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Ordinary women and official statements confuse and conflate perimenopause—the long, complex, life phase of higher and chaotic estrogen levels—with the low and stable estrogen levels of menopause. This paints both perimenopause and menopause with an inaccurate ‘estrogen deficiency’ brush. Menopause is the hormonal, and (except for hot flushes) the experiential opposite of perimenopause. This feminist analysis is from my perspective as physician‐scientist who experienced a perimenopause that was scientifically enlightening, but personally agonizing. Denial of perimenopausal and menopausal differences causes perimenopause to be ‘lost’ in several ways: (1) we may assume that perimenopause is chronic rather than ending in a largely asymptomatic menopause; (2) societal taboos isolate us, depriving us of solidarity with perimenopause ‘survivors’; (3) we are told we have dropping estrogen levels when our experiences, like pregnancy dreams, tell us the opposite; (4) gynaecology treats heavy flow with estrogen despite higher perimenopausal estrogen levels; (5) feminists ignore hormonal changes and attribute perimenopausal symptoms to (real) stresses of inferior social status and ageing; and (6) many of us thus become menopausal without the unique, self‐actualization experience that perimenopause has the potential to provide. Thus perimenopause—a valuable transition into knowing and standing up for ourselves—becomes lost.
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Perimenopause lost—reframing the end of
Centre for Menstrual Cycle and Ovulation Research, University of British Columbia, and
Vancouver Coastal Health Research Institute, Vancouver, Canada
Abstract Ordinary women and official statements confuse and conflate perimenopause—
the long, complex, life phase of higher and chaotic estrogen levels—with the low and stable
estrogen levels of menopause. This paints both perimenopause and menopause with an
inaccurate ‘estrogen deficiency’ brush. Menopause is the hormonal, and (except for hot flushes)
the experiential opposite of perimenopause. This feminist analysis is from my perspective as
physician-scientist who experienced a perimenopause that was scientifically enlightening, but
personally agonizing. Denial of perimenopausal and menopausal differences causes
perimenopause to be ‘lost’ in several ways: (1) we may assume that perimenopause is chronic
rather than ending in a largely asymptomatic menopause; (2) societal taboos isolate us,
depriving us of solidarity with perimenopause ‘survivors’; (3) we are told we have dropping
estrogen levels when our experiences, like pregnancy dreams, tell us the opposite; (4)
gynaecology treats heavy flow with estrogen despite higher perimenopausal estrogen levels; (5)
feminists ignore hormonal changes and attribute perimenopausal symptoms to (real) stresses of
inferior social status and ageing; and (6) many of us thus become menopausal without the
unique, self-actualization experience that perimenopause has the potential to provide. Thus
perimenopause—a valuable transition into knowing and standing up for ourselves—becomes
This feminist critique of current misinformation concerning perimenopause posits that
it is currently (deliberately) misunderstood to mean dropping estrogen levels, wrongly
equated with menopause or, worse yet, entirely ignored. Before describing the six
deficits of ignoring perimenopause, I will provide some historical context for the
dominant estrogen deficiency paradigm. I will also provide and critique current
definitions in women’s ageing. I will put this new knowledge into the context of my own
struggle to personally as well as scientifically understand the hormonal changes of
perimenopause. Finally, I will show that perimenopause, as a unique life phase, is being
Address for correspondence: Professor J. C. Prior, UBC Endocrinology, 2775 Laurel St, Room 4111, Diamond
Health Care Centre, Vancouver, BC V5Z 1M9, Canada. Tel: +1 604 875-5927; Fax: +1 604 875-5915. Email:
Received: 1 May 2006. Accepted: 30 June 2006.
VOL. 24, NO. 4, NOVEMBER 2006, pp. 323–335
ISSN 0264-6838/print/ISSN 1469-672X/online/06/040323-13
#2006 Society for Reproductive and Infant Psychology
DOI: 10.1080/02646830600974071
Perimenopause is defined by gynaecology (the recognized authority on women’s
health) as ‘the time preceding normal menopause during which declining ovarian
function causes oligomenorrhea or dysfunctional uterine bleeding, symptoms of
estrogen deficiency and elevated gonadotrophins’ (Nelson et al., 1996, p. 1393). The
above inaccurate and hormonally incongruous definition
was the only mention of
perimenopause in a two-volume gynaecology text published in 1996. Almost 10 years
later, consensus statements and reviews continue to imply that perimenopause is a time
of dropping estrogen levels (National Institutes of Health, 2005). And menopause
continues to be defined by an inaccurate ‘estrogen deficiency paradigm’ that didn’t
change after the recent randomized controlled trial data showing more harm than
benefit from treatment with estrogen or estrogen/progestin for largely asymptomatic
menopausal women (Beral et al., 2002). Although menopause and its low estrogen and
progesterone levels are a normal part of all women’s life cycle, the estrogen deficiency
paradigm to explain women’s health risks remains as strong as ever. One might even
speculate that perimenopause is constructed as dropping estrogen levels to serve as a
new market for estrogen now that sales for older menopausal women have decreased
(Austin et al., 2003).
But first, we need to discuss language and definitions. Average women call
‘menopause’ any changed experiences (especially hot flushes) in midlife and beyond.
However, officially ‘menopause’ is the literal ‘final menstrual period’ (Soules et al.,
2001; WHO Technical Report Series, 1996). ‘Postmenopause’ begins immediately
following that ‘final’ flow. Perimenopause, or the ‘menopausal transition’ as is now
politically correct, begins when cycles become irregular and pituitary follicle
stimulating (FSH) levels are increased (Soules et al., 2001). The menopausal transition
ends the day before the final menstrual period (McKinlay et al., 1992; Soules et al.,
2001). In both the WHO 1996 and the 2001 STRAW conference recommendations,
perimenopause and ‘postmenopause’ overlap for 1 year beyond the final menstrual
period (Soules et al., 2001; WHO Technical Report Series, 1996). At best, this is
shabby nomenclature.
The above definitions don’t fit with women’s experiences or new scientific data.
