CLIMACTERIC 2014;17:235–241

Menopause or climacteric, just a semantic

discussion or has it clinical implications?
J. E. Blümel, P. Lavín, M. S. Vallejo and S. Sarrá

Facultad de Medicina, Clínica Quilín, Universidad de Chile, Santiago, Chile

Key words: CLIMACTERIC, PREMENOPAUSE, PERIMENOPAUSE, POSTMENOPAUSE

ABSTRACT
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Climacteric and menopause are two terms that are indistinctly used to name clinical expected events related
to the decline in ovarian function. Thus, in the literature and in clinical settings we read and hear ‘menopausal
symptoms’ or ‘climacterics symptoms’. Globally, the term menopause is much more frequently used than
climacteric but, before we use either one, we should consider that ‘menopause’ is referring to a specific event,
the cessation of menses, and ‘climacteric’ to gradual changes of ovarian function that start before the
menopause and continue thereafter for a while. In the premenopause period, hormonal changes will take
place that are associated with symptoms, which deteriorate the quality of life, and with metabolic changes
which increase the risk of chronic diseases. Therefore, the word climacteric (‘steps’ in Greek) seems more
adequate to refer to the symptoms and chronic diseases associated with the gradual decrease of ovarian
function, and we should leave the term ‘menopause’ only for naming the event of cessation of menstruation
that will happen later as the consequence of the decline in ovarian activity. This differentiation has clinical
For personal use only.

importance, because it implies that, during the premenopausal period, the impact that the decrease in estrogen
has on the health status of women must be assessed and, if it is pertinent, we should indicate lifestyle changes,
hormonal therapy, hypolipidemic drugs, etc. It does not seem proper to wait for the cessation of menstrual
bleeding before some intervention is started. The decay of women´s health starts many years before menopause
and prevention of its consequences is a must for us the clinicians.

INTRODUCTION We can see further that, within the 48 societies affiliated

Usually when physicians want to speak about the
symptomatology associated with the age-related decline in
ovarian function – or reproductive aging as it has been called –
they indistinctly use the terms ‘menopausal’ or ‘climacteric’
symptomatology. Two of the world’s largest societies on the
specialty are the North American Menopause Society and
the International Menopause Society; their official Journals
are called Menopause and Climacteric, respectively, although
both societies are named as ‘… Menopause Society’. Is any
real difference implied or is it just semantics? The other very
large international society also has the word ‘menopause’ in
its name – the European Menopause and Andropause Society
(EMAS), and in an eclectic decision they called its journal
Maturitas, but they describe it as an ‘international
multidisciplinary journal concerned with the medical,
sociological and psychological aspects of life in the middle
years and beyond as far as related to the climacteric’.
to the Council of Affiliated Menopause Societies (CAMS) of
the International Menopause Society (IMS), most have
included in their names the word ‘menopause’, and not
‘climacteric’, with the exceptions being the Hellenic Society
for the Study of Climacterium and Menopause (Greece), the
Philippine Society of Climacteric Medicine (The Philippines),
and 16 of 19 Latin American countries that do have the
word ‘climacteric’ in their titles. It may be that societies in
Latin American countries include the word ‘climacteric’
influenced by the fact that the Federation that groups them
together is named ‘Federación de Sociedades de Climaterio
y Menopausia’ (FLASCYM)1, but it also could be just the
other way around – that the Federation is named after the
societies.
If a search for the last 10 years is run for the words ‘meno-
pause’ and ‘climacteric’ in PubMed, filtered by articles with
abstracts, these terms will appear in the title of 2075 and 363
articles, respectively2,3.

Correspondence: Dr J. E. Blümel, Universidad de Chile, Medicina Sur, Gran Avenida 3204, Santiago de Chile, Santiago, 8900085 Chile; E-mail: juan.
blumel@redsalud.gov.cl

