Memorandum 14
Submission from Dr Joel Brind, Professor
of Human Biology and Endocrinology, Baruch College of the City
University of New York
SCIENTIFIC DEVELOPMENTS
RELATING TO
THE EFFECT
OF ABORTION
ON RISK
OF FUTURE
BREAST CANCER
EXECUTIVE SUMMARY
— Higher risk of future breast cancer
in women with abortion versus pregnancy and delivery has been
consistently reported in medical literature since 1970 multinational
study (including the UK) by the World Health Organization (WHO).
— Oxford University epidemiologists
have led the effort to give public false assurance of safety since
1982, with three studies on UK women, and a recent (2004) "reanalysis"
by Valerie Beral et al, of worldwide data, which reported the
false conclusion of no risk increase with abortion.
— The Oxford "reanalysis"
was biased in selecting studies for review, including at least
four large, scientifically invalid studies, and excluding or omitting
15 valid studies for non-scientific reasons.
— The Oxford "reanalysis"
used the clinically impossible standard "of never having
had that pregnancy" to which women who chose abortion are
compared.
— The majority of world-wide published
evidence shows abortion raises breast cancer risk beyond "never
having had that pregnancy", as we reported in our 1996 meta-analysis,
published by the British Medical Association.
— Established facts of breast physiology
support independent effect of abortion in raising breast cancer
risk.
— The flawed methodology used for abortion,
in Oxford "reanalysis" and in general, is compared with
correct methodology used to identify HRT as a significant risk
factor, even by the same Oxford researchers (Beral et al.) in
their 2003 "Million Women Study".
— The same inappropriate standard of
comparison used for abortion would also make HRT appear not to
increase risk, as demonstrated by Million Women Study results.
— Recent US experience with hormone
replacement therapy (HRT) shows honest reportage of risks results
in women avoiding risk, by stopping HRT use.
— Recent US drop in breast cancer shows
striking results of women stopping HRT use, thus avoiding risk.
— RCOG Clinical Guideline No. 7 acknowledges
lower breast cancer risk with pregnancy and delivery, yet it contradicts
its own evidence with the claim of no risk increase, and violates
its own Clinical Governance Advice No. 6 re: obtaining informed
consent.
— RCOG Clinical Guideline No. 7 misrepresents
evidence against their recommendation as "Evidence supporting
recommendation".
— Open disclosure of abortion's effect
in raising breast cancer risk will reduce future medical costs
and demographic decline in the UK.
FOCUS OF
THIS REPORT
1. This report will focus primarily on recent
developments in research as published in the peer-reviewed medical
literature, mostly in the UK, concerning "the relative risks
of early abortion versus pregnancy and delivery" (Select
Committee instruction 2(a)), specifically in relation to "evidence
of (the) long-term ... adverse health" outcome(s) from abortion"
(instruction 3) of breast cancer.
BACKGROUND
2. Compared to pregnancy and delivery, that
the risk of future breast cancer is increased in women who choose
abortion has been documented in the peer-reviewed medical literature
since at least 1970, with the publication of a seven-nation (including
the UK) international epidemiological study in the Bulletin of
the World Health Organization1. That study established that early
full-term—but not aborted—pregnancy confers substantial
protection against future breast cancer. The authors described
the "striking relation ... that women having their first
child when aged under 18 have only about one-third the breast
cancer risk of those whose first birth is delayed until the age
of 35 years or more." Importantly, the authors further observed
that, where differences were observed regarding the frequency
of abortion they "were in the direction which suggested increased
risk associated with abortion—contrary to the reduction
in risk associated with full-term births." Hence, a pregnant
women choosing to abort her first pregnancy was found to be putting
herself at substantially higher risk of future breast cancer,
compared to her choosing to complete the pregnancy.
3. Despite multiple confirmations of higher
risk with abortion compared to full-term pregnancy, many epidemiological
researchers have continued to "reassure" the public
about the safety of induced abortion vis-a"-vis breast cancer
risk. This effort has been most consistently made over the years
by researchers at Oxford University2-5, most recently by a group
headed by Valerie Beral. The quantitative evidence to support
this false claim of safety was inappropriately compiled in several
important ways.