Instead, menopause is the normal life phase beginning 1 year beyond the final
menstrual period—a 45-year-old woman with 1 year without flow has less than a 10%
chance of further flow (Wallace et al., 1979). Perimenopause begins when women
notice experience changes—these indicate the evolving hormonal patterns of ovarian
ageing. Thus perimenopause begins in midlife women with regular menstrual cycles
(Hale et al., 2003; Prior, 2002b, 2005a, 2005b). Women typically notice cycles that are
closer together, sore breasts, mid-sleep wakening, heavier flow and cyclic night sweats
(Prior, 2005a). Menopause begins a year beyond the final menstrual flow.
Why this concept of ‘estrogen deficiency’? It originated early in the 20th century
following the first chemical isolation of estrogen. This new hormone immediately
became a gynaecological therapy to treat women (’s inferiority) (Oudshoorn, 1994). The
construction of perimenopause as a time of dropping estrogen levels comes directly
from the view that menopause is characterized by ‘stigmata of hormone deprivation’
(Byyny & Speroff, 1990). That is not to deny that estrogen levels are low in menopause.
Something that is a normal part of the life cycle cannot at the same time cause major
disease and debility. The normal life cycles for estrogen and progesterone levels are
shown in Figure 1. The low estrogen levels of childhood are mirrored by similar levels
in menopause. Both the adolescent and perimenopausal transitions show higher and
324 J.C. PRIOR
more variable estrogen levels. Progesterone is produced in high levels only during the
luteal phase, the last third of the menstrual cycle following release of an egg (ovulation).
The luteal phase has an optimum length of 10–14 days; however, luteal phases are short
in puberty and perimenopause (Prior, 2002b; Vollman, 1977) (Figure 1).
For the last 10 years, we have known that estrogen levels are higher and less
predictable in perimenopause (Prior, 1998; Santoro et al., 1996). Santoro and
colleagues studied pre- and perimenopausal women in parallel across one menstrual
cycle monitoring daily urinary estrogen and progesterone levels—perimenopausal
women showed significantly higher estrogen and lower progesterone excretions
(Santoro et al., 1996). I performed a meta-analysis of the published comparisons,
within four centres, of serum estradiol levels at two times in the cycle in over 200 pre-
and perimenopausal women (Prior, 1998). Estradiol levels, in these (presumably
asymptomatic) perimenopausal women with regular cycles, averaged 30% higher than
in premenopausal women (Prior, 1998).
I feel a profound sense of personal outrage that ‘experts’ can deny the existence of
perimenopause or portray it as dropping estrogen levels when estrogen is really high
and unpredictable. For me, perimenopause was an extremely difficult time, made
worse because I was experiencing the opposite of what I had expected. I experienced
more than 12 years of sore, swollen and nodular breasts. The premenstrual fluid and
mood symptoms I had learned to control with increased exercise when I was
premenopausal no longer relented no matter how far I ran or walked (Prior, 2002a).
And I dreamed I was pregnant! Both my rational and my unconscious mind knew I was
experiencing high estrogen levels. However, the medical literature at the time asserted
the opposite.
Therefore, I was jubilant when I first saw the data from an excellent population-
based study showing higher-than-premenopausal-normal estrogen levels in perimeno-
pause (Figure 2) (Burger et al., 1995). Estrogen levels were measured at baseline in the
Melbourne Midlife Women’s Health Study, which enrolled 438 women aged 45–55
who had menstruated within the past 3 months, were not taking oral contraceptives or
any hormone therapy, and agreed to join a longitudinal study. The data were shown as
a scatter plot of estrogen levels obtained days 3–8 of the menstrual cycle by midlife
Figure 1. A cartoon-like depiction of the estrogen and progesterone changes across women’s life cycles shows the
chaotic and higher estrogen levels in perimenopausal women and lower progesterone levels during both adolescence and
women classified into five groups: (I) women with regular flow (‘premenopausal’); (II)
those with changes in flow; (III) those with changes in cycle length; (IV) those with
changes in both cycle length and flow; and (V) those who had been 3 but less than 12
months without a period. I have annotated Figure 2 with a lower line for the average
premenopausal follicular phase (cycle days 3–8) estrogen levels, and a higher line
for the highest midcycle peak estrogen level of the normal premenopausal mens-
trual cycle based on published data from Burger’s own lab (McLachlan et al., 1987).
Almost 50% of estrogen values were higher than normal and at least 10% were higher
than the premenopausal midcycle peak, even in group V who were almost a year
beyond their last period (Burger et al., 1995) and were considered ‘postmenopausal’ by
the WHO and STRAW criteria (Soules et al., 2001; WHO Technical Report Series,
My excitement at seeing scientific validation of my high estrogen perimenopausal
experiences, however, was dashed when I read the conclusion for that paper: ‘We
conclude that … decreases in E
(estrogen) … are the major endocrine changes that
characterize the menopausal transition’ (Burger et al., 1995, p. 3537; author’s
emphasis). Although the geometric mean estrogen level is higher for group I than
group V, these authors had not seen the very high estrogen levels that their data so
beautifully showed. They were perhaps unable to see because the data didn’t fit their
paradigm. We wrote a scathing letter to the editor demanding that the authors ‘let the
data speak!’ (Prior et al., 1996).
These higher perimenopausal estrogen levels are associated with lower progesterone
levels or shorter luteal phase lengths (Prior, 2002b; Santoro et al., 1996) as shown in
Figure 1. It is not yet proven, but likely, that the higher, chaotic estrogen levels and
lower progesterone production cause symptoms in perimenopause. However, a case-
control study of perimenopausal women with heavy flow showed significantly higher
estrogen levels than controls. Endometrial (uterine lining) biopsies in the cases showed
Figure 2. This figure, a scatter plot of estradiol levels during days 3–8 of the menstrual cycle from the Melbourne
Midlife Women’s Health Study, shows the mean premenopausal early follicular phase levels in the same lab with a
lower line and mean midcycle estradiol peak levels as a solid line. Groups of women classified I–V are described in the
text. Adapted from Burger (Burger et al., 1995).
326 J.C. PRIOR
hyperplasia consistent with higher estrogen and lower progesterone levels (Moen et al.,
2004). I have made the case that the hormonal changes of perimenopause are
congruent with the troubling experiences of symptomatic women although proof is
currently lacking (Prior, 1998).
Despite its unique hormonal characteristics, perimenopause, as opposed to
menopause, is barely mentioned in books for lay women (O’Leary Cobb, 2005).