REVIEW Received 20-06-2013

© 2014 International Menopause Society Revised 22-08-2013
DOI: 10.3109/13697137.2013.838948 Accepted 26-08-2013
 Menopause or climacteric?
Which is the most proper term to refer to the symptoma-
tology and health consequences related with the natural
age-related decline in ovarian function? To answer this, it is
important first to precisely define the concept embedded in
each term, ‘menopause’ and ‘climacteric’.
DEFINITIONS
Menopause
The word comes from the French, menopause, an expression
created by the physician Charles of Gardanne in the XIX
century, using the Greek words: μη′ν (men ⫽ month) and
παν′ση (pausis ⫽ cessation)4 to refer to the ceasing of the
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monthly vaginal bleeding subsequent to physiological endo-
metrial shedding. The International Menopause Society defines
menopause as ‘the permanent cessation of menstruation
resulting from the loss of ovarian follicular activity’. The inter-
national medical consensus is that natural menopause is rec-
ognized to have occurred after 12 consecutive months of
amenorrhea, for which there is no other obvious pathological
or physiological cause. Menopause happens with the final
menstrual period (FMP), which is known with certainty only
in retrospect at least 1 year after the event. An adequate
biological marker for the event does not exist5. Otherwise,
the Menopause Glossary of the North American Menopause
For personal use only.
Society (NAMS) defines menopause as ‘the final menstrual
period, which can be confirmed after going 12 consecutive
months without a period’. This episode marks the permanent
end of menstruation and fertility. It is a normal natural event
associated with the progressive reduced functioning of the
ovaries; this will result in lower levels of circulating ovarian
hormones (primarily estrogen)6. Therefore, from these defini-
tions, we can conclude that menopause refers to the specific
moment at which menstruation definitively ceases.
Climacteric
The term ‘climacteric’ derives from the Greek κλιμακτήρ
(klimater ⫽ step), indicating a process that has stages7.
The IMS defines it as ‘the phase in the aging of women mark-
ing the transition from the reproductive phase to the
non-reproductive state’, adding, ‘This phase incorporates the
perimenopause by extending for a longer variable period
before and after the perimenopause’5. Furthermore, ‘peri-
menopause’, a term still in common usage that means the time
around menopause, has been a very loose concept that was
recently more precisely defined in the Stages of Reproductive
Aging Workshop (STRAW ⫹ 10, Figure 1) as including all the
‘menopausal transition stage’ (Stages ⫺ 2 and ⫺ 1) plus only
the first year (Stage 1a) of the ‘early postmenopause stage’
(Stage 1)8, i.e. until the diagnosis of menopause is ratified by
12 months of amenorrhea, a period which in this case
is shorter than that defined by the IMS as perimenopause.
Consequent to the STRAW classification, which NAMS has
236
Blümel et al.
adopted, in their Menopause Glossary the word ‘climacteric’
is not shown6. We can conclude that it is clear that, when we
mention the term ‘climacteric’, we are referring to a progres-
sive phenomenon that takes place in an extended period of
time, not in one moment as the menopause is, and that is
longer than the perimenopause stage defined by STRAW.
PHYSIOLOGY
The transition of a fully functional ovary to a postmenopausal
ovary is a physiological process that takes years and reflects
the status of the hypothalamic–pituitary–ovarian function
before and after the FMP. Treloar was the first to define the
concept of ‘menopausal transition’ and considered, based on
the loss of the periodicity of menstruations, that this stage
started at the age of 45.5 years, and menses ceased 4.8 years
afterward9. Nevertheless, this definition is centered in the
changes of the rhythmical pattern of uterine bleeding, i.e. in
changes in the production level of the ovarian hormones dur-
ing the menstrual cycle that will subsequently change the pat-
tern of endometrial shedding. But changes in the ovarian
hormonal levels can precede by years the changes in the men-
strual pattern10. Increases in follicle stimulating hormone
(FSH) and luteinizing hormone (LH) concentrations can be
detected in women with regular ovulatory cycles quite early
during their reproductive life. There is a significant progres-
sive increase in FSH levels as early as age 29–30 years which
continues throughout the thirties and became more marked
in the early forties. LH levels show a significant increase at
the age of 35–36 years which is maintained until the age of
40 years and is followed by a further increase in women older
than 40 years. Lately, the cohort of the Study of Women’s
Health Across the Nation (SWAN, n ⫽ 1215) (data used in the
STRAW ⫹ 10 staging system for ovarian aging) has shown
non-specific age-related changes in mean FSH and estradiol
concentrations, but instead in relation to time in years before
and after the FMP (menopause)11. The FSH level starts to
gradually rise 7 years before the FMP, with a steeper upward
inclination 2 years before. Estradiol decreases markedly
2 years before the FMP. Both hormones continuing their
trends, up and down respectively, for 2 more years after the
FMP (extending well past the end of the perimenopause as
defined by STRAW itself), after which the level of each of these
hormones stabilizes10. Therefore, STRAW ⫹ 10 recommended
that the stage named ‘early postmenopause’ (Stage ⫹ 1) be
subdivided into three substages (⫹ 1a, ⫹ 1b, and ⫹ 1c)8.
STRAW ⫹ 10 ratifies that in the late reproductive stage
(Stage ⫺ 3, which marks the time when fecundability begins to
decline), in what is call Stage ⫺ 3b, the ‘menstrual cycles can
remain regular, although in Stage ⫺ 3a there could be subtle
changes without change in its length or FSH levels in the early
follicular phase; however, anti-Müllerian hormone (AMH)
and antral follicle count (AFC) are low and most studies sug-
gest that inhibin-B is also low.’ The lack of standardized
AMH assays prevents the development of quantitative recom-
mendations for this biomarker. One of the central elements
Climacteric
 Menopause or climacteric? Blümel et al.
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For personal use only.

