Women’s Health Blog

What is the menopause? 

A transitional time, an adaptation challenge


Would you like to know about my approach to helping you through the menopause? 

Scroll to the bottom of this page to learn more about my herbal formulations for menopausal symptoms.

The menopause is the permanent cessation of menstrual periods which is caused by the natural depletion of the ovarian follicle reserves; it marks the end of reproductive function.

During a woman’s reproductive cycle the Follicular Stimulating Hormone (FSH) stimulates the ovarian follicles (ovarian follicular phase) to mature the oocytes needed for the monthly reproductive cycle.  

However, the ovaries have a finite follicle reserve; the menopausal transition commonly starts with irregular or delayed periods reflecting the fact that the pool and function of ovarian follicles is naturally diminishing.  During the transition, FSH fluctuates from normal to higher levels to stimulate the follicles, and remains high post-menopause.  The transition period formally ends after a continuous lack of periods for 12 months and at that point the menopause can be formally confirmed.

The median duration of the menopausal transition is about 4 years but symptoms can be most severe during the first 1-2 years after the final menstrual period, with some women experiencing disturbing symptoms for more than a decade.

 

What happens to estrogen during the menopausal transition?

Contrary to commonly held belief, estrogen fluctuates and varies during the menopausal transition.  During the early menopausal transition, although follicles are smaller with fewer granulosa cells, follicular aromatase activity increases to compensate and maintain estradiol levels (estradiol is the most active form of estrogen).  This can result in equal or greater estrogen levels than even mid-reproductive age women.

Moreover, due to reduced follicle quality, there is diminished production of progesterone during the luteal ovarian phase.  This can lead to FSH rises out of sync, causing out-of-phase ovulation and very high estradiol levels, as follicular estradiol can be ‘stacked’ from two cycles.   

During the late menopausal transition, lasting around 1-3 years, compensatory mechanisms fail and more stark changes are observed: menstrual cycles are more dysregulated, FSH is more consistently elevated, estrogen levels fluctuate but are more persistently low and progesterone continues to decline.  As a result, cycles are less likely to demonstrate luteal activity / ovulation and become longer.  Anovulatory cycles have varying underlying hormonal patterns and sometimes ovulatory cycles can return for a short time.

Estradiol remains the biologically active estrogen in postmenopausal women even if the circulating levels are low. It is synthesized either by reduction of estrone (another type of estrogen) in extragonadal sites including skin, adipose tissue, bone, the brain or alternatively by direct aromatization of circulating testosterone].

  • It is thus not true that post-menopause the body can no longer make estrogen, but it is true that the ovaries can no longer participate, as reproductive organs, in estrogen creation.  

  • The body maintains estrogen balance to address levels of estrogen needed for non-reproductive purposes.

 

Loss of ovarian estrogen underpins symptom onset but does not explain variation of symptoms in the population. 

The menopausal transition can be a miserable time for women due to a variety of symptoms that are linked, but not limited to, to ovarian estrogen deprivation.  

The most disturbing symptoms during the transition are hot flushes, vaginal dryness with higher risk genitourinary infection, depression, anxiety and sleep problems.

Vasomotor symptoms: Hot flushes, sweats, chills and palpitations

Vasomotor symptoms (VMS) affect the majority of women and can significantly impair quality of life.  VMS are hot flushes affecting the face and upper body followed by sweats, chills and often heart palpitations.

  • There is no linear relationship between irregular / declining ovarian function and the start of hot flushes and sweats.   

  • There is no consistent correlation between actual plasma estrogen levels and severity of symptoms.

It is not the absolute level of estrogens, but the rate of estrogen withdrawal that determines the onset and severity of flushes.

 

What are the causes of hot flushes during the menopausal transition?

The hypothesis is that the thermoregulatory zone in the hypothalamus is narrowed in symptomatic postmenopausal women.  This implies that small core temperature elevations are not tolerated and trigger the heat loss mechanisms of the hot flush (cutaneous vasodilation, sweating and the shivering observed following many of them).  This is preceeded by reduced skin resistance suggesting that central hypothalamic regulation is indeed the ‘switch’.  Note that external factors have an effect on increasing core temperature: ambient temperature, coffee, alcohol, spices, stress and anxiety can trigger flushes. 

