Sorry 1Flesh, “The Pill” Still Doesn’t Cause Breast Cancer: Debunking 1Flesh, Episode 1, Round 2

 
 

WARNING: THIS POST IS LOOOOOOONG.

I hate to have to do this, dear readers, but it appears that 1Flesh has slightly updated their post on the Pill and Breast Cancer, and is claiming that I’ve made false statements about what they said (you can see precisely what was written in their earlier post by looking for the italicized paragraphs in my old post – link). But since they’ve nicely (well, sort of nicely, anyway) asked me to update MY post to reflect their updated post, I figured I’d be nice enough to do so. I felt things would be too complicated to just change my other post (and besides, I want that info out there, to show that they actually WERE claiming what I said they had claimed, as well as to provide the background info on breast cancer and statistics), so I’m writing a new post here. 

Some of the info will be copied over (because they’re still trying to make some of the same claims), so don’t be too shocked if something sounds familiar. Also, as always, you can recognize 1Flesh’s statements from my own by the fact that their statements will be in all italics. Further, you can find my responses to their claims made directly to me on Facebook in brackets, and new info will be highlighted in yellow, just in case you don’t feel like reading the whole thing and want to just scroll to see new info.

And now on to Round 2 of Episode 1 of Debunking 1Flesh. Enjoy!

The Pill increases a woman’s risk of triple-negative breast cancer.

[I’m still going to “quibble” with this statement. Because, as I pointed out in my last post, and as I will repeat below, the study you cite (which, by the way, is EXTREMELY outdated) only found an increased risk of triple-negative breast cancer for a very specific subset of women, i.e. women under 40 years of age. For women over 40, there was no increased risk.

ACCURACY IN REPORTING IS IMPORTANT, 1FLESH.]

Why? Because oral contraceptives cause a significantly higher rate of breast cell division, and in general, cells that divide more rapidly are more likely to become cancerous.

[Side note: I have to giggle here because 1Flesh, on their Facebook page, claimed that I was the one using outdated data. Yes, I realize how ridiculous that sounds, as well.]

Using a medical study from 1989? Again with the outdated studies, 1Flesh. How about we look at something more recent, like information from the authors of the 2002 CARE study about what actually happens when hormones interact with breast cells:

Giske Ursin, M.D., Ph.D., associate professor at the Keck School and one of the CARE study authors has explained that the understanding the differences between a woman’s own hormones before and after menopause – and how they interact with hormonal medications – is key.

Prior to menopause, levels of progesterone (the natural version of progestin) and estrogen in a woman’s body rise and fall over the course of her monthly cycle. Estrogen thickens the endometrium, then the ovaries release an egg. After ovulation, progesterone levels increase to prepare the uterus for pregnancy. If pregnancy does not happen, progesterone levels drop.

These hormones don’t just affect the uterus, however; they travel through the blood to breast and other tissues. Estrogen and progesterone stimulate breast cells to divide and multiply. And, as 1Flesh correctly states above (I know, I’m as shocked as you are), the more breast cells multiply, the greater the chance that genetically faulty cells (read: cancer causing cells) survive and multiply out of control.

According to Ursin, “The greatest amount of division and proliferation of breast cells happens when estrogen and progesterone come together…at the end of the cycle. But something interesting happens with women taking oral contraceptives. In these women, the levels of breast cell proliferation remain almost level throughout the month.”

In other words, instead of having the highs and lows of estrogen and progesterone experienced by premenopausal women, women on OCs have more stable hormone levels as the pill “tricks” the body into not ovulating, and maintains a steady level of estrogen and progestin.

This means that the average amount of monthly hormones flowing through a woman taking OC and those not taking OC are about the same, with OC sometimes providing even LESS hormones.  Even more importantly, by the end of a cycle, breast cells in a woman taking OCs have multiplied by as much as – or maybe even slightly less – than a woman not on OC.

Huzzah for studies using more recent data!