Figure 1 The Stages of Reproductive Aging ⫹ 10 staging system for reproductive aging in women. FMP, fi nal menstrual period; FSH, follicle
stimulating hormone; AMH, anti-Müllerian hormone. Reprinted from Harlow SD, Gass M, Hall JE, et al. Executive Summary: Stages
of Reproductive Aging Workshop ⫹ 10: addressing the unfi nished agenda of staging reproductive aging. Climacteric 2012;15:105 –14;
Fertil Steril 2012;97:843 –51; J Clin Endocrinol Metab 2012;97:1159 – 68; Menopause 2012;19:387–95

of ovarian senescence is the decrease in follicular mass, a
change that is important in fertility assessments. The age-
related decrease in ovarian primordial follicle numbers leads
to a decrease in inhibin B, which in turn leads to an increase
in FSH, hypothesized to act as a stimulus to the maintenance
of circulating estradiol in the follicular phase until late in the
‘menopausal transition’ (STRAW stages)8. The marked
decrease in follicle numbers during the late reproductive age
appears to predispose to erratic and unpredictable cycle char-
acteristics (such as ovulation, estradiol level and endometrial
bleeding), with normal ovulatory cycles continuing to occur
episodically. During the follicular phase of an ovulatory cycle,
gradual increases in FSH and estradiol levels and a decrease
in inhibin B concentration are observed; instead, in a non-
ovulatory cycle there is a markedly increased FSH level
with low levels of estradiol and inhibin B. No specific
endocrine change is characteristic of either the early or late
menopausal transition phase (STRAW stages), confirming
the observations of previous studies regarding the unpredic-
tability of cycle characteristics and hormone changes with
the approach of menopause12. The AMH level correlates
with follicle numbers (AFC) and shows a large age-related
decrease to reach undetectable levels 3 years before the
menopause13.
Therefore, the end of ovarian function is a gradual and
slow process that takes years to evolve and, as the SWAN
study shows, there do not seem to be significant differences
in different ethnicities11. The STRAW staging system classifi-
cation and STRAW ⫹ 10 (supported by The North American
Menopause Society, The National Institute on Aging, The
Office of Research on Women’s Health of the National
Institutes of Health, the American Society for Reproductive
Health, The International Menopause Society, and the
Endocrine Society) clearly show this by defining stages of
reproductive aging and stating that menopause is a moment
(Stage 0) of a process that starts some years before8.
SYMPTOMATOLOGY
Nobody doubts that the climacteric triggers different symp-
toms that deteriorate a woman’s quality of life. However,
defining which symptoms pertain to the climacteric stage has
been a difficult problem that up until today still causes discus-
sion. Hot flushes are for both physicians and women one of
the more characteristic symptoms of the decline in ovarian
function14,15. Nevertheless, different studies have shown that
this symptom, hot flushes, is not the most frequent of all the