The narrowing of thermotolerance can be the product of hormonal and structural changes in symptomatic women:

  • it has been linked to elevated central noradrenergic activation which is elevated before and during hot flushes.   The data shows a decline in inhibitory a2-adrenergic receptors leading to increased noradrenaline levels in the brain.  Noradrenaline is a neurotransmitter released predominantly from the ends of sympathetic nerve fibres; when elevated it narrows the band of the thermoregulatory zone.  

  • lower serotonin levels and upregulation of serotonin receptor 5-HT2A can result in an increased central temperature and lead to increased secretion of adrenocorticotropic hormone (ACTH) from the pituitary gland.  ACTH directly implicates the Hypothalamus-Pituitary-Adrenal axis (HPA axis) because it stimulates the adrenals.  

  • KNDy neurons increase in cell size and gene expression during the transition.  As they extend from the infundibular nucleus of the hypothalamus into the preoptic structures they accelerate heat dissipation effectors in those structures.  These neurons express estrogen receptor-a and the peptides kisspeptin and neurokinin B (NKB); activation of the neurokinin 3 receptor (NK3R) reduces body temperature

 

Other symptoms of menopausal transition:

  • Genitourinary symptoms

    Estrogen deprivation causes symptoms of atrophy and dryness of the vagina; dryness and a higher pH can sometimes lead to more frequent urinary infections and dyspareunia (pain during sex).

  • Mood changes 

    Depression or anxiety can appear during the menopause attributed to changes in the gamma amino butyric acid (GABA), norepinephrine and serotonin levels and stimulation of the HPA axis.  

  • Sleep 

    Sleep disturbance appears in the early menopause transition but peaks in the late transition and levels can remain unchanged after postmenopause.  Sleep disturbance can be affected by night-time VMS, but disturbance can also be experienced by women without night-time VMS.

  • Weight management

    For some women weight management can be made trickier due to the complex relationship between the nervous and hormonal systems during the transition.

 

What about Hormone Replacement Therapy (HRT)?

Although the onset of menopausal symptoms is underpinned by loss of ovarian estrogen, this is a naturally programmed transition from the reproductive years.  The body still produces non-ovarian estrogen during the non-reproductive years to keep estrogen homeostasis.  Wider hormonal changes that are not solely restricted to the loss of ovarian estrogen can be seen in the context of a wider adaptation effort.  If there is pre-existing hormonal imbalance this can lead to worse and prolonged menopausal symptoms.  In this context, HRT cannot stop the follicular demise.   

Estrogen is a proliferative hormone and one of its main functions is to grow the endometrium; once the reproductive years are over there are dangers to estrogen replacement.  This is why systemic estrogen formulations must be taken with a progestin or uterine-level estrogen receptor antagonist to reduce the risk of endometrial hyperplasia and cancer from unopposed estrogen exposure.  Additionally, HRT has vascular risks of clotting and is contraindicated for many other conditions; many women’s medical or family history precludes them from using HRT due to those increased risks.

 

The menopausal transition calls for natural adaptation (not opposition).

To recap, the menopause is a natural event due to the programmed loss of ovarian follicles; as a result, estrogen is no longer made by follicles but it can still be made in the body and locally by the enzyme aromatase.  When estrogen is replaced in the form of HRT it does not bring back follicular function.

 

My approach to helping women through the menopause:

Menopausal symptoms cannot be assessed as events outside this programmed transition.  It is the rate of the transition for many women that produces the symptoms, not necessarily the transition itself.  Your previous history will also help identify the areas that may be contributing to the symptoms that are individual to you; of vital importance is the HPA axis and nervous system, the liver, the colon and the thyroid.

As a medical herbalist with a strong focus on female health, I have designed special herbal formulations that smooth the transition, not oppose it, using selected phytoestrogenic, adaptogenic and balancing herbs. 

Phytoestrogens are plant molecules that ‘mimic’ the action of estrogen at estrogen receptor-sites; they can be very useful during the menopause, as the body adapts to not having ovarian estrogen.  Another relevant class of herbs is the adaptogenic herbs, that help the body during periods of excess demand for adaptation.  

My herbal formulations are natural hydro-ethanolic herbal extracts:

  •  They are made for you each time. 

  • They are available directly and can be repeated.

  • They are cost-effective.

If you are interested in finding out more about my approach, please contact me for a -free- exploratory discussion of your situation.