Revision notes for Edexcel A A Level Biology Lipids, cholesterol and CVD treatments. Open the guide for explanations and worked examples. Written against the Edexcel A A Level Biology (9BN0) specification, so the content matches what's examinable rather than general Biology background.
Lipids, cholesterol and CVD treatments
What you'll learn
- How triglycerides, phospholipids and cholesterol differ in structure and function.
- Why saturated and unsaturated fatty acids affect lipid properties.
- How LDL and HDL transport cholesterol in the blood.
- How atherosclerosis develops and how common CVD treatments reduce risk.
Lipids: the starting point
Definition
Lipid
A lipid is a biological molecule that is mostly insoluble in water but soluble in non-polar solvents. Lipids include triglycerides, phospholipids and cholesterol.
Lipids are important because they store energy, form cell membranes, provide insulation, and act as signalling molecules. In this topic, the key link is between lipids in the blood, artery disease, and treatments for cardiovascular disease.
Definition
Cardiovascular disease
Cardiovascular disease, often shortened to CVD, means disease of the heart or blood vessels. Examples include coronary heart disease, heart attack and stroke.
Triglycerides: energy-storage lipids
A triglyceride is made from one glycerol molecule joined to three fatty acids.
A fatty acid has a long hydrocarbon chain and a carboxyl group. The glycerol and fatty acids join by condensation reactions, where water is released. The bond formed is an ester bond. The reverse reaction is hydrolysis, where water is used to break the ester bond.
Saturated and unsaturated fatty acids
A saturated fatty acid has no carbon-carbon double bonds in its hydrocarbon chain, so it is “saturated” with hydrogen atoms. The chain is usually straight.
An unsaturated fatty acid has at least one carbon-carbon double bond. This often creates a kink in the chain, so unsaturated fatty acids cannot pack together as tightly.
Key Idea
Structure affects properties
Fatty acids with more saturated chains pack closely together, so their lipids tend to have higher melting points. Fatty acids with more unsaturated chains pack less tightly, so their lipids tend to have lower melting points.
Example
Predicting lipid properties from fatty acid structure
A food contains lipid A, which has mostly saturated fatty acids, and lipid B, which has mostly unsaturated fatty acids.
- Compare the chain shapes: lipid A has straighter fatty acid chains, while lipid B has more kinked chains due to carbon-carbon double bonds.
- Compare packing: straighter chains in lipid A can pack more closely together, but kinked chains in lipid B leave gaps between molecules.
- Predict the melting point: lipid A is likely to have the higher melting point and is more likely to be solid at room temperature than lipid B.
Phospholipids: membrane lipids
A phospholipid is similar to a triglyceride, but one fatty acid is replaced by a phosphate-containing group. So it has:
- one glycerol backbone
- two fatty acid tails
- one phosphate-containing head
A phospholipid is amphipathic, meaning it has both a water-attracting part and a water-repelling part. The phosphate head is hydrophilic, meaning it interacts with water. The fatty acid tails are hydrophobic, meaning they do not interact well with water.
This is why phospholipids form a bilayer in cell-surface membranes: hydrophilic heads face the watery surroundings, while hydrophobic tails point inwards away from water.
Tip
Phospholipid orientation
If you are asked to explain a membrane diagram, always link the arrangement to water: hydrophilic heads face water, hydrophobic tails avoid water.
Cholesterol: essential, but linked to CVD risk
Definition
Cholesterol
Cholesterol is a small lipid molecule with a ring-based structure. It is found in cell membranes and is also used to make steroid hormones, vitamin D and bile salts.
Cholesterol is not automatically “bad”. Your body needs it. The problem is that high concentrations of cholesterol carried in the blood, especially in certain transport particles, are linked with a higher risk of atherosclerosis.
Because cholesterol is a lipid, it does not dissolve well in blood plasma. Instead, it is transported in particles called lipoproteins.
Definition
Lipoprotein
A lipoprotein is a particle made of lipid and protein that transports insoluble lipids, such as cholesterol and triglycerides, in the blood.
LDL and HDL
LDL, or low-density lipoprotein, transports cholesterol from the liver to body tissues. High LDL concentration is associated with cholesterol deposition in artery walls.
HDL, or high-density lipoprotein, transports cholesterol from body tissues back to the liver. This is called reverse cholesterol transport and is generally associated with lower CVD risk.
Common Mistake
LDL and HDL are not cholesterol
LDL and HDL are lipoprotein particles that carry cholesterol. They are not different types of cholesterol molecule.
Example
Interpreting an LDL to HDL ratio
A person’s blood results change from LDL = 4.0 mmol dm⁻³ and HDL = 1.0 mmol dm⁻³ to LDL = 2.5 mmol dm⁻³ and HDL = 1.2 mmol dm⁻³ after treatment.
- Calculate the original ratio:
- Calculate the new ratio:
- Compare the two values: the LDL to HDL ratio has fallen, so this would usually suggest a reduced CVD risk, although doctors would consider other risk factors too.
Atherosclerosis: how artery disease develops
Definition
Atherosclerosis
Atherosclerosis is the build-up of fatty material, cholesterol, calcium and fibrous tissue in the wall of an artery, forming an atheromatous plaque.
Arteries are blood vessels that carry blood away from the heart. The coronary arteries supply oxygenated blood to the heart muscle itself.
Atherosclerosis often begins when the endothelium, the thin inner lining of an artery, becomes damaged. Risk factors such as high blood pressure, smoking, and high LDL concentration increase the chance of this damage.
