study did was apply a model used by the Dutch Central Bureau of Statistics to determine the proportion of estrogen excretion based on total population figures, which estimated that EE2 accounted for approximately 1% of the total human excretion of estrogens in the Netherlands, to the US. Becaues 43% of Dutch females of reproductive age used OCs during the time of the Dutch analysis, while only 28% of US females of reproductive age used OC’s, the authors determined that excreted EE2 was likely less than 1% of total estrogens.
There. Now was that so hard?
Unfortunately, this study was shown to have drastically understated the potency of ethinylestradiol — the artificial estrogen in oral contraceptives — by approximately a twentieth of its actual strength. When Waldemar Grzybowski of the Institute of Oceanography of the University of Gdansk applied the approximated actual potency of ethinylestradiol to the study’s population, she found that “its share in the total estrogenicity exceeds 50%”.
Second, the authors actually didn’t drastically understate the potency, which they explained in their response to his comment (which you obviously read, because you cite from it below). In their response, the authors provided the source they used to determine potency ratios (that they mistakenly failed to provide in their original paper), which DID provide actual potency references, which matched the potency references they had in their study.
Also, it should be noted that Dr. Grzybowski did not apply the “actual” potency. He applied an ASSUMED potency. Meaning he made up a number and used that number in his analysis. Not really very scientific, but whatever.
The author’s of the original study admitted this flaw: “It is worth noting that the original author’s of the study admitted to this flaw — “if including all methods of potency determination (both in vitro and in vivo), one might estimate a somewhat higher potency for EE2 than we originally reported in our publication.”
First, editors. You guys need editors, like, WHOA. Second, you conveniently leave out the part above this where they prove their original methods were correct, and also conveniently leave out the part below this, where they state:
However, this should still be considered in light of the following findings: (1) wastewater treatment systems have been shown to be highly effective in removing synthetic estrogens before they reach the environment and drinking water treatment removes virtually all of them before reaching our tap; and (2) there are many other sources of estrogens in the environment that enter waterways untreated, including agricultural waste, industrial synthetic estrogens and estrogenic plant compounds.
Anyway, yeah. I’m glad you guys are finally getting the hang of looking at articles, and then comments to articles, and responses to those comments (well, sort of, anyway), it would be even more helpful if you didn’t try to deceive your readers by cherry-picking what information you give them. Oh, and if you learned the difference between the words “actual” and “assumed.”
So while it’s certainly true that oral contraceptives are not the only source of artificial estrogen pollution, they cannot be ignored as having a negligible effect on the environment.
I don’t think anyone’s saying we should ignore the possible impacts of EE2 on the environment. The authors actually made it clear that they think we should be diligent about monitoring ALL sources of estrogen pollution in waterways, and looking for ways to diminish their impact (they actually provide several solutions – you should really look into them if you’re concerned about estrogen pollution in waterways). What this study DID show, however, that the level of EE2 in found in US drinking water is typically lower than the measure used by the USGS, and that the impact of EE2 on the total estrogenicity of waterways IS negligible, largely because wastewater treatment plans can reduce the level of estrogens (both natural and synthetic) by 50 – 98% BEFORE they enter waterways, unlike other sources of estrogens which do not go through this same treatment process.
Is this a reason to ditch the Pill? Maybe, but probably not on its own. We do, however, see this evidence as part of the growing possibility that the Pill, for all the good it does, may be detrimental to the human person and to society as a whole.
No, this is no reason to ditch the Pill. None of the information you presented here, once thoroughly examined, provides ANY proof that oral contraceptives are dangerous to humans or to the environment.
We also see this information as a good reason for men to be involved in the discussion of contraception and reproductive health.
Hey, look! Something we agree upon! I think (as do most people involved in the reproductive health community) that both women AND men should be involved in discussions about contraception and reproductive health.
We understand that couples using the Pill do so in an effort to seek out what’s best for their relationship, and so we’d encourage everyone to consider the use of a natural, side-effect free method of family planning as a better, healthier way.
Seriously, guys – you keep hawking this method. And that’s fine, if you want to use it, that’s great. But you should learn to be honest about its shortcomings (because it has many). I detail them here.
For more on the effects of contraception on the environment, check out our environmental page.
Um, I actually debunked your claims on that page here. I notice you didn’t take any of that to heart.
Join the discussion on the health effects of hormonal contraception in the forum.
And, I would, but you’ve got some crazy guy over there who keeps telling me that I’m the scourge of the earth and other such nonsense, so I’m not really sure why I would want to. But thanks for the offer!
Till next time,