Climacteric 237
 Menopause or climacteric?
symptoms. In the USA the SWAN multicenter study showed
that joint stiffness affects 54.3% of women of 40–55 years of
age, emotional strain affects 51.9% and hot flushes only
27.5%16. An Indian study, using a validated instrument for
assessing climacteric symptomatology, showed that physical
exhaustion and osteomuscular pain are more prevalent that
hot flushes in postmenopausal women17. A Japanese study
showed that, in 50-year-old women, the prevalence of tired-
ness is 64.7%, of joint discomfort 75.4%, while that of hot
flushes is only 36.9%18.
In the last years, many investigators in different regions of
the world have used the Menopause Rating Scale (MRS) to
assess climacteric symptomatology; this has been an important
step forward that allows us to objectivize and compare the
clinical effects of climacteric in different populations19,20. This
scale was used to evaluate climacteric symptomatology in 8373
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healthy women in 18 cities of 12 Latin American countries21.
When studying the symptoms in different climacteric stages, it
was observed that symptoms started very early, even before
menstrual irregularities; thus 29.7% of premenopausal women
younger than 45 years have vasomotor symptoms, 26.1%
heart discomfort, 49.6% sleeping problems and 45.9% joint
and muscular discomforts. Globally, 77.0% reported at least
one rated complaint of the MRS21. It has to be pointed out
that the classic vasomotor symptoms are not the most preva-
lent ones in this reproductive stage for these Latin American
women. These results are in accordance with a study in Finland
For personal use only.
that showed that in young women, 42–46 years old, 64%
presented a myriad of different menopausal symptoms22 (either
sweating, hot flushes, vaginal dryness and tenderness, recur-
rent urinary infections, urinary incontinence, sleeping prob-
lems, depression, irritability, dizziness, palpitation, dyspare-
unia, and/or lack of sexual desire). In the Latin American study
just cited, those symptoms in general are not of great intensity
in premenopausal women between 40 and 44 years of age,
though diverse severe symptoms occur from 3.3 to 9.5%
depending on the specific symptom. Almost all of these symp-
toms had greater prevalence in the postmenopause stage and
were present for 5 or more years. The vasomotor symptoms
most likely to occur during the perimenopause8 are some of
the few that tend to decline in the late postmenopause. This
profile of symptom evolution is repeated also in the psycho-
logical and urogenital domains, with a significant presence of
this type of symptom in premenopausal women of 40–44 years
and a progressive increase with age and years of postmeno-
pause, tending to remain steady or to slightly decline in preva-
lence in women of more than 5 years postmenopause.
One aspect that has complicated the understanding of the
climacteric syndrome has been its link with the cessation of
menstruation. It has been considered that there must be a
causal relationship between menopause and the appearance
of symptoms16. This is true for vasomotor symptoms, which
are seen more in the postmenopause, but not for the psycho-
logical ones, whose prevalence does not change with the
menopause23,24. The reason is that psychological symptoms
have been shown to increase in the period previous to the
menopause21. The link of hypoestrogenism with psychological
238
Blümel et al.
symptomatology is demonstrated in that premenopausal
women who experience hot flushes have greater risks of
depression (odds ratio (OR) 8.1), stress (OR 7.5), sexual dys-
function (OR 7.2) and anxiety (OR 3.7) than premenopausal
women without hot flushes25. The presence of climacteric
symptomatology many years before menopause itself
damages the quality of life, early and sometimes severely, of
a significant proportion of women. In premenopausal women
of 40–44 years, assessed with the MRS scale, it is observed
that 12.9% have severe compromise of quality of life; this
percentage rises progressively, reaching its peak of 31.6% in
the first 4 years of postmenopause, and only declining slightly
afterwards in the late postmenopause.
We can conclude by pointing out that menopausal symp-
tomatology is observed already in women of 40–44 years old
(or younger), even if they still have absolutely regular cycles,
and affects a growing percentage of women as their age
increases and the different stages of the climacteric are passed
through. This symptomatology can last for many years,
as shown in the Latin American study21, where women with
5 or more years of postmenopause continued to have symp-
tomatology equivalent in prevalence and intensity to women
who were in the peri- or early postmenopause stage. This last
period has classically been considered as the one with the
largest menopausal symptomatology16,26.
RISK OF CHRONIC DISEASES
Cardiovascular risk
A paradigm of cardiovascular risk is constituted by the meta-
bolic syndrome27. The prevalence of this syndrome increases
three times in women from 30 to 50 years of age28. Therefore,
it is not surprising that atherosclerotic lesions occur, even in
young women, in a process not dependent on the hormonal
levels but more on age29. However, the influence of age on
cardiovascular risk is not easily isolated from the decline in
