Unit 1: Molecules, Diet, 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.

A gas-exchange surface is effective when it has a large area, a short diffusion distance and a steep concentration gradient. Fick’s law summarises this as rate ∝ surface area × concentration difference ÷ barrier thickness.

Alveoli provide a huge folded surface, a thin moist epithelium and a dense capillary network. Ventilation refreshes alveolar air and blood flow removes oxygen, maintaining the gradient.

If surface area doubles while thickness and gradient stay constant, the predicted diffusion rate doubles. If mucus thickens the barrier, diffusion slows even if oxygen concentration outside remains unchanged.

Small organisms can rely on their body surface because their surface-area-to-volume ratio is high. Larger organisms need specialised surfaces and transport systems to keep internal cells within diffusion distance.

The bilayer is fluid because phospholipids and some proteins move laterally. It is selectively permeable: small non-polar molecules cross the lipid core more readily, while ions and many polar molecules need specific channel or carrier proteins.

Models are interpretations of evidence. Electron micrographs established a very thin layered boundary; freeze-fracture images revealed particles within the bilayer, supporting embedded proteins rather than continuous protein coats. Labelling and mobility experiments showed that proteins are distributed unevenly and some can move laterally.

New data replaced simpler sandwich models with the fluid-mosaic explanation. The model can still be refined when evidence shows proteins anchored to cytoskeleton or organised into local domains.

1. Cut equal beetroot cylinders or discs and rinse until surface pigment is removed.
2. Place equal tissue amounts in equal solution volumes for the same time.
3. For temperature, use thermostatically controlled water baths; for alcohol, prepare a concentration series while holding temperature constant.
4. Remove the tissue and measure solution absorbance with a colorimeter.
5. Use a blank, repeat each condition and calculate a mean.

Higher temperature increases phospholipid movement and can denature membrane proteins; extreme heating disrupts membrane organisation. Alcohol interacts with membrane lipids and proteins, so increasing alcohol concentration can also release more pigment.

Control disc dimensions, beetroot source, rinsing, solution volume, exposure time, pH and colorimeter wavelength. Treat temperature and alcohol as separate independent-variable investigations.

Osmosis is the net movement of water across a partially permeable membrane from higher water potential to lower water potential. Water potential combines pressure effects and solute effects, so it is not simply “water concentration”.

A concentrated solution has a more negative solute potential. Water leaves a cell placed in a lower-water-potential solution, reducing turgor; water enters when the external solution has higher water potential.

If potato cylinders lose mass in a sucrose solution, the solution had a lower water potential than the potato cells. The concentration at which there is no net mass change estimates the tissue’s initial water potential.

Use equal cylinders, blot them consistently, control time and temperature, repeat at several concentrations and plot percentage mass change rather than relying on one sample.

Channels form hydrophilic pores and may be gated. Carriers bind a particular solute and change conformation; the same broad protein type can mediate facilitated diffusion or active transport depending on direction and energy coupling.

Primary structure is the amino-acid sequence. Hydrogen bonding creates secondary structure. Further folding produces tertiary structure through hydrogen bonds, ionic attractions, disulfide bonds and hydrophobic interactions; several polypeptides may form quaternary structure.

The R-group sequence fixes which interactions can form, so a primary-structure change can alter folding, shape and function. Globular proteins expose suitable hydrophilic groups to water; fibrous proteins form long structural assemblies.

In an induced-fit model, substrate binding changes the active site's shape slightly, positioning reacting groups and straining bonds. Products no longer fit and leave, so the enzyme can catalyse another reaction.

Intracellular enzymes catalyse reactions inside cells, such as steps of respiration. Extracellular enzymes are secreted and act outside cells, such as digestive enzymes hydrolysing large food molecules before absorption.

Temperature or pH outside the working range can disrupt bonds that maintain the active site. Substrate may then collide with the enzyme but fail to form a productive complex.

To investigate temperature, pH, enzyme concentration or substrate concentration, measure the initial rate of an enzyme reaction while changing one independent variable and controlling the others.

Use equal volumes, a defined mixing time and a signal that changes predictably, such as colour, gas volume or product concentration. Take several early readings, calculate a gradient and repeat at each condition.

Initial rate avoids later distortion when substrate is depleted or product accumulates. A water bath, buffer and matched enzyme volumes make the comparison fair.

A rate–temperature curve rises while collisions become more frequent, reaches an optimum and falls when the protein begins to lose structure. A plateau with increasing substrate may indicate that active sites are saturated.

A nucleotide contains a pentose sugar, phosphate group and nitrogenous base. DNA nucleotides contain deoxyribose and A, T, C or G; RNA nucleotides contain ribose and A, U, C or G.

Nucleotides join by phosphodiester bonds between the phosphate and sugars, forming a sugar–phosphate backbone. Complementary bases pair through hydrogen bonds: A with T in DNA or U in RNA, and C with G.

The base sequence stores information while the backbone gives the polymer continuity. The 2′ hydroxyl in ribose makes RNA chemically less stable than DNA and suits its shorter-lived information-carrying roles.

