Topic 1 - Molecules, Transport and Health

Ions and other polar solutes are attracted to these partial charges. Water molecules surround them, separate them and keep them dispersed in solution, so the dissolved particles can move with the water.

Blood plasma transports dissolved glucose, amino acids, mineral ions, urea and carbon dioxide-containing species. Plant transport fluids likewise carry dissolved mineral ions and assimilates between organs.

A polysaccharide contains many monosaccharide units. Starch is the plant energy store: amylose is an unbranched, coiled chain and amylopectin is branched. Glycogen is the animal energy store and is more highly branched than amylopectin.

Monosaccharides and many disaccharides are small and soluble, making them suitable for transport and immediate respiration. Starch and glycogen are compact and insoluble, so storing many glucose units has little osmotic effect. Branching supplies many ends where enzymes can release glucose.

1. Prepare a dilution series of known reducing-sugar or starch concentrations.
2. Use equal sample and reagent volumes. Heat every Benedict's tube in the same water bath for the same time; do not heat iodine tests.
3. Test the unknown under identical conditions.
4. Match its final colour to the closest standard and report the corresponding concentration or range.
5. Repeat and include a zero-concentration control.

The standards turn a subjective colour observation into an ordered concentration estimate. Keeping volumes, temperature, heating time and viewing conditions constant makes colour the only intended response to concentration.

Glucose + glucose forms maltose; glucose + fructose forms sucrose; glucose + galactose forms lactose. Repeated condensation of glucose units forms glycogen, amylose or amylopectin.

During digestion, enzyme-catalysed hydrolysis converts disaccharides and polysaccharides into soluble monosaccharides that can be absorbed. In cells, condensation assembles glucose into compact storage polysaccharides.

A triglyceride forms when glycerol reacts with three fatty acids in condensation reactions, creating three ester bonds and releasing three water molecules. Its hydrocarbon tails store substantial chemical energy.

A saturated fatty acid has no carbon–carbon double bond; an unsaturated fatty acid has one or more. Double bonds introduce bends, so unsaturated tails usually pack less tightly and have lower melting points.

Long reduced hydrocarbon chains contain many bonds that can be oxidised, giving lipids a high energy value per gram. Their insolubility also makes them compact stores with little osmotic effect.

A fat rich in saturated tails tends to be solid at room temperature, whereas an oil rich in cis-unsaturated tails is more likely to remain liquid. The physical state reflects tail packing, not simply the word ‘lipid’.

Diffusion is effective over short distances but becomes too slow when an organism is large or metabolically active. A circulatory system moves substances in bulk between exchange surfaces and tissues.

A pump maintains a pressure gradient and vessels provide a controlled route. The heart sends deoxygenated blood to the lungs and oxygenated blood to body tissues in a double circulation, keeping exchange gradients steep.

An active muscle has a high oxygen demand. Blood flow delivers oxygenated blood close to the cells and removes carbon dioxide, while diffusion completes the final short distance across capillary walls and tissue fluid.

Arteries have thick walls containing elastic tissue, smooth muscle and collagen: elastic recoil maintains pressure, muscle changes lumen diameter, and collagen resists overexpansion. Veins have thinner walls, wide lumens and valves; skeletal-muscle contractions squeeze them and valves prevent backflow. Capillary walls are one endothelial cell thick, giving a short diffusion path.

Many capillaries in parallel provide a very large total cross-sectional area, so blood velocity falls through a capillary bed. Their narrow lumen keeps red blood cells close to the wall, while extensive branching supplies a large exchange area.

1. During atrial systole, the atria contract and complete ventricular filling through open atrioventricular valves.
2. During ventricular systole, ventricular pressure closes the atrioventricular valves, then opens the semilunar valves so blood enters the pulmonary artery and aorta.
3. During diastole, the heart relaxes; semilunar valves close and atrioventricular valves reopen as the chambers refill.

The right side pumps through the pulmonary circuit; the thicker left ventricle generates the higher pressure needed for the systemic circuit. The septum prevents mixing, and coronary vessels supply the cardiac muscle.

At the lungs, high oxygen partial pressure favours oxyhaemoglobin formation. At respiring tissues, lower oxygen partial pressure favours unloading. Most carbon dioxide is carried as hydrogencarbonate ions; some binds to haemoglobin, and haemoglobin also buffers hydrogen ions.

Extra carbon dioxide in active tissue lowers blood pH and reduces haemoglobin's oxygen affinity. This Bohr effect shifts the curve to the right, so more oxygen is released at the same oxygen partial pressure.

Fetal haemoglobin has a higher oxygen affinity than adult haemoglobin, so at the placenta fetal blood can load oxygen released from maternal haemoglobin.

Atherosclerosis begins when the arterial endothelium is damaged. An inflammatory response attracts white blood cells, cholesterol-rich deposits and smooth-muscle changes, forming an atheroma in the artery wall.

Endothelial damage → inflammation → low-density lipoprotein enters the wall → macrophages form foam cells → plaque grows and narrows the lumen. A rough plaque can also encourage clot formation.

If a coronary artery lumen narrows, resistance to blood flow rises and cardiac muscle receives less oxygen. A plaque that ruptures may trigger a thrombus that blocks flow suddenly.

The disease links risk factors to a mechanism: high blood pressure can damage the endothelium, while smoking, diabetes and high LDL increase the likelihood of plaque development.

Damage to a blood vessel releases thromboplastin. In the presence of calcium ions, it helps convert soluble prothrombin into thrombin; thrombin converts soluble fibrinogen into insoluble fibrin.

