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The Silent Shift: How Menopause Changes Cholesterol and Heart Health
- Rachel Hubbard BSc
- Oct 29
- 15 min read
One common question is: why do cholesterol levels rise during menopause even when our diet, exercise, and lifestyle have not changed?
Did you know. that oestrogen plays a key role in how the body manages fats and cholesterol?
Many women teach each week have told me how surprised they were to see their cholesterol levels rise after menopause. For some, these changes have been linked to small strokes (TIAs), raised blood pressure, or an increased risk of heart disease.
As fitness professionals, it is essential that we understand the health issues affecting our class members and clients. This blog (taken from one of my Cafe Rachel talks) aims to explain what cholesterol really is, why it changes during menopause, and how lifestyle choices can make a meaningful difference. It also addresses the confusion, mixed messages, and understandable anxiety that often surround this topic.
To begin with cholesterol is not the enemy. - it is a vital fat-like substance that the body requires. Every cell membrane in your body contains cholesterol. It gives structure to those membranes, helps cells communicate, and is vital for producing hormones like oestrogen, progesterone, and testosterone. It’s also a precursor for vitamin D and bile acids, which help digest fats.
Cholesterol travels in the blood as part of particles called lipoproteins.
We often divide these into two categories:
LDL — low-density lipoprotein
HDL — high-density lipoprotein
LDL is often called the “bad” cholesterol, but this label oversimplifies the science. The problem arises when there are too many small, dense LDL particles circulating for too long. These particles can become oxidised and enter the walls of arteries, triggering inflammation and plaque build-up. HDL, in contrast, helps to remove cholesterol from tissues and transport it back to the liver for clearance.
Why Cholesterol Changes with Age and Menopause
Oestrogen supports healthy lipid metabolism by helping helps the liver clear LDL from the blood and maintain higher levels of HDL. When oestrogen levels fall, that protective system weakens. LDL builds up more easily.
Research shows that LDL cholesterol and triglyceride levels often rise, while the beneficial HDL2 — the larger and more protective HDL particle — declines. This shift is largely driven by falling oestrogen levels. Even when blood test results appear “normal”, the type and quality of lipoproteins often change in ways that increase cardiovascular risk. This “silent shift” — or gradual metabolic change that often begins in the menopausal transition.
A study by Akahoshi (1996) followed Japanese women before, during, and after menopause. They found that total and LDL cholesterol levels rose sharply after menopause, while blood pressure and BMI also increased - it wasn’t simply about lifestyle. It was about our hormones.
Anagnostis (2015) went further, showing that menopause doesn’t just raise cholesterol levels — it changes the subfractions. Before menopause, women typically have more HDL2 — the large, buoyant, protective HDL particles. After menopause, HDL2 declines, and HDL3 — which is smaller and less protective — becomes more common. So even if your total HDL number looks good, the quality of that HDL may have changed.
Menopause then becomes a key window for prevention. It is the time to act — not through fear, but through informed, evidence-based choices that protect long-term heart and metabolic health.
Exercise and Cholesterol
Exercise is one of the most reliable ways to improve your cholesterol profile.
Regular physical activity has one of the most powerful effects on cholesterol balance. Both aerobic exercise and resistance training influence how the body produces, transports, and clears fats from the bloodstream.
Aerobic exercise stimulates enzymes that support the transfer and removal of cholesterol from tissues. This process increases HDL levels and improves how HDL functions, particularly its ability to clear cholesterol from artery walls.
Aerobic Exercise and HDL Function
Aerobic activities such as brisk walking, cycling, or swimming stimulate enzymes involved in lipid transport — particularly lipoprotein lipase (LPL) and lecithin-cholesterol acyltransferase (LCAT).
LPL breaks down triglyceride-rich lipoproteins (like VLDL), making their fatty acids available for energy or storage.
LCAT remodels HDL particles, allowing them to collect excess cholesterol from tissues and return it to the liver for removal — a process known as reverse cholesterol transport.
This leads to an increase in both HDL concentration and HDL functionality. The improvement is seen most consistently in the HDL2 subfraction — the larger, more cardioprotective form.
