Ovary and menopause

The ovary during menopause is the organ that makes the completion of female reproductive ageing clinically apparent. Menopause does not merely correspond to a generic “hormonal decline”, but to the functional exhaustion of ovarian follicular competence, namely the reduction to critical levels of the follicular pool capable of responding effectively to gonadotropins and sustaining regular ovulatory cycles. Once this threshold is crossed, the production of oestradiol and progesterone becomes irregular and subsequently insufficient, while FSH secretion tends to increase because ovarian feedback is lost. The result is not only the cessation of menstruation, but a systemic endocrine reconfiguration involving thermoregulation, bone, the urogenital system, metabolism, sleep, sexual function and cardiovascular risk.

In clinical terms, the relationship between the ovary and menopause includes at least three major areas. The first is the physiological menopausal transition, during which the ovary moves from a still active but unstable cyclical function to a state of persistent hypoestrogenism. The second concerns non-physiological or early forms, such as early menopause, primary ovarian insufficiency and iatrogenic loss of ovarian function, which have different implications in terms of age, prognosis and therapeutic indications. The third consists of the long-term consequences of oestrogen deprivation and the need to distinguish symptoms attributable to menopause from concomitant diseases or residual ovarian conditions, such as persistent cysts or neoplasms. For this reason, the management of the ovary during menopause requires continuous integration between endocrinology, gynaecology, metabolic medicine, bone health and cancer prevention.

Menopause is the final outcome of a long, progressive and nonlinear biological process that begins well before the final menstrual period. The ovary is formed with a finite follicular reserve consisting of primordial follicles, which decline continuously throughout life because of atresia and recruitment. Over time, not only does the number of follicles decrease, but the quality of the follicular response to gonadotropins and oocyte competence also deteriorate. This combined quantitative and qualitative decline causes the ovarian cycle to progressively lose its regularity and endocrine precision. Ovarian ageing therefore does not consist of an abrupt cessation, but of a gradual loss of coordination between follicular recruitment, dominant follicle selection, ovulation and luteal function.

During the later stages of reproductive life, the ovary may still produce significant amounts of oestrogen, but it does so in an increasingly unpredictable manner. Follicular cohorts become smaller and less synchronised, the duration of the follicular phase tends to change, cycles may shorten or lengthen and the quality of the corpus luteum may become more variable. At the same time, the secretion of inhibin B and, subsequently, AMH declines, resulting in reduced inhibition of pituitary FSH secretion. The increase in FSH during the initial stages of ovarian decline is therefore one of the first endocrine signs of change, but it does not yet correspond to established menopause.

The menopausal transition includes an initial period dominated by subtle menstrual irregularities and a more advanced period in which menstrual changes become evident, with highly variable intermenstrual intervals and frequent anovulatory cycles. The STRAW+10 system provided a clinical structure for this continuum by distinguishing late reproductive stages, early and late menopausal transition, and the postmenopausal stage, defined after 12 consecutive months of amenorrhoea. This classification is particularly useful because it emphasises that the final menstrual period can only be identified retrospectively and that the clinical manifestations of perimenopause begin before the formal definition of menopause is reached.

From a biological perspective, one of the critical events is the loss of regular ovulation. As cycles become increasingly anovulatory, progesterone production declines even before oestradiol levels fall consistently. This produces phases in which a woman may be exposed to fluctuating or relatively preserved oestrogen levels, but with insufficient progestogenic opposition. Many manifestations of perimenopause arise from this condition, including irregular bleeding, breast tenderness, fluctuating vasomotor symptoms and marked variability in subjective well-being. The transition is therefore not initially a simple state of deficiency, but a state of endocrine instability.

When the follicular pool falls below a critical threshold, the ovary is no longer able to generate competent dominant follicles and oestrogen production declines more persistently. FSH remains consistently elevated, cyclical progesterone production disappears and cyclical ovarian function ends. However, the postmenopausal ovary is not endocrinologically “inactive” in absolute terms. Stromal and theca cells remain capable of producing small amounts of androgens, which may subsequently be converted into oestrogens in peripheral adipose tissue. This explains why the transition to menopause changes the hormonal balance towards a relatively hypoestrogenic state with a new proportion between oestrogens and androgens, rather than producing a complete absence of ovarian steroids.