Worse yet, following the culturally accepted paradigm of estrogen deficiency, even
feminists seeking to empower women describe perimenopause as a time when ‘the
ovaries are no longer producing enough estrogen to result in regular cycles …’ (Boston
Women’s Health Book Collective, 2005, p. 531). Finally, official bodies actively
conflated and confused perimenopause with menopause because both may cause hot
flushes and decreased sexual interest (National Institutes of Health, 2005).
Before I’m accused by my feminist colleagues of medicalizing a normal phase of
women’s lives (Ford & Mains, 2003), let me stress that only about 15–20% experience
importantly negative perimenopausal experience changes (Avis et al., 1993). Further,
perimenopausal symptoms relate to culture, ethnicity, as well as economic status (Gold
et al., 2000).
Having now developed some perspective from my vantage as an asymptomatic
menopausal woman, but given the distress I see in hundreds of ‘Ask Jerilynn’ emails to
the Centre for Menstrual Cycle and Ovulation Research (, I feel
that it is tragic to misunderstand perimenopause as dropping estrogen levels. Knowing
that today 19% of Canadian woman are aged 40–55, I feel that it is urgent to set the
record straight and provide them with accessible scientific and practical information
(Prior, 2005b). Furthermore, it is illogical to treat perimenopausal symptoms with
estrogen therapy when endogenous estrogen levels are high and relatively non-
suppressible (Prior, 1998). Given that perimenopausal progesterone levels are low,
progesterone and progestins are effective therapy for hot flushes (Leonetti et al., 1999;
Schiff et al., 1980) and that oral micronized progesterone improves deep sleep (Friess
et al., 1997), cyclic progesterone therapy should be the first line of therapy for
symptomatic perimenopausal women (Prior, 2005b).
The lack of, or mis-, information we as women receive deprives us of self-knowledge,
alienates us (further) from our own bodies, and leaves us both diseased and dependent.
In the remainder of this analysis I will describe and illustrate six ways in which the
current gynaecological construction of ovarian ageing deprives us of the power of
Perimenopause as a chronic illness
Women lose the potential power of perimenopause, given that perimenopause and
menopause are implied to be the same, because they feel their current, undesirable
experiences (symptoms) will go on forever. This results in women seeking and finding
(disease) diagnoses to explain and legitimize the suffering such as ‘fibromyalgia’,
‘chronic fatigue syndrome’ and ‘PMS’. All may be ways of explaining, in a medically
sanctioned manner, the low energy and mood swings that some women experience
(Kaufert et al., 1987). Consequently, a perimenopausal woman may start viewing
herself as chronically ill. She also commonly ends up missing work with heavy periods
(Cote et al., 2002), and may lose her occupation and/or have to go on long-term
disability. Women currently, from popular literature and their physicians’ advice,
cannot know that perimenopause ends in a kinder and calmer phase of life
appropriately called menopause. Thus competent, valuable women become dependent
on society or others, instead of contributing their creativity and energy.
Perimenopausal isolation
Perimenopausal isolation arises in an information vacuum combined with reticence in
talking with other women. As Sheehy described in 1992, ‘Menopause (sic) may be the
last taboo’ (Sheehy, 1992, p. 4). Lack of accurate, available information isolates women
from each other and often causes women to seek medical help, or pay large sums of
money for preparations that may/may not be helpful. The current increased alternative
and complementary medicine use may be largely because perimenopausal women are
thrilled to find someone (a health food store clerk or self-help speaker) to listen to and
validate their experiences.
Although feminist publications aim to produce solidarity, if these writings con-
fuse menopause and perimenopause, as many do (Boston Women’s Health Book
Collective, 2005; Breen & Hall, 1999; O’Leary Cobb, 2005), they don’t accurately
describe women’s experiences and cannot relieve the sense of isolation. Thus, peri-
menopause becomes a lonely voyage into a frightening future.
Perimenopause as dropping/deficient estrogen levels
From my personal perimenopausal frustrations, I know what it feels like to have your
experiences disbelieved, discounted, or denied. I experienced high estrogen levels in
perimenopause—I knew that because of many more days than usual of stretchy mucus,
breasts that were swollen and tender, not just before flow but for most of the month,
and because of fluid retention and a tendency to feel blue. These experiences occurred
occasionally at my midcycle estrogen peak or premenstrually during my 34
premenopausal years—I had enthusiastically monitored my menstrual cycle experi-
ences and basal temperature for at least 10 years by the time I began perimenopause.
So, when experts said perimenopause was about dropping or deficient estrogen levels, I
secretly scoffed. And then I became angry. I further felt a keen need to scientifically
confirm what I was experiencing.
The most convincing evidence for high estrogen in perimenopause experiences is the
pregnancy dream that women from many backgrounds and cultures report. I had such
a vivid dream early in perimenopause when my cycles were still regular. That pregnancy
dream was also reported by Janine O’Leary Cobb in the 1993 introduction to the first
edition of her book Understanding Menopause (O’Leary Cobb, 2005). Finally, a !Kung
woman from the Kalahari Desert, who was frustrated at regular flow and no pregnancy,
told a woman ethnographer that she had recently dreamed that she was pregnant
(Shostak, 1981). There is nothing about pregnancy that feels like, or means, low
estrogen levels!
I was so eager to prove that I was experiencing higher estrogen levels that I repeated a
mammogram I had about 6 years earlier because of a benign breast lump (in the
opposite breast). I had it done on the same X-ray machine, using identical focal
distances and exposures so that I could, for teaching purposes, contrast the peri-
menopausal increases in my breast size and density with my premenopausal normal
breast (Figure 3).
My further efforts to document the true hormonal changes of perimenopause
culminated in a systematic review of the medical literature that had published
328 J.C. PRIOR
premenopausal and perimenopausal estrogen levels from women within the same
centre (Prior, 1998). I was able to find eight studies and perform a meta-analysis
in four of estrogen levels in the follicular phase in 292 premenopausal versus 415
perimenopausal women and from the premenstrual portion of the cycle in 250
premenopausal versus 69 perimenopausal women (Figure 4). The data analysed
within-centre by chi square testing showed significantly higher estrogen levels in
perimenopausal women during both the follicular and premenstrual phases (F516.12,
p50.041 and F515.46, p50.016), respectively.
Perimenopausal heavy flow—erroneous concepts and inappropriate therapies
Heavy flow doesn’t fit with the concept of dropping estrogen levels in perimenopause.