ovarian function. It seems clear though that the deficit of
ovarian steroids influences the atherosclerosis risk. In female
rabbits fed with a rich cholesterol diet, it was observed
that castration increases by three times the extension of
atherosclerotic aortic lesions compared with normal-diet con-
trols30. In humans, the early menopause or bilateral oophorec-
tomy in young women increases the incidence of cardiovascular
diseases. A meta-analysis of 12 observational studies showed
that early menopause increased the risk of cardiovascular dis-
ease in 25% (relative risk 1.25; 95% confidence interval (CI)
1.15–1.35)31. In the same direction, another meta-analysis
showed that women who have a bilateral oophorectomy
before 45 years of age and who do not take estrogens have
an increased risk of cardiovascular mortality (hazard ratio
1.84; 95% CI 1.27–2.68)32. The impact of the estrogenic defi-
cit is easy to understand if it is considered that estradiol is an
important player in cardiovascular health, exerting its effects
by action at the level of estrogenic receptors, improving lipids,
carbohydrate metabolism and fibrinolysis; and acting also via
Climacteric
 Menopause or climacteric?
a non-genomic pathway, triggering a rapid vasodilatation,
exerting anti-inflammatory actions, regulating the growth and
migration of vascular cells and giving protection to the
cardiomyocytes33.
Different studies suggest that the cardiovascular risk is
increased during the premenopause stage conjointly with the
characteristic hormonal changes in this stage. In female mon-
keys, the decrease in estradiol levels during premenopause is
associated with endothelial dysfunction, an early marker of
atherosclerotic risk34. In humans, there are few studies that
show that, in normal premenopausal women, there is an incre-
ment of the cardiovascular risk that is dependent on the hor-
monal changes present in that reproductive stage. We know
that a chemokine in the etiopathogenesis of atherosclerotic
plaque formation, monocyte chemoattractant protein-1, is
strongly elevated during premenopause35. In the same way, it
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has been observed that the severity of hot flushes, which are
frequently observed in premenopausal women, is the main
determinant of endothelial dysfunction in early menopausal
women36. Finally, the concept of the ‘window of opportunity’
emphasizes the importance of starting early hormonal therapy
for cardiovascular prevention in periods close to menopause
and supports the difference between climacteric and other
stages following the menopause37.
Osteoporosis
For personal use only.
Osteoporosis is a disease that is clearly influenced by ovarian
function. As early as 1940, Fuller Albright communicated
that, of 42 cases of ‘idiopathic’ osteoporosis, 40 were post-
menopausal women; some cases were women of premeno-
pausal age who had had a surgical menopause. He concluded
that idiopathic osteoporosis is in fact postmenopausal osteo-
porosis38. But, in reality, it is not only postmenopausal; bone
mass measurements in young women show that bone loss
starts slowly two decades before the menopause and is
accelerated in the first postmenopausal years. In the hip, there
is a slow loss of bone mass from the age of 30 years; this loss
does not happen in the lumbar spine. Instead, in the post-
menopause stage, there is a rapid bone loss in both sites,
which is more related with the postmenopausal years than
with age39. In the same way, the bone turnover markers also
change before the menopause. Hoshino and colleagues have
found that the increase in bone turnover happens 4 years
before menopause40. All this observations show that bone
loss starts before the menopause and is accelerated from the
perimenopause on.
Genitourinary atrophy
The status of the vaginal mucosa is dependent on estrogenic
levels. Therefore, is not surprising that vaginal lubrication
decreases and subsequent dyspareunia starts at the premeno-
pausal stage, in which the estradiol levels gradually diminish.
A REDLINC study showed that 28.7% of premenopausal
Climacteric
Blümel et al.
women 40–44 years of age noted a decline in vaginal lubrica-
tion, a percentage that rises to 37.5% in premenopausal
women ⫺ ⬎ 45 years of age, and to 49.8% in perimenopausal
women21. Sexual problems and urinary discomfort follow a
similar pattern. Another study shows that around 15% of
women in the perimenopausal stage present with vaginal atro-
phy41. From these data, we can conclude that a significant
percentage of women will experience decay in vaginal health
before menopause itself.
CLINICAL IMPLICATIONS
The fact that most women have a clinical decay during the
premenopausal period leads us to emphasize the need for
women’s health status to be assessed prior to menopause
onset, evaluating the impact that this eventual hormonal
changes could have on their health. Climacteric symptomatol-
ogy damages quality of life very early and we should detect it
very early too. We should first use a set of standardized ques-
tions on symptoms related with the estrogenic deficit, for
which the MRS questionnaire could be a model to follow. In
the same way, we should evaluate weight and especially
abdominal obesity, because an abdominal circumference
⬎ 88 cm is an important marker of metabolic risk. One study
that analyzed the risk of metabolic syndrome in women of