By how much? According to the 2009 study Risk Factors for Triple-Negative Breast Cancer in Women Under the Age of 45 Years, published in the journal Cancer Epidemiology, Biomarkers, and Prevention, after less than one year of taking oral contraceptives, a woman’s risk of triple-negative breast cancer is increased 2.5 fold.

After more than one year of use, her risk is increased 4.2 fold.

Half-truths again, you silly geese over at 1Flesh? This (outdated) study examined the risk association between oral contraceptive usage and triple-negative breast cancer (again, the rarest form of breast cancer) among women who were diagnosed between the ages of 20 and 45 between the years of 1983 and 1992. The actual results of this study are as follows:

Women in this cohort who used OCs for more than one year had a 2.5 fold increase in the risk of triple-negative breast cancer, with the risk of triple-negative breast cancer being higher for women under 40 years of age (a 4.2 odds ratio). However, there was NO significantly increased risk with OC use for non-triple-negative breast cancer among any women, nor for triple-negative breast cancer among women 41-45 years of age.

There we go. That’s better, right? Accuracy in reporting always helps.

Further, it should be noted that the study did not differentiate between various types of hormonal contraception, though it is likely that many of the women in the study (particularly those who had been taking the pill for longer periods of time, and who were more likely to suffer an increased risk) had been taking oral contraceptives containing much higher doses of hormones.

To explain, OC’s available to women in this study would have most likely been first generation (containing more than 35 micrograms of estrogen and more than 2.5 milligrams of progestin) or second generation (containing less than 35 mcg of estrogen and less than 2.5 mg of slightly newer progestins like norethindrone or levonorgestrel).

By contrast, today’s OCs contain even lower amount of estrogen (typically 20mcg to 30mcg) and much lower levels of newer progestins (from .15 mg of second generation progestins like levonorgestral to .18mg of third generation progestins like norgestimate).

As explained in my earlier post, lower levels of hormones (particularly newer formulations of hormones) = lower levels of risk. And, actually, we have some data to back up that assertion:

The largest modern study, published in 2002, enrolled more than 4500 patients with breast cancer and 4500 controls aged 35 to 64 years from the United States from 1994 to 1998. Key findings from this study included no breast cancer risk among current (OR, 1.0; 95% CI, .8 – 1.3) or former (OR, 0.9; 95% CI, .8 – 1.0) OC users and no risks associated with duration of use or dose of estrogen. Moreover, a recent study of OC use in more than 4200 patients with breast cancer found no association between breast cancer mortality and OC use when duration of OC use, time since first use, age at first use, and use of specific formulations was examined. While breast cancer risks of the newest formulations of OCs are still unknown, based on the most recent data, they are predicted to show no association with the newest dosages and compositions of the estrogens and progestins being used.

[1Flesh, in their Facebook response to me, claimed that the more recent formulations haven’t been studied, so I can’t make this claim. Unfortunately for 1Flesh, this response indicates that their reading comprehension skills aren’t that great because the studies talk about that.

But, you know what, I’ll give them another study. This one is from 2002, and was published in the New England Journal of Medicine. It was a multivariate analysis study, including an analysis of different types of OCs. The authors actually researched many second generation OCs (as most women in the study were currently, or had been, taking newer formulations of OCs) and found NO increased risk associated with them. Given that the increased risk of breast cancer was associated largely with first generation OCs, the fact that second generation OCs – the ones with lower dosages and new formulations of progestins – have shown no increased risk has led researchers to conclude, as I state above, that there will be no association with the newest super low dosages and compositions.

Ta Da! ]

This risk is further increased if a woman begins her use of oral contraceptives before the age of 18, or if she smokes. This increased risk decreases immediately after ending the use of the Pill, and is gone approximately 10 years after discontinuation.

