Why Inflammation Matters for Heart Health

When we talk about heart disease, cholesterol often dominates the conversation. But over the last two decades, research has increasingly pointed to another important piece of the puzzle: chronic inflammation.

Inflammation is not inherently harmful. It is a vital part of the immune response. The issue arises when inflammation becomes long-term, low-grade and persistent. This type of chronic inflammation is now recognised as a key contributor to cardiovascular disease, acting alongside cholesterol, blood pressure, blood sugar balance and lifestyle factors.

In this blog, I will explain what chronic inflammation is, how it affects the heart and blood vessels, and what the current evidence shows us about diet and lifestyle changes that may help reduce cardiovascular risk.

What is chronic inflammation?

Inflammation is the body’s natural defence mechanism. When you cut your finger or catch an infection, inflammatory signals help recruit immune cells and promote healing. This short-term response is known as acute inflammation and is both necessary and protective.

Chronic inflammation is different. It refers to a persistent, low-level inflammatory state that can continue for months or years. It often develops quietly, without obvious symptoms, and is influenced by factors such as excess body fat, insulin resistance, smoking, poor sleep, chronic stress, physical inactivity, ultra-processed diets and some long-term health conditions.

In research settings, chronic inflammation is commonly assessed using blood markers such as C-reactive protein (CRP), particularly high-sensitivity CRP (hs-CRP). Elevated hs-CRP has been consistently associated with increased cardiovascular risk, even when cholesterol levels are not markedly raised.

How inflammation affects blood vessels and the heart

The cardiovascular system is lined with a delicate layer of cells called the endothelium. This lining helps regulate blood flow, blood pressure and clotting. Chronic inflammation disrupts normal endothelial function, making blood vessels less flexible and more prone to damage.

Inflammatory signals also play a direct role in the development of atherosclerosis. Rather than cholesterol simply building up passively in artery walls, we now understand that atherosclerosis is an inflammatory process. Cholesterol-containing particles that enter the artery wall trigger an immune response. Over time, this leads to the formation of plaques that can narrow arteries or become unstable and rupture.

Large genetic, observational and interventional studies over the last five years have strengthened the link between inflammation and cardiovascular events. Importantly, these associations persist even after adjusting for traditional risk factors such as LDL cholesterol.

Links with cholesterol and blood pressure

Unsurprisingly, inflammation and cholesterol are closely intertwined.  Inflammation increases the likelihood that cholesterol-containing particles will penetrate and be retained in the artery wall. Plus, it impairs the body’s ability to clear these particles effectively. This may explain why some people experience cardiovascular events despite having LDL cholesterol levels that are not dramatically elevated.

Blood pressure is also affected by inflammatory processes. Chronic inflammation contributes to endothelial dysfunction and arterial stiffness, both of which increase vascular resistance and raise blood pressure over time. Elevated blood pressure, in turn, further damages the vessel wall, creating a reinforcing cycle.

This is why cardiovascular risk assessment increasingly focuses on the broader picture rather than a single number.

Nutritional strategies supported by research

Nutrition cannot remove cardiovascular risk entirely, and it should never be positioned as a replacement for medical care where that is needed. However, a growing body of peer-reviewed evidence shows that diet plays a meaningful role in modulating inflammatory pathways linked to heart disease.

Dietary patterns matter more than individual foods

Recent systematic reviews and meta-analyses consistently show that overall dietary patterns are more predictive of cardiovascular outcomes than individual nutrients in isolation.

Mediterranean-style dietary patterns are associated with lower inflammatory markers, reduced cardiovascular events and improved endothelial function. These benefits appear to be driven by a combination of factors including higher intakes of vegetables, fruit, legumes, wholegrains, nuts, seeds and olive oil, alongside regular fish intake and lower consumption of ultra-processed foods.

Importantly, these effects are observed even when weight loss is modest or absent, suggesting benefits beyond calorie reduction alone.

The role of fats in inflammation

The type of fat consumed influences inflammatory signalling. Replacing saturated fats with unsaturated fats, particularly monounsaturated and omega-3 fats, has been shown to reduce inflammatory markers and improve lipid profiles in controlled trials. Extra virgin olive oil, oily fish, nuts and seeds are key contributors within dietary patterns associated with lower cardiovascular risk.

Omega-3 fatty acids from oily fish appear to have modest anti-inflammatory effects, partly through the production of specialised pro-resolving mediators that help switch off inflammatory responses once they are no longer needed.

Fibre and the gut–inflammation link

Dietary fibre, particularly soluble and fermentable fibre, plays an important role in inflammation regulation.