45–64 years old found that abdominal obesity implies a strong
increment in risk of metabolic syndrome (OR 13.01, 95% CI
10.93–15.49)42. This same study pointed out that an abdomi-
nal circumference ⬎ 88 cm picked up 69.9% of women with
this syndrome.
If the hormonal changes that happen in the years immedi-
ately before the menopause are involved in the genesis of
the symptoms and of the metabolic changes typical of the
climacteric, we should then try to counteract them with some
therapy. It is significant that, in women of 40–44 years of age
with absolutely regular menses, 3.0% of them used hormone
therapy21, a percentage that rises to 4.9% in premenopausal
women of 45–49 years and to 10.4% in perimenopausal
women (STRAW stages). This implies that physicians are
prescribing hormone therapy before menstruation ceases.
Nevertheless, the most relevant scientific societies of the world
do not mention this issue. The IMS, in its ‘Updating of the
recommendations of the IMS on postmenopausal hormonal
therapy and strategies of health prevention for the middle age
of life’, constantly refers to ‘postmenopausal’ women43. The
2012 Position Statement of the North American Society of
Menopause mentions: ‘The recent data support the starting of
hormone therapy around the menopause for treatment of the
symptoms related with menopause and for preventing osteo-
porosis in women with high risk of fracture’44.
There is a lack of straightforward directions on the use of
hormone therapy in premenopausal symptomatic woman.
From the theoretical point of view, if estradiol fluctuations
are involved in the neurochemical changes that give rise to
climacteric symptomatology45, we should try to minimize the
periods of hypoestrogenism by prescribing transdermal
239
 Menopause or climacteric?
estradiol, because the oral route of administration induces in
blood serum a greater level of estrone and a lower level
of estradiol46. There are no studies that indicate whether
progesterone should be added in a symptomatic woman who
menstruates regularly.
Even though climacteric symptomatology and metabolic
changes in the premenopausal woman are due to variations
in the hormone levels, it should not be thought that the sole
therapeutic intervention is hormone therapy; lifestyle
changes that improve the cardiometabolic risk are at least
equal or more important. A systematic review of controlled
trials of lifestyle interventions in adults (diet, physical exer-
cises and behavioral therapies) with body mass index of less
than 35 kg/m2 with at least 2 years of follow-up, in which
the objective was to determine the effectiveness of long-term
lifestyle interventions for the prevention of weight gain in
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adults, showed significant improvement in weight, reduction
in hypertension, and reduction in risk of type 2 diabetes and
metabolic syndrome47. Another meta-analysis, that included
six randomized controlled studies studying premenopausal
women, found that a short exercise – less than 30 min a day
– of high impact exercise improved the bone density of the
hip48. Another positive effect of lifestyle change could be in
breast cancer risk. Most studies found that exercise, weight
reduction, low-fat diet, and reduced alcohol intake were
associated with a decreased risk of breast cancer49. But a
healthy lifestyle not only lowers the risk of chronic diseases
For personal use only.
but also attenuates the climacteric symptomatology, improv-
ing quality of life. Most published studies report that active
cigarette smoking is directly correlated with vasomotor
symptoms and obesity50. Weight loss as part of a healthy
dietary modification may help eliminate hot flushes in
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10. Ahmed Ebbiary NA, Lenan EA, Cooke ID. Hypothalamic-
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Blümel et al.
postmenopausal women51. High dietary fiber intakes were
related to decreased severity of vasomotor symptoms52.
CONCLUSIONS
The decline and cessation of ovarian function is a natural
process that takes years to complete. In this relatively long
process, many women will show symptoms that deteriorate
their quality of life and will have an increase in risk factors
for chronic diseases. Therefore, it is pertinent to evaluate
these symptoms and risks at this reproductive stage to mini-
mize, if possible, the decay of the health status of these
woman. In those women who wish, we should propose thera-
peutic intervention such as changes in lifestyle, hormonal
therapy, hypolipidemic drugs, etc. It does not seem proper
to wait for the disappearance of the menstrual periods
(menopause) before we perform these clinical interventions.
In most cases, menopause and the time after (the postmeno-
pausal period) is not the most appropriate time for starting
therapies; it should be the decrease in quality of life and risk
increments for chronic diseases that trigger the start. There-
fore, if we want to refer to the period of decline and cessation
of ovarian function, it seems more appropriate to use the
word ‘climacteric’.
Conflict of interest The authors report no confl ict of
interest. The authors alone are responsible for the content
and writing of this paper.
Source of funding Nil.
11. Randolph JF Jr, Zheng H, Sowers MR, et al. Change in
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