Therefore it, like sore breasts, is missing from the early questionnaires developed to
assess ‘menopause’ (Greenblatt et al., 1950; Kupperman et al., 1953) and from con-
temporary studies (Dennerstein et al., 2000). However, even the inaccurate gynaeco-
logical definition of perimenopause quoted earlier mentioned ‘dysfunctional uterine
bleeding’, which means abnormally heavy, unexplained, but regular menstrual flow.
That is because heavy flow is a prominent symptom for perimenopausal women
(Kaufert et al., 1987; McKinlay et al., 1992) and commonly the cause for a physician
The currently recommended therapy for heavy flow in perimenopause is an oral
contraceptive (OC) (Greendale & Greendale, 2002) even though the only randomized,
double blind placebo-controlled (pharmaceutical-funded) study showed a significant
Figure 3. This photograph contrasts mammograms of one breast in a woman when she was premenopausal (on the
left) and when she was regularly menstruating with high estrogen levels in early perimenopause (on the right).
worsening of unpredictable bleeding in the first 3 months of perimenopausal OC use
(Casper et al., 1997). Although the flow did improve during cycles four through six of
that study, the medication caused no significant improvements in quality of life using
the SF-36 nor in hot flushes (Casper et al., 1997).
Perimenopausal women with heavy menstrual bleeding, because they may have co-
existent fibroids, ‘hear’ (understand) that these cause the excess flow. Fibroids,
however, arise from the uterine muscle wall and rarely impinge on the lining that is
bleeding. Also, a case-control study of perimenopausal women with heavy bleeding
clearly showed higher estrogen levels compared with premenopausal controls (Moen
et al., 2004). Furthermore, endometrial biopsies documented hyperplasia, an abnormal
result that develops with low progesterone and higher estrogen levels, as commonly
occurs in perimenopause (Moen et al., 2004). The heavy bleeding in perimenopause
often requires therapy. However, effective non-surgical therapies are available
(Baldaszti et al., 2003; Fraser, 1990; Irvine et al., 1998) including non-steroidal anti-
inflammatory drugs, such as ibuprofen,
that decrease flow by 25–45% (Fraser et al.,
Despite these evidence-based, woman-acceptable and available therapies, dilatation
and curettage, and hysterectomy are the most common treatments for heavy flow
(Coulter et al., 1991). Five women in that clinical practice study who were lost to
follow-up no longer had heavy flow when interviewed 5 years later, indicating that the
natural history of perimenopausal menorrhagia is improvement. Average age at
hysterectomy is 42 to 46, based on data from three population-based studies in three
different countries (Maresh et al., 2002; Tuppurainen et al., 1993; Weel et al., 1999).
Figure 4. This bar graph represents data from a meta-analysis of the literature on estradiol levels, within-centre, in
premenopausal and perimenopausal women (Prior, 1998).
330 J.C. PRIOR
Thus ‘heavy flow’ is at a younger age than when irregular cycles start and
perimenopause is diagnosed, age 47.5 (McKinlay et al., 1992; Soules et al., 2001).
This congruence in mean age at hysterectomy across very different populations points
to a common underlying biological process causing it (the hormonal changes of early
perimenopause) and the need to diagnose perimenopause before irregular cycles begin
in symptomatic midlife women (Prior, 2005a).
One of the rarely mentioned results of hysterectomy for perimenopausal women is
that they lose the potential to use bleeding to organize and understand their
experiences. Perhaps for that reason, women who have had hysterectomy visit their
physicians twice as often as those women who haven’t (Johannes et al., 1994;
Oldenhave et al., 1993). Even if the ovaries were not removed, hysterectomized women
were more likely to report hot flushes (Oldenhave et al., 1993) and to be treated with
(inappropriate) estrogen therapy (Guthrie et al., 2003).
Perimenopause as social and cultural loss
Feminists have tended to construct perimenopause as a time of loss of youth and
therefore women’s sexual allure and status. Feminists, ascribing women’s midlife
symptoms to the ‘empty nest’, are now saying we are symptomatic in perimenopause
because of the role conflicts of being wageworkers and also having care-giving functions
for elderly parents and nearly/adult children.
Feminists have rightly been mistrustful of doctors and scientists who construe
‘menopause’ as a deficiency disease (MacPherson, 1985). Furthermore, women have
traditionally understood science to be the domain of men (Keller, 1983) and as anti-
woman because science, in this culture, views men as the primary creators of facts
(Hubbard, 1990). However, social relationships and cultural critiques are well within
the scope of women’s acknowledged expertise (Rossi, 2004). Therefore feminists have
tended to focus on women as social, rather than also as biological, creatures. They have
questioned the existence of perimenopause at all (Ford & Mains, 2003) and ascribed
the discomforts and symptoms primarily to social stress (Page, 1994). As a
perimenopausal woman I was working closely with the author of the above book. I
was upset that she seemed ‘allergic to the body’. However, Page doesn’t deny the
physical changes of perimenopause but instead focuses on the sociocultural and
emotional sides that are part of what is ‘silent’ about ‘menopause’ in this culture (Page,
1992). She wisely observed that previous personal reproductive issues tended to surface
and need attention in perimenopause (Page, 1994). But to ascribe all of the emotional
turmoil that perimenopause can produce to the social inequities inherent in this
culture, to changed domestic responsibilities or past experiences, is to maintain an
anachronistic, dualistic and inaccurate view that separates body from soul or spirit. I
believe that there is no way to understand health in its totality as physical, emotional,
and social well-being without understanding and integrating the essential, multi-
directional hypothalamic connections among social stress, nutritional, sleep and
exercise changes, and physical and emotional responses (Prior et al., 1999).
Two examples illustrate the complex connections among perimenopausal physical
and emotional changes: the role of high estrogen levels in amplifying the hormonal
responses to social stress; and the complex interactions among estrogen exposure, PMS
and hot flushes. The first is an experiment using the Trier Social Stress Test, a
standardized test of neuroendocrine responses to the social stress of speaking and doing
math in front of an audience. Researchers assessed the effect of estrogen on stress
responses by randomizing young men to wear a 100-mg estrogen patch or identical
placebo before and during the test (Kirschbaum et al., 1996). Estrogen-treated men
showed significantly higher levels of the stress hormones, ACTH, cortisol and
norepinephrine compared with the placebo-treated (Kirschbaum et al., 1996). Thus,
the high estrogen levels of perimenopause amplify the stress responses of women to
their existing social/emotional stressors.