Evidence supports this:
Kodama et al. (2007, JAMA) conducted a meta-analysis of 25 randomised trials and found that aerobic exercise significantly increased HDL-C by an average of 2.5 mg/dL (0.06 mmol/L), independent of weight loss. The greatest improvements occurred with higher total weekly energy expenditure (>900 kcal/week).
Durstine et al. (2001, Sports Medicine) reported that regular endurance training enhances HDL particle size and improves its cholesterol efflux capacity — the ability to clear cholesterol from arterial walls.
In short, aerobic training doesn’t just raise HDL levels; it improves how HDL works.
Resistance exercise also plays an important role.
Building and maintaining muscle improves insulin sensitivity, which helps the liver regulate fat metabolism more efficiently.
Resistance exercise contributes to lipid health through several pathways:
It increases muscle mass, which raises resting metabolic rate and improves insulin sensitivity.
Improved insulin sensitivity reduces the liver’s production of triglyceride-rich lipoproteins (VLDL).
Muscle contraction itself stimulates AMP-activated protein kinase (AMPK), enhancing fat oxidation and triglyceride clearance.
Scientific evidence supports this mechanism:
Tambalis et al. (2009, Lipids in Health and Disease) found that a 12-week resistance training programme reduced fasting triglycerides by up to 15% and improved HDL function, particularly in adults with metabolic syndrome.
Kelley and Kelley (2009, Atherosclerosis) conducted a meta-analysis of resistance training and showed that it consistently lowered triglycerides, especially when sessions were performed 2–3 times per week, targeting major muscle groups.
Research shows that combining aerobic and strength-based exercise produces the greatest benefit, reducing triglycerides, improving HDL function, and supporting stable blood glucose.
Combining aerobic and resistance exercise produces synergistic effects — aerobic work improves lipoprotein metabolism, while resistance training improves insulin handling and body composition. Together, they create a metabolic environment that supports lower triglycerides, higher HDL, and more stable blood glucose levels.
The evidence suggests:
150 minutes of moderate-intensity aerobic activity per week (or 75 minutes vigorous) is the threshold for significant improvement.
Adding 2 or more resistance sessions per week further enhances triglyceride control and HDL quality.
The benefits are dose-dependent — meaning the more consistent you are, the greater the effect. But even small increases in activity yield measurable lipid improvements.
Nutrition and Lipid Balance
Diet is another crucial factor. A way of eating that supports heart and metabolic health focuses on balance, fibre, and healthy fats, rather than strict restriction.
Dietary composition directly affects how cholesterol and lipoproteins are produced, transported, and cleared from the bloodstream.
Dietary Fibre and LDL Reduction
Soluble fibre — found in oats, beans, lentils, fruit, and vegetables — binds to bile acids in the gut.
Since bile acids are made from cholesterol, the body must draw on its internal cholesterol stores to replace them.
This process lowers circulating LDL cholesterol.
Soluble fibre also slows carbohydrate absorption, improving insulin sensitivity and reducing liver fat accumulation — both of which support better lipid metabolism.
Scientific evidence:
Brown et al. (1999, American Journal of Clinical Nutrition) conducted a meta-analysis of 67 controlled trials and found that each additional 10 g of soluble fibre per day lowered LDL cholesterol by approximately 5%.
Jenkins et al. (2011, Archives of Internal Medicine) confirmed that diets high in viscous fibre reduce LDL and non-HDL cholesterol without adverse effects on HDL or triglycerides.
Beyond the numbers, fibre-rich diets also reduce oxidative stress and inflammation, key drivers of atherosclerosis.
Omega-3 Fatty Acids and Triglyceride Regulation
Omega-3 fats — particularly EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) found in oily fish such as salmon, sardines, and mackerel — reduce triglycerides by limiting the liver’s production of very-low-density lipoproteins (VLDL)
This reduces both plasma triglycerides and the number of ApoB*-containing particles.
Scientific evidence:
Bays et al. (2008, American Journal of Cardiology) and Mozaffarian & Wu (2011, Journal of the American College of Cardiology) show that omega-3 supplementation consistently lowers triglycerides by 20–30% and can modestly reduce ApoB by decreasing VLDL particle production.