[1Flesh, again, in their Facebook response to me, claims that I am arguing semantics in the following paragraphs. If insisting on accuracy when reporting on women’s health issues is semantics, then I’m guilty as charged. Because I’m sorry, 1Flesh, but you simply can’t tie the results of multiple different studies together and claim that they mesh. You just can’t. It’s intellectually dishonest and unethical.]

While it is true that it is recommended that women taking OCs not smoke, particularly if they are 35 years of age or older, that fact was not mentioned in this study. And, actually, data from this study showed that smoking did NOT increase the risk for triple-negative-breast cancer. In addition, according to this study’s data, the risk for women who began taking OC’s before age 18 was heightened, but not “further increased” beyond the risks listed above. Again, accuracy matters, particularly when you’re playing with women’s health.

Also, the idea that increased risk persisted for 10 years after discontinuation was definitely not mentioned in this study, as they didn’t break the data down that way. It would be helpful if 1Flesh cited a source for this “fact.”

Actually, you know what, 1Flesh, here, I’ll help you. The data on OC use and increased risk for ten years prior to discontinuation comes from this study. First, it should be noted (again) that this study was a meta-analysis of 54 previous studies, many of which involved women using early generations of OCs containing higher levels of hormones. Second, the results of the study are far from damning:

[W]hile women are taking combined oral contraceptives and in the 10 years after stopping there is a small increase in the relative risk of having breast cancer diagnosed (relative risk [95 percent CI] in current users 1.24 [1.15-1.33], 2p<0.00001; 1-4 years after stopping 1.16 [1.08-1.23], 2p=0.00001; 5-9 years after stopping 1.07 [1.02-1.13], 2p=0.009). Second, there is no significant excess risk of having breast cancer diagnosed 10 or more years after stopping use (relative risk 1.01 [0.96-1.05], NS).

In layman’s terms, this means that even using data on OCs with extremely high levels of hormones, the increased risk of breast cancer was only 24% for current users, dropping to 16% in years 1-4 after discontinuation, to 7% in years 5-9 after discontinuation, and finally dropping to no increased risk at year ten and beyond.

[Finally, the study I cited above, the more recent one that showed NO increase in the risk of breast cancer, also found that early age at first use of contraception did not increase the risk. Again, huzzah for research! So that statement that women who started using OCs before age 18 have a heightened risk (again, I ask heightened from what baseline, to encourage 1Flesh to be intellectually honest), is no longer true.]

Triple-negative breast cancer is a particularly aggressive subtype of breast cancer, with little treatment available outside of chemotherapy and mastectomy. It makes up between 10% and 19% of breast cancer cases.

[Glad to see here, 1Flesh, that you picked up on the research I did for you to show you how rare this particular type of cancer actually is].

Ohemgee. A completely true sentence. Be still my heart! Yes, triple-negative breast cancer is a particularly aggressive subtype of breast cancer, for which treatment options are severely limited. HOWEVER, as noted above, this particular type of cancer is fairly rare – comprising only 10 – 19% of cases.

[In 1Flesh’s original post, they inserted another study about a DIFFERENT type of breast cancer (double negative cancer) among African-American women, but it’s no longer there. I’m assuming that’s because, upon a full reading of the study, one can see that, though the authors found a SLIGHTLY elevated risk of this particular type of breast cancer among African-American women, they also stated, “Because the prevalence of oral-contraceptive use is similar or perhaps even lower among African-American women than white women, oral-contraceptive use by itself is unlikely to explain the higher proportion of ER− breast cancers among African-American women.” Unfortunately, 1Flesh deleted this part of their post, and then accused me on Facebook of dismissing the study. Sorry, 1Flesh, but if the authors of a study tell you that contraceptive use is unlikely to explain the increase in breast cancer, I’m fully within my rights to tell you that you can’t use that study to claim that OCs increase that type of breast cancer.]