2004 OXFORD "REANALYSIS"
OF WORLDWIDE
DATA
4. While purporting to be comprehensive
in having "brought together worldwide epidemiological evidence"
on abortion and breast cancer, the Oxford group's 2004 "collaborative
reanalysis" in the Lancet comprising 52 studies4, was highly
selective. Although 41 studies with abortion-breast cancer data
had been published by that time, the total of 52 was arrived at
by the exclusion or omission of 17 published studies and the inclusion
of 28 studies' worth of previously unpublished data.
5. Of the 13 studies excluded in the 2004
Beral "reanalysis", only two were excluded for valid
scientific reasons, ie, specific information on "induced
abortions had not been recorded systematically for women with
breast cancer and a comparison group." However, an additional
three large published studies—should have been excluded
under the same criterion, to wit: a 1997 study in Denmark6 in
which all the data on legal abortions before 1973 were missing
(80,000 abortions on 60,000 women), a 2001 study of Oxford women3,
in which over 90% of the abortions in the study population were
unrecorded, and a 2003 Swedish study7, in which data on all abortions
after the most recent childbirth (ie, a majority of abortions)
were missing. All of these inappropriately included studies reported
no increased breast cancer risk associated with induced abortion,
and substantially biased the "reanalysis" in the negative
direction.
6. An additional large but unpublished (subsequently
published in 2005) study on women in Scotland5 included in the
"reanalysis, should also have been excluded on the same grounds.
In fact, the Scotland study by Brewster et al, which was co-authored
by Beral herself, distorted an otherwise excellent database and
arrived at an entirely invalid result. Specifically, the database
of NHS reproductive histories of women in Scotland, had been computerized
in 1981. Since pre-1981 events were also incorporated into the
database in 1981, such events could also be included in the Brewster
study. But inexplicably, Brewster et al. included only "those
with some reproductive events occurring before 1981, and (for
whom) number of pregnancies equalled number of births—that
is, no miscarriages or induced abortions before 1981". This
egregious application of selection bias eliminated over 90% of
the women for whom abortion preceded the first live birth; a majority
of abortions in Scotland. The resulting analysis consequently
embodied such a thorough distortion of the database as to render
the study's negative result entirely invalid. I have published
a detailed deconstruction of the Brewster study elsewhere8.
7. A bias in the Beral et al. "reanalysis"
in the same direction (of finding no risk increase with induced
abortion) is evidenced by the pattern of exclusion of valid studies.
Specifically, 11 studies were excluded from the analysis for non-scientific
reasons, ie: "Principal investigators ... could not be traced,
original data could not be retrieved", or "researchers
declined to take part in the collaboration" or "judged
their own information on induced abortion to be unreliable"
(this last justification being particularly remarkable, as the
data in question had been published in a prominent peer-reviewed
journal9 and never retracted). Four additional studies simply
never appeared in the analysis, with no justification given, even
though they had been previously published as abstracts or included
in other reviews.
8. That the Beral et al.4 "reanalysis"
was severely biased by these 15 inappropriate and unscientific
exclusions and omissions is clear from the fact that this excluded
group includes all the large studies which had reported overall
relative risks in excess of two (ie, double the risk). The "reanalysis"
therefore gives the false impression that no single, substantial
study in the published record reported an overall relative risk
in excess of 1.41, when in fact, four of the studies had reported
overall relative risks greater than two; one as high as 3.110.
9. Despite the conclusion of Beral et al.4 in
their 2004 reanalysis that induced abortions "do not increase
a woman's risk of developing breast cancer", and notwithstanding
the substantial selection bias inherent in the "reanalysis",
Beral et al. still reported a summary, statistically significant
relative risk of 1.11 for all studies based on retrospective data,
in contrast to a slightly negative association (RR = 0.93) for
studies based on prospective data. Finding the difference between
the prospective and retrospective study results "highly significant"
(despite the egregious flaws in four of the prospective studies,
described in paragraph 5 and 6 above), Beral et al. reported that
the difference was likely attributable to "the systematic
difference in reporting induced abortion between cases and controls
indicated by the Swedish retrospective study". The Swedish
study11 to which Beral et al. refer, however, was based on the
presumption that women who had reported abortions which did not
appear in the computerized registry had "overreported"
them, ie, imagined them to have taken place. This preposterous
assumption of "overreporting" was retracted in 199812,
a fact not mentioned in the "reanalysis".