Thrombin activates more clotting reactions and fibrin fibres form a mesh across the wound. Platelets become trapped, the mesh contracts and a clot reduces blood loss while tissue repair begins.

A cut exposes tissue and activates the cascade locally. The resulting fibrin network stays near the damaged vessel rather than turning all circulating fibrinogen into a body-wide clot.

The cascade amplifies a small trigger, but inhibitors and the intact endothelium limit clotting to the injury. If a clot forms inside an artery it can obstruct blood flow and cause thrombosis.

Smoking damages endothelium, raises blood pressure and increases clot risk. High blood pressure increases mechanical damage to artery linings. Inactivity and an energy-rich diet can promote obesity, hypertension and an adverse blood-lipid profile. Inherited alleles can alter lipid handling or blood pressure.

Age, biological sex and inherited susceptibility are non-modifiable, whereas smoking, activity and diet are modifiable. A non-modifiable factor can identify higher baseline risk; a modifiable factor offers a route to reduce risk.

Antioxidants can react with reactive molecules and may reduce oxidative damage. This gives a plausible link between diet and cardiovascular disease, but plausibility is not the same as demonstrated protection.

Oxidative damage can affect lipids and the arterial endothelium, yet CVD is also shaped by blood pressure, LDL, smoking, diabetes and activity. A single nutrient cannot be treated as an isolated cause.

A study may find that people who eat more fruit have lower CVD risk. The result could reflect antioxidants, fibre, lower saturated-fat intake or other lifestyle differences, so the design must address confounding.

Prefer evidence from controlled interventions or well-adjusted longitudinal studies over a single correlation. Report the strength and limits of the evidence before recommending a behaviour.

1. Prepare or obtain a vitamin C solution of known concentration.
2. Place a fixed volume and concentration of DCPIP in a tube.
3. Add the standard dropwise while mixing until the blue colour just disappears; record the volume and repeat.
4. Prepare each food or drink sample by the same extraction and dilution method.
5. Titrate each sample to the same endpoint, repeat and calculate a mean.

For a fixed DCPIP amount, the vitamin C amount reaching the endpoint is constant. Compare the mean standard and sample volumes, including every dilution factor, to calculate vitamin C concentration; report appropriate units such as $\mathrm{mg\,cm^{-3}}$.

Keep DCPIP volume/concentration, extraction mass, dilution, temperature and endpoint judgement constant. Minimise heating and air exposure because vitamin C oxidises.

Describe what the data show before explaining it: identify the population, units, trend and comparison. A correlation means two variables change together; it does not by itself show that one causes the disease.

Confounders such as age, income, activity or access to healthcare can influence both the risk factor and the outcome. Relative risk, absolute risk and sample size answer different questions.

If disease prevalence rises with smoking exposure, state the size and direction of the association, then ask whether dose, timing, biological mechanism and alternative explanations support a causal interpretation.

Use confidence intervals or statistical tests where supplied, avoid extrapolating beyond the population studied, and distinguish an individual prediction from a population estimate.

Judge a study by asking who was sampled, how exposure and outcome were measured, whether comparison groups are appropriate, and whether the time sequence can support the claim. A large sample cannot rescue a biased design.

Check representativeness and sample size; define variables consistently; control or stratify confounders; use blinding or randomisation where possible; and report drop-outs and measurement uncertainty.

A questionnaire finding that diet and CVD are associated may suffer recall bias and self-selection. A prospective cohort with repeated measurements gives stronger temporal evidence but still cannot control every confounder.

Validity concerns whether the design supports the intended inference; reliability concerns consistency. Ethical limits may make a randomised exposure impossible, so conclusions should match the design.

People often judge risk using vividness, familiarity and perceived control rather than the measured probability alone. Rare dramatic events can feel more likely than common gradual hazards.

Actual risk is estimated from population data and an agreed time frame; perceived risk is an individual judgement that can be shifted by media coverage, personal experience and trust in the source.

A person may fear a rare treatment side effect after seeing a news story but underestimate the cumulative CVD risk of smoking because it is familiar. The decision changes when absolute risk and comparison groups are made explicit.

Good communication does not simply replace perception with a number: it explains denominator, time horizon, uncertainty and the action that can change risk.

When analysing a graph or table, identify units, groups, sample size and uncertainty. Describe how CVD incidence changes with total cholesterol, LDL or HDL, then distinguish relative from absolute risk and association from causation.

A causal case is stronger when several lines agree: risk rises with sustained LDL exposure, inherited conditions that raise LDL produce early CVD, and interventions that lower LDL also lower later cardiovascular events. A plausible mechanism links LDL entry and modification in artery walls to inflammation and atheroma.

Reducing coronary heart disease (CHD) risk combines biological knowledge with an evidence-based decision: improve diet and activity, avoid smoking, manage blood pressure and interpret body-composition measures in context.

Body mass index and waist-to-hip ratio are screening indicators, not complete diagnoses. They can help identify groups for further assessment, but muscle mass, age, sex and ethnicity affect their meaning.

A high BMI may reflect muscle rather than excess adipose tissue; a central fat pattern may still signal metabolic risk. A sensible conclusion uses the measurement with blood pressure, lipids, family history and activity data.

When comparing an intervention, check whether risk-factor changes are measured over a relevant time and whether the study controls confounding. Translate the evidence into a proportionate recommendation rather than a guarantee.

A person at high thrombotic risk may gain a large absolute benefit from clot prevention, while the same drug may be unsuitable when bleeding risk is high. Treatment combinations require monitoring because benefits and harms can add.