Cardiovascular diseases (CVDs) are a group of disorders of the heart and blood vessels many of which are related to a process called atherosclerosis.
Atherosclerosis is a condition that develops when plaque builds up in the walls of the arteries. This buildup narrows the arteries, making it harder for blood to flow through (higher pressure)
If a plaque ruptures a blood clot can form, blocking the flow of blood and causing a heart attack or stroke.
High blood pressure and rigid arterial walls can also cause vessels in the brain to burst (hemorrhagic stroke,) lack of blood to the heart muscle itself is called Coronary heart disease and when enough blood can’t reach the lower limbs this is called peripheral arterial disease (PAD).
KEY STATISTICS
Cardiovascular diseases (CVDs) are the leading cause of death globally.
An estimated 17.9 million people died from CVDs in 2019, representing 32% of all global deaths. Of these deaths, 85% were due to heart attack and stroke.
Over three quarters of CVD deaths take place in low- and middle-income countries.
Most cardiovascular diseases can be prevented by addressing behavioural risk factors.
It is important to detect cardiovascular disease as early as possible so that management with counselling and medicines can begin.
Source: WHO
RISK FACTORS FOR CVD
Modifiable:
Diet
physical inactivity
tobacco use
harmful use of alcohol
Socioeconomic status*
Stress
High BMI
Non modifiable:
Genetics - If your dad/ brother developed heart disease before they were 55, or your mum/ sister before they were 65, then you’re at higher risk
Sex - men are more likely to get CVD earlier than women
Age - the older you are, the more likely you are to get CVD.
ethnic background - E.g. South Asian people have a higher risk of developing Type 2 diabetes, which is a risk factor for atherosclerosis.
*partially
LDL-C AS A CAUSAL PATHWAY FOR CVD
LDL-C (low density lipoprotein cholesterol) has a clearly identified Causal role in the development of atherosclerosis.
Small, dense lipoproteins can pass into and out of the arterial wall, and in doing so they react and oxidise initiating pathogenesis.
We focus mainly on LDL-C as it constitutes ~90% of ApoB (apolipoprotein b) containing atherogenic lipoproteins in body circulation and is the principle carrier of cholesterol.
(Boren et al. European Heart Journal 2020)
What is a lipoprotein?
A molecule that is a combination of lipid and protein. Lipids do not travel in the blood by themselves, but they are carried through the bloodstream as lipoproteins.
Size matters
The size and density of lipoproteins is critical to understanding the capacity of these compounds to enter into the artery wall.
Lipoproteins with a diameter of >75nm are too large to penetrate the artery, so chylomicrons and large VLDL particles are not atherogenic.
The smaller particles: VLDL, IDL, LDL, and Lp(a), are all pro-atherogenic lipoproteins.
Due to its small size and density, HDL is also capable of penetrating the arteries, however, it also has the capacity to exit via the adventitia of the artery (see image) and so HDL does not build up in the artery.
small VLDL, IDL, LDL, and Lp(a) are all small enough to penetrate into the arteries, but large enough that they cannot exit via the adventitia. The only way for these to be removed is via the same route of entry, however this reverse transport goes against the blood pressure gradient, and consequently these lipoproteins and their cholesterol contents become trapped within the arterial wall, initiating the processes of atherosclerosis.
Source: Sigma nutrition
Source: Sigma Nutrition
PART 2:
Reducing my risk through diet
CVD risk increases linearly with increasing levels of LDL-C and non-HDL-C
When measured, high LDL-C at one point in time infers greater risk than lower LDL-C but we also need to consider that longer exposures to high levels overtime drive risk up.
as such we must aim to reduce our cumulative exposure to LDL-C over the lifespan, warranting early action and sustained behavioural change for modifiable risk factors.
Clinical benefit of lowering LDL-C is determined by both the absolute reduction in LDL-C and duration of exposure to lower LDL-C.
Lower LDL-C is better
Lifelong plasma level of <2.1mmol/L LDL-C protects against atherosclerotic plaque development.
ASTEROID trial reduced LDL-C from 3.3mmol/L (130mg/dL) to achieved levels of LDL-C 1.5mmol/L (60mg/dL) and achieved regression of atheroma (statin therapy).
Lifestyle intervention
Saturated fat
The is strong evidence for a saturated fat cut off at 10% of total calorie intake for reducing risk of CVD events.
The current recommendation is to consume <10% kcal from SFA.
For a 2000 calorie diet this looks like 22g or less saturated fat per day, for a 2500kcal diet: 27g or less.
Nutrient replacement
replacing saturated fat (SFA) with other things can reduce risk. Replacement nutrients that have shown reductions in risk are wholegrain carbohydrate and unsaturated fats, with polyunsaturated (PUFA) sources in particular offering the greatest risk reduction.
Replacing SFA with refined carbohydrate or trans fats (TFA) increased risk.
Replacing 5% of energy intake from saturated with PUFA confers a 10% reduction in heart disease risk.
There is also benefit to replacing refined carbohydrate with wholegrains and unsaturated fats.
In order of greatest risk reduction when replacing SFA: PUFA (from plant and marine sources, MUFA (from plant sources), wholegrain carbohydrate.
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