The second illustration of social–emotional–hormonal connection relates to
premenstrual symptoms and hot flushes. Premenstrual symptoms, although poorly
understood, are worse when estrogen levels are higher and progesterone levels are
lower, in a within-woman analysis (Wang et al., 1996). Evidence suggests that
premenopausal premenstrual symptoms are decreased by exercise of increasing
intensity (Prior et al., 1987) but become resistant to the physiological feedback of
exercise in perimenopause (Prior, 2002a). Several prospective studies have shown that
midlife women with increased premenstrual symptoms were more likely to have hot
flushes later in perimenopause (Freeman et al., 2004; Guthrie et al., 1996; Morse et al.,
1989). To understand these relationships, one must realize that hot flushes occur
because the hypothalamus has been exposed to higher levels of estrogen (hence
premenstrual symptoms). The brain then reacts when estrogen levels decrease at all,
even from extremely high to high (Gangar et al., 1993). Such swings are common
during perimenopausal hormonal chaos. Therefore, women with premenstrual
symptoms and the highest estrogen levels early in perimenopause were more likely to
experience troublesome night sweats/hot flushes later. It is also clear that stress
increases hot flushes (Gold et al., 2000; Swartzman et al., 1990). Thus, stress
responses, premenstrual symptoms, and hot flushes in perimenopause cannot be
understood without integration of biological and cultural variables. Therefore,
feminists and social scientists do women a disservice to focus only on social and
cultural losses.
Perimenopause without self-actualization
It would be a tragedy to live through perimenopause thinking that you had a chronic
disease from which you would never recover, and to never learn that many others had
survived similar symptoms in perimenopause. It would also be ultimately sad to feel
further devalued in perimenopause because your experiences didn’t fit with the
dropping estrogen levels you were told you had, or to have undergone hysterectomy
when the bleeding could have been treated medically. There would also be major loss if
a woman were to blame herself for her inability to cope with the estrogen-related
amplification of life’s midlife stresses. The biggest loss of all would be to avoid the self-
learning intrinsic to perimenopause—that is the final of the six losses related to
There is surprising unanimity among many thoughtful authors that perimenopause
‘requires’ a fundamental life re-evaluation. This concept is best expressed by author
Ursula Le Guin:
There are things the Old Woman can do, say, and think which the Woman cannot
do, say, or think. The Woman has to give up more than her menstrual periods
before she can do, say, or think them. She has to change her life … The woman
who is willing to make that change must become pregnant with herself, at last.
(LeGuin, 1991, p. 4)
332 J.C. PRIOR
In summary, this paper has reframed perimenopause and described six reasons why
perimenopause may be ‘lost’. It is an important loss to have become menopausal
without experiencing the perimenopause ‘graduation’ that implies new and essential
self-knowledge. Each of these six reasons can have tragic consequences for a woman’s
well-being. These reasons include not knowing that perimenopause is self-limited and
we all survive, that it can be a time of solidarity with the millions of women present and
past, and that our symptoms are related to higher rather than dropping estrogen levels.
There will be irreversible loss if perimenopausal heavy bleeding is treated by surgery
when it could be treated with effective, acceptable medications, and its natural history
is improvement. If we don’t learn how our physical and sociocultural responses are
linked in perimenopause, we will likely not learn this later. All of the above may cause
women to survive perimenopause without gaining the self-awareness and confident
assertiveness that are this life phase’s endowment for women.
1. Incongruous because estrogen deficiency and declining ovarian function are diametrically opposite to
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... However, it is not clear why an adaptive menopause should be such a long and difficult process, rather than a rapid and smooth transition from the reproductive to the non-reproductive phases of a woman's life. Specifically, menopause is preceded by a peri-menopausal period of 10-15 years, during which fertility decline is not driven by the demise of hormone production due to ovarian senescence but rather by dramatic fluctuations in oestrogen levels, resulting in irregular menstrual cycles and skipped ovulations (Prior 1998(Prior , 2006Douma et al. 2005) (Fig. 1). Indeed, oestrogen reaches its highest levels in a woman's lifetime during peri-menopause; as high as 30% above the average level during the regular reproductive period (Santoro et al. 1996;Prior 1998Prior , 2006Douma et al. 2005) (Fig. 1). ...
... Specifically, menopause is preceded by a peri-menopausal period of 10-15 years, during which fertility decline is not driven by the demise of hormone production due to ovarian senescence but rather by dramatic fluctuations in oestrogen levels, resulting in irregular menstrual cycles and skipped ovulations (Prior 1998(Prior , 2006Douma et al. 2005) (Fig. 1). Indeed, oestrogen reaches its highest levels in a woman's lifetime during peri-menopause; as high as 30% above the average level during the regular reproductive period (Santoro et al. 1996;Prior 1998Prior , 2006Douma et al. 2005) (Fig. 1). This hormonal deregulation during peri-meno- (Austad 1997) Good Mother Trade-off between giving up own reproduction (when there is a growing age-related mortality) in exchange of greater survival of depending children (Williams 1957;Alexander 1974) Grandmother Hypothesis ...
... painful intercourse, vaginal dryness) disorders (Gold et al. 2000;Avis et al. 2001). Interestingly, these symptoms often appear to be working at cross-purposes (Prior 1998(Prior , 2006. Duration, hormonal chaos and contradictory symptoms, taken together, suggest that peri-menopause is a detrimental process, from a woman's perspective. ...
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Menopause is the transition from reproductive to non-reproductive life well before natural death. Rather than involving a smooth, rapid change, it is normally preceded by a long period of erratic hormonal fluctuation that is accompanied by a plethora of unpleasant symptoms. Here, we (1) suggest that this turbulent period owes to conflict, between a woman's maternally inherited (MI) and paternally inherited (PI) genes, over the trade-off between reproduction and communal care; (2) perform a theoretical analysis to show that this conflict is resolved either through silencing or fluctuating expression of one of the genes; (3) highlight which of the symptoms preceding menopause may result from antagonistic co-evolution of MI and PI genes; (4) argue that ecological differences between ancestral human populations may explain the variability in menopause among different ethnic groups; (5) discuss how these insights may be used to inform family planning and cancer risk assessment based on a woman's ancestral background.