Adding further support to this research, The International Agency for Research on Cancer (IARC) lists combined oral contraceptives as Group 1 carcinogens. ‘Group 1’ includes carcinogens in which “the agent (mixture) is definitely carcinogenic to humans.” Other Group 1 carcinogens include asbestos, mustard gas, ultraviolet radiation, and formaldehyde.

You know what else is categorized as a Group 1 carcinogen? Alcoholic drinks, wood dust, oh, and the sun (among about about 99 other things). Also, not to be picky (oh, hell, who am I kidding, yes, to be picky), the preamble for the IARC lists contains the REAL definition for when items are to be placed in Group 1, and it’s this:

This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent acts through a relevant mechanism of carcinogenicity.

Ever so slightly different, but enough to matter to those of us concerned with accuracy.

It’s true that the Pill reduces the risk of other cancers, most notably ovarian cancer. However, according to a 2010 study published in Breast Cancer Research: 

Lifetime risk of triple-negative breast cancer is highest in black women (1.98%, 1.80-2.17%), compared to 0.77% (0.67-0.88%) for Asians, 1.04% (0.96-1.13%) for Hispanics and 1.25% (1.20-1.30%) for whites.

A woman’s lifetime risk for ovarian cancer is only 1.38%. The Pill increases a woman’s risk of triple-negative breast cancer by 4.2 after just 1 year, and only decreases a woman’s risk of ovarian cancer by half after 10 years of use.

[On Facebook, 1Flesh wholeheartedly disagrees with my claim that OCs don’t lead to an increased risk of breast cancer, even though ALL of the newer studies support my assertion. They also state that, “we simply believe that it’s demeaning to women to say, ‘Here’s a pill that will increase your risk of breast cancer, cervical cancer, heart problems, blood clotting, and HIV infection, while reducing your risk of ovarian cancer, endometrial cancer and colorectal cancer.’”

I have a lot of information on the benefits of OCs below, but since 1Flesh has raised new claims in their Facebook post about other possible harms – and seriously? They think it’s demeaning to give women all of the information about the benefits and possible risks of a medication? – I’ll address those below my old post notes, as well as add in some of the other uber cool things about OCs. Hope you enjoy learning about how absolutely fan-freaking-tasting OCs can be.]

Oh goodie! Now we get to the part where I get to talk about all of the completely awesome things about OCs!

First, I just have to mention this because it’s just THAT amazingly cool. Two recent studies, including on ongoing study following 45,000 women for up to 39 years and a completed study including 17,000 women followed through 2009 both found that ever use of OCs resulted in a lower relative risk of mortality (RR .88, CI 95%, .82-.93 and RR, .87, CI 95%, .79 – .96). If you’ve been following along with all this statistics mumbo jumbo, you’ll realize that that means that women who have ever used oral contraceptives have a 12 to 13% relative risk of mortality than women who have never used OC. Now we ALL know that correlation is not causation, but that’s still pretty freaking cool, is it not?

I could talk about lots of other awesome things about OCs, but since 1Flesh chose specifically to talk about cancers in this post, that’s what I’ll talk about hear, too.

1Flesh is right (I know, twice in one post? I feel faint) in that a woman’s lifetime risk of developing breast cancer being 12%. And they’re only slightly wrong about the lifetime risk of ovarian cancer (it’s actually 1.42%). But that’s where we part ways on this one.

We’ve already talked about how the 4.2 fold increased risk is bunk, as it only applies to triple-negative-breast cancer for women under age 40 who were most likely using older generation OCs which might higher hormone levels, so I won’t go into that again.

What I will take issue with is 1Flesh’s reporting half-truths, once again. The study 1Flesh cites clearly states (even in just the abstract) that:

The overall estimated protection from cohort and case-control studies is approximately 30% for ever OC users, and increases with duration of use by approximately 5% per year of use to about 50% for long-term (≥10 years) users. The favourable effect of OC against ovarian cancer risk persists for at least 20 years after OC use has ceased, and it is not confined to any particular type of OC formulation. The reduced risk among OC users is observed in women without or with family history or genetic predisposition to ovarian cancer, and for most histological types of epithelial ovarian cancer, although the pattern of risk is less consistent for mucinous than for other types. The protection of OC on ovarian cancer risk, also in view of its long-term persistence, corresponds to the avoidance of 3000-5000 ovarian cancers (and 2000-3000 deaths) per year in Europe, and a similar figure in North America.