In summary, the ovary during menopause passes through three main phases: initial reproductive ageing, with a reduced reserve and changes that remain subclinical, a menopausal transition characterised by marked endocrine and menstrual irregularity, and stable postmenopause, in which chronic oestrogen deprivation predominates. Understanding this sequence is essential for interpreting symptoms, hormone test results and therapeutic indications in a manner consistent with the actual biology of the process.

Physiological menopause occurs on average during the early years of the sixth decade of life, but the age at which it occurs shows broad and clinically significant individual variability. This variability mainly depends on the rate at which the follicular reserve is depleted and the endocrine resilience of the ovarian compartment. The genetic component is highly relevant: maternal age at menopause, chromosomal characteristics, the efficiency of DNA repair systems and genes involved in follicular recruitment substantially influence the timing of ovarian exhaustion. Menopause is therefore not merely a matter of chronological age, but the individual outcome of a biologically determined trajectory of gonadal ageing.

Among environmental factors, cigarette smoking is the factor most classically associated with earlier menopause. Tobacco toxins have harmful effects on follicles and accelerate the loss of ovarian reserve, resulting in menopause occurring earlier than in women who do not smoke. Environmental exposures, nutritional status, chronic diseases and conditions of biological stress may also contribute, although their influence is more variable and less consistent. Obesity does not necessarily lead to earlier menopause in a consistent manner, but it modifies the perception and clinical impact of the transition through peripheral aromatisation of androgens, low-grade inflammation and interaction with cardiometabolic risk.

A distinct epidemiological area concerns early menopause and, above all, primary ovarian insufficiency. Loss of ovarian function before the age of 40 should not simply be considered an “early” menopause, because it represents a specific biological and clinical condition that is often intermittent, may retain a limited degree of reversibility and has more severe consequences for bone health, the cardiovascular system, sexual health and psychological well-being. Recent international guidelines emphasise that this condition requires a diagnostic and therapeutic pathway distinct from that used for physiological menopause in middle age.

Iatrogenic factors are particularly important among non-physiological causes of early ovarian cessation. Bilateral oophorectomy, chemotherapy, pelvic radiotherapy, repeated ovarian surgery and gonadotoxic treatments may cause an abrupt or progressive loss of ovarian function. In these cases, the gradual endocrine transition of natural menopause does not occur. Instead, deprivation develops more rapidly, is often more symptomatic and carries a greater burden of systemic consequences. This is particularly important in younger women, in whom chronological age does not mitigate, but rather increases, the clinical significance of oestrogen deficiency.

Certain genetic and autoimmune conditions also substantially alter ovarian prognosis. X chromosome abnormalities, FMR1 premutation, galactosaemia, autoimmune oophoritis and autoimmune polyglandular syndromes are examples of conditions that may result in early ovarian insufficiency. In these women, menopause does not represent the normal completion of reproductive life, but the clinical manifestation of an ovarian or systemic disease requiring an aetiological diagnosis and specific follow-up.

The epidemiological summary is that menopause depends on the interaction between the initial follicular reserve, the rate of follicular loss, genetic susceptibility, environmental toxicity and iatrogenic factors. Clinicians must therefore always distinguish between expected physiological menopause, early menopause and primary ovarian insufficiency, because prognosis and treatment depend on this distinction.

Follicular ageing is the central pathophysiological mechanism of menopause. The human ovary does not regenerate its follicular pool to a clinically relevant extent, and its function therefore depends on the progressive utilisation of a finite reserve. Over time, the number of antral follicles responsive to FSH declines, inhibin B and AMH secretion decreases, circulating FSH increases and cyclical endocrine activity loses stability. During this phase, the ovary may still produce high oestrogen levels during some cycles, but the quality of this secretion becomes unpredictable and less closely coordinated with ovulation. The menopausal transition is therefore initially dominated more by variability than by absolute deficiency.

The practical consequence of this instability is an increasing frequency of anovulatory cycles. Without ovulation, a functional corpus luteum does not form, and progesterone production becomes irregular or absent. This disrupts the physiological proliferative and secretory sequence of the endometrium and produces many of the dysfunctional bleeding patterns typical of perimenopause. The endometrium may be exposed to fluctuating oestrogen levels without regular progestogenic opposition, a condition that explains both the variability of menstrual flow and the need, in some cases, to distinguish functional bleeding from pathological bleeding requiring diagnostic investigation.