... Perimenopause profoundly disturbs the premenopausal estradiol-progesterone balance in favor of estradiol 4 . We previously documented that oral micronized progesterone therapy was effective for menopausal VMS 12 , thus we postulated progesterone would also be effective for perimenopausal VMS and significantly decrease perimenopausal night sweats and/or hot flushes. ...
... "Women's Perceived Change" as reported previously 12 assessed changes between treatment groups on a -5 to +5 scale with zero as no change using Wilcoxon rank-sum test. Statistical software included SAS 9·4 (SAS Institute Inc., Cary, NC) and R 3·3·3 (R Foundation for Statistical Computing, Vienna, Austria). ...
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Background Oral micronized progesterone (progesterone) has been shown superior to placebo for vasomotor symptoms (VMS, night sweats and/or hot flushes) in menopausal women (>1 year after final flow). A VMS Score difference ≥3 was clinically important. VMS begin in perimenopause; however, all but two VMS randomized placebo-controlled trials (RCT) were in menopausal women. No well-performed RCT has proven any therapy to be effective for perimenopausal VMS.Methods To test progesterone for perimenopausal VMS, we ran a quadruple masked, randomized (1:1), placebo-controlled trial (2012-2016) with 28-day run-in and 84 days’ experimental phases. Our academic medical centre recruited locally/nationally for women ages 35-58 with cycle irregularity but menstruation within 12 months plus untreated, problematic VMS. Our primary, intent-to-treat outcome was participant-recorded daily VMS Score ([# night sweats x intensity]+[#daytime hot flushes x intensity]) days 56-84, adjusted for run-in VMS Score. Our secondary outcome was Women’s Perceived VMS Change (-5 to +5) on day 84.Findings We randomized 189 women of mean (SD) age 49·9 (4·6) years to progesterone, 300 mg/bedtime [n=93], vs placebo [n=96]. The mean run-in VMS Score (n=189) was 12·2 (11·3). VMS Scores days 56-84 were not different by progesterone vs placebo (Rate Ratio [RR] 0·79 [95% CI 0·54, 1·15]; Rate Difference [RD] -1·51 [95% CI -3·97, 0·95]; P=0·222). RD 95% CI included -3, thus did not exclude a clinically important effect. Perceived VMS Change indicated progesterone significantly improved night sweats over placebo (-3 vs -2, P=0·023). No serious adverse events occurred.Interpretation Progesterone-treated perimenopausal women perceived significantly improved night sweats. These results show trends toward clinically important VMS benefits from perimenopausal progesterone. Given the previously undocumented high perimenopausal VMS variability, a larger RCT of progesterone for perimenopause VMS is still needed. Registered: NCT0146469. Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation This preprint research paper has not been peer reviewed. Electronic copy available at: Preprint not peer reviewed
... The neuroendocrine system presides over the significant hormonal changes occurring in the HPG axis during puberty and perimenopause (see Table 1 for a summary). In particular, both of these periods are characterized by major changes in the production of luteinizing hormone (LH) and follicle stimulating hormone (FSH), which together regulate ovarian follicle growth and ovulation, and estradiol, the most abundant form of endogenous estrogen (Albin et al., 2012;Archibald et al., 2003;Burger, 2008;Burger et al., 2007a;Burger et al., 2007b;Nelson, 2008;Prior and Hitchcock, 2011;Prior, 2006). Mean levels of estradiol increase across pubertal development until menarche, when estradiol levels stabilize and then cycle regularly through the menstrual cycle each month. ...
... (Fluctuations do not correlate to precise changes in estrogen levels). Adapted fromPrior (2006) and reprinted with permission. ...
... While there is a great deal of variation in menopause symptom experience, they are a ubiquitous complaint among menopausal women, with common symptoms including hot flashes, vaginal dryness, joint and muscle pain, and anxiety Islam, Bell, Rizvi, & Davis, 2017). Mechanistically, menopause symptoms can be understood to be largely the result of hormonal fluctuations (Douma, Husband, O'Donnell, Barwin, & Woodend, 2005;Prior, 1998Prior, , 2006, but there is little understanding of whether there is any adaptive evolutionary rationale underlying the presentation of these symptoms. ...
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All human females who reach midlife experience menopause, however, it is currently unclear why women experience this period of infertility, and why it is accompanied by many unpleasant symptoms. Using primary data from four ethnic groups in China, we test an existing theory that age of menopause and its symptoms are the result of intragenomic conflict between maternally and paternally inherited genes, with the outcome of such conflict predicted to be contingent on the ancestral postmarital residence pattern of the female (Úbeda, Ohtsuki, & Gardner, Ecology Letters, 17, 2014, 165). The model predicts that being ancestrally patrilocal results in less intragenomic conflict, causing a shorter, less symptomatic perimenopause that terminates in a later menopause. Our findings show no support for this hypothesis and suggest current, rather than ancestral, residence patterns better predict aspects of the menopausal transition. Furthermore, current patrilocality when compared to duolocality is associated with more severe menopause symptoms, which may be due to sexual, rather than intragenomic, conflict. Open research badges: This article has earned an Open Data Badge for making publicly available the digitally-shareable data necessary to reproduce the reported results. The data is available at
... Within the medicine-centered discourse, menopause has been characterized for decades as a medical condition, specifically an estrogen deficiency disease that requires monitoring and treatment by a physician (Dickson, 1993;Kaufert & McKinlay, 1985;Martin, 1987;Murtagh & Hepworth, 2003;Prior, 2006;Wilson, 1966). Not surprisingly, given the multi-billion dollar industry surrounding it, the medicine-centered discourse views prescription treatment as the most effective or desirable way to manage this deficiency. ...
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This article focuses on unpacking dominant cultural discourses about menopause in the United States and examining their impact on women's personal menopause narratives. Recently, two contrasting menopause discourses have emerged in the U.S.: the medicine-centered discourse and the women-empowerment discourse. While both discourses were reflected in women's accounts in this study, the medicine-centered discourse continues to play a dominant role in women's understandings of their menopause experiences. Women also seem to embrace changing notions of "natural" and "safe" as components of their menopause management decision making including whether or not to take synthetic or bioidentical menopause hormone therapy (MHT) or to use over-the-counter and herbal supplements to manage symptoms they find troublesome. In addition, women's experience of symptoms are critical to their menopause narratives; those with more troubling symptoms buy more heavily into the medicine-centered discourse than those untroubled by or minimally inconvenienced by symptoms.