The REDUCE-IT trial (Bhatt et al., 2019, NEJM) demonstrated that high-dose EPA (4 g/day) reduced cardiovascular events by 25% in high-risk individuals — even when LDL levels were already well-controlled.
These effects stem from improved lipid clearance and reduced lipoprotein oxidation, both of which stabilise the arterial environment.
Replacing saturated fats, such as butter and processed meats, with unsaturated fats from olive oil, avocados, nuts, and seeds also supports healthy lipid metabolism. These fats encourage the liver to clear LDL particles more efficiently, improving overall cholesterol balance.
Together, these nutritional habits lower LDL and ApoB, reduce inflammation, and improve the resilience of blood vessels. Two portions of oily fish per week, plenty of plant fibre, and the regular use of unsaturated oils in cooking can all make a measurable difference within a few months.
Scientific evidence:
Mensink et al. (2003, American Journal of Clinical Nutrition) reviewed over 60 dietary trials and found that replacing 1% of total energy intake from saturated fat with unsaturated fat lowers LDL cholesterol by about 0.05 mmol/L.
Jenkins et al. (2005, AJCN) showed that a portfolio diet — rich in unsaturated fats, fibre, plant sterols, and soy — reduced LDL cholesterol by 28%, comparable to low-dose statin therapy.
Clifton et al. (2004, European Journal of Clinical Nutrition) demonstrated that monounsaturated fat from olive oil reduced ApoB concentrations more effectively than carbohydrate substitution.
These findings support the Mediterranean dietary pattern, which consistently lowers cardiovascular risk through improved lipid ratios and reduced systemic inflammation.
For most adults, the following daily habits achieve meaningful changes within 8–12 weeks:
At least 25–30 g of fibre per day, including 10 g from soluble sources (oats, beans, fruit, vegetables).
Two portions of oily fish per week, or plant-based omega-3s (flaxseed, chia, walnuts) if vegetarian.
Replacing butter, lard, or coconut oil with olive or rapeseed oil in cooking.
Including a handful of nuts or seeds daily for sustained unsaturated fat intake.
When sustained, these changes can lower LDL cholesterol by 10–20% and ApoB by 15–25%, depending on baseline levels and genetic factors.Sleep, Stress, and Hormonal Regulation
Sleep, Stress, and Hormonal Regulation
Sleep and stress regulation are often overlooked, yet both have a major impact on cholesterol metabolism.
When we are under chronic stress or not sleeping well, cortisol levels rise. This leads to higher blood sugar, elevated triglycerides, and a reduction in HDL. Over time, these changes contribute to the production of smaller, denser LDL particles, which are more likely to cause arterial damage.
Sleep as a Metabolic Regulator
Sleep is not simply rest; it is an active biological process that recalibrates hormones, metabolism, and cellular repair.
During deep sleep, growth hormone and melatonin rise while cortisol falls. This supports lipid processing in the liver and enhances insulin sensitivity. In contrast, when sleep is shortened or fragmented, the opposite happens — cortisol, adrenaline, and inflammatory cytokines increase, and insulin sensitivity drops.
Scientific evidence:
Spiegel et al. (1999, The Lancet) showed that restricting sleep to 4 hours per night for six nights caused a 40% reduction in glucose tolerance — mimicking early diabetes.
St-Onge et al. (2016, Journal of the American Heart Association) reviewed human trials and found that poor sleep quality or duration consistently raised LDL cholesterol and triglycerides, while lowering HDL, even when diet and weight were controlled.
Chasens & Luyster (2016, Sleep Health) reported that restoring regular sleep patterns for just two weeks improved fasting lipid profiles and insulin function in middle-aged adults.
Mechanistically, poor sleep disrupts the hypothalamic–pituitary–adrenal (HPA) axis — the body’s master stress and hormone control system. When this axis is overstimulated, cortisol remains elevated during the night, interfering with lipid clearance by the liver and promoting fat storage around the abdomen.