10. Last but not least in the list of methodological
flaws of the Oxford "reanalysis" is the manner in which
the relative risk estimates were inappropriately calculated, ie,
the assignment of an artificial and clinically irrelevant comparison
between choosing abortion v. the literally impossible situation
of "never having had that pregnancy"4.
WORLD-WIDE
PUBLISHED EPIDEMIOLOGICAL
AND BIOLOGICAL
EVIDENCE OF
ABC LINK
11. The accumulated epidemiological evidence
of the independent effect of induced abortion in raising breast
cancer risk was compiled by my own research team and published
in the British Medical Association's Journal of Epidemiology and
Community Health in 199613. In that report, we compiled all available
published data, which dated as far back as 195714, and documented,
in our meta-analysis, an average increased risk (beyond "never
having had that pregnancy") of approximately 30%.
12. Denials of the independent link—indeed
any link—between induced abortion and breast cancer notwithstanding,
even the largest, most often cited study6 to claim "induced
abortions have no overall effect on the risk of breast cancer"
shows a clear elevation in risk (beyond no pregnancy at all) among
women with abortions beyond the first trimester. Thus, Melbye
et al, in their nationwide prospective study on Danish women12
reported a clear, significant trend of increasing risk with gestational
age at abortion, the risk increase reaching 89% beyond 18 weeks'
gestation. The same Danish research group confirmed this trend
for premature livebirths, reporting more than a twofold risk increase
for livebirths delivered before 32 weeks' gestation15. There is
no difference between a premature livebirth and an induced abortion,
in terms of hormonal effects on the breasts and the future risk
of breast cancer. This effect is well understood in terms of the
lack of breast maturation into cancer-resistant lobules before
32 weeks, and argues for a careful reevaluation of the safety
of late term abortions (before as well as after 24 weeks) and
the regulations regarding such abortions.
13. Since induced abortion has also been
established as a risk factor for subsequent premature and very
premature births (ie, before 32 weeks) 16, it secondarily increases
the risk of breast cancer in such women.
14. In addition to the effect of abortion
in raising future breast cancer risk by abrogating the protective
effect of full-term pregnancy, is the well-documented independent
effect of abortion in raising risk even beyond that of "never
having had that pregnancy" (see paragraph 11, above). This
effect is attributable to the growth-stimulating effects of sharply
elevated levels of oestrogen and progesterone during pregnancy;
these hormones causing the formation of greater numbers of immature
type 1 and 2 breast lobules, where almost all breast cancers start17.
(During pregnancy, milk-producing lobules only mature to cancer-resistant
type 3 and 4 lobules after 32 weeks gestation, resulting in full-term
pregnancy's long-term protective effect.)
COMPARISON OF
ABORTION WITH
ANOTHER AVOIDABLE
RISK: HORMONE-REPLACEMENT
THERAPY (HRT)
15. The absurdity of the claim of abortion's
safety vis-a"-vis "never having had that pregnancy"
is underscored by comparison of this flawed methodology with the
correct methodology used to quantify the breast cancer risk increase
attributable to combination (ie, oestrogen-progestogen) hormone
replacement therapy (HRT). This therapy is used by many postmenopausal
women, and its breast cancer danger was documented in another
large study (among others)—"the Million Women Study"—published
by Beral's group18 in The Lancet in 2003.
16. In striking contrast to the comparison
made in the 2004 "reanalysis" on induced abortion and
breast cancer, the 2003 HRT study appropriately compared postmenopausal
women taking HRT to women of the same age not taking HRT. As other
groups have amply confirmed, the risk of future breast cancer
was significantly increased—in fact, doubled—among
combination HRT users.
17. Had Beral and co-workers instead applied
an inappropriate standard for HRT risk as they had applied in
the case of induced abortion, little if any risk increased would
have been observed. Specifically, the analagous comparison would
have been between HRT users and premenopausal women of comparable
age; women in the position of "never having had that"
menopause. The analogy between the two types of methodology is
strictly correct, as both full-term pregnancy and menopause have
similar effects on a woman's future breast cancer risk: They lower
risk in inverse proportion to the woman's age at which the event
(full-term pregnancy or menopause) occurs.