Fibre supports gut microbiota diversity and the production of short-chain fatty acids, such as butyrate. These compounds help maintain gut barrier integrity and modulate immune activity. Poor gut barrier function has been linked to increased systemic inflammation and cardiometabolic risk.

Higher fibre intakes are consistently associated with lower CRP levels and reduced cardiovascular events in large prospective studies, with benefits seen across a range of populations.

Ultra-processed foods and inflammatory load

Diets high in ultra-processed foods are associated with higher inflammatory markers and increased cardiovascular risk. These foods often combine refined carbohydrates, industrial fats, additives and excess sodium, while displacing fibre-rich, nutrient-dense foods.

Reducing ultra-processed food intake does not require perfection. Even partial replacement with whole or minimally processed foods has been shown to improve inflammatory profiles in controlled feeding studies.

Alcohol, stress and sleep also matter

Inflammation does not arise from diet alone. Alcohol intake, chronic psychological stress and poor sleep quality all influence inflammatory pathways that directly affect cardiovascular risk.

Alcohol and inflammation

Alcohol has a complex relationship with cardiovascular health, but recent evidence has shifted the conversation away from the idea that alcohol is protective.

Large observational studies and Mendelian randomisation analyses published in the last five years suggest that lower alcohol intake is associated with lower cardiovascular risk, with no clear threshold at which alcohol becomes beneficial. Alcohol consumption is linked to higher blood pressure, raised triglycerides and increased systemic inflammation, even at moderate intakes.

Alcohol can increase gut permeability, sometimes referred to as “leaky gut”. This allows inflammatory compounds to pass into the bloodstream more easily, activating immune responses that contribute to chronic low-grade inflammation. Alcohol metabolism also generates oxidative stress, further amplifying inflammatory signalling.

From a practical perspective, people concerned about heart health may benefit from:

• Having regular alcohol-free days each week
• Reducing portion sizes and frequency rather than aiming for perfection
• Being mindful that alcohol can worsen sleep quality and blood pressure even when intake feels modest

Stress, the nervous system and inflammation

Chronic stress is a powerful but often underestimated driver of inflammation.

Persistent activation of the stress response leads to dysregulation of cortisol and other stress hormones. Over time, this can promote insulin resistance, abdominal fat accumulation and increased production of pro-inflammatory cytokines. Chronic stress is also associated with higher CRP levels and increased cardiovascular event risk, independent of traditional risk factors.

Stress influences cardiovascular health through both biological and behavioural pathways. It can directly affect blood vessels and immune signalling, while also increasing the likelihood of poor sleep, irregular eating patterns, higher alcohol intake and reduced physical activity.

Supportive strategies do not need to be complicated. Evidence suggests that even modest, regular practices can help reduce inflammatory load, including:

• Daily movement, particularly walking, which has been shown to lower inflammatory markers
• Breathing practices or mindfulness-based approaches that support parasympathetic nervous system activity
• Creating predictable meal patterns, which can reduce stress-related blood sugar fluctuations

Importantly, stress reduction is not about removing stress entirely, but about improving the body’s ability to recover after stress.

Sleep and cardiovascular inflammation

Sleep plays a central role in regulating immune and inflammatory processes.

Short sleep duration and poor sleep quality are both associated with higher CRP levels, increased blood pressure, impaired glucose regulation and greater cardiovascular risk. Experimental studies show that even a few nights of restricted sleep can raise inflammatory markers and impair endothelial function.

Sleep disruption also alters appetite-regulating hormones, increasing hunger and cravings for ultra-processed foods, which can further exacerbate inflammation.

From a heart health perspective, supportive sleep strategies include:

• Aiming for consistent sleep and wake times, even at weekends
• Reducing alcohol intake in the evening, as alcohol fragments sleep architecture
• Prioritising exposure to natural daylight earlier in the day to support circadian rhythm
• Ensuring evening meals are balanced and not overly late or heavy, which can disrupt sleep and blood pressure regulation

For individuals experiencing ongoing sleep problems, addressing sleep quality can be just as important as dietary changes when aiming to reduce cardiovascular risk.

Why this matters in practice

When alcohol intake, stress and sleep are overlooked, people can do everything “right” nutritionally and still see limited improvement in inflammatory markers or cardiovascular risk factors.

The most effective approach to heart health recognises that inflammation sits at the intersection of diet, lifestyle and physiology. Supporting recovery, regulation and resilience is often what allows nutritional strategies to work more effectively.

Bringing it together

Chronic inflammation is not a vague or theoretical concept. It is a measurable biological process that plays a central role in cardiovascular disease development.

For individuals concerned about heart health, the most effective approach is rarely about eliminating a single food or chasing one marker. Instead, it involves supporting the body’s inflammatory balance through consistent, sustainable changes that address diet quality, metabolic health, lifestyle stressors and overall cardiovascular risk.