At the same time, the reduction in mean oestradiol levels and the greater fluctuation in oestrogen concentrations profoundly alter central autonomic systems. Vasomotor symptoms are not simply the expression of “low hormones”, but result from changes in the stability of hypothalamic thermoregulatory circuits caused by the abrupt reduction or fluctuation of oestrogen signalling. This produces hot flashes, night sweats, fragmented sleep and a substantial proportion of the discomfort experienced during the menopausal transition. Mood, subjective cognitive function and vulnerability to insomnia are also affected by this neuroendocrine reorganisation.

The postmenopausal ovary retains a degree of stromal and androgenic activity, but permanently loses the ability to sustain ovulatory cycles and adequate systemic oestrogenisation. Cyclical progesterone production disappears, oestradiol falls to consistently low levels and the relationship with gonadotropins changes persistently, with elevated FSH and often elevated LH because negative feedback is lost. These changes have effects beyond the reproductive system. Bone turnover accelerates, the genitourinary tract loses oestrogen-dependent trophism, the lipid profile tends to deteriorate and body fat distribution becomes more central.

A particularly important point is the distinction between physiological menopause and primary ovarian insufficiency. In physiological menopause, ovarian ageing is consistent with age and with the natural trajectory of the follicular reserve. In primary ovarian insufficiency, ovarian functional failure occurs before the age of 40 and may present with intermittent ovarian activity, amenorrhoea or menstrual irregularity and biochemical confirmation. Updated guidelines emphasise this distinction because the consequences of oestrogen deficiency at a young age are more profound and require replacement therapy at least until the average age of natural menopause, unless contraindications are present.

In summary, menopause represents the redefinition of ovarian function from a cyclical ovulatory system to a chronic hypoestrogenic state with residual stromal activity. The transition is the most biologically unstable phase, and this instability explains the wide range and heterogeneity of clinical symptoms.

Not every cessation of menstruation at a relatively young age corresponds to physiological menopause. Primary ovarian insufficiency is a condition characterised by loss of ovarian function before the age of 40, with irregular or absent menstrual cycles and biochemical confirmation of ovarian insufficiency. It differs from natural menopause because it may follow an intermittent course, with possible residual follicular activity, and because its age of onset makes it a pathological condition in every respect. Its consequences concern not only fertility and menstruation, but also bone health, cardiovascular risk, sexual function, quality of life and mental health.

The causes of primary ovarian insufficiency are numerous and heterogeneous. Some are genetic, including X chromosome abnormalities, gonadal dysgenesis and FMR1 premutation. Others are autoimmune, with possible associations with adrenal disease, thyroid disease or polyglandular syndromes. Others remain idiopathic even after comprehensive investigation. This heterogeneity is highly important in clinical practice, because identifying hypoestrogenism is not sufficient. It is also necessary to establish whether associated comorbidities, familial risk, residual reproductive implications and the need for broader endocrine follow-up are present.

Secondary or iatrogenic losses of ovarian function also occur. Bilateral oophorectomy, chemotherapy, radiotherapy, antioestrogen treatments or extensive ovarian surgery may cause an abrupt cessation of ovarian activity. Symptoms may be particularly severe in these cases because the gradual adaptation phase typical of physiological menopause is absent. The sudden decline in oestrogen rapidly leads to severe hot flashes, insomnia, mood changes, vulvovaginal dryness and accelerated bone loss. From a clinical perspective, this represents surgical or toxic ovarian deprivation, not simply a variant of the climacteric period.

Another relevant category is early menopause between the ages of 40 and 45. Although it does not strictly meet the definition of primary ovarian insufficiency, it shares some of its clinical implications. These women experience a longer duration of exposure to oestrogen deficiency than women who undergo menopause at the population average age and may benefit from a therapeutic approach closer to that used for early forms than to that used for later physiological menopause. Contemporary scientific societies therefore emphasise the need not to standardise treatment solely according to the presence of amenorrhoea, but to consider the biological age at which ovarian function is lost.

From a prognostic perspective, early recognition of these conditions is essential. In younger women, prolonged untreated oestrogen deficiency may impair bone mass, cardiovascular health, sexual function and psychological well-being to a greater extent than physiological menopause. Furthermore, in forms with intermittent ovarian activity, contraceptive and reproductive counselling must be explicit, because fertility is not always completely absent and prognosis may be more complex than the menstrual pattern suggests.