So, quality sleep is not simply recovery — it’s metabolic alignment. It ensures that hormones regulating appetite (like leptin and ghrelin), stress (cortisol), and energy storage (insulin) stay in rhythm.
Scientific evidence:
Rosmond & Björntorp (2000, Psychoneuroendocrinology) showed that individuals with chronic stress had higher cortisol levels, greater abdominal fat, and elevated triglycerides — independent of calorie intake.
Vitaliano et al. (2002, Psychosomatic Medicine) found that long-term caregiving stress raised both LDL cholesterol and inflammatory markers such as IL-6 and CRP.
Black et al. (2018, Psychosomatic Medicine) demonstrated that mindfulness-based stress reduction lowered cortisol, improved sleep, and led to favourable changes in HDL and triglycerides.
Daily practices such as deliberate breathwork, mindful walking, or even short visual focus exercises — help activate the parasympathetic nervous system. This branch of the nervous system slows the heart rate, lowers blood pressure, and promotes recovery — restoring the body to metabolic equilibrium. When parasympathetic tone is strong, cortisol rhythms normalise: high in the morning to promote alertness, and low in the evening to allow rest. This rhythm is essential for lipid regulation, inflammation control, and cardiovascular health.
To support hormonal and nervous-system balance:
Aim for 7–8 hours of quality sleep each night, ideally within a consistent schedule.
Create a calm, dark, and cool sleep environment.
Reduce stimulants after mid-afternoon, and limit alcohol in the evening.
Practise daily stress regulation — this could be a short walk, a breathing session, or a brief mindfulness check-in.
Prioritise morning daylight exposure to stabilise circadian rhythm and cortisol release.
These small daily behaviours recalibrate the body’s hormonal rhythm, allowing cortisol, insulin, and melatonin to operate in sync. Over time, this lowers triglycerides, improves HDL function, and reduces vascular inflammation.
Liver Health and Alcohol
The liver plays a central role in cholesterol control. It produces, processes, and removes lipoproteins from the blood. When the liver is healthy, this system works efficiently. When it is under strain — from excess alcohol, fatty infiltration, or inflammation — cholesterol and triglycerides tend to rise.
The liver produces about 80% of the cholesterol circulating in the body. It packages cholesterol and triglycerides into lipoproteins (VLDL and LDL) for transport to other tissues. It also removes excess cholesterol by converting it into bile acids that are excreted through the digestive tract.
When liver function is optimal, there is a steady cycle of production and clearance. But when it is impaired — through fatty infiltration, alcohol excess, insulin resistance, or inflammation — this balance breaks down. The liver begins to overproduce VLDL and under-clear LDL, leading to higher ApoB and triglyceride levels.
Non-Alcoholic Fatty Liver Disease (NAFLD) and Lipid Dysfunction
NAFLD is now the most common liver disorder in Western populations and is linked with menopausal metabolic changes - and it is characterised by the accumulation of fat within liver cells, unrelated to alcohol intake.
Scientific evidence:
Chalasani et al. (2018, Hepatology) identified NAFLD as a major contributor to dyslipidaemia, independent of obesity or diabetes.
Jung et al. (2014, Journal of Hepatology) found that individuals with NAFLD had significantly higher triglycerides and ApoB concentrations than those with healthy livers, even when matched for age and BMI.
Yki-Järvinen (2014, Diabetologia) described NAFLD as the “hepatic manifestation of metabolic syndrome”, emphasising its central role in cholesterol and glucose imbalance.
In short: when the liver becomes fatty, it cannot clear LDL efficiently, nor regulate cholesterol synthesis properly. The result is a cascade of elevated lipids, inflammation, and insulin resistance.
Liver health is highly responsive to lifestyle choices. Improvements can occur within weeks through:
Reducing alcohol intake to within or below recommended limits, with several alcohol-free days each week.
Maintaining a healthy body weight and waist circumference to reduce fat deposition in the liver.
Engaging in regular aerobic and resistance exercise, which enhances hepatic fat oxidation.
Eating a diet rich in unsaturated fats, fibre, and antioxidants, while limiting added sugars and processed foods — especially fructose-containing drinks, which strongly contribute to liver fat.