A DNA template with the base A pairs with a T in the complementary strand; an RNA transcript uses U instead. Replacing T with U is a molecule-level difference, not a change in the genetic message by itself.

Before cell division, DNA strands separate and each acts as a template. Free nucleotides pair by complementarity, DNA polymerase joins them into new strands, and each daughter DNA molecule contains one original and one new strand.

Helicase separates the strands; complementary nucleotides align; DNA polymerase forms phosphodiester bonds in the new strand. The two molecules then carry the same base sequence, apart from copying errors.

Meselson and Stahl grew bacteria with heavy nitrogen, moved them to light nitrogen and separated DNA by density. An intermediate-density band after one generation supported semi-conservative replication; later generations produced light and intermediate DNA.

The density pattern distinguishes semi-conservative replication from conservative and dispersive alternatives because it tracks old and newly synthesised DNA together.

The genetic code is a triplet code: each three-base codon specifies one amino acid or a start/stop signal. Codons are read sequentially and non-overlapping on mRNA.

There are more codons than amino acids, so the code is degenerate: several codons can specify the same amino acid. This can make some substitutions silent but does not make every mutation harmless.

Changing a base in a codon may leave the amino acid unchanged, replace it with another, or create a stop codon. The outcome depends on the codon and on where it occurs in the coding sequence.

Translate from the correct start codon in the correct reading frame, then stop at a stop codon. A one-base insertion can shift every downstream triplet.

The order of DNA bases determines the complementary mRNA codons made during transcription. Ribosomes read those codons during translation, and tRNAs bring amino acids in the corresponding order. Peptide bonds then join the amino acids into a polypeptide.

Changing one DNA base can alter an mRNA codon and therefore one amino acid. If that change affects folding or an active site, the protein's function may change; degeneracy means some base substitutions do not change the amino acid.

Protein synthesis has two linked stages: transcription copies a gene into mRNA, then translation reads the mRNA to assemble a polypeptide. The DNA template (antisense) strand is used for transcription; codons are read on mRNA and anticodons pair on tRNA.

During transcription, RNA polymerase opens the DNA locally and joins complementary RNA nucleotides. The mRNA leaves the nucleus and binds to a ribosome. In translation, tRNA brings amino acids whose anticodons match successive mRNA codons; peptide bonds join the chain from the start codon until a stop codon.

A template triplet TAC produces an mRNA codon AUG. The ribosome recognises AUG as the start signal and the matching tRNA brings methionine; later codons determine the rest of the sequence.

Many mutations have no observable effect because they occur outside a relevant coding sequence, produce the same amino acid, or do not alter protein function. Others cause genetic disorders when a required protein changes. Mutations affecting cell-cycle control genes can contribute to cancer.

A dominant allele determines the heterozygous phenotype; a recessive phenotype appears when no dominant allele is present. In codominance, both different alleles contribute distinctly to the heterozygous phenotype.

For monohybrid inheritance, assign allele symbols, write parental genotypes, derive gametes and combine them in a genetic cross. In a pedigree, use affected offspring, parental phenotypes and sex distribution to test possible genotypes; probabilities are not guarantees for a small family.

Red-green colour blindness is commonly caused by a recessive allele on the X chromosome. A male expresses the allele on his single X chromosome; a heterozygous female is usually a carrier. Fathers pass their X to daughters and their Y to sons, so there is no father-to-son transmission of an X-linked allele.

Cystic fibrosis is caused by recessive CFTR alleles that produce faulty chloride ion channels. Reduced chloride transport changes water movement by osmosis, making mucus unusually thick in several body systems.

In the airways, sticky mucus is harder for cilia to clear, so infection risk rises and blocked airways reduce gas exchange. In the digestive system, mucus can block pancreatic ducts and hinder enzyme delivery and nutrient absorption. In the reproductive system, thick mucus can obstruct sperm movement or passage.

Two unaffected carrier parents can each pass the recessive allele: the child-risk calculation is 1/4 affected, 1/2 carrier and 1/4 non-carrier. The inheritance probability and the physiological symptoms are linked but are not the same claim.

Genetic screening tests DNA to identify a carrier, assess an embryo before implantation, or test a foetus during pregnancy. It informs a decision; it does not by itself predict every aspect of a person's future health.

Carrier testing checks an asymptomatic person's allele status. Pre-implantation genetic diagnosis analyses embryo cells during IVF before implantation. Prenatal testing uses chorionic villus sampling or amniocentesis to obtain foetal DNA during pregnancy.

Chorionic villus sampling is earlier than amniocentesis, while both can provide information about a familial disorder. A result may help parents prepare or consider options, but sampling carries procedure risks and tests can give false results.

The social and ethical question is not simply whether screening is possible, but how its information should be used. Judgements can concern autonomy, disability, privacy, fairness, pregnancy decisions and the interests of a future child.

Different viewpoints may weigh the same result differently: a family may value preparation or avoiding a severe disorder, while another may stress the risk of pressure, discrimination, unequal access or a narrow idea of which lives are worthwhile.

A carrier result can help a couple plan, yet sharing genetic data with insurers or employers could create harm. Prenatal or embryo results may support informed choice, but false positives, false negatives and procedure risks limit certainty.