In summary, early menopause, primary ovarian insufficiency and iatrogenic loss of ovarian function represent distinct areas of ovarian medicine. Their correct identification is crucial because it changes the definition, aetiological investigation, intensity of follow-up and indications for hormone therapy.

Alongside hot flashes and menstrual irregularities, symptoms may occur during the menopausal transition that women do not immediately associate with ovarian changes. These include palpitations, difficulty concentrating, a sensation of brain fog and fatigue. These manifestations may reflect interactions between hormonal fluctuations, disturbed sleep, vasomotor symptoms and psychosocial factors, but their temporal association with menopause does not automatically establish a hormonal cause. In particular, persistent palpitations or those accompanied by syncope, chest pain or dyspnoea require appropriate cardiac assessment; progressive cognitive difficulties or those affecting independence require assessment in their own right, rather than being generically attributed to the climacteric period.

Musculoskeletal pain is another frequently underestimated manifestation. Diffuse joint pain, stiffness, tendon and muscle discomfort, or worsening of pre-existing conditions may be reported at this stage; changes in oestrogen levels may contribute through effects on connective tissues, pain perception and inflammatory processes. However, the available evidence is heterogeneous and does not allow every chronic pain condition to be attributed to menopause. Osteoarthritis, inflammatory arthritis, thyroid disorders and other musculoskeletal causes must be considered according to the clinical presentation. Joint swelling, prolonged morning stiffness, functional impairment or persistent localised pain require targeted investigation rather than treatment based solely on presumed oestrogen deficiency.

The skin and its appendages are affected by ageing and changes in the hormonal environment. Declining oestrogen levels may contribute to dry skin, itching, reduced elasticity and changes in dermal collagen; photoageing, genetics and environmental factors act simultaneously and often play a substantial role. Hair thinning, especially in a female-pattern distribution, may also become more noticeable in peri- and postmenopause, but its aetiology is multifactorial. Marked or rapid hair loss, patchy alopecia or signs of hyperandrogenism require targeted dermatological and endocrinological assessment. Systemic hormone therapy is not a routine treatment for cosmetic changes in skin or hair alone.

Sleep disorders include difficulty falling asleep, repeated awakenings and unrefreshing sleep. Night sweats can fragment sleep, but chronic insomnia, obstructive sleep apnoea, restless legs syndrome, mood disorders and stressors unrelated to ovarian function may coexist. Irritability and vulnerability to anxiety and depressive symptoms may also increase during this period; assessment should distinguish transient fluctuations, sleep disorders and psychiatric conditions that require treatment in their own right. For chronic insomnia, cognitive behavioural therapy specifically for insomnia is a reference treatment; when hot flashes are a major contributing factor, treating them can also improve sleep.

Menopause does not eliminate the need to consider the ovary as a potential site of organic disease. Although follicular function has ceased, the postmenopausal ovary may still harbour residual cysts, benign masses, stromal tumours or epithelial neoplasms. During this stage of life, the detection of an adnexal lesion has a different significance than during the reproductive years, because most of the functional cystic physiology typical of reproductive age is no longer present. For this reason, an ovarian mass after menopause requires greater attention in terms of ultrasound characterisation and risk stratification.

Not all postmenopausal cysts are malignant. Small, simple and stable cysts may occur and often have limited clinical significance, particularly when they lack thick septa, papillary projections, solid components or suspicious vascularisation. Nevertheless, the postmenopausal context requires caution because the pretest probability of malignancy is higher than in younger women and the range of physiological functional conditions is narrower. Assessment must therefore integrate expert ultrasound examination, symptoms, size, bilaterality, the possible presence of ascites and changes over time.

Stromal or androgen-secreting tumours represent a specific category. Because the postmenopausal ovary retains stromal and theca cell activity, certain neoplasms arising from these compartments may present with late-onset hyperandrogenism, alopecia, hirsutism or signs of virilisation. In these patients, the problem is no longer oestrogen decline, but pathological androgen production that must be distinguished from the modest physiological hormonal changes of postmenopause. The clinical presentation therefore requires a targeted endocrine and oncological assessment of the ovary and, when necessary, the adrenal glands.