... 19 Before the cessation of menses, women enter the menopausal transition (perimenopause); cycle lengths become variable as hormone levels begin to fluctuate and gradually fall. 20 With fewer follicles maturing in the aging ovaries, levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) become elevated due to disinhibition, although 17b-estradiol (E 2 ) levels become highly variable. On average, the perimenopausal period lasts about 4 years. ...
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Objective: Recent evidence suggests that early or induced menopause increases the risk for cognitive impairment and dementia. Given the potential for different cognitive outcomes due to menopause types, it is important that present research on menopause and cognition distinguishes between types. The aim of this project was to determine to what extent research looking at cognition in postmenopausal women published in one year, 2016, accounted for menopausal type. Methods: We searched MEDLINE, EMBASE, and PsychINFO using keywords and MeSH terms for menopause and cognition. We included any research paper reporting a cognitive outcome measure in a menopausal human population. Differentiation between the types of menopause was defined by four categories: undifferentiated, demographic differentiation (menopause type reported but not analyzed), partial differentiation (some but not all types analyzed), and full differentiation (menopause types factored into analysis, or recruitment of only one type). Results: Fifty research articles were found and analyzed. Differentiation was distributed as follows: undifferentiated, 38% (19 articles); demographic differentiation, 16% (8); partial differentiation, 28% (14); and full differentiation, 18% (9). Conclusions: This review revealed that although some clinical studies differentiated between the many menopauses, most did not. This may limit their relevance to clinical practice. We found that when menopause types are distinguished, the differing cognitive outcomes of each type are clarified, yielding the strongest evidence, which in turn will be able to inform best clinical practice for treating all women.
... Additionally, some scholars argue that medical intervention during menopause serves only to increase the medical profession's control over women's bodies and health (Cousins & Edwards, 2002;Voda, 1993). For decades, menopause was described in medicine as a deficiency disease (Dickson, 1993;Martin, 1987;Murtagh & Hepworth, 2003;Prior, 2006;Wilson, 1966) that needed treatment, and advocates for demedicalizing menopause argue that it is a natural life change or transition that can be managed naturally by women themselves (Hunt, 1994;Kaufert, 1982;McCrea, 1983). ...
The number of women approaching menopausal age in the U.S. is increasing, making menopause an important health topic. Historically, menopausal hormone therapy (MHT) was the accepted method for treating the symptoms of menopause; however, in recent years several studies raised questions about the efficacy and safety of MHT, resulting in debate over appropriate ways to view and treat menopause. This qualitative study examined the role of discourse in shaping women's menopausal experiences and menopause-management decisions. By applying social constructionism and discourse theory, this study uncovers how communication shapes the dominant discourses of menopause within U.S. culture. Twenty-five perimenopausal and menopausal women who were either taking or not taking MHT participated in semi-structured interviews. Grounded theory and the constant comparative method informed the data collection process. Using inductive thematic analysis, the major themes and subthemes of each of these dominant cultural discourses were identified. These themes were used to analyze semi-structured interviews with women who were and women who were not taking MHT. Additionally, inductive analysis was used to discover emergent themes within women's accounts that did not fit within either of the two dominant cultural discourses. The analysis revealed that both dominant cultural discourses influenced how women described their menopausal experiences. Furthermore, women integrated these discourses into their menopause-management decision-making process in unique ways. Theoretical and practical and theoretical implications of this study are discussed.^
Women show a heightened risk for psychosis in midlife that is not observed in men. The menopausal transition (i.e. perimenopause) and accompanying changes in ovarian hormones are theorized to account for this midlife increase in risk. This narrative review aims to empirically examine these theories by reviewing studies of midlife and perimenopausal psychosis risk in women and potential ovarian hormone mechanisms of effects. Clinical and pre-clinical studies examining the effects of midlife age, menopausal stage, and ovarian hormones across adulthood on psychosis risk were identified. Synthesis of this body of work revealed that the peak ages of midlife psychosis risk in women overlap with the age range of key menopausal stages (especially the perimenopausal transition), although studies directly assessing menopausal stage are lacking. Studies examining ovarian hormone effects have almost exclusively focused on earlier developmental stages and events (e.g. pregnancy, the menstrual cycle) and show increases in psychotic symptoms in women and female rats during periods of lower estradiol levels. Estrogen treatment also tends to enhance the effects of neuroleptics in females across species at various reproductive phases. Initial data are promising in suggesting a role for menopausal stage and ovarian hormones in psychosis risk. However, critical gaps in our knowledge base remain, as there is a tendency to rely on indirect and proxy measures of menopausal status and hormones. Opportunities for future research are discussed with the goal of increasing research in this critical area of women's health.
The female genital tract undergoes anatomic changes from birth through menopause. Concurrently, the relative levels and roles of estradiol and progesterone dramatically change during the female life cycle. This review provides a conceptual overview of clinically relevant anatomic and hormonal changes in the female genital tract, and how these changes may affect HIV-1 pathogenesis, transmission, and mucosal immunology and protection against HIV and STIs across the female life cycle. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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Perimenopause, rather than a time of declining estrogen, is characterized by three major hormonal changes that may begin in regularly menstruating women in their mid-thirties: erratically higher estradiol levels, decreased progesterone levels (in normally ovulatory, short luteal phase or anovulatory cycles), and disturbed ovarian-pituitary-hypothalamic feedback relationships. Recent data show that approximately a third of all perimenopausal cycles have a major surge in estradiol occurring de novo during the luteal phase. This phenomenon, named "luteal out of phase (LOOP)" event, may explain a large proportion of symptoms and signs for symptomatic perimenopausal women. Large urinary hormone data-sets from women studied yearly over a number of years in the Study of Women Across the Nation (SWAN) and in the Tremin data will eventually provide a more clear prospective understanding of within-woman hormonal changes. Predicting menopause proximity with FSH or Inhibin B levels is documented to be ineffective. Anti-Mullerian hormone levels may prove predictive. Finally, there is an urgent need to change perimenopause understandings, language and therapies used for midlife women's symptoms to reflect these hormonal changes.