LDL particles can enter the artery wall. White blood cells called macrophages take up lipid and become foam cells. Over time, a plaque develops. This narrows the lumen, which is the central space through which blood flows.
If blood flow through a coronary artery is reduced, heart muscle receives less oxygen for aerobic respiration. This can cause angina, which is chest pain during exertion. If a plaque ruptures, platelets and clotting factors may form a thrombus, which is a blood clot inside a blood vessel. A complete blockage can cause a myocardial infarction, commonly called a heart attack.
Key Idea
Why plaques are dangerous
Plaques reduce blood flow, but the most serious event is often plaque rupture followed by clot formation, which can suddenly block an artery.
Example
Explaining how high LDL can lead to a heart attack
- Link LDL to the artery wall: high LDL concentration increases the chance that cholesterol-rich material enters and remains in damaged artery walls.
- Link deposition to narrowing: lipid accumulation contributes to atheromatous plaque formation, reducing the lumen diameter and restricting blood flow.
- Link plaque rupture to clotting: if the plaque ruptures, platelets stick to the damaged area and a thrombus may form.
- Link blockage to symptoms: if a coronary artery is blocked, heart muscle cells receive too little oxygen, aerobic respiration decreases, and cells may die in a myocardial infarction.
Risk factors: probability, not certainty
A risk factor is anything associated with an increased probability of developing a disease. Risk factors for CVD include:
- high LDL concentration
- low HDL concentration
- high blood pressure, called hypertension
- smoking
- diets high in saturated fats, trans fats or salt
- low physical activity
- obesity
- age, sex and inherited alleles
Some risk factors are modifiable, meaning you can change them, such as smoking or diet. Others are non-modifiable, such as age or inherited genetic risk.
Common Mistake
Risk is not destiny
A risk factor does not guarantee disease, and absence of one risk factor does not guarantee health. CVD risk depends on multiple interacting factors.
Treatments for CVD
CVD treatment aims to reduce risk, improve blood flow, lower blood pressure, or reduce clot formation. In exams, focus on the mechanism: what the treatment changes and why that reduces disease risk.
Lifestyle changes
Lifestyle changes may include:
- reducing saturated and trans fat intake
- replacing some saturated fats with unsaturated fats
- reducing salt intake to lower blood pressure risk
- increasing aerobic exercise
- stopping smoking
- maintaining a healthy body mass
These changes can reduce risk, but they may not be enough for someone with very high inherited risk or established artery disease.
Statins
Definition
Statin
A statin is a cholesterol-lowering drug that inhibits an enzyme involved in cholesterol synthesis in the liver.
Statins reduce cholesterol production in the liver, which tends to reduce blood LDL concentration. This can slow atherosclerosis and reduce the risk of heart attacks and strokes. Statins may also help stabilise existing plaques, making rupture less likely.
Possible limitations include side effects such as muscle pain, liver enzyme changes, and the need to take the drug long-term.
Antihypertensives
Definition
Antihypertensive
An antihypertensive is a drug that lowers high blood pressure.
High blood pressure increases force on artery walls and can damage the endothelium, increasing atherosclerosis risk. Antihypertensives reduce this pressure.
Examples include:
- ACE inhibitors, which reduce vasoconstriction
- beta-blockers, which reduce heart rate and force of contraction
- calcium channel blockers, which relax artery smooth muscle
- diuretics, which increase salt and water loss in urine, reducing blood volume
Anticoagulants and platelet inhibitory drugs
An anticoagulant is a drug that reduces the clotting cascade, so clots are less likely to form or grow. Examples include warfarin and heparin.
A platelet inhibitory drug reduces platelet activation or platelet aggregation. Aspirin is a common example.
These treatments are especially useful when clot formation is a major risk, such as after a heart attack, after some surgery, or in people at high risk of thrombosis.
Common Mistake
Do not mix up clotting drugs
Anticoagulants affect clotting factors in the clotting cascade. Platelet inhibitory drugs affect platelet sticking and aggregation. Both reduce thrombosis risk, but by different mechanisms.
Surgical treatments
In angioplasty, a small balloon is inflated inside a narrowed artery to widen it. A stent, which is a mesh tube, may be inserted to keep the artery open.
In a coronary artery bypass graft, a healthy blood vessel is used to create a new route around a blocked coronary artery. This restores blood flow to heart muscle beyond the blockage.
Example
Choosing a treatment from the problem
A patient has high LDL, high blood pressure, and a narrowed coronary artery causing angina.
- Match high LDL to treatment: a statin would help reduce LDL concentration and slow further plaque development.
- Match high blood pressure to treatment: an antihypertensive would reduce pressure on artery walls and lower further endothelial damage risk.
- Match narrowed artery to treatment: angioplasty with a stent, or bypass surgery in severe cases, could improve blood flow to the heart muscle.
- Consider clot risk: if plaque rupture or a previous clot is a concern, a doctor may prescribe an anticoagulant or platelet inhibitory drug, balancing benefit against bleeding risk.
Exam technique
In the exam
- For lipid structure questions, use precise terms: glycerol, fatty acid, ester bond, saturated, unsaturated, hydrophilic and hydrophobic.
- For CVD mechanism questions, build the chain clearly: endothelial damage → LDL deposition → plaque formation → narrowed lumen → reduced blood flow → clot/blockage.
- For treatment questions, always state both the treatment and its mechanism, not just the drug name.
Self review
Check yourself
- Why does an unsaturated fatty acid usually make a lipid less able to pack tightly?
- How do LDL and HDL differ in the direction they transport cholesterol?
- How does a statin reduce the risk of a myocardial infarction?
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