Another relevant consideration is that some symptoms generically attributed to menopause may actually conceal adnexal disease. Abdominal distension, a sensation of pelvic pressure, early satiety, worsening bowel habits or persistent pelvic pain should not automatically be attributed to the climacteric period or ageing. In postmenopausal women, these symptoms always justify a low threshold for gynaecological and ultrasound assessment, because ovarian neoplasms must be detected as early as possible.

Postmenopausal uterine bleeding, although primarily an endometrial warning sign, may occasionally occur in the context of an oestrogen-secreting ovarian disorder or pathological endocrine imbalance. This is less common than primary endometrial disease, but it forms part of the differential diagnosis when an oestrogen-secreting ovarian mass is present. Clinicians should therefore not regard the ovary as an “inactive” organ, but as a possible site of new disease with endocrine or compressive manifestations.

In summary, postmenopause reduces the frequency of functional ovarian disorders but increases the clinical significance of persistent masses and neoplastic risk. The quality of ultrasound assessment and correct interpretation of symptoms are essential for distinguishing between cautious observation, structured follow-up and the need for specialist treatment.

The diagnostic assessment of the ovary during menopause should be structured as a pathway beginning with the menstrual history and extending to evaluation of systemic and oncological risk. The first step is to establish whether the patient is undergoing the menopausal transition, has established menopause or has an early form of ovarian insufficiency. This requires a detailed history of menstrual regularity, duration of amenorrhoea, onset of vasomotor symptoms, previous ovarian surgery, oncological treatments, family history of early menopause and the presence of autoimmune or genetic diseases. Chronology is essential because 12 months of amenorrhoea define menopause only in the absence of other causes and at an age consistent with the physiological process.

From a laboratory perspective, physiological menopause in middle age is often a clinical diagnosis and does not necessarily require routine biochemical confirmation. However, measurement of FSH and oestradiol may be useful in selected situations, particularly when age is atypical, the menstrual pattern is unclear or primary ovarian insufficiency is suspected. The most recent guidelines emphasise that a single hormone measurement, particularly during perimenopause, may be misleading because endocrine levels fluctuate markedly. Diagnosis in physiological forms is therefore based more on the clinical context than on an isolated test, whereas biochemical confirmation is more important in early forms.

Two common diagnostic misconceptions should be clarified. Symptoms of perimenopause may begin several years before the final menstrual period: waiting for 12 months of amenorrhoea before recognising and treating clinically significant symptoms unnecessarily delays care. Moreover, in women older than 45 years with a typical clinical presentation, a single normal FSH result does not rule out the menopausal transition, just as an occasionally elevated value does not by itself establish a stable postmenopausal state. The need for contraception must be assessed separately, because sporadic ovulations remain possible during perimenopause.

When the patient is younger than 40 or there is a strong suspicion of early loss of ovarian function, the diagnostic pathway must be expanded. According to updated international guidelines on primary ovarian insufficiency, diagnosis requires documentation of menstrual irregularity or absence associated with biochemical confirmation of ovarian insufficiency, followed, when appropriate, by genetic, autoimmune and iatrogenic aetiological investigations. This approach prevents diagnosis from being reduced to a symptomatic label and allows associated conditions relevant to prognosis and treatment to be identified.

Pelvic ultrasound is the principal imaging examination when abnormal bleeding, pelvic pain, a palpable mass, abdominal symptoms or suspected adnexal disease are present. After menopause, ultrasound is used primarily to characterise ovarian cysts or masses, whereas during perimenopause it may help assess irregular bleeding, endometrial thickness and associated disease. The objective is not to “diagnose menopause” by ultrasound, but to exclude organic diseases that may be concealed by symptoms attributed to ovarian decline.

Follow-up must be personalised according to the clinical profile. In physiological menopause with mild symptoms, it may be limited to periodic reassessment of symptoms, cardiovascular risk, bone health and therapeutic indications. Women receiving hormone therapy require regular reassessment of efficacy, tolerability and the balance between risks and benefits. In patients with primary ovarian insufficiency or early menopause, follow-up should be more structured and include bone health, cardiometabolic risk, sexual well-being, psychological support and reproductive or contraceptive counselling when indicated. In women with adnexal masses, surveillance depends on ultrasound morphology and changes over time.