That makes OC sound a hell of a lot better at preventing ovarian cancer, doesn’t it? See what a little honest reporting can do?

Further, oral contraceptives have also been found to have significant positive effects in preventing endometrial cancer. For instance, studies have found the risk of endometrial cancer to be 30 to 50% less among OC users than non-users.

Oh, and lest we forget about colorectal cancer, note that a meta-analysis of 11 controlled studies and 7 cohort studies found a RR of .81 (CI 95%, .72-.92) in OC users compared to never users, with the reduction in risk being greatest among recent users.

Finally, as we’ve spent much of this blog talking about breast tissue, now might be a good time to mention that current users of OC’s have at least a modest reduction in the risk of benign breast disease (which can potentially progress to cancer).

Still not worth it, 1Flesh?

[As noted above, 1Flesh first claims (again) that OCs increase the risk of breast cancer, a theory that has been thoroughly debunked by more recent research, some of which I site in this post.

1Flesh then claims that OCs increase the risk of cervical cancer. And, again 1Flesh may be right (I know, I’m about to have a heart attack, too); however, I think this might be the time for 1Flesh to learn the mantra: correlation does not equal causation.  It’s also a good time for them to remember the difference between relative risk and absolute risk I pointed out in my previous post.

An article published in the Lancet in 2007 found that, among women currently using OCs, the risk for invasive cervical cancer increased with increasing duration. For instance, women who had been using OCs for 5 or more years had approximately twice the risk versus women who had never used them (relative risk). BUT when the researchers applied this relative risk to the absolute risk, they found that using oral contraceptives for ten years (e.g. from age 20 to 30) raised the cumulative incidence of invasive cervical cancer from 3.8 to 4.5 per 1000 women in industrialized countries, and from 7.3 to 8.3 per 1000 for women in developing countries.  Further, that whole, “correlation does not equal causation” thing is particularly important here as oral contraceptive users may have more unprotected sexual encounters and an increased exposure to the human papillomavirus, a known risk factor for cervical cancer.

Further, the study authors noted that the slightly increased risk of cervical cancer needed to be weighed against the roughly 50% reduction in the risks of ovarian and endometrial cancers. One model actually estimates that for every 100,000 women, 44 fewer reproductive cancers would occur amongst users than in nonusers.

With regard to cardiac issues, there are four primary concerns: coronary artery disease, venous thromboembolism, hypertension, and stroke. I’ll take these one by one. In regards to coronary artery disease, low-dose oral contraceptives were developed in response to increased cardiovascular events associated with higher-dose oral contraceptives. Studies of low-dose OCs (i.e. contraceptiveswith less than 50  µg estrogen) havefound no increased risk of myocardial infarction (MI) among healthy, nonsmokingwomen. In women over age 35, smoking 15 or more cigarettes per day increases the risk of heart attack, but such risks were not evidenced for women under 35, or thosewho smoked less or did not smoke.

One cardiac risk which has been consistently tied to OC use is the risk of venous thromboembolism (VTE). The risk of VTE istwo to six times higher in oral contraceptive users than in nonusers. However, the absolute risk of VTE in otherwise healthy women is low, at about 1 or 2 persons in 1,000 to 10,000, depending on age, which means that OC use would increase the number of women diagnosed with VTE to, at most, 6 or 12 per 1,000 or 10,000, depending on age.

While many women may have an increase in blood pressure with OC use, readings usually remain within the normal range. Low-dose oral contraceptives are not contraindicated in otherwise healthy women with well-controlled hypertension, but women over age 35 who have hypertension and who smoke or have end-organ vascular disease should not use oral contraceptives.