If you would like support translating this evidence into a personalised plan that fits your health history, preferences and test results, why not get in touch?

Confused by Cholesterol? Here’s What Really Matters

If you’ve ever been told your cholesterol is “a bit high”, you are not alone. Many of my clients leave the GP surgery with a print-out of numbers and very little explanation of what they actually mean, or what is worth focusing on first. This can be quite worrying, particularly if you have a family history of heart disease. 

This blog will walk you through the basics in a practical way. We will take a look at what cholesterol actually is, how to interpret the key markers on a standard lipid panel (cholesterol report), and look at why two additional tests, lipoprotein(a) (Lp(a)) and apolipoprotein B (ApoB), can add some important context. And then we’ll look beyond cholesterol, because heart health is about far more than just a single number.

Cholesterol: friend, not foe

Cholesterol is a waxy, fat-like substance that your body uses to build cell membranes, make vitamin D, and produce hormones and bile acids. It is super important for your wellbeing! Your liver makes most of the cholesterol you need, and you also get a small amount from food.

Cholesterol only becomes a problem when cholesterol-containing particles build up in artery walls over time, contributing to atherosclerosis (narrowing and hardening of the arteries). This process is influenced by many things - including blood pressure, blood sugar balance, inflammation, smoking, genetics, menopause, stress, sleep and how much exercise you do.

What is a lipid profile actually measuring?

A standard lipid profile usually includes:

Total cholesterol

This is the overall amount of cholesterol in your blood. It is a broad measure and does not tell you how cholesterol is being carried.

LDL cholesterol (often called “bad cholesterol”)

LDL stands for low-density lipoprotein. LDL particles carry cholesterol from the liver out to tissues. When LDL particles are present in higher numbers, or are circulating for longer, the risk of cholesterol being deposited in artery walls may be increased.

HDL cholesterol (often called “good cholesterol”)

HDL stands for high-density lipoprotein. HDL particles are involved in reverse cholesterol transport, moving cholesterol away from tissues back towards the liver – they are like the rubbish truck coming and taking away the waste. HDL is not a simple “the higher the better” marker, but in general, low HDL can be a sign of metabolic risk.

Triglycerides

Triglycerides are a type of fat used for energy storage. They often rise with insulin resistance (when blood sugar isn’t under control), excess alcohol intake, high intakes of ultra-processed foods, and low activity levels. They can also rise if the blood test is taken soon after eating, which is why your GP may request a fasting test.

Non-HDL cholesterol

This is not always reported, but it is easy to calculate: total cholesterol minus HDL cholesterol. It represents the cholesterol carried by all potentially atherogenic particles (not just LDL), ie the particles that are linked to potential heart disease. In UK practice, non-HDL cholesterol is often used in risk assessment and monitoring. 

Why “LDL cholesterol” is not the whole story

LDL cholesterol tells you how much cholesterol is being carried inside LDL particles. But it does not tell you how many particles are carrying it.

This matters because atherosclerosis is driven by the number of atherogenic particles entering the artery wall. Two people can have the same LDL cholesterol but a very different number of LDL particles. This is one reason why measuring something called ApoB can actually be more helpful in ascertaining your risk of heart disease.

ApoB: the marker many people have never heard of

Apolipoprotein B (ApoB) is a protein found on the surface of atherogenic lipoproteins (including LDL, VLDL and remnants), ie the cholesterol carriers that may lead to heart disease. Each particle carries one ApoB, so ApoB is effectively a count of the number of “risk-carrying” particles.

Recent expert discussions and guideline conversations increasingly highlight ApoB as a strong predictor of cardiovascular risk, particularly when LDL cholesterol alone may underestimate risk (for example, in insulin resistance or higher triglycerides). 

When might ApoB testing be useful?

ApoB is not essential for everyone, but it is worth discussing with your GP (or clinician) if any of these apply:

• A family history of early heart disease
• Type 2 diabetes, prediabetes, PCOS, fatty liver, or metabolic syndrome
• Higher triglycerides
• “Normal” LDL cholesterol but ongoing concern about risk, especially if other markers or symptoms suggest metabolic strain

This is something you can request from your GP, or there are many private labs that offer this measurement. If this is something that you’d like to look at, please do get in touch as this is something that I can potentially help with.

Lp(a): a genetic risk factor worth knowing about

Lipoprotein(a), written as Lp(a), is an LDL-like particle with an additional protein attached (apolipoprotein(a)). Lp(a) is largely genetic and remains fairly stable across your lifetime.

However, elevated Lp(a) is now recognised as an independent risk factor for cardiovascular disease. It can contribute to risk even when other cholesterol markers look “fine”. European guidance and consensus documents support measuring Lp(a), often at least once in adulthood, to identify inherited elevation and refine risk assessment. 