In summary, diagnosis of the ovary during menopause is not limited to confirming the cessation of menstruation. It includes distinguishing between a physiological process and early pathological ovarian failure, excluding concomitant conditions and planning follow-up proportionate to the systemic consequences of ovarian deficiency.

Treatment of the loss of ovarian function during menopause is based on a central principle: menopause itself, as an inevitable biological event, is not treated. Instead, symptoms are managed and clinically significant consequences of oestrogen deprivation are prevented when the balance between benefits and risks is favourable. Menopausal hormone therapy remains the most effective treatment for vasomotor symptoms and genitourinary syndrome, and it also contributes to the prevention of bone loss. Contemporary scientific societies emphasise that treatment must be individualised according to age, time since menopause, presence of the uterus, thrombotic profile, cardiovascular risk, symptoms and patient preferences.

In women with an intact uterus, systemic oestrogen administration requires adequate progestogenic protection to prevent endometrial hyperplasia. In women who have undergone hysterectomy, oestrogen therapy may be used without a progestogen. The choice between oral and transdermal administration and the choice of progestogen depend on the individual clinical profile. The key concept is that there is no single regimen suitable for every woman. Instead, the strategy must minimise risks and maximise symptomatic and skeletal benefits within the specific clinical context.

Hormone therapy has specific clinical indications: symptoms that impair well-being, the need for bone protection in selected women and, with a different rationale, endocrine replacement in early forms of ovarian insufficiency. It is not a universal anti-ageing treatment and should not be prescribed solely to prevent cardiovascular events or dementia. Conversely, the idea that it is always contraindicated after menopause is also incorrect: in suitable symptomatic women, particularly those younger than 60 years or within 10 years of the final menstrual period, the benefit-risk balance is often favourable; this balance changes in the presence of contraindications and with increasing age or time since the onset of menopause.

When genitourinary syndrome of menopause is the main problem, local treatment with vaginal oestrogens or other targeted therapies may be preferable to systemic therapy if vasomotor symptoms are not significant. Conversely, systemic therapy may have a central role in patients with severe hot flashes, night sweats, insomnia and impaired quality of life. For women who cannot or do not wish to use hormones, non-hormonal options with varying efficacy are available and should be selected according to the predominant symptoms and comorbidities.

The therapeutic rationale changes profoundly in primary ovarian insufficiency and early menopause. In these women, hormone therapy is not merely a symptomatic treatment, but genuine replacement of ovarian function that has been lost prematurely. Its purpose is to protect bone, the cardiovascular system, sexual function and overall well-being until at least the average age of natural menopause, unless contraindications are present. This principle is shared by recent guidelines and clearly distinguishes these conditions from the management of physiological menopause in middle age.

Treatment of metabolic and skeletal consequences represents another important area. Oestrogen deprivation is associated with increased bone turnover and a greater risk of osteoporosis and fractures. Physical activity, adequate calcium and vitamin D intake, smoking cessation, weight control and pharmacological antiosteoporotic strategies when indicated are therefore part of comprehensive management. Cardiovascular risk, sleep disorders, sexual health and quality of life also require an integrated approach, because ovarian loss is not expressed through a single symptom, but through a new systemic equilibrium.

From a nutritional perspective, cardiometabolic and musculoskeletal prevention requires a sustainable dietary pattern that meets energy requirements and is rich in plant foods, legumes, whole grains and sources of predominantly unsaturated fats, with adequate protein intake to preserve muscle mass. Control of abdominal adiposity should go hand in hand with preservation of lean mass: excessive calorie restriction, particularly when combined with a sedentary lifestyle, may aggravate muscle loss. For bone health, it is important to ensure adequate calcium intake, preferably through diet, and to assess vitamin D according to risk factors and clinical indications. Supplements and products marketed to 'rebalance hormones' do not restore ovarian follicular function and cannot replace treatments with demonstrated efficacy.

Physical activity should combine aerobic exercise with resistance training. As a general target, at least 150-300 minutes per week of moderate-intensity aerobic activity, or an equivalent amount of vigorous activity, are recommended, together with muscle-strengthening exercises involving the major muscle groups on at least two days each week. Resistance training is particularly useful for counteracting loss of muscle mass and function, while weight-bearing exercise, when appropriate, supports skeletal health; balance training and fall prevention become increasingly important with age. Exercise type and intensity should be adapted to functional capacity, frailty, fracture risk and comorbidities. These interventions have documented benefits for overall health, but are not an equally effective alternative to hormone therapy for controlling hot flashes.