Finally, studies evaluating OCs and stroke are difficult to interpret. Many studies have had small sample sizes, have not differentiated between hemorrhagic and thromboembolic stroke, and have not controlled for major risk factors. Most evidence suggests, however, thatthere is no increased risk in oral contraceptive users, except in those who smoke. The risk of stroke from use of these agents in migraine patients is also controversial. Studies of older, high-dose oral contraceptives showed anincreased risk of stroke whereas studies of low-dose formulations have not.

As for the risk of HIV infection, if 1Flesh is unschooled enough to believe that OCs actually CAUSE HIV infection, I don’t know what to say.  Again, correlation =/= causation. As the risk of HIV infection is ALWAYS present when engaging in sex with an infected partner when not properly using a barrier method, I’m not sure how this point is relevant. If there is a concern about HIV transmission, a barrier method should always be used, whether or not a woman is using OCs. ALWAYS.

And now to quickly share some of the other awesome GOOD things that OCs can do FOR you. We’ve already talked about the cancer preventative properties of oral contraceptives, but there are also benefits in terms of decrease in symptoms or a decreased risk of several conditions, such as dysmenorrhea, anemia, acne, hirsutism, ectopic pregnancy, ovarian cysts, and pelvic inflammatory disease (research shows a 10 – 70% reduction in PID).

Oral contraceptives can also help prevent osteopenia and osteoporosis, a subject near and dear to my heart (I was diagnosed with osteopenia at age 24 due to low estrogen levels). Studies have shown that because oral contraceptives provide a consistent dose of estrogen, they may increase bone mineral density by promoting higher peak bone mass. This benefit has been reported even with ultra-low-dose formulations, and the positive effect increases with higher doses and longer use.

Finally, OC’s that contain third-generation progestins improve dyslipidemia by improving serum lipoprotein profiles by increasing HDL and decreasing LDL.

I’m hoping by this point that what 1Flesh writers are gathering is that OCs are actually pretty damn safe for women who are otherwise healthy, and who don’t smoke, but that doctors should always share the risks AND benefits of any medication when prescribing it to patients.]

It is entirely likely — though currently unproven — that the increase in breast cancer cases around the world since the 1970′s has been aided by the likewise massive increase in the use of oral contraception, and its subsequent effects on the environment.

Key words in that paragraph? “Though currently unproven.” I’d change that to won’t be proven, but otherwise, yes, there HAS been a massive increase in breast cancer cases.

And you know what’s also interesting? We have proven causes for this, even hormonal ones. Want to hear a few:

As for the effect of OCs on the environment, sorry 1Flesh, but that theory’s been thoroughly debunked by others. Try harder.

Adding further support to this research, The International Agency for Research on Cancer (IARC) lists combined oral contraceptives as Group 1 carcinogens. ‘Group 1’ includes carcinogens in which “the agent (mixture) is definitely carcinogenic to humans.” Other Group 1 carcinogens include asbestos, mustard gas, ultraviolet radiation, and formaldehyde.

Please take note that the IARC is telling us that there is convincing evidence that OCs confer a protective benefit against cancer.

You know what else is categorized as a Group 1 carcinogen? Alcoholic drinks, wood dust, oh, and the sun (among about about 99 other things). Also, not to be picky (oh, hell, who am I kidding, yes, to be picky), the preamble for the IARC lists contains the REAL definition for when items are to be placed in Group 1, and it’s this:

This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent acts through a relevant mechanism of carcinogenicity.

Ever so slightly different, but enough to matter to those of us concerned with accuracy.

These are the facts.

Well, NOW there are some facts thrown in there.

We at 1Flesh beg that pharmaceutical companies clearly label their oral contraceptive products as increasing breast cancer risk. We beg that pharmaceutical companies inform doctors of the risks contained in the pills advertised to them. We beg that doctors inform their patients of the risk of breast cancer conferred by their prescriptions.