Evidence from animal studies and clinical observations suggest that the activity of the pituitary-adrenal axis is under significant influence of sex steroids. The present study investigated how a short term elevation of estradiol levels affects ACTH, cortisol, norepinephrine, and heart rate responses to mental stress in healthy men. In a double blind study, 16 men received a patch delivering 0.1 mg estradiol/day transdermally, and age- and body mass index-matched control subjects received a placebo patch. Twenty-four to 48 h later, they were exposed to a brief psychosocial stressor (free speech and mental arithmetic in front of an audience). In response to the psychosocial stressor, ACTH, cortisol, norepinephrine, and heart rate were increased in both experimental groups (all P < 0.0001). However, the estradiol-treated subjects showed exaggerated peak ACTH (P < 0.001) and cortisol (P < 0.002) responses compared to the placebo group. Also, the norepinephrine area under the response curve was greater in the estradiol group (P < 0.05). Although heart rate responses differences failed to reach statistical significance, they, too, tended to be larger in the estradiol group. Neither mood ratings before or after the stressor, nor ratings of the perception of the stressor could explain the observed endocrine response differences. In conclusion, short term estradiol administration resulted in hyperresponses of the pituitary-adrenal axis and norepinephrine to psychosocial stress in healthy young men independent of psychological effects, as assessed in this study.
Six months of exercise training was associated with decreased premenstrual symptoms in two groups of women. There was no change in symptoms in nontraining women. Eight sedentary (ST) women increased running from 0 to 76.±26 kmlcycle (mean±standard deviation) over 6 months and seven runners (MT) trained for a marathon (422 km). Six normally active, nontraining (C-NT) women kept their activity constant. Each subject completed monthly intensity-graded questionnaires or kept daily symptoms diaries concerning premenstrual symptoms. All monitored basal body temperature, weight, and exercise. Gonadal steroids were measured in ST women. For ST subjects, breast ( P =0.005), fluid ( P =0.01), and personal stress ( P =0.025) decreased. MT women experienced decreased fluid ( P =0.034) and depression ( P =0.014). Anxiety tended to decrease ( P =0.087). ST and MT subjects experienced decreases in premenstrual symptoms without documented hormonal, menstrual cycle, or weight changes. These symptom changes appear to be the earliest evidence of the effects of conditioning exercise on the reproductive system.
The menopause is probably the least glamorous topic imaginable; and this is interesting, because it is one of the very few topics to which cling some shreds and remnants of taboo. A serious mention of menopause is usually met with uneasy silence; a sneering reference to it is usually met with relieved sniggers. Both the silence and the sniggering are pretty sure indications of taboo.
Objective: To determine effectiveness of transdermal progesterone cream for controlling vasomotor symptoms and preventing postmenopausal bone loss. Methods: We randomly assigned 102 healthy women within 5 years of menopause to transdermal progesterone cream or placebo. Study subjects and investigators were masked until data analysis was completed. An initial evaluation included complete history, physical examination, bone mineral density determination, and serum studies (TSH, FSH, lipid profile, and chemistry profile). Subjects were instructed to apply a quarter teaspoon of cream (containing 20 mg progesterone or placebo) to the skin daily. Each woman received daily multivitamins and 1200 mg of calcium and were seen every 4 months for review of symptoms. Bone scans and serum chemistries were repeated after 1 year. Results: Thirty of the 43 (69%) in the treatment group and 26 of the 47 (55%) in the placebo group complained initially of vasomotor symptoms. Improvement or resolution of vasomotor symptoms, as determined by review of weekly symptom diaries, was noted in 25 of 30 (83%) treatment subjects and five of 26 (19%) placebo subjects (P < .001). However, the number of women who showed gain in bone mineral density exceeding 1.2% did not differ (α = 05, power of 80%). Conclusion: Although we found no protective effect on bone density after 1 year, we did see a significant improvement in vasomotor symptoms in the treated group. Progesterone from diosgenin, extracted from Mexican yams, is identical to the natural progesterone of the human ovary or placenta. 1 Transdermal progesterone has been used cosmetically for over 20 years; however, recently those preparations have been used as alternatives to traditional hormone replacement therapy (HRT). Because of its organic origin and lack of side effects, use of transdermal progesterone cream has increased dramatically. Studies using cell culture and animal models suggest that progesterone might function as an osteotrophic hormone. 2 Anecdotal evidence and human noncontrolled trials suggested daily use of transdermal progesterone cream might increase lumbar spine bone mineral density in postmenopausal women and improve overall well-being. Lee noted, in reviewing his personal files, an increase in spinal bone mineral density in 63 of 100 menopausal women treated daily with 20 mg of transdermal progesterone cream. 3 He also reported an increase in well-being and excellent compliance, owing to ease of use and lack of side effects. Recent data also suggest that natural progesterone might have theoretical advantages over oral medroxyprogesterone acetate based on lipid profiles and coronary vascular experiments in primates. 4,5 We designed a randomized, double-masked, placebo-controlled trial to investigate the effectiveness of transdermal progesterone cream for controlling vasomotor symptoms and preventing menopausal bone loss.
Of the 19% of women now between ages 45 and 60, 20% are experiencing perimenopausal symptoms and seeking medical help. Primary health care is under economic stress and specialists are often not available. Furthermore, confusion reigns about the major hormonal changes of perimenopause and the language used to describe them. Menopause, for example, can mean three different things - everything miserable from midlife onward, the final menstrual period, and a normal life phase beginning after 1 year without flow. The transition to menopause or perimenopause was formerly thought to involve dropping estrogen levels. Estrogen levels are now known to average 30% higher, to be chaotic, and to be associated with less progesterone. Perimenopause begins in women with regular periods and includes characteristic experiences such as heavy flow or flooding, midsleep disturbance, and cyclic hot flushes. There is no consensus and little evidence-based data about treatment of symptomatic perimenopausal women. Oral contraceptives eventually improve flow but don't help with hot flushes or quality of life. In this context, a University of British Columbia research group has initiated a comprehensive long-distance endocrine specialist consultation program called the Perimenopause Experiences Project. The project aims to educate physicians about the physiology and management of symptomatic women in perimenopause and to improve medical care for perimenopausal women. A successful pilot has been completed and health care providers are now being recruited to a 1-year study that will compare consultation with usual care and the outcomes of both. The study will involve physicians' self-assessment of their clinical competence and women's self-assessment of how perimenopause interferes with their usual activity.