18. The proof that inappropriate comparison
of postmenopausal women who took HRT to comparably aged premenopausal
women, would have resulted in little or no increased risk, actually
appears in the Million Women Study18. Specifically, "among
never users of HRT the relative risk of invasive breast cancer
was ... 0.63 (95% CI 0.58-0.68) (ie, significantly reduced by
an average 37%) for postmenopausal, compared with premenopausal
women." Hence, the (higher) risk of premenopausal women was
similar to the risk of postmenopausal women who used HRT. That
late menopause increases the risk of breast cancer is well established,
and attributable to the risk-increasing effect of ovarian sex
hormones, whether made by a woman's own ovaries (before the menopause),
or taken exogenously (as HRT).
19. The HRT-breast cancer link is of particular
relevance to the abortion-breast cancer link in that both are
avoidable risks, and recent events in the US have illustrated
how women take these risks seriously when accurate information
is given. A large, five-year randomized trial—the Women's
Health Initiative study19—begun in 1999 to test HRT's putative
effect in lowering heart attack risk—was terminated in 2002
after only three years because heart attack risk was found to
be significantly elevated, rather than reduced. News of the study's
termination included confirmation of HRT's carcinogenic effect
on the breasts, which most women on HRT found out for the first
time. Over the next two to three years, use of HRT declined by
70%.20
20. Strikingly, within a year of the WHI
study's termination, the breast cancer incidence rate for women
in the US over 50 years old began to decline in parallel with
the decline in HRT use, the extent of the decline reaching almost
12% within three years. That the breast cancer incidence decline
was due to the massive cessation of HRT use is widely accepted
as the only likely explanation20.
RCOG GIVES INACCURATE
AND CONTRADICTORY
CLINICAL ADVICE
TO ABORTION
PRACTITIONERS
21. Importantly, The RCOG Clinical Guideline
No. 721 on "the care of women requesting induced abortion"
acknowledges the Beral reanalysis4 as "a major systematic
review ... which lent further support to these conclusions (of
no association between induced abortion and breast cancer risk)",
despite the fact that the very first line of text in the Beral
reanalysis states: "Pregnancies that result in a birth are
known to reduce a woman's long-term risk of developing breast
cancer".
22. Hence, false reassurance of the safety
of abortion vis-a"-vis future breast cancer risk is embodied
in the RCOG's Clinical Guideline No. 721 (Recommendation 16.7):
"Induced abortion is not associated with an increase in breast
cancer risk." This advice, if taken by abortion practitioners
when advising patients and obtaining their consent, results in
the flagrant violation of the RCOG's own Clinical Governance Advice
No. 622 which describes the requirements for "obtaining valid
consent." This Advice clearly advises the practitioner: "You
should already have: ... discussed with the patient the risks
and benefits of having no treatment. These points should be reinforced
at the time of signing of the consent form." As it is unequivocal
that "having no treatment", ie, carrying the pregnancy
to term, results in a lower long-term risk of breast cancer, the
practitioner clearly has a duty to inform the patient of this
fact not once, but twice, in order to obtain valid consent for
abortion.
23. Yet another stark contradiction in the
RCOG Clinical Guideline on induced abortion practice21 is the
recommendation (No. 16.7) of no association between induced abortion
and breast cancer risk in the face of the same Guideline's acknowledgement,
under "Evidence supporting recommendation 16.7" of our
1996 meta-analysis13. Specifically, the Guideline cites our summary
conclusion "that induced abortion was a significant, independent
risk factor for breast cancer, with an odds ratio of 1.3 (95%
CI 1.2-1.4)", and further acknowledges that our review had
been "carefully conducted", "and that the Brind
et al. study had no major methodological shortcomings and could
not be disregarded." Clearly, our review constitutes credible
evidence against rather than "supporting" the Guideline's
unequivocal recommendation of induced abortion's being "not
associated with an increase in breast cancer risk."
CONCLUSIONS
24. It is therefore likely that providing
full and accurate information on the effect of abortion in raising
future breast cancer risk substantially, compared to pregnancy
and delivery, is likely to reduce the abortion rate substantially.
Such a reduction in numbers of a procedure which is not safe for
women as originally thought in 1967, will provide benefits in
terms of improved future health for British women, lower costs
for cancer treatment and treatment of other sequelae, as well
as amelioration of the alarming demographic decline evident in
the UK in recent years.
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22. RCOG Clinical Governance Advice No. 6. http://www.rcog.org.uk/index.asp?PageID=478
August 2007
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