Research shows that high Lp(a) increases heart disease risk by acting like "sticky" LDL cholesterol, promoting plaque buildup (atherosclerosis) and blood clots in arteries, potentially leading to heart attacks and strokes, even with normal cholesterol. This is because its unique protein (Apo(a)) hinders plaque breakdown and encourages clot formation. This genetic factor causes more aggressive plaque, calcification, and inflammation, independently raising cardiovascular danger, especially with other risk factors present. 

Levels are largely determined by genetics (inherited from your parents), explaining why some people develop severe heart disease early without typical risk factors. It's often overlooked in routine checks but is a major contributor to premature cardiovascular disease, according to UK experts like the British Cardiovascular Society. Your level of Lp(a) is believed to be the same from the age of 5 onwards and can’t be massively changed by diet and lifestyle. That’s why it’s worth getting it checked at least once in your lifetime to help determine your risk. 

A note on numbers and units

Lp(a) can be reported in mg/dL or nmol/L. You cannot reliably convert between the two because the particles vary in size between individuals.

A commonly used threshold for increased risk is around 50 mg/dL or 125 nmol/L, but your full clinical picture matters too. 

Can you lower Lp(a) with diet?

Because Lp(a) is genetic, lifestyle changes tend not to shift the number very much. The focus is usually on lowering overall risk by improving other modifiable factors (LDL cholesterol, blood pressure, blood sugar, inflammation, smoking status, fitness, sleep). 

Specialist medications specifically targeting Lp(a) are under investigation, but lifestyle still matters because it reduces the total risk burden. 

How can you test ApoB and Lp(a) in the UK?

Both tests are simple blood tests. They are not always included in routine NHS lipid panels, so you may need to request them.

A practical approach is:

1. Ask your GP whether ApoB and/or Lp(a) are appropriate for you, based on your family history and overall risk.
2. If they are not available locally, a private blood test may be an option, and this is something I can organise for you if you are interested.

If you have a known high Lp(a), it is also worth telling close relatives, as this can run strongly in families and testing can be helpful for them too. 

Cholesterol is one piece of heart health. Blood pressure is another

High blood pressure increases strain on artery walls and is a major driver of cardiovascular risk. Nutrition and lifestyle changes can make a meaningful difference.  A large meta-analysis of randomised trials found the DASH dietary pattern reduces blood pressure in adults with and without hypertension. 

Separately, a dose response meta-analysis of clinical trials shows that reducing sodium intake lowers blood pressure, with stronger effects in those with higher starting blood pressure. 

As we age, keeping an eye on your blood pressure can be very useful. Blood pressure increases with age largely because arteries naturally become stiffer, thicker, and less flexible due to biological aging and wear-and-tear, forcing the heart to work harder to pump blood through them. This stiffening, known as arteriosclerosis, means blood vessels can't expand as well as they once did, leading to higher pressure against artery walls, even with healthy habits. Other contributing factors include lifestyle changes, genetics, and other medical conditions, but the vascular stiffening is the main physiological driver.  Using a home blood pressure kit can be helpful but make sure to test your blood pressure three times in a row – taking an average of the three – and try to take it at the same time of day each time. Take these results to your GP to discuss.

What actually helps in real life? Evidence-based priorities

Cardiovascular disease affects more than 7 million people in the UK alone, causing about a quarter of all deaths and 1 in 4 premature deaths. So, it’s super important to keep an eye on our heart health! There are number of changes that we can make to our diet and lifestyle to help improve our odds. If you are trying to support cholesterol, blood pressure and overall cardiovascular risk, these are the foundations I prioritise with my clients.

• Build meals around a heart-supportive pattern

A Mediterranean-style dietary pattern has consistently been associated with improved cardiovascular outcomes across multiple high-quality reviews. 

In practice, this looks like:
Plenty of vegetables, beans and lentils, fruit, extra virgin olive oil, nuts and seeds, wholegrains where tolerated, and regular fish, alongside much less ultra-processed food.

• Focus on the fats that genuinely move the needle

The strongest nutrition evidence is not about “low fat” diets. It is about the type of fat.

When we talk about fats and heart health, the conversation often becomes overly simplistic. Saturated fat is frequently grouped together as something to avoid, but the evidence does not support treating all saturated fats as equal.

Whole-food fats such as butter, ghee and coconut oil have been part of traditional diets for generations and are chemically stable, particularly at higher cooking temperatures. In contrast, the strongest evidence of harm relates to industrial trans fats and highly processed sources of saturated fat, such as those found in commercially baked goods, pastries, deep-fried foods and processed meats.