And I beg that pharmaceutical companies clearly label their oral contraceptive products with correct information, i.e. that their products do NOT increase breast cancer risk. I beg that pharmaceutical companies inform doctors that their oral contraceptive products do not carry an increased risk of breast cancer, but do carry the benefits of preventing certain other types of cancers. And I beg that doctors inform patients of the truth of the risk between the use of oral contraceptives and breast cancer – namely that the risk does not exist.

We beg women to consider natural and more effective alternatives to carcinogenic birth control.

AND…again with the pitch to a form of natural family planning that isn’t really all that effective. But now I get it. Dr. Creighton has an honorary degree from the Franciscan University of Steubenville, where several of the founders of 1Flesh are currently students, and where the Creighton Model is taught as part of a premarital counseling program.  Sometimes it’s easiest to promote what you know…even when what you know isn’t always the best.

Till next time,

-H

© Heather Parker and Antigone Awakens, 2012-2013.

2 thoughts on “Sorry 1Flesh, “The Pill” Still Doesn’t Cause Breast Cancer: Debunking 1Flesh, Episode 1, Round 2

  1. fuckthestatquo

    From 1Flesh's FB:

    The study “showed that the risk of breast cancer was not significantly related to the duration of oral-contraceptive use or to the dose of estrogen.” While there are a lot of issues with this study, this would seem to indicate that the claim you're making — that third generation pills, because of their lower dose of estrogen, have a lower risk of breast cancer — is not yet valid.

    As for the study itself, there have been valid complaints about it's methodology that render us skeptical. For instance: “Seventy-six percent of the case subjects and 78 percent of the controls had used oral contraceptives, and 38 percent and 41 percent, respectively, had used hormone-replacement therapy. How many of the 4575 case subjects and 4682 controls had never taken hormones? It is impossible to know the effects of hormones without comparing women who have used them with women who have never used them.

    The United Kingdom National Case–Control Study Group's report on women younger than 36 may be more reliable, since few younger women use hormone-replacement therapy. There was a significantly increasing trend in the risk of breast cancer with longer use of combined-formulation pills. The risk in nulliparous women with longer use was 2.3 times the risk in women with no use. However, when women who had used progestin-only pills were compared with those who had never used combined-formulation pills, the former group was found to have a 60 percent greater risk of breast cancer after as little as 1 to 12 months of use, mostly during lactation. This increase in a very short time is worrisome, especially since intermittent, large doses of progestins are being promoted for emergency contraception.” Ellen C.G. Grant, M.B., Ch.B.

    And from the National Cancer Institute:
    Similarly the National Cancer Institute's analysis of the study found it wanting: “In the Women's Contraceptive and Reproductive Experiences (Women's CARE) Study, Marchbanks et al. (June 27 issue) carefully verified previous investigations showing that there is no association between combination oral contraceptives and the risk of breast cancer among women older than 45 years of age. However, when data from women 35 to 44 years old are combined for analysis, the risk of breast cancer associated with recent use of oral contraceptives may not be fully apparent among the youngest women. The investigators report that they found a higher risk of breast cancer among the women 35 to 39 years old than among the older women. However, because the risk of breast cancer associated with recent oral-contraceptive use is greatest among very young women, and may be twice that among nonusers in some subgroups, closer examination of the women 35 to 39 years old in this study is warranted.
    Although oral-contraceptive use does not appear to increase the risk of breast cancer among older women, the findings need to be interpreted within the context of risk over the course of a lifetime. For example, oral contraceptives may cause nascent tumors to become clinically evident earlier in women who use contraceptives than in those who do not. Consequently, oral-contraceptive users in whom cancer does not develop at a young age (e.g., before the age of 40 years) may be less susceptible at older ages to the promotional effects of oral contraceptives. The results of the Women's CARE Study sparked media reports that oral contraceptives should no longer be considered a risk factor for breast cancer, when in fact there may be some evidence that recent use increases risk in very young women.