Managing sleep disturbances and psychological distress also requires specific interventions. Sleep hygiene and regular daily rhythms are supportive measures, whereas persistent insomnia benefits above all from a structured cognitive behavioural programme and investigation of any coexisting disorders. Treatment of vasomotor symptoms, sleep apnoea and depressive disorders should address their respective causes. This approach integrates prevention of pathological ageing with symptom control, without attributing every midlife complaint solely to oestrogen deficiency.

In summary, treatment of the ovary during menopause is based on personalised medicine. Management ranges from observation and counselling in patients with few symptoms to systemic or local hormone therapy, and to true endocrine replacement in early forms. The guiding criterion is the clinical significance of ovarian loss for the individual patient, not merely the presence of amenorrhoea.

The complications of ovarian functional loss during menopause are not limited to immediately perceived symptoms. Hot flashes, night sweats and insomnia are the most evident manifestations, but the greatest clinical concern involves the medium and long-term effects of oestrogen deficiency. Bone is one of the main target tissues. After menopause, bone turnover accelerates, mineral loss increases and the risk of osteopenia, osteoporosis and fractures rises significantly. This consequence is particularly marked in women with early menopause or primary ovarian insufficiency, who spend more years in a state of oestrogen deprivation.

The cardiovascular profile also changes. Menopause is not the sole cause of cardiovascular disease, but the end of the reproductive oestrogen environment coincides with deterioration in some lipid parameters, increased central adiposity, greater vascular stiffness and interactions with age, blood pressure, diabetes and lifestyle. In early forms of ovarian loss, this risk becomes even more important because it is combined with a prolonged duration of endocrine deficiency. This is why scientific societies emphasise the preventive value of diagnosis and appropriate treatment in younger women with ovarian insufficiency.

Body composition also changes during the menopausal transition. Longitudinal studies indicate that around the final menstrual period, gains in fat mass may accelerate while lean mass tends to decline, without overall weight necessarily increasing at the same rate. Redistribution towards abdominal fat occurs alongside ageing, physical inactivity, diet and sleep, contributing to metabolic risk to varying degrees from woman to woman. For this reason, body weight alone, or BMI in isolation, may underestimate a deterioration in body composition. Waist circumference, blood pressure, blood glucose, lipid profile and muscle strength assessment provide more useful information for tailoring prevention.

The genitourinary tract is another important target. Persistent reduction in oestrogen leads to progressive thinning of the vaginal epithelium, reduced lubrication, increased susceptibility to pain during intercourse, urinary urgency, dysuria and recurrent urinary tract infections in some patients. These symptoms are not merely a local disorder, but profoundly affect sexuality, self-esteem, relationships and quality of life. They are often underreported or underestimated, particularly when consultation focuses exclusively on hot flashes.

Psychological and subjective cognitive well-being represents another central area. Sleep disturbances, irritability, mood fluctuations, reduced energy, difficulty concentrating and a perception of cognitive decline are common during the menopausal transition. They are not all caused exclusively by ovarian changes, because age, comorbidities, psychosocial stress and sleep disorders make substantial contributions, but the loss of stable ovarian endocrine function remains one of the main vulnerability factors during this phase. In women with primary ovarian insufficiency, the psychological impact may be even greater because it is associated with unexpected loss of fertility, a sense of premature ageing and the need for prolonged treatment.

The complications of treatment must be considered with the same attention as the complications of untreated menopause. Hormone therapy requires periodic assessment of efficacy and safety because benefits and risks depend on age, timing of initiation, route of administration, duration and comorbidities. Failure to personalise treatment may result either in insufficient treatment, with persistent symptoms and bone damage, or in choices that are disproportionate to the individual risk profile. The success of menopausal medicine is measured precisely by its ability to avoid these extremes.

In summary, ovarian endocrinology during menopause does not end with the cessation of menstrual cycles, but continues as the management of functional outcomes. The true objective is not merely to confirm that the ovary has completed its reproductive function, but to protect bone health, the genitourinary system, cardiovascular health, psychological well-being and quality of life during a phase of life that may last for decades.