Hot flushes

More than 90% of women transitioning through menopause experience hot flashes, defined as transient sensations of heat, sweating, flushing, anxiety, and chills lasting for 1 – 5 min, constituting one of the most common symptoms of menopause.

Hot flashes primarily arise from dysregulation of hypothalamic thermoregulatory control. The hypothalamus normally maintains body temperature within a stable “thermoneutral zone,” but this zone narrows significantly in menopausal women experiencing withdrawal of estrogen, which then destabilizes the thermoregulatory system. With destabilisation, even minimal elevations in core temperature are enough to trigger an intense heat-loss response, where peripheral vasodilation and sweating occur rapidly. [17]

Sleep Disturbances

Sleep disturbances are a core symptom of the menopausal transition affecting 40 - 60% of women. Sleep disturbances often arise from the onset of hot flashes and night sweats, these episodes often cause abrupt awakenings, leading to sleep fragmentation and impairments in sleep continuity. Objectively, they are also associated with reduced slow-wave sleep (SWS), and delayed onset of rapid eye movement (REM) sleep, all of which reduce overall sleep efficiency.

Estrogen plays a role in modulating melatonin production and influences thermoregulatory centers in the brain. Therefore during the menopausal transition, the decline in estrogen hormones impairs thermoregulation and is associated with a reduction in nocturnal melatonin secretion, which contributes to circadian rhythm disruption, and subsequent poor sleep initiation and maintenance.[15]

Accelerated Skin Aging
 

Estrogen plays a key role in maintaining skin structure, primarily by promoting type I collagen synthesis in dermal fibroblasts. With reduced estrogen, matrix metalloproteinases (MMPs) increase, degrading existing collagen, while new collagen synthesis fails to keep up, accelerating visible aging. The result is deeper wrinkles and compromised skin integrity, especially in the dermis.[21]

Abdominal Weight Gain

During the menopausal transition, women experience profound and adverse changes in body composition, primarily driven by a sharp decline in estrogen levels. Estrogen normally promotes subcutaneous fat storage and helps preserve lean muscle mass. Its loss results in a redistribution of fat from peripheral regions to central, most notably increasing abdominal fatty tissue.

On average, women gain approximately 6 kilos over the 8 years spanning the menopausal transition. Specifically MRI based studies have demonstrated the following after menopause

• 10% increase in visceral fat 

• 36% increase in fat over the entire torso

• 49% increase in abdominal cavity fat

• 22% rise in subcutaneous abdominal fat [22]

Cognitive Impairment

Estrogen and progesterone are hormones that normally:
 

• Stimulate neurogenesis

• Support synaptic plasticity

• Modulate BDNF, supporting neuronal survival, growth

• Modulate cholinergic function, critical for attention, learning, and memory
   

After Menopause there is significant cognitive impairments which have been Quantified via brain scans illustrating: 

• 1.7% Reduction in Total Brain Volume

• 2.2% reduction in Grey Matter

• 5 - 7% reduction in Frontal regions size

• 3 - 5% reduction in Temporal cortex size

• 4 - 8% in hippocampal volume

• 5 - 7% reduction in Amygdala volume 

• 2 - 4 % reduction in the Basal Ganglia volume [26]
   

Overall this constitutes a significant effect on cognitive decline, including up to 15% decline in memory recall, but also in working memory, language and executive function. Indicating an imperative need to begin hormone support as soon as possible. 

Irritability / Low Mood

Estrogen deficiency disrupts key neurotransmitter systems involved in mood regulation. Specifically, it reduces central serotonin availability, heightens norepinephrine activity, and alters dopamine and GABA signaling, neurochemical changes that collectively contribute to mood disturbances. These alterations are linked to increased irritability, low mood, and heightened anxiety, which are commonly reported during the menopausal transition. [16]
 

Compromised Bone Health / Osteoporosis

Bone health is significantly affected by the decline in estrogen. Estrogen normally inhibits osteoclast activity via suppression of RANKL. Although with menopause, unopposed RANKL stimulation leads to increased bone resorption and reduced bone mineral density, heightening the risk of osteoporotic fractures, particularly in the vertebrae and femoral neck.[23]

It is estimated after menopause, bone loss accelerates up to 5% per year, especially in the first decade. 1 in 3 women over 50 will suffer a fracture, with hip and vertebral fractures leading to significant morbidity. [16]
 

Vaginal Dryness

Vaginal dryness affects up to 93% of postmenopausal women, stemming from oestrogen deficiency. Oestrogen plays a critical role in maintaining vaginal lubrication through its stimulation of mucus production, vascular perfusion, and epithelial integrity. 

Loss of oestrogen also reduces glycogen content in the vaginal epithelium, which in turn decreases the presence of Lactobacilli bacteria that produce lactic acid and maintain an acidic vaginal pH. This microbial shift causes thinning of mucosa and insufficient lubrication, leading to dryness and discomfort.[15]

Vaginal Itching, Burning, and Irritation

These sensations are due to epithelial atrophy and microtrauma, both consequences of reduced oestrogen levels. As the vaginal walls lose collagen, elastin, and moisture, nerve endings become more exposed and sensitive. This hypersensitivity, combined with inflammation and altered microbiota, results in itching and burning, which are often mistaken for infections. [15]

Dyspareunia (Painful Intercourse)

Oestrogen deficiency causes loss of vaginal rugae, elasticity, and lubrication. The resulting dry, fragile, and narrow vaginal canal increases friction and pain during intercourse. Fissuring and inflammation may occur, especially in the posterior fornix. Deep pelvic pain may also arise from pelvic floor dysfunction or prolapse secondary to tissue weakening.[15]

Urinary Urgency, Frequency, Incontinence

Oestrogen receptors are abundant in the urethra and bladder trigone. Hypoestrogenism leads to urethral thinning and mucosal inflammation, increasing urgency, frequency, and incontinence. Bladder instability may mimic or worsen overactive bladder symptoms. Additionally, pelvic floor weakening contributes to stress incontinence.[15]

Recurrent Urinary Tract Infections (UTIs)

The loss of Lactobacilli and rise in vaginal pH create an environment where uropathogens (like E. coli) flourish. Without the protective acidic environment, pathogen adhesion to uroepithelial cells increases, leading to frequent UTIs. The urethral epithelium, now thinner and less elastic, becomes more vulnerable to colonization and trauma.

Decreased Libido

Declines in both oestrogen and androgens (especially testosterone) lead to reduced genital sensitivity, diminished arousal, and loss of spontaneous sexual desire. Oestrogen also affects dopaminergic signalling in the brain’s reward system, and its absence impairs sexual motivation and satisfaction. Beyond this, the sensation of vaginal pain and dryness alongside emotional distress further reduces libido.[15]

Causes