    I'm curious how a 2002 study with this kind of criticism isn't outdated, but a 2009 study from the NCI is. Either way, there's simply not enough evidence for you to be making the claim that third generation pills come with no increased risk of breast cancer.

    Reply
  2. Heather

    Dear anonymous user,

    Thank you for reposting 1Flesh's response from their FB page here, even though it was clear that we were conversing quite well on their page. In any case, here is my response to their comments, which is also posted on their FB page for your perusal:

    “Hi 1Flesh,

    First, thanks again for your responses to my blog posts, and to the studies (well, one study in particular – the 2002 CARE study – that I listed therein). It seems, from your concerns, that you copied and pasted information from the Letters to the Editor page in response to that article.

    Unfortunately, it doesn’t look as if you scrolled down far enough to see the study authors’ response to those criticisms.

    In response to your first question, if you actually read the study and the appendices, you’ll notice that the authors DO give you data on the number of women who had never used any type of hormonal contraceptives or hormonal-replacement therapy (you can find it here: http://www.nejm.org/doi/full/10.1056/NEJMoa013202#t=article). However, in the interest of firmly establishing their analysis, the authors actually repeated their analysis with a completely new reference group consisting of women who had never used oral contraceptives, hormone-replacement therapy, or contraceptive shots or implants, and found that the relative risks of breast cancer associated with any, current, or former use of combined OCs among women aged 35-64 years old were 1.0 (95% CI, 0.8 to 1.1), 1.0 (95% CI, 0.8 to 1.3), and 0.9 (95% CI, .8 to 1.0). In case that isn’t clear, that means that OC use among women aged 35 – 64 years was NOT associated with any increase in the risk of breast cancer for any or current users, and was actually associated with a LOWERED risk of breast cancer for former OC use.

    The UK study is published in the Lancet (here: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(89)92627-5/abstract) is interesting – thank you for drawing it to my attention – though I will point out that it was published in 1989 and had a much smaller sample size. Further, if you read the study I cite below (in the second paragraph below this one), you’ll see that more recent studies have not found an increased risk; in fact OCs have been show to LOWER the risk of early onset breast cancer in BRAC1 mutation carriers.

    In response to the second LTE from the NCI (concerning OC use and the risk of breast cancer about women who receive a diagnosis at an early age), the authors admitted that their data was not fully informative on the topic because they restricted their study to women aged 35-64 because they were primarily interested in resolving the question of whether use of OCs during reproductive years would increase the risk of breast cancer later in life, where the incidence is highest. When the authors examined the data from their youngest subgroup of women (aged 35-39 years old), the discovered that the relative risks associated with any, current, and former use of combined OCs were: (1.3, 95% CI, 0.9-1.8), (1.2, 95% CI, 0.8-.8), and (1.3, 95% CI, 0.9-1.8), respectively, indicating a slightly elevated risk.

    HOWEVER, Another more recent study, conducted solely on premenopausal women, found, however, that oral contraceptive use not only did NOT increase the risk of early onset breast cancer for OC users, but use for at least 12 months was associated with a DECREASED risk of cancer for BRCA1 mutation carriers [OR, .22, 95% CI, 0.10 – 0.49; p <0.001]. BRCA2 mutation carriers and noncarriers did see this same benefit, but were not at any higher risk (OR, 1.02; 95% CI, 0.34 – 3.09) and (OR, .93; 95% CI, 0.69-1.24 with an exception being those users who began taking OCs prior to 1976 (again, with the hormone levels in OCs were much higher), who had an increased risk (OR, 1.52; 95% CI, 1.22-1.91; p < 0.001) You can read that study here: http://cebp.aacrjournals.org/content/14/2/350.full.pdf+html

    If you have any further questions, you know how to reach me.”

    Best,

    Heather

    Reply

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