This week we've invited the wonderful Lauren Dyer - clinical functional nutrition practitioner - to write for Medicine Central.

Her subject is one you'll recognise in clinical practice: a perimenopausal or menopausal patient, routine bloods, and an LDL that's crept up.

Lauren masterfully explains why LDL in this context rarely tells the full story on its own, and that hormonal changes, sleep disruption, stress physiology, and even dietary patterns can all shift the numbers in ways that don't necessarily signal increased CV risk.

It’s well worth the read!

PLUS…

→ NICE backs first non-hormonal drug for hot flushes.

→ Early menopause linked to 41% higher heart risk.

→ Long-term HRT use shows no increase in mortality.

Written by Lauren Wallis Dyer - BSc (Hons) Nutritional Biochemistry | MSc Medical Molecular Biology DipCLN | FNTP | IFM Certified Health Coach Clinical Functional Nutrition Practitioner Lauren Wallis Nutrition | Bedfordshire | UK & International Clients

LDL cholesterol often rises during the menopausal transition. This is well described in the literature and occurs independently of age. It reflects changes in oestrogen signalling.

Oestrogen has a direct effect on lipid metabolism. It influences LDL receptor activity in the liver, cholesterol clearance and bile production. As oestrogen levels fall, LDL receptor activity reduces and circulating LDL increases. This is a predictable physiological response and is seen consistently across different populations.

When HRT is started, lipid levels can become unstable in the early phase. The liver is adjusting to a new hormonal signal and that process is not immediate. It is not unusual to see LDL rise or fluctuate during the first few months.

The route of administration also plays a role. Oral oestrogen passes through the liver and can alter lipid handling differently to transdermal preparations. Transdermal oestrogen tends to produce a more stable response. The addition of progesterone or testosterone can also influence lipid levels.

LDL should not be interpreted in isolation. In clinical practice, many women in this phase present with low triglycerides and high HDL. This pattern is commonly seen alongside preserved insulin sensitivity. LDL elevation can sit within this profile without other metabolic markers being raised.

Sleep and stress are highly relevant. Many menopausal women report disrupted sleep, early waking and vasomotor symptoms. Cortisol influences hepatic cholesterol production and can raise LDL. Lipid changes are often seen alongside poor sleep and increased sympathetic activation.

Physical activity also needs to be considered carefully. Reduced activity can affect lipid handling. At the same time, a number of women experience impaired recovery and reduced tolerance to exercise during this phase. Higher intensity exercise can aggravate symptoms and may not improve lipid markers.

Interpretation of LDL should sit alongside other markers, including HbA1c, CRP and fasting glucose, as well as an understanding of the individual’s symptoms and lifestyle. Where available, ApoB or particle number can provide additional insight into cardiovascular risk.

From a nutritional perspective, changes in LDL at this stage are not usually driven by dietary fat intake alone. Blanket recommendations to reduce fat or increase fibre do not reflect the underlying physiology. A more useful approach is to support overall metabolic stability, including adequate protein intake, regular meals and avoidance of significant under-fuelling, particularly in physically active individuals.

Very low carbohydrate diets require a shift in fuel utilisation away from glucose towards fat. This is accompanied by lower insulin levels, increased lipolysis and greater reliance on circulating lipoproteins to transport fatty acids. In this state, LDL can rise as part of normal lipid trafficking rather than as a marker of impaired metabolism. This is more commonly seen in individuals with low triglycerides and high HDL, where insulin sensitivity is preserved.

In menopausal women, this effect can be more pronounced. Reduced oestrogen influences hepatic LDL receptor activity and cholesterol clearance. When combined with increased lipid mobilisation from very low carbohydrate intake, circulating LDL levels may increase further. This can occur in the absence of other adverse metabolic markers.

Very low carbohydrate intake can also influence cortisol and sleep in some individuals. Lower glycogen availability and increased reliance on gluconeogenesis can contribute to early waking and reduced exercise recovery. Where sleep is already disrupted, this can reinforce the physiological drivers associated with changes in lipid handling.

In practice, dietary patterns that support stable energy availability, recovery and hormonal regulation tend to be more relevant than targeting LDL directly.

LDL elevation during menopause and early HRT is common. These changes are frequently observed alongside hormonal transition, altered sleep and changes in stress physiology. Interpretation requires consideration of the wider clinical picture.

Read more of Lauren’s work

NICE has recommended fezolinetant (Veoza) for NHS prescribing. It's the first NK3 receptor antagonist approved for moderate to severe vasomotor symptoms in women who can't take HRT.

Around 500,000 women in England are estimated to be eligible. It works by blocking neurokinin B signalling in the hypothalamus, targeting the mechanism behind hot flushes directly. No hormones involved.

The catch? Liver function tests are needed before starting, monthly for three months, then periodically. HRT stays first line. But for women who can't use it, this is the first real alternative.

A JAMA Cardiology study pooling data from over 10,000 women found that natural menopause before 40 was associated with 41% higher lifetime risk of coronary heart disease.

Premature menopause was three times more common in Black women (15.5% vs 4.8%). A UCL study from the same month found Black women in the UK face significant barriers to menopause care, including misdiagnosis and reluctance to prescribe HRT.

NICE NG23 already says: offer HRT for premature ovarian insufficiency, even without symptoms. This data backs that up.

A Danish cohort study in the BMJ followed 876,805 women over 14 years. Among the 104,086 who used HRT, there was no difference in all-cause mortality. Even after ten or more years of use. No signal for heart disease, stroke, or cancer deaths either.

One standout finding: women who had bilateral oophorectomy between 45 and 54 for non-cancerous reasons had 27 to 34% lower mortality with HRT. That's mortality-level evidence, not just symptom relief.

The updated BMS Practice Standards say the same thing: no arbitrary limits on duration, dose, or age.