Scientific evidence:
Keating et al. (2015, Journal of Hepatology) showed that a 12-week exercise programme reduced liver fat content by 20–30%, independent of weight loss.
Brouwers et al. (2020, Diabetologia) reported that replacing saturated fats with monounsaturated and polyunsaturated fats reduced liver fat and improved VLDL secretion rates.
Dongiovanni et al. (2016, Trends in Molecular Medicine) found that dietary antioxidants — particularly from vegetables, coffee, and polyphenol-rich foods — reduce hepatic inflammation and fibrosis progression.
Fortunately, the liver responds quickly to positive changes. Reducing alcohol intake, increasing daily movement, eating a diet rich in fibre and unsaturated fats, and maintaining a healthy weight can improve liver function within weeks. A healthy liver is one of the most powerful tools for maintaining good cholesterol balance.
Putting It All Together
Cholesterol management is not about restriction or short-term fixes. It is about creating an internal environment where the body can regulate its lipids naturally.
Regular exercise, balanced nutrition, restorative sleep, effective stress management, and good liver health all work together to reduce ApoB, improve HDL function, and protect the heart.
For some, lifestyle changes alone may not be enough, and evidence-based medication* can play a crucial role. What matters most is combining scientific understanding with practical action — improving health through informed, sustainable choices.
Cholesterol is not something to fear. It is a system to understand and manage, especially through midlife and menopause, when small adjustments can protect both heart and metabolic health for years to come.
oh....and all of this applies to men too as they are often at risk!
Cafe Rachel
This is the type of topic we explore in Café Rachel — my online programme designed to help you improve your health and fitness through understanding and action. The Café Conversations are at the heart of the programme. They provide clear, evidence-based information to help you understand why we exercise and how it supports your overall health and wellbeing.
Each session is delivered live in a private Facebook group, with open access to all recordings on my YouTube channel so you can watch whenever it suits you — with no time limits. Click the link below to find out more about upcoming sessions and how to join.
Footnote:
A more precise way to assess cardiovascular risk is by measuring Apolipoprotein B (ApoB). Each potentially harmful LDL or related particle carries one ApoB molecule, so measuring ApoB gives a clearer picture of how many of these particles are in circulation. Higher ApoB levels indicate more cholesterol-carrying particles moving through the bloodstream, which increases the likelihood of arterial damage.
In the UK, ApoB testing is not yet part of routine NHS cholesterol screening, but it can be arranged privately or through specialist referral. For reference, an ApoB level below 0.8 g/L is generally considered low risk, while a level below 0.6 g/L may be ideal for individuals with existing cardiovascular concerns or additional risk factors, such as menopause-related lipid changes.
What About Statins?
Statins are among the most commonly prescribed medications for lowering cholesterol in the UK. They work by reducing the liver’s production of cholesterol and increasing its ability to clear LDL from the bloodstream. Research shows they can significantly reduce the risk of heart attack and stroke, especially in people with known cardiovascular disease or very high LDL levels.
However, statins are not without drawbacks. Some people experience side effects such as muscle aches, fatigue, or digestive discomfort, although severe reactions are rare. For women in midlife, statins can sometimes affect energy levels, recovery from exercise, or muscle function — factors worth discussing with a GP or specialist if they occur. It is also important to remember that statins mainly target LDL levels and do not directly address the broader metabolic changes seen during menopause, such as shifts in triglycerides, HDL quality, or insulin sensitivity.
For many, lifestyle interventions remain the foundation — regular movement, strength training, balanced nutrition, and stress management all support heart and metabolic health. Statins, when used appropriately, can then complement these strategies rather than replace them.
📚 Reference List
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Anagnostis, P., Stevenson, J.C., Crook, D., Johnston, D.G. and Godsland, I.F., 2015. Effects of menopause, gender and age on lipids and high-density lipoprotein cholesterol subfractions. Maturitas, 81(1), pp.62–68.https://doi.org/10.1016/j.maturitas.2015.02.262
Attia, P., 2023. Outlive: The Science and Art of Longevity. London: Vermilion.
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